·      https://youtu.be/dp6d3yH7AJs

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I review the NICE guideline on Type 2 diabetes in adults: management, always focusing on what is relevant in Primary Care only.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The NICE clinical guideline on Type 2 diabetes in adults: management [NG28] can be found here:

·      https://www.nice.org.uk/guidance/ng28

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I’m Fernando, a GP in the UK. Today we are looking at the new updated NICE guideline on type 2 diabetes in adults, always focusing on what is relevant in Primary Care only.

The diabetes guideline is a comprehensive document, so I am breaking it down into clear and practical sections.

Today, we are focusing on how to introduce medicines, how to review them, and what to do when further treatment is needed after the initial regimen.

In recent episodes, we covered the earlier sections of the guideline. In future episodes, we will move on to insulin-based treatment in more detail and the management of complications.

Right, let’s jump into it.

First, let’s look at introducing medicines.

We should introduce medicines one at a time and check tolerability and effectiveness before moving on.

When starting initial therapy with modified release metformin and other medicines, we should begin with metformin and confirm it is tolerated.

If we are using an SGLT 2 inhibitor, we should start it once metformin is at the maximum tolerated dose.

If we are also planning to use a GLP 1 receptor agonist or tirzepatide, we should introduce this once the SGLT 2 inhibitor is at the maximum tolerated dose.

So even though the initial plan may involve more than one medicine, we still introduce them sequentially one at a time and monitor carefully.

Now, let’s look at preventing diabetic ketoacidosis with SGLT 2 inhibitors.

Before starting an SGLT 2 inhibitor, we should assess the risk of DKA.

Risk factors include a previous episode of DKA, acute illness, dehydration, or following a very low carbohydrate or ketogenic diet.

We should address modifiable risks before starting treatment. For example, if someone is on a ketogenic diet, we may need to delay the SGLT 2 inhibitor until their diet changes.

We should also advise people that a very low carbohydrate diet increases the risk of DKA while on an SGLT 2 inhibitor. They should speak to a healthcare professional before starting such a diet, and treatment may need to be temporarily suspended.

Next, let’s look at general principles when reviewing treatment.

Before switching or adding medicines, we should optimise the current regimen. That means checking doses, adherence, side effects, and revisiting lifestyle advice.

Now, let’s look at reviewing metformin.

If someone is already taking standard release metformin, we can continue it.

If it is not tolerated, or if the person prefers, we should switch to modified release metformin.

Now, let’s look at reviewing other medicines.

If a person has reached their target, we should consider continuing the medicines that contributed to that success.

We should consider continuing SGLT 2 inhibitors for their cardiovascular or renal benefits, even if HbA1c targets are not fully achieved.

We should stop GLP 1 receptor agonists or tirzepatide if the person becomes underweight, with a BMI below 18.5.

We should also stop them if they are not helping the person reach glycaemic targets and they are not being used for cardiovascular benefit.

We must take into account adverse effects from combinations, such as hypoglycaemia and we should not combine a GLP 1 receptor agonist or tirzepatide with a DPP 4 inhibitor.

Now let’s move on to further medication, group by group.

For people with no relevant comorbidity who need further treatment, we should add a DPP 4 inhibitor.

If this is contraindicated, not tolerated, or not effective, we should add a sulfonylurea, pioglitazone, or insulin-based treatment.

For people with heart failure who need further treatment, we should also add a DPP 4 inhibitor.

If that is not suitable or not effective, we should add a sulfonylurea or insulin-based treatment.

For people with atherosclerotic cardiovascular disease who develop this after initial treatment, we should add subcutaneous semaglutide, up to 1 mg once weekly, for cardiovascular and renal benefit.

If further glycaemic control is needed, we should add a sulfonylurea, pioglitazone, or insulin-based treatment.

For people with early onset type 2 diabetes who need further treatment, we should consider adding a GLP 1 receptor agonist or tirzepatide.

If these are not suitable, we should add a DPP 4 inhibitor.

If that is also not suitable or not effective, we should add a sulfonylurea, pioglitazone, or insulin-based treatment.

If they are already taking a GLP 1 receptor agonist or tirzepatide and still need further control, we should add a sulfonylurea, pioglitazone, or insulin.

For people living with obesity, if weight management is a key issue, we should follow the obesity guidance.

If after at least 3 months of initial therapy further glycaemic control is needed, and they are not already on a GLP 1 receptor agonist or tirzepatide, we should consider adding one.

If these are contraindicated, not tolerated, or ineffective, we should add a DPP 4 inhibitor.

If that is not suitable, we should add a sulfonylurea, pioglitazone, or insulin.

If they are already on a GLP 1 receptor agonist or tirzepatide and still need further control, we should add a sulfonylurea, pioglitazone, or insulin.

For people with chronic kidney disease who need further treatment, we should consider adding a DPP 4 inhibitor.

If they are already on one, or it is not suitable, we should consider adding pioglitazone, or a sulfonylurea if eGFR is above 30, or insulin.

Finally, for people with frailty who need further treatment to control symptoms and reach targets, we should consider adding a DPP 4 inhibitor.

If they are already on one or it is not suitable, we should consider adding pioglitazone, a sulfonylurea, or insulin.

When choosing in frailty, we must remember that sulfonylureas and insulin increase the risk of hypoglycaemia and falls.

So that is it, a review of a section of the NICE guideline on type 2 diabetes.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/-kla7F8yibM

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through new and updated recommendations published in March 2026 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The Full NICE News bulletin for February 2026 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2026-03-01&to=2026-03-31&ndt=Guidance&ndt=Quality+standard

The new guideline on Kidney cancer: diagnosis and management [NG256] can be found here:

·      https://www.nice.org.uk/guidance/ng256

The guideline on suspected cancer: recognition and referral can be found here:

·      https://www.nice.org.uk/guidance/ng12/

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we’ll look at the NICE updates published in March 2026, focusing on what is relevant in Primary Care only.

This month, none of the updated guidelines were relevant to primary care. Only one new guideline had some relevance: kidney cancer: diagnosis and management.

We will cover this briefly, focusing mainly on diagnosis and referring to the relevant section of the NICE guideline on suspected cancer, recognition and referral.

Right, let’s jump into it.

Before we go into kidney cancer itself, let’s briefly set the scene by looking at the NICE suspected cancer guideline. It is designed to help us recognise when symptoms may represent cancer and when to refer patients urgently.

In urological cancers, we need to be aware that many cancers, including kidney and bladder cancer, may present with relatively non-specific symptoms.

However, one symptom stands out as particularly important: that is, haematuria.

Visible haematuria is the single most important red flag symptom for urological cancers.

NICE recommends that we should make an urgent suspected cancer referral for bladder or renal cancer in adults aged 45 and over with unexplained visible haematuria, either without a urinary tract infection, or if it persists or recurs after treatment of a urinary tract infection.

So, this is an important point. Visible haematuria, especially when unexplained, should always be taken seriously.

At the same time, we should remember that haematuria can also be associated with prostate cancer. NICE advises that we should consider a PSA test and a digital rectal examination in patients with visible haematuria as well as those with lower urinary tract symptoms or erectile dysfunction.

However, prostate cancer assessment follows a separate pathway, so today we will just focus on renal cancer.

Now, what about non-visible haematuria?

This is less specific, but still important in certain groups.

NICE recommends that we should consider an urgent suspected cancer referral in people aged 60 and over with unexplained non visible haematuria if this is associated with symptoms such as dysuria, or abnormal blood results such as a raised white cell count.

So the threshold is higher, but it is still clinically relevant.

However we should note that this relates to suspected bladder cancer rather than kidney cancer, as the urgent criteria for renal cancer are based on visible haematuria.

And while we are here, NICE also advises that we should consider a non urgent referral for bladder cancer, I repeat, a non urgent referral for bladder cancer in people aged 60 and over with recurrent or persistent unexplained urinary tract infection.

Additionally, the suspected cancer guideline also emphasises safety netting.

If a patient does not meet the referral criteria but symptoms persist or evolve, we should reassess and reconsider referral, always using our clinical judgement alongside the guideline.

Now, with that context in mind, let’s move on to the new kidney cancer guideline itself.

Diagnosing kidney cancer in Primary Care can be challenging. In fact, patients with kidney cancer may present late or with non-specific symptoms which may overlap with other conditions.

So in practice, the diagnosis pathway for kidney cancer in Primary Care relies heavily on the features that trigger referral under the guideline on suspected cancer.

This means that visible haematuria remains central.

In addition, we also need to be aware that kidney cancer may present with more general symptoms, like flank or abdominal pain, weight loss, or fatigue.

However, these are non-specific, and on their own may not meet referral thresholds.

So again, clinical judgement and safety netting are really important.

Another important point is the role of incidental findings.

Some kidney cancers are detected incidentally on imaging performed for other reasons, although, in these cases, the pathway is usually driven by secondary care.

In Primary Care, our role is mainly in recognising the features and making the referral and after that, most of the diagnostic pathway takes place in secondary care. There, once kidney cancer is suspected, the main test used is a CT scan of the abdomen and pelvis, or, if necessary, an MRI scan. On occasions, a contrast-enhanced ultrasound scan can be considered.

So to summarise this section.

Kidney cancer diagnosis in Primary Care is largely based on recognising features that trigger referral under the suspected cancer guideline.

Visible haematuria remains the most important red flag symptom.

Non-visible haematuria can also be relevant for bladder cancer in higher risk groups.

And because symptoms can be vague, safety netting and clinical judgement are essential.

So that is it, a review of the NICE updates relevant to primary care.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/7LiKkriN9tc

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I review the NICE guideline on Type 2 diabetes in adults: management, always focusing on what is relevant in Primary Care only.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The NICE clinical guideline on Type 2 diabetes in adults: management [NG28] can be found here:

·      https://www.nice.org.uk/guidance/ng28

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I’m Fernando, a GP in the UK. Today we are looking at the new updated NICE guideline on type 2 diabetes in adults, always focusing on what is relevant in Primary Care only.

The diabetes guideline is a comprehensive document, so I am breaking it down into clear and practical sections.

Today, we are focusing on medicines management, including sick day rules and choosing initial medicines.

In recent episodes, we covered the initial sections of the guideline and in future episodes, we will move on to further drug treatment and the management of complications.

Right, let’s jump into it.

When discussing medicines, we should go through the benefits and risks of each option. This includes:

·      The effect on HbA1c and weight.

·      The effect on cardiovascular and renal outcomes.

·      Whether there are contraindications, such as pioglitazone in heart failure or metformin when eGFR is below 30.

·      Practical issues that might affect adherence.

·      And cost. If two medicines from the same class are equally suitable, we should use the least expensive option.

If a person has more than one comorbidity, for example atherosclerotic cardiovascular disease and obesity, we should make a shared decision about which condition to prioritise.

When discussing GLP 1 receptor agonists or tirzepatide we should explain the guidance on use in pregnancy and breastfeeding. We should explain that weight loss may improve fertility and that effective contraception must be used while taking these medicines. And if pregnancy is planned, contraception should continue for a period after stopping treatment.

Now let’s move on to sick day rules.

We should include clear sick day guidance in each person’s individual treatment plan.

Depending on the medicines they are taking, this should cover:

·      Whether medicines need to be adjusted during illness or surgery.

·      Whether medicines such as metformin or SGLT 2 inhibitors should be temporarily stopped if there is a risk of dehydration, vomiting, or diarrhoea.

·      How to adjust insulin doses.

·      And how to restart treatment after recovery.

Before initiating treatment, we should assess cardiovascular and renal status, and the person’s future cardiovascular risk.

If frailty is a concern, we should assess this before starting medicines. Frailty can change the balance between benefits and harms.

Let’s now move on to initial medicines.

This section sets out what we should start at diagnosis, before insulin is needed. The recommendations are grouped by clinical profile.

Let’s go through them one by one.

First, people with no relevant comorbidities.

For them, we should offer dual therapy with modified release metformin and an SGLT 2 inhibitor from the outset.

If metformin is contraindicated or not tolerated, we should offer an SGLT 2 inhibitor alone.

So the default starting point is dual therapy, not metformin alone.

Next, people with heart failure.

For adults with type 2 diabetes and heart failure, regardless of ejection fraction unless otherwise specified, we should again offer modified release metformin and an SGLT 2 inhibitor.

If metformin cannot be used, we should offer an SGLT 2 inhibitor alone.

Now let’s look at people with atherosclerotic cardiovascular disease.

Here, we should offer modified release metformin, an SGLT 2 inhibitor, and subcutaneous semaglutide, up to 1 mg once weekly, for its cardiovascular, renal, and glycaemic benefits.

If metformin is contraindicated or not tolerated, we should offer an SGLT 2 inhibitor plus subcutaneous semaglutide.

So in this group, initial therapy is triple therapy, reflecting the very high cardiovascular risk.

Next, people with early onset type 2 diabetes.

Early onset means diagnosis under the age of 40.

For these adults, we should offer modified release metformin and an SGLT 2 inhibitor, and we should consider adding either a GLP 1 receptor agonist for its cardiovascular, renal, and glycaemic benefits, or tirzepatide for its glycaemic benefits.

If metformin is not suitable, we should offer an SGLT 2 inhibitor and consider adding a GLP 1 receptor agonist or tirzepatide.

This reflects the higher lifetime risk in early onset disease and the need for more intensive early management.

Now, let’s look at people living with obesity.

For adults with type 2 diabetes who are living with obesity, we should offer modified release metformin and an SGLT 2 inhibitor.

If metformin is contraindicated or not tolerated, we should offer an SGLT 2 inhibitor alone.

Obesity itself does not automatically change the initial dual therapy recommendation, but it will influence later choices.

Next, people with chronic kidney disease.

We need to tailor treatment according to eGFR.

If eGFR is above 30, we should offer modified release metformin and an SGLT 2 inhibitor.

If metformin is not suitable, we should offer an SGLT 2 inhibitor alone.

If eGFR is between 20 and 30, we should offer either dapagliflozin or empagliflozin, together with a DPP 4 inhibitor.

If eGFR is below 20, we should consider a DPP 4 inhibitor.

If a DPP 4 inhibitor is contraindicated, not tolerated, or not effective, we should consider pioglitazone or an insulin-based treatment.

So in advanced kidney disease, the pathway shifts away from metformin and SGLT 2 inhibitors, depending on renal function.

Finally, people with frailty.

For adults with type 2 diabetes and frailty, we should offer modified release metformin.

We should only offer an SGLT 2 inhibitor if the person’s level of frailty does not place them at risk of adverse effects, such as volume depletion or hypotension.

If metformin is contraindicated or not tolerated, we should assess frailty carefully.

If frailty does not increase the risk of adverse events, we should consider an SGLT 2 inhibitor alone.

If frailty does increase risk, we should consider a DPP 4 inhibitor instead.

So that is it, a review of a section of the NICE guideline on type 2 diabetes.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/LsB8J96adC0

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I review the NICE guideline on Type 2 diabetes in adults: management, always focusing on what is relevant in Primary Care only.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

 There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The NICE clinical guideline on Type 2 diabetes in adults: management [NG28] can be found here:

·      https://www.nice.org.uk/guidance/ng28

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I’m Fernando, a GP in the UK. Today we are looking at the new updated NICE guideline on type 2 diabetes in adults, always focusing on what is relevant in Primary Care only.

The diabetes guideline is a comprehensive document, so I am breaking it down into clear and practical sections.

Today, we are focusing on blood glucose management, including HbA1c targets and glucose monitoring.

In the last episode, we covered patient education, dietary advice, and bariatric surgery. In future episodes, we will move on to further drug treatment and the management of complications.

Right, let’s jump into it.

Let’s start with HbA1c measurement and targets.

We should measure HbA1c every 3 to 6 months, tailored to the person, until levels are stable on unchanging therapy. Once HbA1c and treatment are stable, we should measure it every 6 months.

If HbA1c is unreliable, for example because of abnormal haemoglobin or altered red cell turnover, we should use alternative methods. These include quality-controlled plasma glucose profiles, total glycated haemoglobin if abnormal haemoglobins are present, or fructosamine.

If there is a mismatch between HbA1c and other glucose readings, we should investigate and seek specialist advice if needed.

Now let’s talk about targets.

We should agree an individual HbA1c target with each person. This should be a shared decision. We should encourage people to reach and maintain their target, unless doing so causes adverse effects, including hypoglycaemia, or reduces their quality of life.

For people managed with lifestyle alone, or with medicines that do not cause hypoglycaemia, we should support them to aim for an HbA1c of 48 mmol per mol, or 6.5 percent.

For people taking medicines associated with hypoglycaemia, we should support them to aim for 53 mmol per mol, or 7 percent.

If HbA1c rises to 58 mmol per mol, or 7.5 percent or higher, we should reinforce advice about diet, lifestyle and adherence, and intensify treatment, aiming again for 53 mmol per mol or 7 per cent.

We should consider relaxing HbA1c targets on a case-by-case basis. This is particularly important for older or frail adults, people with reduced life expectancy, those at high risk of hypoglycaemia, or those with significant comorbidities.

If someone achieves an HbA1c lower than their agreed target and is not having hypoglycaemia, we should encourage them to maintain it. However, we should remember that a low HbA1c may sometimes be a sign of other issues, such as weight loss or deteriorating kidney function.

Now let’s move to self-monitoring of capillary blood glucose.

We should not routinely offer self-monitoring to everyone with type 2 diabetes.

We should offer it if the person is on insulin, has hypoglycaemic episodes, is taking medicines that increase the risk of hypoglycaemia while driving or operating machinery, or is pregnant or planning pregnancy.

Additionally, we should consider short term self-monitoring when starting corticosteroids, or to confirm suspected hypoglycaemia.

During acute illness, we should review treatment because blood glucose levels can worsen.

If someone is self-monitoring, we should carry out a structured review at least once a year. This should include checking their technique, how often they test, whether they understand the results, the impact on their quality of life, whether it is still beneficial, and the equipment they are using.

Now let’s look at continuous glucose monitoring.

NICE says that we should offer intermittently scanned continuous glucose monitoring, often called flash monitoring, to adults on multiple daily insulin injections if they have recurrent or severe hypoglycaemia, impaired hypoglycaemia awareness, a disability that prevents finger prick testing, or if they would otherwise need to test at least eight times a day.

We should also offer flash monitoring to adults on insulin who would otherwise need help from a care worker or healthcare professional to monitor their glucose.

We should consider real time continuous glucose monitoring instead of flash if it is available at the same or lower cost.

Continuous glucose monitoring should be provided by a team with expertise, and it must be part of a wider self-management plan.

People using continuous glucose monitoring still need to check capillary blood glucose at times. This is to confirm accuracy and as a back up if the device fails or glucose levels are changing quickly. They should be given enough test strips to do this safely.

If someone cannot or does not want to use continuous monitoring, we should offer capillary blood glucose monitoring instead.

We should review the use of continuous monitoring regularly as part of the diabetes care plan. If there are concerns about how it is being used, we should explore any problems and offer further education or support.

Finally, a word on hyperglycaemia.

If an adult with type 2 diabetes develops symptoms of hyperglycaemia, we should consider insulin or a sulfonylurea, and then review treatment once blood glucose returns to target.

So that is it, a review of the first section of the NICE guideline on type 2 diabetes.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/y-hTBUYkInk

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I review the NICE guideline on Type 2 diabetes in adults: management, always focusing on what is relevant in Primary Care only.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The NICE clinical guideline on Type 2 diabetes in adults: management [NG28] can be found here:

·      https://www.nice.org.uk/guidance/ng28

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I’m Fernando, a GP in the UK. Today we are looking at the new updated NICE guideline on type 2 diabetes in adults, always focusing on what is relevant in Primary Care only.

The link to the NICE guideline is the episode description.

Right, let’s jump into it.

The diabetes guideline is a comprehensive document, so I am going to break it down into manageable sections.

Today, we will focus on the first part of the NICE guideline, covering tailoring care, structured education, dietary advice, and bariatric surgery.

In future episodes, we will move on to drug treatment and the management of complications.

First, let’s start with tailoring care to the person.

NICE recommends an individualised approach for adults with type 2 diabetes. Care should be tailored to the person’s needs and circumstances. This includes their personal preferences, their other medical conditions, the risks from polypharmacy, and their likelihood of benefiting from long term treatments.

This is especially important for people with multimorbidity. At each review, we should reassess the person’s situation and think about whether any medicines are no longer effective and could be stopped.

When planning care, we should take into account any disabilities, including visual impairment.

For discussions about overweight and obesity, NICE directs us to the guideline on overweight and obesity management, including how to classify overweight and obesity and how to address the drivers behind it. There is also a specific section in the guideline on eating disorders for those who have both type 2 diabetes and an eating disorder, covering advice on collaborative care, blood glucose management, and insulin use.

Next is structured education.

NICE says we should offer structured education to all adults with type 2 diabetes at diagnosis. Family members or carers should also be involved where appropriate. Education should be reinforced and reviewed every year and it should be explained clearly that structured education is a core part of diabetes care.

Education programmes should be evidence based and suitable for the person. They should have clear aims and learning objectives, and support people to develop the knowledge and skills to self-manage their diabetes.

Programmes should follow a structured curriculum, be delivered by trained educators, and outcomes should be regularly monitored.

Group education is the preferred option, but there must be an alternative of equal standard for people who cannot attend or prefer not to take part in group sessions.

Education programmes should meet local cultural, language, cognitive and literacy needs. All members of the diabetes team should know what programmes are available locally, and these programmes should be integrated into the overall care pathway.

Now let’s move on to dietary advice.

Adults with type 2 diabetes should receive individualised and ongoing nutritional advice from a healthcare professional with expertise in nutrition.

Dietary advice should be sensitive to the person’s culture, beliefs, willingness to change, and the impact on quality of life.

In general, people with type 2 diabetes should follow the same healthy eating advice as the general population. This includes choosing high fibre, low glycaemic index carbohydrates such as fruit, vegetables, wholegrains and pulses, choosing low fat dairy products, eating oily fish, and limiting saturated and trans fats.

For low energy or very low energy diets aimed at remission, the guideline directs us to the specific guidance on the NHS Type 2 Diabetes Path to Remission Programme and the overweight and obesity management guideline.

Dietary advice should be integrated into a personalised diabetes management plan, including physical activity and weight management.

Carbohydrate intake, alcohol intake, and meal patterns should be individualised. Reducing the risk of hypoglycaemia is particularly important for people using insulin or insulin secretagogues.

People can substitute a limited amount of sucrose containing foods for other carbohydrates in their meal plan, but they should avoid excess calorie intake.

NICE advises against using foods marketed specifically for people with diabetes.

For people admitted to hospital or another care setting, there should be a meal planning system that provides consistency in carbohydrate content.

Finally, let’s talk about bariatric surgery.

For people with recent onset type 2 diabetes, we should follow the recommendations on surgical interventions in the overweight and obesity management guideline.

This guideline is separate to the diabetes guideline but we will cover it briefly here. It says that we should offer adults a referral for a comprehensive assessment by a specialist multidisciplinary overweight and obesity management service to see whether bariatric surgery is suitable if they have a BMI of 40 or more, or a BMI between 35 and 39.9 with a significant health condition that could improve with weight loss. These conditions include cardiovascular disease, hypertension, fatty liver disease, obstructive sleep apnoea, and type 2 diabetes. The person must also agree to long term follow up after surgery, including lifelong annual reviews.

For people of South Asian, Chinese, other Asian, Middle Eastern, Black African, or African Caribbean background, we should use a BMI threshold that is 2.5 lower than these values, because cardiometabolic risk occurs at lower BMI in these groups.

We should refer for expedited assessment for bariatric surgery to people with a BMI of 30 or more who have recent onset type 2 diabetes, defined as diagnosed within the past 10 years, provided they are also being assessed within a specialist overweight and obesity management service.

For people from South Asian, Chinese, other Asian, Middle Eastern, Black African, or African Caribbean backgrounds, we should use BMI thresholds that are 2.5 lower when deciding on expedited assessment.

So that is it, a review of the first section of the NICE guideline on type 2 diabetes.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/YX_YmP-yRfM

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through new and updated recommendations published in February 2026 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The Full NICE News bulletin for February 2026 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2026-02-01&to=2026-02-28&ndt=Guidance&ndt=Quality+standard

The updated guideline on Type 2 diabetes in adults: management [NG28] can be found here:

·      https://www.nice.org.uk/guidance/ng28

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we’ll look at the NICE updates published in February 2026, focusing on what is relevant in Primary Care only.

This month there is just one updated guideline relevant to us, but it’s a major one: type 2 diabetes.

A few months ago we reviewed the draft version of the guideline. Now that the final version has been published, over the next few weeks I’ll be creating separate episodes covering the different sections in more depth.

So today, I’ll just give you an overview, highlighting the differences between the draft recommendations and the final version.

Right, let’s jump into it.

Firstly, let’s have a look at the first line treatment in people with no relevant comorbidities.

In the draft guideline, NICE recommended starting metformin plus an SGLT2 inhibitor from the outset, with SGLT2 monotherapy if metformin was not tolerated.

The final guideline confirms this, but now specifies that patients should be started on modified release metformin rather than just metformin.

This change applies throughout the guideline. Wherever standard release metformin was previously recommended, it now says modified release metformin.

Is this the death of the standard release preparation? Possibly in the long term. Anyone starting treatment should be on the modified release version, so numbers on standard release metformin will gradually fall. However, NICE also states that patients already on standard release can continue, or switch if necessary.

Now let’s look at first line treatment in specific clinical groups, starting with heart failure.

In the draft guideline, the recommendation was metformin plus an SGLT2 inhibitor, and it suggested that semaglutide could be added for weight management in selected people with preserved ejection fraction and no frailty.

In the final guideline, it’s still modified release metformin plus an SGLT2 inhibitor, with SGLT2 monotherapy if metformin is not tolerated.

However, for people with heart failure who need further treatment, the guideline moves straight to adding a DPP4 inhibitor first, then a sulfonylurea or insulin if needed. There is no recommendation in this section to add a GLP1 receptor agonist specifically for heart failure.

Next, people with atherosclerotic cardiovascular disease.

The draft guideline recommended early triple therapy with metformin plus an SGLT2 inhibitor plus semaglutide, continuing for cardiorenal benefit even if glycaemic targets were not met.

In the final guideline, this is confirmed but made more specific. Here, we should offer modified release metformin plus an SGLT2 inhibitor plus subcutaneous semaglutide up to 1 milligram once a week for cardiovascular, renal and glycaemic benefits. If metformin is not tolerated, we will use an SGLT2 inhibitor plus semaglutide. It also explicitly recommends starting semaglutide if atherosclerotic cardiovascular disease develops at any stage after initial therapy.

Next is the obesity group.

In the draft guideline, semaglutide was recommended after three months, with additional filters such as preserved ejection fraction and no frailty.

In the final guideline, NICE broadens this. It recommends either a GLP1 receptor agonist or tirzepatide after at least three months of initial therapy if further treatment is needed.

Now let’s look at chronic kidney disease.

There are three eGFR bands here: above 30, 20 to 30, and below 20.

For eGFR above 30, we will use modified release metformin. SGLT2 inhibitors are still prioritised early for kidney and cardiovascular protection, and dapagliflozin and empagliflozin are specifically named because of licensing reasons.

The 20 to 30 eGFR band is where we see a change.

In the draft guideline, if eGFR was between 20 and 30, NICE advised offering dapagliflozin or empagliflozin alone.

In the final guideline, it now says that if eGFR is 20 to 30, we should offer dapagliflozin or empagliflozin plus a DPP4 inhibitor. So, this is now explicit dual therapy rather than SGLT2 monotherapy. The rationale explains why. If the eGFR is below 30, cardiorenal protection of SGLT2 inhibitors remains, but the glucose lowering effect is reduced, so a DPP4 inhibitor is recommended for HbA1c control.

For eGFR below 20, the draft guideline advised using a DPP4 inhibitor first, then considering pioglitazone or insulin, and it stated that sulfonylureas should not be used if eGFR was below 30.

In the final guideline it remains the same, a DPP4 inhibitor first and then pioglitazone or insulin. However, there is no blanket rule about sulfonylureas in the CKD section although we need to know that hypoglycaemia risk increases as renal function falls. .

The draft also recommended not using empagliflozin or dapagliflozin if eGFR was less than 20. The final guideline does not phrase it that way. It simply directs us to DPP4 inhibitors rather than a blanket ban of SGLT2 inhibitors when eGFR is below 20.

And now, the final group is frailty.

The draft guideline recommended metformin alone, effectively deprioritising SGLT2 inhibitors as frailty increases SGLT2 risks.

In the final version, modified release metformin remains first line, but there is no automatic ban of SGLT2 inhibitors at baseline. Instead, the escalation sequence is first a DPP4 inhibitor and then consider pioglitazone, a sulfonylurea or insulin, taking into account hypoglycaemia and falls risk.

Regarding GLP1 receptor agonists and tirzepatide, the draft implied they were generally inappropriate in frailty due to weight loss and gastrointestinal effects.

However, the final guideline is more neutral. It does not specifically recommend them for frailty, but it states there is no inherent safety risk. If another indication exists, they can still be used even in frailty.

Now, let’s look at some other sections of the guideline.

Looking at GLP1 receptor agonists, the draft recommended stopping them if glycaemic or weight goals were not achieved, unless the person had atherosclerotic cardiovascular disease or early onset diabetes.

In the final guideline, NICE recommends stopping GLP1 receptor agonists or tirzepatide if BMI falls below 18.5 or if they do not help with the glycaemic targets as long as they are not being taken for cardiovascular benefit. So, the emphasis shifts from weight thresholds towards glycaemic targets and cardiovascular benefit.

Regarding combining GLP1 receptor agonists and DPP4 inhibitors, both the draft and the final guideline advise against it. The final guideline also extends this to tirzepatide.

In the insulin section, the draft stated that GLP1 receptor agonists could be combined with insulin in Primary Care without specialist approval.

The final guideline does not explicitly restate the specialist approval point. It simply states that when initiating insulin, we should continue metformin, stop other medicines used solely for glycaemic control, and discuss continuing medicines used for cardiovascular protection or weight management.

So that is it, a review of the NICE updates relevant to primary care.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/tdY5bOFmzbg

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

This video refers to the clinical guideline by the National Osteoporosis Guideline Group. (details below). Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by them.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I review the treatment of osteoporosis, always focusing on what is relevant in Primary Care only. The information is based on the clinical guideline by the National Osteoporosis Guideline Group. The link to it is below.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The NICE clinical guideline on osteoporosis can be found here:

·      https://www.nice.org.uk/guidance/cg146

The Clinical guideline for the prevention and treatment of osteoporosis by the National Osteoporosis Guideline Group can be found here:

·      https://www.nogg.org.uk/sites/nogg/download/NOGG-Guideline-2024.pdf?v3

The NICE technology appraisal on Bisphosphonates for treating osteoporosis can be found here:

·      https://www.nice.org.uk/guidance/ta464

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I’m Fernando, a GP in the UK. Today we are going to review the treatment of osteoporosis, always focusing on what is relevant in Primary Care only.

I have based this episode on the clinical guideline by the National Osteoporosis Guideline Group. The link to it is the episode description.

Right, let’s jump into it.

We will start by saying that we need a strategy to decide who gets treated, which is what we call “intervention thresholds.”

We need to remember that the NICE guideline on assessing the risk of fragility fracture and Osteoporosis does not itself define fixed treatment thresholds. Instead, we are advised to follow local or national guidance when deciding when to treat. So, for the purpose of this video, I will explain the thresholds given by the National Osteoporosis Guideline Group.

Here the intervention threshold (for people under 70) is set at a fracture risk equivalent to a same-age woman who has already had a fracture. As people age, the threshold for treatment rises, so at the age 70 years and above, fixed thresholds are applied.

When FRAX is calculated we can get a result that shows low risk, intermediate risk, high risk and very high risk of a Major Osteoporotic Fracture.

If the fracture risk is low, we will offer lifestyle advice.

If a person’s calculated risk sits near that intervention threshold, then that is intermediate risk and we should consider a bone mineral density (BMD) measurement with DXA to refine the estimate. If after the bone mineral density result the risk is high, we move forward with treatment otherwise, we will reassess later.

If the fracture risk meets or exceeds the intervention threshold, that person is considered high risk and eligible for treatment.

If the risk is very high, for example if they have multiple risk factors — we may consider referral for more aggressive treatment.

Let’s now focus on the non-drug measures recommended for preventing and managing osteoporosis. They should be recommended for everyone, whether or not we eventually use drugs.

First — diet and nutrition, ensuring adequate calcium intake. Ideally this is achieved through food, but if needed, we can use supplements to reach recommended levels.

We should also make sure vitamin D is addressed. For people at risk of low vitamin D — for example, those with limited sun exposure, people who are housebound, or living in care homes — we should offer vitamin D supplementation.

Next —We should encourage regular weight-bearing and muscle-strengthening exercise, tailored to each person’s ability. This supports bone strength, maintains muscle mass, and helps prevent falls.

Speaking of falls — for those with osteoporosis or fragility fractures, or at risk of fracture, we must assess their fall risk. For patients identified as at risk of falling, we should offer an exercise programme to improve balance and muscle strength.

We must also address lifestyle factors. We should advise smoking cessation in smokers and recommend moderation of alcohol intake.

For all patients we should also screen for and manage other medical conditions that may contribute to bone fragility, such as endocrine problems, malabsorption, chronic illness or immobility.

Now let’s move on to the pharmacological treatment options for osteoporosis, based on the National Osteoporosis Guideline Group recommendations, and the NICE Technology Appraisal on Bisphosphonates for treating osteoporosis

There are several effective drug treatments available, but for most patients, bisphosphonates remain the first-line option. These include oral alendronic acid, risedronate and ibandronate, as well as intravenous zoledronic acid and ibandronate if recommended by a specialist.

How do bisphosphonates work?

Bisphosphonates slow down the rate of bone breakdown by inhibiting osteoclast activity. This helps stabilise bone density and reduces the risk of fractures.

What about risks and how do we minimise them?

Common side effects include gastrointestinal irritation with oral bisphosphonates, and muscle or joint aches. Much rarer risks include atypical femoral fractures and osteonecrosis of the jaw. To minimise these, we ensure correct administration: oral tablets should be taken with a full glass of water on an empty stomach, with the patient remaining upright for at least 30 minutes. We also maintain good dental hygiene, have a dental check-up and complete major dental work before starting treatment where possible, and reassess the need for long-term therapy at appropriate intervals.

Alongside bisphosphonates, denosumab is another established anti-resorptive option. If we use denosumab, we must plan from the start how we will eventually stop or switch treatment, because stopping it abruptly without follow-up therapy can lead to rebound bone loss and an increased risk of vertebral fractures.

For patients at the highest fracture risk, we should seek specialist input. These patients may benefit from anabolic, or bone-forming treatments such as romosozumab, or other anabolic or sequential regimens.

Now let’s look at how we manage osteoporosis treatment over time, that is, the long-term strategy.

First: when we start a drug treatment for osteoporosis — for example a bisphosphonate or denosumab — we need a clear plan for how long that treatment should continue, how we’ll monitor it, and when we’ll reassess risk.

For oral bisphosphonates, we generally treat for at least five years and for intravenous bisphosphonates, at least three years.

In patients at higher risk — for instance people over 70, or those who’ve had hip or vertebral fractures, or patients on high-dose steroids — longer treatment might be needed. Also, if they sustain a further fragility fracture while on treatment, we will also keep going.

In lower-risk patients, after five years of oral bisphosphonates (or three years of IV bisphosphonates), we may consider a treatment pause for 18 to 36 months, depending on individual risk.

Second: we must reassess fracture risk periodically. This means that we should repeat the fracture risk assessment if the patient has a new fracture, regardless of when the treatment started.

If we paused treatment, we should re-assess the fracture risk after 18 months to 3 years — depending on individual circumstances.

Third: some situations require special consideration.

• In people starting long-term glucocorticoids (for example ≥ 7.5 mg prednisolone daily for 3 months or more), we should begin bone-protective therapy immediately — we don’t wait for a DXA scan.
• For patients receiving hormone therapy that impacts bone — for instance androgen-deprivation therapy in men or aromatase inhibitors in women — we should manage fracture risk proactively, often also with bone-protection from the start.

And finally, fourth: after a fragility fracture or in people at high or very high fracture risk, treatment should start promptly, because the risk of re-fracture is often greatest soon after the first event.

So that is it, a review of the treatment of osteoporosis.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/GmCg9TskZNA

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

This video refers to a number of medical articles on ADHD published by a number of organisations (details below). Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by any of them.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I cover ADHD increasing incidence, especially in adults, always focusing on what is relevant in Primary Care only. The information is based on a number of published medical articles. The links to them are below.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The NICE clinical guideline on osteoporosis can be found here:

·      https://www.nice.org.uk/guidance/cg146

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I’m Fernando, a GP in the UK. Today we are looking at the NICE guideline on osteoporosis, specifically how we diagnose it and how we assess the risk of fragility fractures, always focusing on what is relevant in Primary Care only.

The links to the NICE guideline is the episode description.

Right, let’s jump into it.

Let’s start by saying that we should consider assessing fracture risk in all women aged 65 and over, and all men aged 75 and over.

Additionally, we should also consider assessing fracture risk in women under 65 and men under 75 if they have risk factors. Examples of these risk factors include:

• a previous fragility fracture,

• current or frequent recent use of oral or systemic glucocorticoids,

• a history of falls,

• a family history of hip fracture,

• a low BMI, below 18.5,

• smoking,

• drinking more than 14 units of alcohol per week

• and any cause of secondary osteoporosis

Causes of secondary osteoporosis can include endocrine conditions such as hypogonadism in either sex — including untreated premature menopause — and treatment with aromatase inhibitors or androgen-deprivation therapy. They also include hyperthyroidism, hyperparathyroidism, hyperprolactinaemia, Cushing’s disease, and diabetes.

Other causes include gastrointestinal conditions such as coeliac disease, inflammatory bowel disease, chronic liver disease, chronic pancreatitis, and other causes of malabsorption.

Then we have rheumatological conditions like rheumatoid arthritis and other inflammatory arthropathies as well as haematological diseases such as multiple myeloma, and haemoglobinopathies.

And finally we have respiratory conditions like cystic fibrosis and COPD and other conditions like CKD and immobility due to neurological disease or injury.

We should not routinely assess fracture risk in people under the age of 50 unless they have major risk factors — such as current or recent glucocorticoid use, untreated premature menopause, or a previous fragility fracture — because they are unlikely to be at high risk.

Now, how should we actually assess the risk of fracture?

We can use either FRAX — which we can use without a bone mineral density (BMD) value if a DXA scan hasn’t been done — or QFracture, to estimate the ten-year absolute risk. FRAX can be used for people aged 40 to 90, with or without a bone mineral density (BMD) value. QFracture can be used for people aged 30 to 84, but a bone mineral density (BMD) value cannot be added into that tool. If someone is older than the age range covered by these tools, we should assume they are at high risk.

Additionally. we should interpret fracture-risk estimates with caution in people over 80, because a ten-year prediction may underestimate their short-term risk.

We should not routinely measure bone mineral density with a DXA scan before doing a FRAX or QFracture assessment. These tools estimate a ten-year fracture risk using simple clinical information and help us decide whether a scan is actually needed.

Skipping this step can lead to unnecessary DXA scans in people who are clearly low risk. It can also lead to missed scans in those whose risk is borderline, and it is therefore an inefficient use of resources.

We only need to measure bone density when the FRAX or QFracture score is close to the intervention threshold, where a DXA result could change the treatment decision.

So, the NICE guideline recommends using FRAX or QFracture first, and then requesting a DXA scan only if it is likely to influence management. If we do a DXA scan, once we have the bone mineral density result, we should recalculate the absolute risk using FRAX with the bone mineral density value included.

The intervention threshold is the level of risk at which treatment is recommended. The NICE guideline does not define that threshold; instead, we, as clinicians, should follow local protocols or national guidance. I will cover this in a different episode on osteoporosis treatment.

We should also consider measuring BMD before starting treatments that can rapidly reduce bone density, such as sex-hormone deprivation therapy for breast or prostate cancer.

People under 40 should have BMD measured to assess fracture risk only if they have a major risk factor, such as multiple fragility fractures, a major osteoporotic fracture, or current or recent use of high-dose oral or systemic glucocorticoids — meaning more than 7.5 milligrams of prednisolone, or equivalent, per day for three months or longer.

We should consider recalculating fracture risk in the future if the original risk was close to the intervention threshold and only after at least two years, or if the person’s risk factors change. Again, for intervention thresholds we will need to follow local protocols or national guidelines.

We should also remember that risk-assessment tools can underestimate fracture risk in certain situations. This includes people with multiple fractures, previous vertebral fractures, high alcohol intake, high-dose glucocorticoid use, or other causes of secondary osteoporosis.

As mentioned earlier, causes of secondary osteoporosis include endocrine, gastrointestinal, rheumatological, haematological, respiratory, metabolic, renal, and neurological conditions, as well as prolonged immobility.

Finally, we should keep in mind that fracture risk can also be affected by factors not included in the risk tools — for example, living in a care home, or taking drugs that impair bone metabolism, such as anticonvulsants, SSRIs, thiazolidinediones, proton-pump inhibitors, and antiretroviral medications.

So that is it, a review of the NICE guideline on osteoporosis.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/V93jdGfnLIk

This video refers to guidelines produced by a number of organisations (details below). Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by any of them.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I cover what to do if eosinophilia is found, always focusing on what is relevant in Primary Care only. The information is based on Haematological guidance by Camden CCG, Manchester Foundation Trust and King’s Health Partners.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

My summary of the guidance consulted can be found here:

·      https://1drv.ms/b/s!AiVFJ_Uoigq0mQ4ZjYGRH1wkGBdc?e=Zuxx84

The resources consulted can be found here:

·      Camden CCG guidance: 1456246258-2f3891e610beaa6533f2c0ad7866e776.pdf(Review) - Adobe cloud storage

·      Manchester Adult anaemia guide: https://acrobat.adobe.com/id/urn:aaid:sc:EU:f96fe528-0a47-457c-b29a-a7efb87221e0

·      Manchester Haematology GP guide: https://mft.nhs.uk/app/uploads/2021/02/MFT-Haematology-GP-Pathway-Guide-v4-11.2.21.pdf

·      King’s Health Partners: https://www.kingshealthpartners.org/assets/000/002/294/KCH_-_king_s_health_partners_-_quick_guide_to_haematology_original.pdf

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I’m Fernando, a GP in the UK. Today we are going to cover what to do when we encounter eosinophilia on a full blood count, always focusing on what is relevant in Primary Care only.

I have based this episode on Haematological guidance by Camden CCG, Manchester Foundation Trust and King’s Health Partners. The links to them are in the episode description.

Right, let’s jump into it.

Eosinophilia refers to an increased number of eosinophils in the blood. Although thresholds may vary slightly between laboratories, eosinophilia is generally defined as an eosinophil count greater than 0.5 × 10⁹ per litre. Eosinophils are white blood cells involved in allergic responses, parasitic infections, and various inflammatory processes, so an elevated count can indicate a wide range of underlying conditions.

Let’s have a look at some of the possible causes of eosinophilia. They include:

• Asthma: particularly allergic asthma, which commonly has high eosinophil levels because of their role in airway inflammation and hypersensitivity reactions.

• Then we have Skin disease such as eczema, atopic dermatitis, urticaria, and psoriasis: because these conditions involve allergic or immune-mediated inflammation, which often stimulates eosinophils.

• Infections, especially those due to parasites, as well as fungal infections, tuberculosis and malaria. Parasitic infections are a very typical cause, but some fungal and bacterial infections can also trigger eosinophilia through chronic inflammation.

• Another possible cause is Drugs, including penicillin, allopurinol, amitriptyline, and carbamazepine, although virtually any medication can be a possible trigger.

Drug-induced eosinophilia often occurs as part of a hypersensitivity reaction.

• Then we have Connective tissue diseases such as rheumatoid arthritis given that autoimmune and vasculitic conditions can increase eosinophils due to chronic inflammation.

• We also have Solid malignancies, for example breast, renal, stomach, and lung cancer. This is because certain cancers release cytokines that stimulate eosinophil production. In some cases eosinophilia may be a paraneoplastic manifestation.

• Then, Myeloproliferative disorders including leukaemia and lymphoma. Here eosinophilia can happen either because eosinophils are part of the malignant clone or due to cytokine-driven overproduction.

• another cause, Respiratory diseases such as bronchiectasis and cystic fibrosis, again caused by the ongoing inflammatory response.

• Then, Endocrine conditions such as Addison’s disease. This is because cortisol suppresses eosinophils and in Addison’s, the low cortisol will result in a high eosinophil count.

• and finally we have Post-splenectomy. This is because the spleen normally helps regulate and remove eosinophils from circulation, so splenectomy will result in an increased eosinophil count.

If the eosinophil count is greater than 2.5 × 10⁹/L, we will look for signs of organ damage. This is because very high eosinophil levels can lead to direct tissue injury. Activated eosinophils release toxic inflammatory mediators, and cytokines that can cause inflammation and fibrosis in virtually any organ. The heart, lungs, skin, gastrointestinal tract, and nervous system are particularly vulnerable. Damage can progress rapidly and we should consider urgent admission if there are red flags

Red flags include:

• Severe symptoms secondary to organ involvement, such as

• difficulty breathing,

• chest pain,

• abdominal pain, or

• neurological symptoms.

• as well as other complications, including tissue damage, venous thromboembolism, or evidence of end-organ injury such as acute kidney injury or heart failure.

Even in the absence of red flags, criteria for urgent referral to haematology are:

• A leucoerythroblastic blood film, which suggests bone marrow infiltration, haematological malignancy or severe bone marrow stress.

• And absolute eosinophil count greater than 5 × 10⁹/L, as this level significantly increases the risk of hypereosinophilic syndromes and progressive organ damage.

If the urgent criteria are not met and the patient is clinically well, we will check the travel and drug history and assess for any evidence of atopy, such as asthma, eczema, or allergic rhinitis. We will then repeat the blood test within one to two weeks to confirm whether the eosinophilia is persistent and to look for possible underlying causes.

Initial investigations will include:

• As already mentioned, a repeat full blood count, to confirm that the eosinophilia is persistent and to check for other abnormalities which may suggest a bone marrow disorder.

• A blood film, which can reveal abnormal cell morphology, blast cells, or features suggesting reactive versus clonal eosinophilia.

• Inflammatory markers such as ESR and CRP, which help identify underlying infection, inflammation, or autoimmune disease.

• Immunoglobulin E, as a high IgE is common in allergic disease, parasitic infections, and some hypereosinophilic syndromes.

• An autoimmune profile, since eosinophilia can occur in connective tissue diseases and vasculitis.

• Renal and liver function tests, because organ dysfunction can be both a cause and a consequence of eosinophilia.

• A bone profile, as a high calcium may suggest granulomatous disease such as sarcoidosis or certain malignancies. This is because granulomatous conditions and some cancers increase the production of active vitamin D or stimulate bone breakdown, both of which increase calcium levels.

• We will also check for LDH, which can be high in haematological malignancies and in high cell turnover.

• Vitamin B12 and folate, since a raised B12 can be a clue to myeloproliferative disease, while a deficiency can contribute to abnormal blood counts.

• A chest X-ray, particularly if tuberculosis, pulmonary eosinophilia, or sarcoidosis are suspected.

• Stool culture and microscopy for ova, cysts, and parasites, as parasitic infections are a common and important cause of eosinophilia worldwide.

• Serological antibodies for threadworm or other nematode infections, especially if there are suggestive symptoms.

• and finally, Serological antibodies for schistosomiasis, depending on travel history and ideally after discussion with microbiology, as the timing can influence accuracy. Schistosomiasis is a parasitic infection acquired through contact with freshwater in endemic regions in Africa, the Middle East, South America, and parts of Asia, which emphasises why travel history is so important.

If the cause is found, we will treat it accordingly. However, we will refer to haematology routinely if the eosinophilia remains unexplained and it is greater than 1.5 × 10⁹/L for three months or longer, or if it is rising without an obvious cause. These patterns raise concern for hypereosinophilic syndromes or underlying haematological disease.

So that is it, a review of the assessment and management of eosinophilia.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/us-qmMn8gsk

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through new and updated recommendations published in January 2026 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The Full NICE News bulletin for January 2026 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2026-01-01&to=2026-01-31&ndt=Guidance&ndt=Quality+standard

The updated guideline on Suspected cancer: recognition and referral [NG12] can be found here:

·      https://www.nice.org.uk/guidance/ng12

The updated guideline on Overweight and obesity management [NG246] can be found here:

·      https://www.nice.org.uk/guidance/ng246

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we’ll look at the NICE updates published in January 2026, focusing on what is relevant in Primary Care only.

And this time we have two updated guidelines relevant to us in General Practice: the guidelines on Suspected cancer and on Overweight and obesity management. The changes are minimal so today we have a very short episode.

Right, let’s jump into it.

And let’s start with the guideline on obesity and overweight management.

The update is narrow and specific and clarifies that height-to-weight ratios should only be used to classify the degree of central adiposity in children and young people aged 5 years and over.

Before this amendment, the guideline included height-to-weight ratios for children, but it did not explicitly state that these ratios should not be used in under 5s.

This is because height-to-weight ratios in younger children, may not be validated or appropriate. In fact, in children under 5 years:

·      Body proportions change very rapidly as part of normal growth and development

·      There is wide normal variation in body shape and fat distribution and

·      Height to weight ratios do not accurately reflect central adiposity in this age group and therefore using these ratios risks overestimating or underestimating adiposity

However, in children aged 5 years and over:

·      Body proportions become more stable

·      Patterns of central fat distribution are more consistent

·      And the available evidence supports height to weight ratios in this age group as they are more likely to reflect true central adiposity

No other recommendations, were changed. Everything else remains as it was in the previous published guideline.

Now let’s move to the guideline on suspected cancer.

In January 2026 the update information for the NICE guideline on suspected cancer states that NICE has removed an incorrect recommendation related to blood tests for suspected myeloma. However, when you look at the guideline as it stands, things appear a little confusing, so it is worth looking at this in more detail.

Originally, the guideline listed a broad panel of blood tests for suspected myeloma in primary care. This included serum protein electrophoresis and serum free light chain testing, alongside a full blood count, calcium, and plasma viscosity or ESR. Bence Jones urine testing was suggested as an alternative if serum free light chain testing was not available. These tests were recommended for people with features such as persistent bone pain or an unexplained fracture.

Subsequently, NICE amended the wording of this section to place greater emphasis on serum protein electrophoresis and serum free light chain testing as the key initial investigations.

So the obvious question is this. Has NICE really now removed the recommendation to offer blood tests for suspected myeloma altogether? At face value this looks like guidance that is moving backwards and forwards.

The confusion is increased by the fact that if you look at the recommendations organised by site of cancer, under haematological cancers, the guideline still clearly lists blood tests for suspected myeloma.

So what is actually happening here?

In theory, the update information reflects the official and authoritative change to the guideline. It may be that parts of the published recommendations text have not yet been fully revised or synchronised on the NICE website.

However, I have also reviewed other sections of the NICE website, including committee discussions and rationale documents, and I have not been able to find any explanation for this change. That also raises the possibility that the update statement itself may be an error.

In practical terms, my view is that we should probably continue to request blood tests for suspected myeloma until the guideline text has been fully updated and this discrepancy is clarified. That is, we should request a full blood count, calcium, plasma viscosity or ESR, paraprotein, using serum protein electrophoresis and serum free light chains. If serum free light chain testing is not available, we can use a Bence–Jones test to check for free light chains contained in urine.

I have raised a query directly with NICE, and we should have further clarification soon. For now, this is very much a case of watching this space.

So that is it, a review of the NICE updates relevant to primary care.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/4NysH3aEPMM

This video refers to guidelines produced by a number of organisations (details below). Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by any of them.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I neutropenia always focusing on what is relevant in Primary Care only. The information is based on Haematological guidance by Camden CCG, Manchester Foundation Trust and King’s Health Partners.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

My summary of the guidance consulted can be found here:

·      https://1drv.ms/b/s!AiVFJ_Uoigq0mQ4ZjYGRH1wkGBdc?e=Zuxx84

The resources consulted can be found here:

·      Camden CCG guidance: 1456246258-2f3891e610beaa6533f2c0ad7866e776.pdf(Review) - Adobe cloud storage

·      Manchester Adult anaemia guide: https://acrobat.adobe.com/id/urn:aaid:sc:EU:f96fe528-0a47-457c-b29a-a7efb87221e0

·      Manchester Haematology GP guide: https://mft.nhs.uk/app/uploads/2021/02/MFT-Haematology-GP-Pathway-Guide-v4-11.2.21.pdf

·      King’s Health Partners: https://www.kingshealthpartners.org/assets/000/002/294/KCH_-_king_s_health_partners_-_quick_guide_to_haematology_original.pdf

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I’m Fernando, a GP in the UK. Today we are going to cover what to do when we encounter a high haematocrit, including initial assessment, follow up and management, always focusing on what is relevant in Primary Care only.

I have based this episode on Haematological guidance by Camden CCG, Manchester Foundation Trust and King’s Health Partners. The links to them are in the episode description.

Right, let’s jump into it.

And we will start by saying that haematocrit measures the proportion of blood volume taken up by red blood cells. It can be expressed either as a percentage—from 0 to 100 or as a decimal proportion, from 0 to 1. Because it reflects the relative volumes of red cells and plasma, the haematocrit is influenced not only by the absolute number of red blood cells but also by the amount of circulating plasma. Any change in either component will affect the final value.

A high haematocrit raises the possibility of polycythaemia. Polycythaemia can be diagnosed when the haematocrit is greater than 0.52 in men and greater than 0.48 in women. These thresholds help identify affected people, but they do not, by themselves, tell us the cause.

Polycythaemia is sometimes referred to as erythrocytosis, but this is not entirely accurate. Erythrocytosis specifically refers to an increased number of red blood cells in the circulation. Polycythaemia, on the other hand, is defined by a raised haematocrit, not by a direct count of red blood cells. As a result, it is possible to have a high haematocrit without true erythrocytosis.

This distinction matters because there are two types of polycythaemia. The first is absolute polycythaemia, where an increased red cell mass is genuinely present, that is, true erythrocytosis. The second is relative or apparent polycythaemia, where the haematocrit is high not because there are more red cells, but because the plasma volume is reduced. Dehydration, diuretics, or plasma loss can all create this picture, leading to a raised haematocrit despite a normal red cell mass. It is also common in obese men, and it is also associated with smoking, alcohol, hypertension and stress. Despite the potentially reversible causes of relative or apparent polycythaemia, these patients are also at risk of occlusive vascular episodes.

On the other hand, we have absolute polycythaemia, which reflects a true increase in red cell mass. This can be divided into primary and secondary causes.

The primary cause is Polycythaemia Vera (PV). Well over 90% of patients with PV have an acquired mutation in the JAK2 gene, which plays an important role in regulating erythropoiesis. Because of this mutation, the bone marrow becomes hypersensitive to growth signals and produces red blood cells even when erythropoietin levels are low. In other words, these patients do not need as much erythropoietin to drive red cell production.

The main features of Polycythaemia Vera are therefore:

• a positive JAK2 mutation test,

• a low serum erythropoietin level.

Polycythaemia Vera is also commonly associated with low ferritin, because the accelerated and unregulated production of red cells consumes large amounts of iron.

Being a myeloproliferative disorder, Polycythaemia Vera may also show raised white blood cells and/or platelets, reflecting the involvement of the bone marrow.

Secondary polycythaemia, on the other hand, results from a physiological increase in erythropoietin production. The kidneys release more erythropoietin in response to reduced oxygen levels, so secondary polycythaemia can be an appropriate response to chronic hypoxia, as seen in COPD, congenital or acquired heart disease, and in smokers.

It can also be an inappropriate response when erythropoietin is produced by tumours, such as certain renal or liver tumours, or even uterine fibroids, which can secrete erythropoietin autonomously.

Other possible causes of secondary polycythaemia include anabolic steroids and testosterone therapy, as androgens stimulate erythropoietin production through hormonal pathways.

In cases of secondary polycythaemia, the pattern is different:

• the JAK2 mutation is negative,

• erythropoietin levels are high, and

• ferritin, white blood cells and platelets are normal.

So what do we do when we receive a high haematocrit result? Well, Criteria for urgent referral are a haematocrit greater than 0.60 in men or greater than 0.56 in women. We should also refer urgently if the patient has had a recent thrombosis, shows any abnormal bleeding, or reports neurological or visual symptoms. These features raise concern for hyperviscosity or an underlying myeloproliferative disorder, both of which require immediate specialist assessment.

If the criteria for urgent referral are not met, the next step is to confirm the result by repeating the blood test. In order to differentiate between apparent and absolute polycythaemia, the blood sample should be taken without a tourniquet, and we should ensure that the patient has not been fasting, is well hydrated, and has been advised about alcohol intake and smoking, as these factors can artificially raise the haematocrit.

In this repeat blood test, we should request:

• A repeat full blood count, to confirm whether the raised haematocrit is persistent and to check for associated abnormalities in white cells or platelets.

• A blood film, which can reveal morphological clues to myeloproliferative disease or other haematological disorders.

• We should screen for diabetes, hyperlipidaemia and hypertension, as these cardiovascular risk factors often coexist with secondary causes of polycythaemia and may contribute to vascular complications.

• As mentioned earlier, we should also check Ferritin, to assess iron stores, which may be depleted in Polycythaemia Vera due to increased red cell production.

• and finally renal and liver function tests, since kidney or liver disease may contribute to secondary polycythaemia or influence erythropoietin production.

Additionally, if we suspect absolute polycythaemia, the following tests should be done:

• Genetic testing for the JAK2 mutation, which is positive in the great majority of patients with Polycythaemia Vera.

• And erythropoietin levels, which help distinguish primary from secondary causes, being low in PV and elevated in secondary polycythaemia.

However, in the UK, JAK2 mutation testing and serum erythropoietin levels are not routinely available in primary care. In most areas, these investigations are carried out by haematology teams, as they form part of the specialist work-up for myeloproliferative disorders. While some regions may allow primary-care access, this is not standard practice, and therefore, if absolute polycythaemia is suspected or the haematocrit remains persistently elevated, the appropriate course of action is to refer the patient to haematology, who will then arrange JAK2 and erythropoietin testing as part of their assessment.

So, let’s summarise these patients’ management again:

If we encounter someone with a high haematocrit, we will see if they meet the urgent referral criteria, that is, a haematocrit greater than 0.60 in men or greater than 0.56 in women. We should also refer urgently if the patient has had a recent thrombosis, shows any abnormal bleeding, or reports neurological or visual symptoms.

If the urgent criteria are not met, we will repeat the FBC and arrange routine screening investigations.

Criteria for routine referral are an unexplained, persistently elevated haematocrit above 0.52 in men or above 0.48 in women, taking into account that referral should be considered at lower thresholds if there is associated iron deficiency. “Persistently” means at least two readings above these levels taken four weeks apart.

Alternatively, routine referral is also justified if the haematocrit is above 0.52 in men or above 0.48 in women without waiting for a second test if there are associated symptoms of concern such as pruritus, raised white cell count and/or platelets, splenomegaly, or if there is a past, not recent history of arterial or venous thrombosis.

From a clinical perspective, we will suspect apparent polycythaemia if there is a history of factors such as dehydration, smoking, alcohol excess, diuretics, or other causes of haemoconcentration.

We will suspect absolute secondary polycythaemia if there is chronic hypoxia from conditions such as COPD, smoking, or cardiac disease, if the patient is taking anabolic steroids or testosterone therapy, or if there is a possibility of erythropoietin -producing tumours in the kidney or liver.

If none of these clues is present, we may be dealing with absolute primary polycythaemia, or Polycythaemia Vera. These patients should be referred to haematology, since confirming the diagnosis requires tests that are not routinely available in general practice, ike JAK2 mutation testing and serum EPO levels.

So that is it, a review of the initial assessment and management of neutropenia.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/TQB5tJvM0VM

This video refers to guidelines produced by a number of organisations (details below). Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by any of them.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I cover what to do if thrombocytopenia is found, always focusing on what is relevant in Primary Care only. The information is based on Haematological guidance by Camden CCG, Manchester Foundation Trust and King’s Health Partners.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

My summary of the guidance consulted can be found here:

·      https://1drv.ms/b/s!AiVFJ_Uoigq0mQ4ZjYGRH1wkGBdc?e=Zuxx84

The resources consulted can be found here:

·      Camden CCG guidance: 1456246258-2f3891e610beaa6533f2c0ad7866e776.pdf(Review) - Adobe cloud storage

·      Manchester Adult anaemia guide: https://acrobat.adobe.com/id/urn:aaid:sc:EU:f96fe528-0a47-457c-b29a-a7efb87221e0

·      Manchester Haematology GP guide: https://mft.nhs.uk/app/uploads/2021/02/MFT-Haematology-GP-Pathway-Guide-v4-11.2.21.pdf

·      King’s Health Partners: https://www.kingshealthpartners.org/assets/000/002/294/KCH_-_king_s_health_partners_-_quick_guide_to_haematology_original.pdf

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I’m Fernando, a GP in the UK. Today we are going to cover what to do when we encounter thrombocytopenia on a full blood count, always focusing on what is relevant in Primary Care only.

I have based this episode on Haematological guidance by Camden CCG, Manchester Foundation Trust and King’s Health Partners. The links to them are in the episode description.

Right, let’s jump into it.

Thrombocytopenia is the platelet count is low, which is defined as a platelet count below 150 × 10⁹ per litre.

But before we assume a true low platelet count, we need to remember that thrombocytopenia can often be an artefact. This happens when platelets clump together in the EDTA sample tube, giving a falsely low automated count.

So, the first step is always to confirm the result with a repeat full blood count and a blood film. The blood film not only rules out platelet clumping but can also provide important clues about the underlying cause.

There are many potential causes of thrombocytopenia so, let’s have a look at them:

First, we have alcohol excess. Chronic alcohol use can directly suppress bone marrow production and shorten platelet lifespan. It is also frequently associated with chronic liver disease, where the spleen often becomes enlarged due to portal hypertension destroying more platelets than usual — a process known as hypersplenism.

Then we have recreational drugs, which can also impair platelet production or trigger immune-mediated destruction.

Then, travel history is also very important. Malaria, for example, often presents with thrombocytopenia, sometimes even before fever or parasitaemia becomes obvious.

Tuberculosis can also cause thrombocytopenia, either through bone marrow involvement or immune-mediated mechanisms.

Then we should consider liver and renal disease.

In chronic liver disease we have already explained that hypersplenism is the most common cause of thrombocytopenia in liver disease.

In renal disease, platelet lifespan is reduced because uraemia makes platelets more fragile, causing them to break down more quickly. In addition, bone marrow suppression may also occur.

Then we have medications as another common culprit.

NSAIDs, heparin, digoxin, quinine, anti-epileptics, antipsychotics and proton pump inhibitors are all recognised causes. Most drug-induced thrombocytopenia is caused by either:

• immune-mediated platelet destruction, or

• direct suppression of platelet production in the bone marrow.

Heparin is the main exception because it causes thrombocytopenia through a unique immune reaction that activates platelets, leading to their consumption and a fall in the platelet count.

Another possible cause are nutritional deficiencies, especially vitamin B12 and folate deficiency, which can impair bone marrow production and lead to thrombocytopenia, often alongside other cytopenias.

We also need to consider viral causes. For example, Epstein–Barr virus frequently causes a temporary drop in platelets, which typically resolves within a few weeks.

HIV and hepatitis B or C can cause persistent thrombocytopenia either through direct bone marrow suppression, immune-mediated destruction, or associated splenomegaly.

Then, malignancy is also on the list, because both haematological cancers and solid tumours can infiltrate or suppress the bone marrow.

Then we have bone marrow failure syndromes, such as aplastic anaemia, which will often present with thrombocytopenia together with anaemia and neutropenia.

Another cause is immune thrombocytopenic purpura, or ITP, which is an autoimmune condition that destroys platelets. In adults, ITP can be acute or chronic, and the platelet count can fall to very low levels even when the patient looks otherwise well.

Finally, autoimmune conditions such as SLE can present with thrombocytopenia as part of a broader immunological process.

Now that we have had a look at the causes, how should we manage these patients?

We have already mentioned that we should confirm thrombocytopenia with a repeat FBC and blood film. If the thrombocytopenia is confirmed, we will need to check if there are urgent criteria.

First of all, we should arrange urgent same-day hospital assessment when the platelet count is below 20 × 10⁹ per litre and any concerning clinical features are present. These include:

• Active bleeding, even if minor, because bleeding risk rises sharply at very low platelet levels.

• An abnormal blood film, such as the presence of blasts suggesting acute leukaemia, or red cell fragments suggesting microangiopathic haemolysis, as these findings indicate potentially life-threatening conditions.

• And finally an altered consciousness or confusion, which may point to serious systemic illness, intracranial bleeding, severe infection, or thrombotic microangiopathy.

We should make an urgent outpatient haematology referral if the platelet count is below 50 × 10⁹ per litre, even without symptoms. This is because at this level, the risk of spontaneous bleeding increases, and many underlying causes — such as ITP, bone marrow failure, or haematological malignancy — require urgent assessment.

Additionally, when the platelet count is below 50, it is unsafe to continue antiplatelet agents or anticoagulants, so these should be stopped unless a specialist advises otherwise.

We should also make an urgent outpatient haematology referral when the platelet count is between 50 and 100 and certain concerning features are present. These include splenomegaly, lymphadenopathy, other cytopenias, pregnancy, or planned surgery. This is because all of these situations increase the risk of serious underlying disease or increase the risk of bleeding.

However, if the platelet count is above 50 and none of the urgent referral criteria are present, we should then arrange the following baseline investigations:

Firstly, we begin with a repeat full blood count and a blood film to confirm the thrombocytopenia, rules out platelet clumping, and look for abnormal cell morphology.

Then we will check Vitamin B12 and folate levels to rule out deficiency.

Ferritin and iron studies are also helpful, given that iron deficiency can occasionally contribute to low platelets.

Inflammatory markers, such as ESR and CRP, which can suggest infection, inflammation, or an underlying autoimmune process.

An autoimmune profile to exclude autoimmune-mediated platelet destruction.

Renal, liver and thyroid function tests to identify chronic liver disease, renal failure and thyroid disease given that both hypo- and hyperthyroidism — can contribute to thrombocytopenia.

Then, viral serology for HIV, hepatitis B and hepatitis C as these viruses can be associated thrombocytopenia.

And finally, we should perform any other investigations suggested by the history or examination, for example, malaria testing after relevant travel, a TB workup, coagulation studies if there is bleeding, etc.

After the initial baseline investigations, if no obvious cause is found, the platelet count is above 50 and none of the urgent referral criteria are present, we can repeat the full blood count after 4 to 6 weeks.

If thrombocytopenia persists and remains unexplained, we should then refer the patient routinely to haematology.

So that is it, a review of the assessment and management of thrombocytopenia.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/lhtciu3O8tc

The video on raised bilirubin pattern can be found here:

·      https://youtu.be/ndAus37PfsE

The video on hepatitic pattern abnormal LFTs can be found here:

·      https://youtu.be/rIX46swVSfg

This episode refers to guidelines on the management of abnormal liver function tests by the British Society of Gastroenterology. Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by them.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I cover what to do when we encounter abnormal LFTs with a cholestatic pattern, always focusing on what is relevant in Primary Care only. 

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

My summary guide can be downloaded here:

·      https://1drv.ms/b/s!AiVFJ_Uoigq0mQ8MRxaNYnA1_pzh?e=H2U7rS

The resources consulted can be found here:

BSG- British Society of Gastroenterology:

·      bsg.org.uk/clinical-resource/guidelines-on-abnormal-liver-blood-tests

·      Guidelines on the management of abnormal liver blood tests (bsg.org.uk)

o  First published on:

o  BMJ article:

o  Guidelines on the management of abnormal liver blood tests | Gut (bmj.com)

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I’m Fernando, a GP in the UK. Today we are going to cover what to do when we encounter abnormal LFTs with a cholestatic pattern, always focusing on what is relevant in Primary Care only.

This episode is based on the British Society of Gastroenterology guidelines on abnormal Liver function tests. A link to it is in the episode description.

Right, let’s jump into it.

And let’s start by remembering that there are three common patterns of abnormal liver function tests or LFTs:

1. A cholestatic pattern, normally showing a high ALP and GGT, which is what we will concentrate on today.
2.  An isolated raised bilirubin with otherwise normal liver tests.
3. And a hepatitic pattern, with a raised ALT and AST indicating hepatocellular injury. By the way, if you are interested in finding out more about the last two types, make sure to watch the corresponding episodes on this channel. The links are in the episode description.

As we have said, LFTs showing a cholestatic pattern normally present with a high ALP and GGT.

Alkaline phosphatase, or ALP, is produced mainly in the liver but is also found in bone, intestines, kidneys and the placenta. Levels are physiologically higher in childhood because of rapid bone growth, and in pregnancy due to placental production. Raised ALP can come from either hepatic or non-hepatic sources.

The main source of non-hepatic ALP is bone. ALP increases in bone disease because it is produced by osteoblasts, the cells responsible for forming new bone. Any condition that increases osteoblast activity or bone turnover—such as healing fractures, Paget’s disease, bone metastases, or vitamin D deficiency—causes osteoblasts to increase their activity, releasing more ALP into the circulation.

We should remember that the most common cause of an asymptomatic, non-hepatic raised ALP is vitamin D deficiency. And let’s remember that vitamin D deficiency increases bone turnover because low vitamin D reduces calcium absorption from the gut. To maintain normal calcium levels, parathyroid hormone rises and stimulates bone breakdown to release calcium. This increase in bone remodelling activates osteoblasts leading to a rise in ALP.

But as we are focusing on liver function tests, what is the source of a raised hepatic ALP? From a pathophysiological perspective, hepatic ALP rises when bile flow is impaired, also known as cholestasis. And, why does cholestasis cause a rise in ALP? It happens because alkaline phosphatase is found in high concentration in the cells lining the bile ducts. When bile flow is impaired, pressure builds up in the biliary system and the bile duct epithelium becomes irritated. This stimulates these cells to produce and release more ALP into the bloodstream. This is the reason why ALP rises in, for example, gallstone disease, strictures, or cholangitis.

On the other hand, γ-glutamyltransferase, or GGT, is found in the liver but not in bone. Therefore, when ALP is raised, measuring GGT helps determine whether the source is hepatic or non-hepatic. A raised ALP with a normal GGT suggests a bone-related cause, whereas a raised ALP with a raised GGT supports a hepatic origin and should prompt further assessment of cholestatic liver disease.

GGT rises in cholestasis because it is also highly concentrated in the cells lining the bile ducts. When pressure builds up in the biliary system, these cells release more GGT into the bloodstream. In addition, cholestasis causes oxidative stress because retained bile acids are toxic to liver cells. In response, the liver increases GGT production, as GGT is involved in antioxidant and detoxification pathways, leading to the characteristic rise in cholestatic liver disease.

A high GGT can also be due to obesity, excess alcohol, or medications. In obesity and NAFLD, fat accumulation within the liver creates oxidative stress, so the liver up-regulates GGT to protect hepatocytes from free radical damage. In this context, an elevated GGT reflects metabolic stress rather than structural cholestasis. In alcohol use, ethanol metabolism produces toxic intermediates that also generate oxidative stress, which further stimulates GGT production as part of the liver’s detoxification response.

We will not go into detail on how to proceed with an isolated raised ALP, that is, with a normal GGT, as today we are focusing on cases where there is clear hepatic involvement, meaning that both ALP and GGT are high in a true cholestatic pattern.

How should we investigate and manage these patients?

When we manage patients with any abnormal liver function tests, we must begin by recognising red flags that require urgent action. According to the British Society of Gastroenterology guidelines, if there are signs of synthetic liver failure – such as unexplained clinical jaundice, a low albumin, or a raised INR – or if there is a suspicion of malignancy, for example unexplained weight loss or marked cholestasis, then the patient should be urgently referred or admitted for specialist assessment.

If the pattern is cholestatic, we will proceed with a full liver screen. This is because cholestatic abnormalities are often related to structural biliary disease, autoimmune cholestatic conditions, or infiltrative disorders, and these require a broader diagnostic approach than simple repeat testing.

What tests should be done in a full liver screen?

A full liver screen should include an ultrasound scan of the liver and biliary tree, which is the first-line imaging test. Ultrasound helps identify biliary dilatation, gallstones, strictures, masses, or features of chronic liver disease. In addition to imaging, blood tests should include hepatitis B and C screening, an autoantibody screen, serum immunoglobulins, ferritin and transferrin saturation, and, often and where clinically appropriate, a coeliac screen, alpha-1 antitrypsin levels, and caeruloplasmin. These tests collectively help detect autoimmune cholestatic diseases such as primary biliary cholangitis, metabolic conditions such as haemochromatosis or Wilson’s disease, and chronic viral hepatitis.

It is also worth emphasising that this full liver screen is recommended not only for cholestatic abnormalities but also for patients who present with a hepatitic pattern, as the BSG guideline advises a comprehensive assessment irrespective of the pattern or the degree of derangement once initial red flags have been excluded.

The management in primary care is fairly simple, because the British Society of Gastroenterology recommends that once initial investigations have been completed, these patients should be referred to secondary care for further assessment. This applies both when a cholestatic picture come with abnormalities in the liver screen and also if the ALP and GGT remain persistently high even in the context of normal investigations.

Referral is indicated because persistent cholestatic abnormalities indicate underlying pathology that usually cannot be adequately diagnosed or managed in primary care and requires specialist input.

So that is it, a review of abnormal LFTs with a cholestatic pattern.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/3QL2R2IV83o

This video refers to guidelines produced by a number of organisations (details below). Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by any of them.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I cover what to do if thrombocytosis is found, always focusing on what is relevant in Primary Care only. The information is based on Haematological guidance by Camden CCG, Manchester Foundation Trust and King’s Health Partners.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

My summary of the guidance consulted can be found here:

·      https://1drv.ms/b/s!AiVFJ_Uoigq0mQ4ZjYGRH1wkGBdc?e=Zuxx84

The resources consulted can be found here:

·      Camden CCG guidance: 1456246258-2f3891e610beaa6533f2c0ad7866e776.pdf(Review) - Adobe cloud storage

·      Manchester Adult anaemia guide: https://acrobat.adobe.com/id/urn:aaid:sc:EU:f96fe528-0a47-457c-b29a-a7efb87221e0

·      Manchester Haematology GP guide: https://mft.nhs.uk/app/uploads/2021/02/MFT-Haematology-GP-Pathway-Guide-v4-11.2.21.pdf

·      King’s Health Partners: https://www.kingshealthpartners.org/assets/000/002/294/KCH_-_king_s_health_partners_-_quick_guide_to_haematology_original.pdf

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I’m Fernando, a GP in the UK. Today we are going to cover what to do when we encounter thrombocytosis on a full blood count, always focusing on what is relevant in Primary Care only.

I have based this episode on Haematological guidance by Camden CCG, Manchester Foundation Trust and King’s Health Partners. The links to them are in the episode description.

Right, let’s jump into it.

Thrombocytosis is when the number of platelets is high, which is usually defined as a raised platelet count above 450 × 10⁹/L.

But before moving on, let’s clarify the terminology: should we call it thrombocytosis or thrombocythemia? There is an important difference. Thrombocytosis is much more common and arises as a secondary response to another condition, which is why it is also known as reactive thrombocytosis. In contrast, thrombocythemia, also called primary or essential thrombocythemia, is far less common and represents a myeloproliferative disorder in which the bone marrow produces platelets in an uncontrolled, abnormal way.

Another important distinction is that patients with reactive thrombocytosis have normal platelets, so their risk of thrombosis and bleeding is relatively low. On the other hand, patients with thrombocythemia have abnormal platelets, which increases their risk of both blood clots and bleeding complications. From a clinical perspective, thrombocythemia often presents with splenomegaly and a platelet count greater than 1000 × 10⁹/L.

So, let’s have a look at the possible causes. Causes of thrombocytosis include:

• Iron Deficiency Anaemia: which is one of the most common causes of reactive thrombocytosis. When iron levels are low, the bone marrow increases its overall activity in an attempt to compensate for the anaemia. Although iron deficiency limits the production of red blood cells, platelet production is not restricted in the same way. As a result, the bone marrow produces more platelets. In addition, inflammatory signals associated with chronic iron deficiency can further stimulate thrombopoietin pathways, increasing platelet numbers even more. This is why thrombocytosis often resolves once the iron deficiency is corrected.

• Another cause is Malignancy, because some tumours release inflammatory cytokines that eventually increase platelet formation. This reactive response is common in several solid cancers, particularly the “LEGO” cancers, that is:

• Lung

• Endometrium

• Gastric

• and Oesophageal cancer

• Another cause is general Inflammation, where cytokines stimulate excessive platelet production.

• Also Infection, which can cause transient reactive thrombocytosis.

• Post-splenectomy and hyposplenism, such as in coeliac disease, since the spleen normally helps remove circulating platelets.

• Post-operative states, where inflammation and stress responses increase platelet counts.

• And finally, a primary myeloproliferative disorder, such as essential thrombocythemia.

How should we respond to thrombocytosis?

The criteria for urgent haematology referral are:

• A platelet count exceeding 1000 × 10⁹/L, which raises concern for a myeloproliferative disorder and a significant risk of thrombosis.

• Splenomegaly, which may indicate a primary haematological process such as essential thrombocythemia or myelofibrosis.

• A recent history of thromboembolism, as thrombocytosis can contribute to recurrent clotting events.

• A platelet count above 600 × 10⁹/L in a patient at high risk of thromboembolism or cardiovascular disease, since the combination significantly increases clinical risk.

• Neurological symptoms, which may reflect microvascular complications associated with very high platelet counts.

• Any signs of malignancy, given that multiple cancers can cause reactive thrombocytosis.

• any other significant abnormal full blood count indices, which may suggest a bone marrow disorder rather than a reactive process.

• And finally, if there is Abnormal bleeding. And let’s stop here for a moment and discuss how it is possible that thrombocytosis can be associated to a high risk of both thrombosis and bleeding.

On one hand, thrombosis risk in thrombocytosis is due to the high number of circulating platelets, which makes clots more likely. In addition, inflammation causing reactive thrombocytosis can also create a prothrombotic environment. Together, these factors increase the thrombosis risk.

On the other hand, bleeding risk in thrombocytosis can occur for two main reasons. First, in primary or essential thrombocythemia, the platelets produced by the bone marrow are structurally and functionally abnormal and these abnormal platelets do not work effectively, so clot formation is impaired. Secondly, thrombocytosis may affect the von Willebrand factor. Von Willebrand factor is a protein that helps platelets stick to damaged blood vessels and to each other, making it essential for the first steps of clot formation. However, when platelet counts become very high, the excess platelets bind and remove the most active forms of von Willebrand factor from the circulation. This leads to a functional depletion known as acquired von Willebrand syndrome. It explains the paradoxical situation in which a patient can have thrombocytosis and yet be at increased risk of bleeding.

If none of the urgent referral criteria are present, we will investigate for underlying causes by arranging the following initial tests:

• A repeat full blood count, to confirm that the thrombocytosis is persistent.

• A blood film, which may reveal abnormal platelet morphology or other features suggestive of a myeloproliferative process.

• Inflammatory markers such as ESR and CRP, since inflammation is a common cause of reactive thrombocytosis.

• Ferritin and iron studies, as iron deficiency frequently elevates platelet counts.

• And we will consider a coeliac screen, because coeliac disease can lead to hyposplenism or iron deficiency, both of which are associated with thrombocytosis.

If the patient is asymptomatic and no obvious cause is identified, we will repeat the full blood count 4 to 6 weeks later. If the thrombocytosis persists above 450 × 10⁹/L, we will refer to haematology routinely for further assessment.

So that is it, a review of the assessment and management of thrombocytosis.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/p6YSowcUuEo

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through new and updated recommendations published in December 2025 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The Full NICE News bulletin for December 2025 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2025-12-01&to=2025-12-31&ndt=Guidance&ndt=Quality+standard

The updated guideline on Child maltreatment: when to suspect maltreatment in under 18s [CG89] can be found here:

·      https://www.nice.org.uk/guidance/ng253

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we’ll look at the NICE updates published in December 2025, focusing on what is relevant in Primary Care only.

And this time we have just one updated guideline that is relevant to us in General Practice: the guideline on when to suspect maltreatment in children.

Right, let’s jump into it.

In December 2025, NICE updated the guideline Child maltreatment: when to suspect maltreatment in under 18s. The core change in this update is the addition of a definition of the term “independently mobile.”

Before this update, the NICE guideline used the term “independently mobile” in several key recommendations, but did not define what that term meant. We were expected to interpret it based on our own judgement. This led to variation in practice, particularly when assessing injuries such as bruises, lacerations, and abrasions. Different clinicians could reasonably reach different conclusions about whether a child met this threshold, even when looking at the same clinical picture.

The term was sometimes difficult to interpret as to whether it meant rolling, crawling, bottom-shuffling, cruising, or walking, given that there was no shared or agreed definition in the guideline.

The definition has been developed using a formal consensus process and “independently mobile” is now clearly defined as a child who can move around independently without support, rather than relying on being placed or carried.

Therefore, a child should be considered independently mobile if they can do any of the following:

• crawl
• bottom shuffle
• pull themself up into a standing position using an object, for example, furniture
• move into a standing position unaided
• cruise (that is, move from place to place holding onto an object, for example, furniture)
• climb, for example onto furniture or stairs
• walk using a push-along walker
• or walk unaided.

Children under 12 weeks typically lack the muscle strength, coordination and neurological maturity needed for independent mobility. However, age alone should not be used to determine whether a child is independently mobile. 

This definition has now been added in three areas, specifically in recommendations on:

• bruising and petechiae,

• lacerations, abrasions and scars,

• and burn or scald injuries.

Compared with the previous version, the key difference is clarity, not threshold. The level of concern for injuries has not been raised or lowered. Instead, we now have a shared understanding of which children fall into the higher-risk group when assessing unexplained or concerning injuries.

Otherwise no other major changes were made to recommendations on child abuse and neglect.

Right, this is the end of the update itself.

And, as we have a brief episode today, let’s now look at a brief summary of this guideline. And the first thing to say is that the aim of the guideline is to help us recognise features that should raise concern and prompt further safeguarding action. We are not expected to confirm abuse, but to recognise the risks and act appropriately.

Let’s now briefly review some examples of when to suspect or consider maltreatment. These are situations that may need urgent safeguarding action or discussion with local safeguarding leads.

We should suspect maltreatment when there are injuries with no explanation, or an explanation that does not fit, especially:

– bruising, cuts, abrasions, burns or scalds in a child who is not independently mobile,

– bruises with clear shapes, such as hands, grips, or ligatures,

– burns or scalds with clear patterns or signs of forced immersion,

– multiple injuries or injuries of different ages,

– injuries that are symmetrical or in unusual locations,

– and injuries that are in areas normally covered by clothing.

We should also suspect maltreatment with serious injuries without adequate trauma, including:

– fractures, especially multiple fractures or rib fractures in infants,

– fractures of different ages,

– intracranial injury without a major accidental cause,

– retinal haemorrhages or unexplained eye injuries,

– and spinal, abdominal, or chest injuries that are unexplained, even if there are no external signs.

Additionally, we should suspect sexual abuse when there are clear indicators, including:

– genital, anal, or perianal injury without an accidental explanation,

– and pregnancy in a child under 13 years, which is a strong indicator of maltreatment.

Pregnancy in 13- to 15-year-olds should prompt assessment for sexual abuse.

We should suspect neglect when there are strong indicators, such as:

– repeated failure to provide basic care, food, warmth, or safety,

– and failure to seek medical help that puts the child at risk.

We should also consider possible neglect, if there is, for example:

– poor hygiene or inappropriate clothing,

– an unsafe home environment,

– missed immunisations or health reviews,

– and severe or ongoing infestations,

And we should be concerned if parents or carers:

– fail to give essential medication,

– repeatedly miss important appointments,

– or do not seek medical help when appropriate.

Also, Poor school attendance without a clear reason and repeated or unusual healthcare attendances, especially across multiple services, should also raise concern.

Additionally, we should consider fabricated or induced illness when:

– reported symptoms do not match clinical findings,

– and when symptoms only occur in the presence of carers, and investigations are repeatedly normal.

We should consider maltreatment when there are behavioural or emotional concerns, such as:

– sudden changes in behaviour,

– extreme fear, withdrawal, or aggression,

– self-harm or eating problems without a clear cause,

– sexualised behaviour that is not age appropriate,

– repeated self-harm, and ongoing wetting or soiling not explained by a medical condition.

We should also consider maltreatment when there are concerning parent–child interactions, including:

– hostility, rejection, or lack of emotional warmth,

– unrealistic expectations of the child,

– and refusal to allow the child to speak alone when appropriate.

Running away from home or living away from caregivers without agreement should also raise concern.

And to end, the key messages for us are that we should follow safeguarding procedures and seek advice early. A pattern over time is often more important than a single event and we should trust our professional judgement and discuss concerns if we are unsure.

Remember that this is not an exhaustive list, but a summary of some relevant cases to be aware of.

So that is it, a review of the NICE updates relevant to primary care.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/ndAus37PfsE

The video on hepatitic pattern abnormal LFTs can be found here:

·      https://youtu.be/rIX46swVSfg

This episode refers to guidelines on the management of abnormal liver function tests by the British Society of Gastroenterology. Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by them.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I cover what to do when in respect of an isolated high bilirubin with otherwise normal liver function tests, always focusing on what is relevant in Primary Care only.  

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

My summary guide can be downloaded here:

·      https://1drv.ms/b/s!AiVFJ_Uoigq0mQ8MRxaNYnA1_pzh?e=H2U7rS

The resources consulted can be found here:

BSG- British Society of Gastroenterology:

·      bsg.org.uk/clinical-resource/guidelines-on-abnormal-liver-blood-tests

·      Guidelines on the management of abnormal liver blood tests (bsg.org.uk)

o  First published on:

o  BMJ article:

o  Guidelines on the management of abnormal liver blood tests | Gut (bmj.com)

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I’m Fernando, a GP in the UK. Today we are going to cover what to do when we encounter an isolated high bilirubin with otherwise normal liver function tests, always focusing on what is relevant in Primary Care only.

This episode is based on the British Society of Gastroenterology guidelines on abnormal Liver function tests. A link to it is in the episode description.

Right, let’s jump into it.

And let’s start by remembering that there are three common patterns of abnormal liver function tests or LFTs:

1. An isolated raised bilirubin with otherwise normal liver tests, which is what we will concentrate on today.
2. A cholestatic pattern, normally showing a high ALP and GGT.
3. And a hepatitic pattern, with a raised ALT and AST indicating hepatocellular injury. By the way, if you are interested in finding out more about this particular type, make sure to watch the corresponding episode on this channel. The link is in the episode description.

Let’s also remember that bilirubin is the by-product of the breakdown of haemoglobin. When red blood cells are broken down, bilirubin is produced and released into the bloodstream. It exists in two forms: unconjugated bilirubin and conjugated bilirubin. Unconjugated bilirubin is water-insoluble and travels to the liver bound to albumin. Once in the liver, it is converted into conjugated bilirubin, making it water-soluble so it can be excreted into bile.

A high unconjugated bilirubin level is usually due to increased production, as in haemolysis, or reduced conjugation within the liver. A high conjugated bilirubin level, on the other hand, is normally due to liver disease or biliary obstruction, where the liver is unable to process or excrete bilirubin normally.

Many path labs will routinely report only the total bilirubin, but they will provide a breakdown into conjugated and unconjugated fractions if the level is abnormal or if it is specifically requested.

Under normal circumstances, the majority of bilirubin should be conjugated. Therefore, if most of the bilirubin is unconjugated, and there is no evidence of haemolysis, the cause is almost always Gilbert’s syndrome. In Gilbert’s syndrome, the enzyme responsible for conjugating bilirubin has reduced activity. As a result, unconjugated bilirubin accumulates, often fluctuating with fasting, stress, illness, or dehydration. Importantly, it is not associated with liver disease or ill health, and patients should be fully reassured that it is a benign lifelong condition.

But we will come back to that a little later.

How do we manage these patients?

When we manage patients with any abnormal liver function tests, we must start by recognising red flags that require urgent action. According to the BRITISH SOCIETY OF GASTROENTEROLOGY guidelines, if there are signs of synthetic liver failure – for example, unexplained clinical jaundice, a low albumin, or a raised INR – or if there is a suspicion of malignancy, such as unexplained weight loss or marked cholestasis, then these patients should be urgently referred or admitted for specialist assessment.

For patients whose only abnormality is an isolated raised bilirubin, and who have no worrying clinical signs, we can follow a more measured primary care approach:

1. First, we will request a full blood count (FBC) and repeat liver function tests (LFTs) on a fasting sample, asking specifically for the breakdown of conjugated and unconjugated bilirubin.
2. The repeat sample should be fasting because in conditions like Gilbert’s syndrome the unconjugated bilirubin tends to rise further when the liver’s conjugating capacity is challenged.

So, why does fasting raise bilirubin in Gilbert’s syndrome?

Firstly, because there is reduced hepatic energy availability. During fasting, blood glucose falls and the liver prioritises essential metabolic functions. Bilirubin conjugation is not a high-priority process, so the already-reduced enzyme activity present in Gilbert’s syndrome becomes even less effective.

Secondly, there is increased bilirubin production because fasting slightly increases the breakdown of haemoglobin and other haem-containing proteins, increasing bilirubin entering the system.

And thirdly, there is reduced hepatic uptake of bilirubin from the bloodstream because of changes in liver blood flow and transporter activity.

1. If after the repeat sample, the unconjugated bilirubin rises further on a fasting sample, and there is no evidence of haemolysis (for example, no anaemia), then Gilbert’s syndrome is the likely diagnosis.

The BRITISH SOCIETY OF GASTROENTEROLOGY guidelines emphasise that for the pattern “isolated raised bilirubin with otherwise normal liver tests”, Gilbert’s syndrome is the most common cause.

1. If there is associated anaemia, this should prompt consideration of haemolysis rather than Gilbert’s. In that scenario we should request a reticulocyte count and LDH (and possibly haptoglobin). This is because when haemolysis occurs, red blood cells are broken down more quickly than normal. This increased red-cell turnover releases large amounts of haemoglobin, which is then converted into unconjugated bilirubin. As a result, the unconjugated bilirubin rises in the bloodstream. To confirm haemolysis, we check a reticulocyte count, which will be high because the bone marrow is trying to replace the destroyed red cells, and LDH, which is released from damaged red cells and therefore increases too. We may also check haptoglobin, which binds free haemoglobin and becomes low when haemolysis is present.

If haemolysis is suspected, the patient should be referred to a haematologist, because haemolysis can have many underlying causes and diagnosing the exact cause requires specialist tests that are not usually available in primary care.

However, if the isolated raised bilirubin persists and the cause remains unclear, or if any additional liver function test abnormalities emerge, then we should follow the British Society of Gastroenterology guideline recommendation for further investigation. This may mean following the pathway for a hepatitic pattern or a cholestatic pattern, depending on the case.

But in any event:

• We should consider a liver ultrasound scan to exclude biliary obstruction or structural liver disease.
• We will consider a full liver screen. And what is a full liver screen? Apart from the ultrasound scan already mentioned, this should include hepatitis B and C screening, an autoantibody screen, serum immunoglobulins, both ferritin and transferrin saturation and, often, a coeliac screen, alpha-1-antitrypsin levels and caeruloplasmin.
• And finally, we will consider re-checking whether there is any evidence of haemolysis by repeating the reticulocyte count and LDH if haemolysis is still suspected.

And eventually, the decision will be between monitoring versus referral.

If after all of the above investigations the clinical picture remains consistent with Gilbert’s syndrome, we can continue with periodic monitoring in primary care.

On the other hand, if the isolated raised bilirubin is persistent and unexplained, we should refer the patient for specialist assessment.

So that is it, a review of an Isolated raised bilirubin with otherwise normal liver function tests.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·     https://youtu.be/w4d4qc7aHn4

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

This video also refers to a number of medical articles on ADHD published by a number of organisations (details below). Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by any of them.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I cover ADHD treatment options, especially in adults, always focusing on what is relevant in Primary Care only. The information is based on a number of published medical articles. The links to them are below.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The resources consulted can be found here:

1. NICE. Attention deficit hyperactivity disorder: diagnosis and management (NG87):

https://www.nice.org.uk/guidance/ng87?utm

2. Ostinelli EG et al. “Comparative efficacy and acceptability of pharmacological, psychological, and neurostimulatory interventions for ADHD in adults: a systematic review and component network meta-analysis.” The Lancet Psychiatry, 2025.

https://www.thelancet.com/journals/lanpsy/article/PIIS2215-0366(24)00360-2/fulltext?utm

3. Gosling CJ et al. “Benefits and harms of ADHD interventions: umbrella review of systematic reviews and meta-analyses.” BMJ, 2025.

https://www.bmj.com/content/391/bmj-2025-085875?utm

4. Cortese S et al. “Attention-deficit/hyperactivity disorder (ADHD) in adults.” World Psychiatry, 2025.

https://pmc.ncbi.nlm.nih.gov/articles/PMC12434367/?utm

5. Wakelin C et al. “A review of recent treatments for adults living with attention-deficit/hyperactivity disorder.” 2023.

https://pmc.ncbi.nlm.nih.gov/articles/PMC10730462/?utm

6. Kooij JJS et al. “Updated European Consensus Statement on diagnosis and treatment of adult ADHD.” European Psychiatry, 2019.

https://pubmed.ncbi.nlm.nih.gov/30453134/?utm

https://www.cambridge.org/core/journals/european-psychiatry/article/updated-european-consensus-statement-on-diagnosis-and-treatment-of-adult-adhd/707E2A36539213CF85EACCA576F47427?utm

7. Nimmo-Smith V et al. “Non-pharmacological interventions for adult ADHD: a systematic review.” Psychological Medicine, 2020.

https://pubmed.ncbi.nlm.nih.gov/32036811/?utm

https://www.cambridge.org/core/journals/psychological-medicine/article/nonpharmacological-interventions-for-adult-adhd-a-systematic-review/538F70FB89C5B687F4A75E7431E63B38?utm

8. Mechler K et al. “Evidence-based pharmacological treatment options for ADHD in children, adolescents and adults.” Neuroscience & Biobehavioral Reviews, 2022.

https://www.sciencedirect.com/science/article/pii/S016372582100142X?utm

9. AWMF S3 Guideline. “Attention-Deficit/Hyperactivity Disorder (ADHD) in Children, Young People and Adults.” 2020.

https://register.awmf.org/assets/guidelines/028_D_G_f_Kinder-_und_Jugendpsychiatrie_und_-psychotherapie/028-045eng_S3_ADHS_2020-12-abgelaufen.pdf?utm

10. Wolraich ML et al. “Clinical practice guideline for the diagnosis, evaluation, and treatment of attention-deficit/hyperactivity disorder in children and adolescents.” Pediatrics, 2019.

https://publications.aap.org/pediatrics/article/144/4/e20192528/81590/Clinical-Practice-Guideline-for-the-Diagnosis?utm

11. Faraone SV et al. “The World Federation of ADHD International Consensus Statement: 208 evidence-based conclusions about the disorder.” Neuroscience & Biobehavioral Reviews, 2021.

https://pubmed.ncbi.nlm.nih.gov/33549739/?utm

https://www.sciencedirect.com/science/article/pii/S014976342100049X?utm

https://www.adhd-federation.org/publications/international-consensus-statement.html?utm

12. CADDRA. Canadian ADHD Practice Guidelines, Version 4.1. 2020.

https://www.caddra.ca/canadian-adhd-practice-guidelines/?utm

13. Therapeutics Initiative. “ADHD in adults.” Therapeutics Letter 144, 2023.

https://www.ti.ubc.ca/2023/09/29/144-adhd-adults/?utm

14. May T et al. “The Australian evidence-based clinical practice guideline for ADHD.” Australian Journal of General Practice / AADPA, 2023.

https://adhdguideline.aadpa.com.au/?utm

https://pmc.ncbi.nlm.nih.gov/articles/PMC10363932/?utm

15. Coghill D & colleagues / Australian Prescriber. “Pharmacological management of attention deficit hyperactivity disorder in children and adolescents.” Australian Prescriber, 2025.

https://australianprescriber.tg.org.au/articles/pharmacological-management-of-attention-deficit-hyperactivity-disorder-in-children-and-adolescents.html?utm

16. Thapar A et al. “Attention-deficit/hyperactivity disorder.” Nature Reviews Disease Primers, 2024.

https://www.nature.com/articles/s41572-024-00495-0?utm

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I’m Fernando, a GP in the UK. Today we are going to talk about ADHD treatment options, especially in adults, always focusing on what is relevant in Primary Care only.

I have based this episode on a number of published medical articles. The links to them are in the episode description.

Right, let’s jump into it.

Modern guidelines emphasise that ADHD management is multimodal — including psychoeducation, environmental adaptations, psychological interventions, and, where indicated, medication.

For children and adolescents, NICE and other guidelines recommend starting with psychoeducation and behavioural or parent training, then adding medication when impairment remains significant.

However, for adults, guidelines are very clear: medication is usually first-line when symptoms cause persistent, moderate to severe impairment, supported by psychoeducation and practical help.

So, when is medication indicated?

For children and adolescents, medication — usually methylphenidate — is recommended only when ADHD is clearly diagnosed, the impairment is significant, and non-drug approaches aren’t enough. In other words, it’s generally reserved for moderate to severe ADHD, rather than mild cases.

However, for adults, medication is indicated when there is a clear diagnosis of ADHD with symptoms present since childhood, even if they were never recognised at the time. The symptoms must be causing clinically significant impairment, and other conditions — like depression, bipolar disorder, or substance misuse — shouldn’t fully explain what’s going on. And finally, the person needs to want to try medication after discussing the risks and benefits.

Guidelines such as NICE and the European consensus explicitly state that, in adults, medication is the main evidence-based treatment for core ADHD symptoms, offered alongside education and support.

Which medications should we use, and how effective are they?

There are two main classes.

First, stimulants, such as methylphenidate in various modified-release forms, and amphetamine formulations like lisdexamfetamine.

Second, non-stimulants, including atomoxetine, guanfacine—which has more evidence in children and adolescents—and others like bupropion, clonidine, and viloxazine, though adult data for these are more limited.

A landmark meta-analysis of randomised trials found that, in adults, amphetamines produced the largest improvements in clinician-rated symptoms. They were at least as well tolerated as methylphenidate, and more effective than atomoxetine and modafinil.

A recent BMJ umbrella review, which examined multiple meta-analyses, concluded that in the short term—up to about twelve weeks—both stimulants and some non-stimulants produce medium to large reductions in symptoms. Evidence beyond one year is more limited, but it does not suggest a loss of effect.

The World Federation of ADHD consensus summarises this by stating that ADHD medication is clearly effective for reducing symptoms, and that stimulants are more effective than non-stimulants.

Are there any long-term benefits of regular medication use?

Well, in terms of symptom control, longitudinal studies and reviews show that continued medication is associated with sustained improvements in symptoms and functioning in both children and adults, as well as improvements in overall life satisfaction.

Furthermore, there is also evidence for broader life outcomes. The World Federation of ADHD consensus concluded that drug treatment is linked to substantial reductions in a range of adverse outcomes, including transport accidents, substance misuse and cigarette smoking, educational underachievement, depression and suicide attempts, and even criminal behaviour and teenage pregnancy.

Taken together, this suggests that for many patients, long-term use of ADHD medication does more than just reduce symptoms. It appears to lower the risk of serious negative life events and improve quality of life.

And now, let’s touch briefly on non-drug treatments.

For children and adolescents, guidelines emphasise psychoeducation and parent-training programmes, school-based interventions, and behavioural approaches such as reward systems and structured routines.

For adults, the main non-drug options include psychoeducation about ADHD, CBT tailored to ADHD, that is, focusing on time management, planning, and emotional regulation, and finally, coaching and skills training, along with workplace or academic adaptations.

So how effective are these approaches? A systematic review of non-pharmacological interventions in adults found that particularly CBT and skills training produce small to moderate improvements in symptoms and functioning.

However, the World Federation consensus is quite blunt: non-medication treatments are generally less effective than medication for core ADHD symptoms, although they remain very useful for addressing residual difficulties once medication has been optimised.

Now that we know the benefits of treatment, what are the possible side effects, and how do we monitor treatment?

Common side effects of both stimulants and atomoxetine include reduced appetite and weight loss, sleep disturbances, mild increases in heart rate and blood pressure, headache, dry mouth, gastrointestinal symptoms, and occasionally irritability or mood lability.

There are also possible psychiatric adverse effects. Rarely, stimulants and atomoxetine can precipitate anxiety, irritability, mood elevation, or even psychotic symptoms, particularly in vulnerable people or at higher doses. To reduce this risk, guidelines recommend careful monitoring, dose adjustments, and stopping the medication if significant symptoms appear.

Overall, the World Federation consensus concludes that “the adverse effects of medications for ADHD are generally mild and can be addressed by changing the dose or the medication,” while the consequences of untreated ADHD are often serious and long-lasting.

In terms of cardiovascular safety, for most people without pre-existing heart disease, stimulants and atomoxetine cause only small increases in blood pressure and heart rate, and serious cardiovascular events are rare.

So what does this mean in practice? Guidelines recommend taking a brief cardiac and family history, checking blood pressure and pulse, and making sure there are no red flags before starting medication. If someone has a known heart condition, or if the assessment raises any concerns, then we should ger cardiology input before prescribing.

Regarding misuse, diversion, and dependency we need to be aware that stimulants have abuse potential, particularly in fast-acting formulations, which is why long-acting preparations and careful monitoring are recommended. However, the consensus statement notes that while stimulants can be diverted or misused, therapeutic doses in people with ADHD are actually associated with lower rates of later substance-use disorders, not higher.

In summary, for adults with significant ADHD, medication is the most effective treatment for core symptoms. When used long-term with proper monitoring, it’s associated not only with better concentration, but with lower rates of other serious negative outcomes. At the same time, side effects are common but usually mild and manageable.

So that is it, a review of ADHD treatment options.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/aDbEwtY3hw0

This video refers to a number of medical articles on ADHD published by a number of organisations (details below). Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by any of them.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I cover ADHD increasing incidence, especially in adults, always focusing on what is relevant in Primary Care only. The information is based on a number of published medical articles. The links to them are below.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The resources consulted can be found here:

1.   Shah P et al. “Potential impact of social media and COVID-19 restrictions on adult attention-deficit rates.” BJPsych Bulletin, 2025.

https://pubmed.ncbi.nlm.nih.gov/41208391/

2.   Adult Psychiatric Morbidity Survey 2023–24, Chapter 9: ADHD (NHS England, 2024).

https://digital.nhs.uk/data-and-information/publications/statistical/adult-psychiatric-morbidity-survey/survey-of-mental-health-and-wellbeing-england-2023-24/attention-deficit-hyperactivity-disorder?utm

3.   McKechnie DGJ et al., UK primary-care database study, 1998–2018 – summarised by NIHR as “Significant rise in ADHD diagnoses in the UK” (2023).

https://www.nihr.ac.uk/news/significant-rise-adhd-diagnoses-uk?utm

4.   Gimbach S et al. “ADHD medicine consumption in Europe after COVID-19.” Public Health / Pharmacoepidemiology, 2024.

https://pmc.ncbi.nlm.nih.gov/articles/PMC10854136/?utm

5.   Rzeszutek M et al. “Global Trends in ADHD Medication Use: Multiple Contexts and Populations.” Journal of Clinical Medicine, 2025.

https://www.mdpi.com/2077-0383/14/20/7338?utm

6.   Martin AF et al. “The changing prevalence of ADHD? A systematic review.” Journal of Affective Disorders, 2025.

https://www.sciencedirect.com/science/article/pii/S0165032725008638?utm

7.   Staley BS et al. “ADHD Diagnosis, Treatment, and Telehealth Use in Adults — United States, 2023.” MMWR (CDC), 2024.

https://www.cdc.gov/mmwr/volumes/73/wr/mm7340a1.htm?utm

8.   Butt DA et al. “Prevalence and Incidence Trends of Attention Deficit Hyperactivity Disorder in Canada.” Canadian Journal of Psychiatry, 2024.

https://journals.sagepub.com/doi/10.1177/07067437231213553?utm

9.   Therapeutics Initiative. “ADHD in adults.” Bulletin 144, 2023.

https://www.ti.ubc.ca/2023/09/29/144-adhd-adults/?utm

10. Bradlow RCJ et al. “Adult attention deficit hyperactivity disorder in Australia: how its current commercial model for diagnosis and treatment is encouraging misdiagnosis.” Medical Journal of Australia, 2025.

https://www.mja.com.au/journal/2025/223/8/adult-attention-deficit-hyperactivity-disorder-australia-how-its-current?utm

11. Woon LSC et al. “Online interest in ADHD predicts ADHD medication prescriptions in Australia from 2004 to 2023: a time-series analysis revealing COVID-19-related acceleration.” (2025).

https://pmc.ncbi.nlm.nih.gov/articles/PMC12138142/?utm

12. May T et al. “The Australian evidence-based clinical practice guideline for ADHD.” Australian Journal of General Practice / Australian guidelines consortium, 2023.

https://pmc.ncbi.nlm.nih.gov/articles/PMC10363932/?utm

13. Cortese S et al. “Attention-deficit/hyperactivity disorder (ADHD) in adults.” World Psychiatry / World Psychiatric Association, 2025. PMC+2Wiley Online Library+2

https://pmc.ncbi.nlm.nih.gov/articles/PMC12434367/?utm

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I’m Fernando, a GP in the UK. Today we are going to talk about the increasing number of ADHD diagnoses, especially in adults, always focusing on what is relevant in Primary Care only.

I have based this episode on a number of published medical articles. The links to them are in the episode description.

Right, let’s jump into it.

And the first question to ask is: why are we covering this topic now?

You may be aware that in the UK, the government has recently announced a formal review into surging mental-health and neurodevelopmental diagnoses, including ADHD and autism. This has sparked media coverage and public debate: are we seeing a real increase in ADHD, or are normal struggles being unnecessarily medicalised?

In other words, is this an epidemic of overdiagnosis, or does the rise in cases simply reflect that we’re starting to catch up with reality?

So now, it’s more important than ever to look at what the research actually shows, especially around adult ADHD diagnoses. And although we in primary care are not directly responsible for the full diagnosis and treatment process, the way we assess and support these patients at their first point of contact can make a huge difference. It shapes how they experience their care, whether they feel understood, and whether they receive the guidance and support they need.

Let’s start by reminding ourselves that attention-deficit/hyperactivity disorder, or ADHD, is a neurodevelopmental condition that affects a person’s ability to regulate attention, manage impulses, and maintain consistent levels of activity.

In adults, ADHD often looks very different from the stereotype of a hyperactive child. Adults tend to present with chronic distractibility, difficulty organising tasks, emotional impulsivity, forgetfulness, restlessness, and problems sustaining attention at work or in relationships. These symptoms can have real-world consequences, including difficulties with work and relationships, financial problems, and a persistent sense of underachievement.

The consensus is that ADHD is highly heritable and is associated with higher rates of anxiety, depression, and substance misuse. It’s also linked to measurable differences in executive brain function. And by this, we mean that the prefrontal cortex — the area responsible for focus, planning, impulse control, and emotional regulation — works differently in people with ADHD. Brain-imaging studies have repeatedly shown altered activity in this area.

So what this really means is that ADHD symptoms aren’t just behavioural. They reflect real differences in brain function.

Importantly, ADHD is not a condition people usually “grow out of.” For around two-thirds of children with ADHD, symptoms continue into adulthood, although sometimes in a more subtle or internalised form.

So, why are adult ADHD diagnoses increasing?

Research shows that adult ADHD is now better recognised. Historically, many adults — especially women — were simply missed in childhood because their symptoms were less disruptive, or because diagnostic criteria were focused on school performance rather than adult functioning.

A recent study from the UK found that adult referrals for ADHD assessment increased threefold between 2019 and 2023, with peaks during and after the COVID-19 pandemic. This is likely because the pandemic disrupted daily routines and removed coping structures, making previously manageable symptoms more difficult, and prompting more adults to seek help.

As diagnoses have increased, some people — including medical professionals — have expressed concerns that the condition might be overdiagnosed. After all, clinicians have always been wary of patients self-diagnosing, and the fact that some ADHD assessments rely on self-reported symptoms can create doubts for those who aren’t familiar with how structured and evidence-based these assessments actually are.

The numbers are stark. A large 20-year UK primary-care cohort study found that recorded ADHD diagnoses increased roughly twenty-fold, while ADHD medication prescribing rose fifty-fold. Some of the biggest proportional increases were seen in adults, particularly men aged 18 to 29.

Is this surprising? Not necessarily. ADHD is more common than many people realise. Multiple published reviews estimate the prevalence in children and adolescents to be between two and eight percent, and a major 2023 re-analysis placed it at 5.41 percent.

However, many studies showing steep increases in diagnosis have still reported prevalence rates well below this expected five percent.

Additionally, the most recent Adult Psychiatric Morbidity Survey shows that in England, although 13.9 percent of adults screened positive for probable ADHD, only 1.8 percent reported receiving a formal diagnosis. That suggests that many adults with ADHD still remain unidentified.

So, while there may be some isolated overdiagnosis, overall, the evidence suggests that ADHD remains underdiagnosed — particularly in adults.

What about internationally? Have there been similar rises across other Western countries?

The short answer is yes. Across Europe and other high-income countries, studies consistently show that ADHD medication use among adults has grown sharply, often by several hundred percent over the last decade, with a particularly striking rise in adult women. And a recent analysis in the United States showed that six percent of adults report a current ADHD diagnosis, and importantly, about half of them were first diagnosed in adulthood.

This increase in diagnosis, which may simply reflect that we are catching up with the reality of neurodivergence. Factors contributing to this better recognition include:

• greater understanding that ADHD persists into adulthood,

• the use of more adult-appropriate diagnostic criteria, and

• higher public awareness with reduced stigma.

What does an ADHD diagnosis actually mean for patients?

For many adults, receiving a diagnosis finally helps them make sense of lifelong challenges. And research consistently shows that after diagnosis, people often experience:

• improved self-esteem,

• better workplace functioning,

• more stable relationships, and

• a reduced risk of comorbid anxiety and depression.

It also gives them the opportunity to seek treatment. Treatment for ADHD is multimodal and includes:

• education and coaching,

• CBT,

• lifestyle structuring,

• and, when appropriate, medication — which remains one of the most effective interventions for ADHD symptoms in adults.

And by the way, if you want to learn more about ADHD treatment options, stay tuned — a full video on ADHD treatment is coming soon.

So that is it, a review of the increased number of ADHD diagnoses.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/dZpq3W-lkSQ

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through new and updated recommendations published in November 2025 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The Full NICE News bulletin for November 2025 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2025-11-01&to=2025-11-30&ndt=Guidance&ndt=Quality+standard

The new guideline on suspected sepsis in people aged 16 or over can be found here:

·      https://www.nice.org.uk/guidance/ng253

The new guideline on suspected sepsis in under 16s can be found here:

·      https://www.nice.org.uk/guidance/ng254

The new guideline on suspected sepsis in pregnant or recently pregnant people can be found here:

·      https://www.nice.org.uk/guidance/ng255

The visual summary for suspected sepsis: evaluation and management, all ages, settings and population groups can be found here:

·      https://www.nice.org.uk/guidance/ng253/resources/suspected-sepsis-managing-and-evaluating-risk-all-settings-pdf-15494830813

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we’ll look at the NICE updates published in November 2025, focusing on what is relevant in Primary Care only.

And this time we have three brand-new guidelines on a single topic: Sepsis. There are three separate guidelines because each one focuses on a different group: people aged 16 and over, children and young people under 16, and those who are pregnant or recently pregnant.

Right, let’s jump into it.

And we will start by saying that we will focus on the recommendations for people over 16 but I’ll also point out what’s different for the under-16 group and for pregnant people.

If infection is suspected, the first question to ask ourselves is: Could this be sepsis? And then assess for a potential source, for risk factors, and for any signs of clinical concern in circulation, breathing, or behaviour, ideally using a structured system.

The main 6 observations that we should assess are: temperature, heart rate, respiratory rate, blood pressure, level of consciousness and oxygen saturation. However, we need to remember that some groups of people with sepsis may not develop a raised temperature and that, in terms of oximetry, poor peripheral circulation due to shock can make peripheral oxygen saturation difficult to measure. Additionally, we need to be aware that some pulse oximeters can underestimate or overestimate readings, especially if the level is borderline and that overestimation has been reported in people with dark skin.

Additionally, we should examine for:

• mottled or ashen appearance
• cyanosis
• skin rashes, particularly non-blanching petechial or purpuric rashes
• and any breach of skin integrity as the source of infection

We should always keep in mind groups who are more vulnerable: people over 75, those with frailty or co-morbidities, learning disabilities, immunosuppression, indwelling lines or catheters, recent surgery or invasive procedures, and those with adverse social or economic factors that may delay presentation.

In hospital or ambulances, the National Early Warning Score 2, or NEWS2, is recommended. NEWS2 measures the same six values, temperature, heart rate, respiratory rate, blood pressure, level of consciousness and oxygen saturation.  and then assigns points based on how abnormal they are. I will not go through every score and its clinical implications but there is NEWS2 calculator app reproduced from the Royal College of Physicians that I would really recommend downloading.

However, in primary care we can consider NEWS2 or any other structured observation tool. The guideline gives us a set of criteria to assess the risk of severe illness. There are high risk and moderate risk criteria. The high-risk criteria for people over 16 are as follows:

·      A new altered mental state

·      A respiratory rate of 25 breaths per minute or more

·      New need for oxygen to maintain saturation more than 92% (or more than 88% in chronic hypercapnic respiratory failure)

·      A Systolic BP of 90 mmHg or less or more than 40mmHg below normal

·      A heart rate of more than 130 beats per minute

·      Not passed urine in previous 18 hours, or for catheterised patients, passed less than 0.5 ml/kg of urine per hour

·      Mottled or ashen appearance

·      Cyanosis and

·      A non-blanching petechial or purpuric rash

These are the high-risk criteria only. For simplicity, I will not go through all the moderate risk criteria, but they are similar to the high-risk ones but with values slightly less abnormal.

Once sepsis is suspected, for primary care, the key point is to arrange rapid referral or admission to hospital. In remote or rural areas where transfer exceeds one hour, the guideline states that systems should exist so GPs can give the first dose of antibiotics when high-risk criteria are met.

For borderline or uncertain cases, we should provide clear safety-netting, and ensure patients and carers understand warning symptoms and when to seek help.

Let’s quickly touch on sepsis in children.

Risk stratification for children is a lot more complex and is based on age bands — under 5, 5 to 11, and 12 to 15 — each with its own physiological thresholds. Because of the complexity, I will not go through all the high-risk criteria here, but we need to remember that severity is judged not just on vital signs, but on age-appropriate risk criteria combined with history, examination and clinical judgement.

Adult early-warning scores such as NEWS2 should not be applied to children.

If a child meets any high-risk criterion, they require urgent admission to hospital.

For lower-risk children, we must still decide between safe management in the community with safety-netting or urgent admission if concerns arise. For this, communication must be tailored to the child and their carers, with clear explanations as to what to do if the situation does not improve.

Let’s now move to people who are pregnant, or within six weeks postpartum. They fall under a separate guideline because pregnancy changes physiology and the pattern of infection.

For pregnant or recently pregnant people, NEWS2 is not appropriate either. Instead, we should use a pregnancy-specific risk table with high-risk, moderate-to-high-risk, and low-risk criteria.

These criteria include the usual physiological markers but they use pregnancy-specific thresholds and they also emphasise obstetric sources of infection, such as endometritis, wound infections, urinary infection, retained products, and mastitis.

Again, I will not go through all the criteria here but NICE has produced a visual summary of the risk criteria for all groups. The link to it is in the episode description.

Going back to the assessment of suspected sepsis for people that are pregnant or recently pregnant, if any high-risk criterion is present, emergency admission will be required.

For us in primary care, the key points are that pregnancy or up to six weeks postpartum automatically places the patient in a higher-risk group, we must use pregnancy-specific criteria rather than adult scores, the threshold for calling an ambulance and pre-alerting services is lower, and finally, we should always think of obstetric sources of infection alongside the usual ones.

So that is it, a review of the NICE updates relevant to primary care.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/rIX46swVSfg

This episode refers to guidelines on the management of abnormal liver function tests by the British Society of Gastroenterology and a number of NHS organisations in the UK. Here I focus on the hepatitic pattern of abnormal LFTs. Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by them.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I review the interpretation, initial follow up management, of adults presenting with a hepatitic pattern in their LFT’s, always focusing on what is relevant in Primary Care only.

This episode is based on the British Society of Gastroenterology guidelines on LFTs. A link to it is in the episode description..

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

My summary guide can be downloaded here:

·      https://1drv.ms/b/s!AiVFJ_Uoigq0mQ8MRxaNYnA1_pzh?e=H2U7rS

The resources consulted can be found here:

BSG- British Society of Gastroenterology:

·      bsg.org.uk/clinical-resource/guidelines-on-abnormal-liver-blood-tests

·      Guidelines on the management of abnormal liver blood tests (bsg.org.uk)

o  First published on:

o  BMJ article:

o  Guidelines on the management of abnormal liver blood tests | Gut (bmj.com)

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I’m Fernando, a GP in the UK. Today we are going to go through the interpretation, initial follow up management, of adults presenting with a hepatitic pattern in their LFT’s, always focusing on what is relevant in Primary Care only.

This episode is based on the British Society of Gastroenterology guidelines on LFTs. A link to it is in the episode description.

Right, let’s jump into it.

We have to start by remembering that liver disease develops silently and at earlier stages liver enzymes may be normal, and, if they are high, the degree of abnormality is not necessarily related to the severity of the underlying condition.

We also need to remember that AST and ALT are enzymes present in the liver cells and the levels increase in response to cell injury or death. ALT is considered more liver-specific while AST is also present in skeletal, cardiac and smooth muscle and so may be elevated in patients with an MI or myositis.

An AST:ALT ratio of >1 is a non-invasive marker of liver fibrosis. In early liver disease, AST and ALT can be normal, but the high AST:ALT ratio is usually present even if both values are normal.

So, what should we do when confronted by abnormal LFTs?

First of all, we should not think that the extent of abnormality of the LFTs correlates necessarily with the severity of the problem. Common conditions leading to chronic liver disease like NAFLD, and hepatitis C are frequently associated with only mild or moderate LFT abnormalities.

Also, we should not think that the duration of the abnormal LFTs is a reflection of clinical significance, so repeating the LFTs hoping that they will improve is not necessarily the way to go. We need to remember that in many chronic liver diseases such as hepatitis C and NAFLD, the LFTs returning to normal do not necessarily imply the resolution of the disease.

Therefore, the recommendation is that most patients with abnormal LFTs should have a full liver screen irrespective of level and duration of the abnormality.

What is a full liver screen?

This should include an USS, hepatitis B and C screening, an autoantibody screen, serum immunoglobulins, both ferritin and transferrin saturation and, often, a coeliac screen, alpha-1-antitrypsin levels and caeruloplasmin.

And finally, let’s remember that there are three common patterns of abnormal LFTs:

1. An Isolated raised bilirubin with otherwise normal liver tests
2. A Cholestatic pattern: normally showing a high ALP and GGT
3. A Hepatitic pattern: with a raised ALT and AST indicating hepatocellular injury, like, for example, viral hepatitis, NAFLD, and ARLD. The hepatitis pattern is the section that we will concentrate on today.

The three most common causes of liver disease are alcohol-related liver disease, non-alcoholic fatty liver disease and viral hepatitis.

How do we manage these patients?

First of all, if there are signs of synthetic liver failure like unexplained clinical jaundice, a low albumin or a high INR or if there is suspicion of malignancy, for example because of weight loss or marked cholestasis, we should urgently refer or admit the patient.

If the patient has a hepatitic picture with a high ALT and AST, the management will depend on the level of liver fibrosis, which we can estimate using non-invasive fibrosis markers.

The majority of patients presenting with a hepatitic pattern will have either NAFLD or ARLD.

So let’s start with NAFLD.

Following a liver USS, for patients with NAFLD or liver disease of unknown cause, we will estimate the risk of fibrosis using the FIB4 or NAFLD fibrosis score. These scores have cut off points for low, intermediate and high risk of fibrosis.

If there is a low risk of advanced fibrosis, we will just manage the risk factors in Primary Care and reassess periodically, generally every 2 to 5 years. In primary care, the treatment for NAFLD is weight loss, alcohol advice, the reduction of cardiovascular risk and the management of co-morbidities.

If the risk of fibrosis is intermediate, these patients should have second-line tests such as an enhanced liver fibrosis blood test, also known as an ELF test, or imaging such as a FibroScan or elastography.

However, patients with very high scores representing a high risk of fibrosis, should be referred to hepatology without waiting to do an ELF test, Fibroscan or elastography.

Let’s now look at ARLD. For patients with ARLD we will assess their alcohol intake, using the AUDIT C or the full AUDIT questionnaire if necessary. Depending on the severity of the alcohol intake, we will give them a brief intervention, refer them to alcohol services or to hepatology for further investigations.

The treatment of ARLD is to stop drinking harmfully, and for many this usually means complete abstinence. Weight loss sometimes also helps because there is a synergy between alcohol and obesity. For example, when the BMI is >35, the risk of liver disease doubles for any given alcohol intake.

But, finally, what should we do if the patient has a hepatitic pattern with a high ALT and AST without an obvious cause, that is, when the liver screen is normal and there is no evidence of NAFLD on USS or excess alcohol?

In those cases, we will need to re-examine the history to exclude potential drug-induced causes. Also, ultrasound is only sensitive for steatosis when hepatocytes are more than 30% steatotic so patients with milder steatosis might have a normal USS. So, if these patients are obese or have metabolic risk factors and we suspect that they may still have NAFLD despite the normal USS, we should assess them in accordance with the NAFLD pathway.

But at the end of the day, if AST or ALT remain high without an obvious cause, we will need to refer them to secondary care for further investigations.

So that is it, a review of abnormal LFTs with a hepatitic pattern.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/goK_Q4P2qpk

This video refers to guidelines produced by a number of organisations (details below). Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by any of them.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I neutropenia always focusing on what is relevant in Primary Care only. The information is based on Haematological guidance by Camden CCG, Manchester Foundation Trust and King’s Health Partners.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

My summary of the guidance consulted can be found here:

·      https://1drv.ms/b/s!AiVFJ_Uoigq0mQ4ZjYGRH1wkGBdc?e=Zuxx84

The resources consulted can be found here:

·      Camden CCG guidance: 1456246258-2f3891e610beaa6533f2c0ad7866e776.pdf(Review) - Adobe cloud storage

·      Manchester Adult anaemia guide: https://acrobat.adobe.com/id/urn:aaid:sc:EU:f96fe528-0a47-457c-b29a-a7efb87221e0

·      Manchester Haematology GP guide: https://mft.nhs.uk/app/uploads/2021/02/MFT-Haematology-GP-Pathway-Guide-v4-11.2.21.pdf

·      King’s Health Partners: https://www.kingshealthpartners.org/assets/000/002/294/KCH_-_king_s_health_partners_-_quick_guide_to_haematology_original.pdf

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I’m Fernando, a GP in the UK. Today we are going to cover neutropenia, including initial assessment, follow up and management, always focusing on what is relevant in Primary Care only.

I have based this episode on Haematological guidance by Camden CCG, Manchester Foundation Trust and King’s Health Partners. The links to them are in the episode description.

Right, let’s jump into it.

Neutrophils are the most numerous subtype of white blood cell and they are the body’s first responders to bacterial infections.

Neutropenia is when the neutrophil count is low. A normal neutrophil count in adults ranges from 2.0 to 7.5. However, an isolated low neutrophil count is extremely common in clinical practice. A result between 1.5 and 2.0 × 10⁹/l, while technically below the normal reference range, is rarely clinically significant. Many healthy people fluctuate in this borderline range due to factors such as minor viral infections, recent exercise, or simply natural day-to-day variation in blood counts.

We also have to remember that normal ranges differ across populations. People of Afro-Caribbean or Middle Eastern heritage often have a normal baseline neutrophil count between 1.0 and 1.8 × 10⁹/l. This is known as constitutional or ethnic neutropenia, which is of no clinical consequence. It is a benign, lifelong finding and does not increase susceptibility to infection. For these patients, referral is usually only needed if the neutrophil count falls below 1.0 × 10⁹/l on repeat testing.

For everybody else and for the purpose of this episode, we will define neutropenia as a neutrophil count below 1.5.

Possible causes of neutropenia are as follows:

• first we have drugs: such as phenytoin, carbimazole, antipsychotics, and co-trimoxazole, which can suppress neutrophil production in the bone marrow or trigger immune-mediated neutrophil destruction. Some drugs are directly toxic to the bone marrow, while others induce antibody formation against neutrophils.

• then we have Malignancy: including conditions like myeloma or any cancer that infiltrates the bone marrow. This reduces the marrow’s ability to produce neutrophils. Additionally, chemotherapy and radiotherapy further compound this by damaging rapidly dividing cells, leading to predictable and sometimes profound neutropenia.

• Also Vitamin B12 and folate deficiency: which impair DNA synthesis. Because neutrophils and their precursors divide rapidly, they are particularly sensitive to this.

• then we have Iron deficiency: which reduces the efficiency of haematopoiesis in general. Although iron deficiency is normally associated with anaemia, iron is also required for normal development of all blood cell lines, including neutrophils. Severe or prolonged deficiency can therefore lead to mild neutropenia.

•Another cause ca be Autoimmune diseases: which can cause neutropenia through immune-mediated destruction by autoantibodies that target neutrophils or their precursors.

• then we have viral infections: including EBV, HIV, and hepatitis B and C, which can directly suppress bone marrow activity or cause redistribution of neutrophils from the bloodstream into tissues. Many other viruses also transiently inhibit neutrophil production during acute illness, making mild neutropenia very common.

• Also, another possible cause is excess alcohol: which is toxic to the bone marrow and can impair the proliferation and differentiation of myeloid precursors. Chronic alcohol use is also associated with nutritional deficiencies, particularly folate, compounding the effect on marrow function.

• then we have Liver disease and cirrhosis: which can lead to neutropenia through hypersplenism causing increased sequestration and destruction of blood cells in the spleen. Another mechanism is metabolic effect of cirrhosis on overall bone marrow function. And finally, as we have already explained there is:

• Ethnic variation: like constitutional or ethnic neutropenia in people of Afro-Caribbean and Middle Eastern descent. Again, this is a benign inherited pattern without any impairment in immune function.

How should we manage these patients? We should send the patient to hospital as an emergency if:

• There is any evidence of sepsis, because neutropenic patients are at high risk of overwhelming infection. This means they can deteriorate rapidly, often without the typical signs of infection.

• Additionally, we should also send the patient to hospital as an emergency if the neutrophil count is below 1.0 × 10⁹/l and any of the following factors are present:

– First, if the patient is on chemotherapy.

This is because chemotherapy-induced neutropenia can progress quickly, and these patients are at particularly high risk. In this setting, infection can become severe within hours leading to sepsis.

– Also, if there is lymphadenopathy because enlarged lymph nodes raise concern for an underlying haematological malignancy, such as lymphoma or leukaemia, or for a significant viral infection causing significant bone marrow involvement.

– Also if there is splenomegaly because an enlarged spleen suggests increased sequestration and destruction of blood cells, or infiltration by malignancy or infection. Splenomegaly with neutropenia can be suggestive of serious conditions such as myeloproliferative disorders, autoimmune cytopenias, or advanced liver disease with hypersplenism.

– And finally, we should also send the patient to hospital as an emergency if the neutrophil count is below 1.0 × 10⁹/l if there are other cytopenias.

For example, if anaemia or thrombocytopenia is also present, this points toward a significant bone marrow problem which increases the risk of complications.

We should make an urgent haematological referral on a cancer pathway if:

• The neutrophil count is below 0.5 × 10⁹/l and the patient is otherwise well.

This is because a neutrophil count this low is concerning even in the absence of symptoms. Counts below 0.5 significantly increase the risk of serious infection, and they also raise the possibility of an underlying bone marrow disorder. Conditions such as acute leukaemia, myelodysplastic syndromes, or bone marrow infiltration can initially present with isolated severe neutropenia before other clinical signs appear.

If the neutrophil count is above 0.5 × 10⁹/l and the patient is clinically well, we can safely take a stepwise approach. The first action is to repeat the blood test within one week, as many cases of mild neutropenia are transient. At the same time, and as part of the initial work-up, which other investigations should we request?

We should investigate the underlying cause by organising the following tests:

• As already mentioned, a repeat full blood count.

This in order to confirm whether the neutropenia is sustained and to check for other full blood count abnormalities.

• A blood film: which can identify abnormal cell morphology, immature cells, or blasts suggestive of bone marrow disease. It can also help detect features consistent with infection, nutritional deficiency, or autoimmune processes.

• Vitamin B12 and folate: because as we said earlier, deficiency can lead to ineffective neutrophil production.

• Ferritin and iron studies: given that iron deficiency not only causes anaemia, but can also reduce neutrophil production.

• Autoimmune screen because some autoimmune conditions can cause immune-mediated destruction of neutrophils or affect bone marrow function.

• HIV testing: because HIV can lead to neutropenia through direct bone marrow suppression, chronic immune activation, or associated infections. In these cases, HIV treatment can reverse the neutropenia and improve overall immunity.

• and finally, we should also request Hepatitis B and C serology: given that chronic viral hepatitis can impair bone marrow function and is also associated with splenomegaly, hypersplenism, and autoimmune cytopenias.

After we have done these tests, if the patient is well and the cause of the neutropenia remains unknown, our next steps will depend on the degree and persistence of the low neutrophil count.

Firstly, if the neutrophil count remains below 1.0 × 10⁹/l we will refer urgently to outpatient haematology. This is because even in the absence of symptoms, this level carries a meaningful risk of infection and warrants specialist assessment.

If the neutrophil count is between 1.0 and 1.5 × 10⁹/l, we will monitor the full blood count for 4–6 weeks. This is because many cases in this borderline range are temporary, and monitoring over several weeks helps determine whether the neutropenia is improving, stable, or worsening.

Then we will refer to haematology routinely if any of the following occur:

– First, if the neutrophil count remains below 1.5 × 10⁹/l

(or below 1.0 × 10⁹/l in African-Caribbean patients, due to constitutional neutropenia). This is to rule out the possibility of a chronic underlying cause.

– Also if there are other full blood count abnormalities suggesting that more than one blood cell line may be affected, raising concern for broader marrow pathology.

– and finally, if there is a history of infections or ulcers. This is because recurrent infections, mouth ulcers, or delayed healing are clinical signs that the neutropenia may be functionally significant, even if the absolute count is only mildly reduced. These symptoms suggest impaired neutrophil activity or insufficient neutrophil reserves, and they strengthen the case for specialist review.

So that is it, a review of the initial assessment and management of neutropenia.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/IzuigE4BNVM

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through new and updated recommendations published in October 2025 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The Full NICE News bulletin for October 2025 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2025-10-01&to=2025-10-31&ndt=Guidance&ndt=Quality+standard

The updated Quality standard on head injury [QS74] can be found here:

·      https://www.nice.org.uk/guidance/qs74

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we’ll look at the NICE updates published in October 2025, focusing on what is relevant in Primary Care only.

And this time there hasn’t been an awful lot that is relevant to Primary care, only an update to the quality standard on head injury.  

Right, let’s jump into it.

The updated quality standard on head injury covers the assessment, management and rehabilitation after a head injury. While much of it applies to secondary care, there are important areas where we play an important role in general practice

This updated quality standard focuses on the NICE guideline on head injury and rehabilitation for chronic neurological disorders.

For GPs, the main message is on recognition and referral. When a patient presents after a head injury, the standard reinforces the importance of same-day assessment and appropriate referral for imaging. The thresholds for CT scans are unchanged, but we should ensure rapid referral if the criteria are met.

But what exactly are these referral criteria? Let’s have a look at them.

The criteria can be divided between emergency referrals and urgent referrals, depending on whether imaging should be done within 1 hour or within 8 hours.

Let’s look at the emergency referral criteria first. They may appear fairly obvious but it is still worthwhile going through them:

• For those aged 16 and over, we need to do a CT head scan within 1 hour if any of the following risk factors are present:
• a Glasgow Coma Scale (GCS) score of 12 or less on initial assessment
• a GCS score of less than 15 at 2 hours after injury
• a suspected skull fracture
• A post-traumatic seizure
• a focal neurological deficit
• more than one episode of vomiting and
• any worrying signs of a basal skull fracture such as haemotympanum, “panda” eyes, cerebrospinal fluid leakage from the ear or nose and bruising over the mastoid process, also known as Battle’s sign
• For children under 16, in addition to what has already been mentioned, we also need to do a CT scan of the head within 1 hour if any of the following apply:
• a suspicion of non-accidental injury
• GCS < 14 or < 15 for babies on initial assessment
• GCS < 15 at 2 h
• a tense fontanelle and
• for babies under 1 year also a head swelling or laceration > 5 cm
• Additionally, a CT should be done within 1 hour if children have more than one of the following risk factors:
• witnessed loss of consciousness >5 minutes
• abnormal drowsiness
• 3 or more episodes of vomiting
• dangerous mechanism of injury
• amnesia >5 minutes and
• any bleeding disorder

Now, let’s look at the urgent referral criteria, that is, when a CT head scan should be done within 8 hours:

• For adults we will do a CT head scan within 8 hours of the head injury, or within one hour if they present more than 8 hours after the injury, if they have had loss of consciousness or amnesia and they also have any of the following factors:
• age 65 or over
• any bleeding or clotting disorder (including anticoagulants) and
• a dangerous mechanism of injury, for example, a pedestrian/cyclist being hit by car, a fall from >1 m or >5 stairs, or more than 30 minutes’ retrograde amnesia before the injury
• Additionally, even if there is no other indication, we should consider a CT head scan within 8 hours of injury (or within 1 hour if presenting >8 hours after injury) for anyone on anticoagulant treatment. This includes warfarin, DOACs, heparin, and antiplatelet treatment excluding aspirin monotherapy

In practice this means that if a patient comes with head trauma, we will need to identify if any of these thresholds are met and refer them appropriately via A&E for imaging. Our role is not to decide whether a CT is indicated or not, but to pick up risk factors, and expedite referral.

Now, going back to the quality statements, the rest of them simply emphasise the role of rehabilitation. In this respect in Primary Care, we should ensure that referral to community neuro-rehabilitation or therapy services happens in a timely fashion and that rehabilitation plans, and shared care arrangements are in place.

In summary: the update doesn’t change the imaging thresholds but for us, it emphasises follow-up, rehabilitation, and long-term management after a head injury.

So that is it, a review of the NICE updates relevant to primary care.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/30qLbVnKHW8

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I give a brief overview of the mechanism of action of sacubitril valsartan for heart failure.

The NICE guidance on Chronic Heart Failure is covered in these episodes:

Part 1- Diagnosis: https://youtu.be/hjKE4JAQM6c

Part 2 – Drug management: https://youtu.be/UGD7-osSlv0

Part 3 – Additional management: https://youtu.be/i0L-Nv4bJzs

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The NICE guideline on Chronic heart failure in adults: diagnosis and management [NG106] can be found here: 

·      https://www.nice.org.uk/guidance/ng106

Additional information on ARNIs can be found here:

·      https://www.ncbi.nlm.nih.gov/books/NBK507904/#:~:text=Mechanism%20of%20Action,-The%20pathophysiology%20of&text=Valsartan%20is%20an%20angiotensin%20receptor,neprilysin%20will%20accumulate%20angiotensin%20II

Transcript

Hello and welcome! I’m Fernando, a GP in the UK.

What are Angiotensin receptor–neprilysin inhibitors? They are a relatively new class of medications used specifically in the management of heart failure with reduced ejection fraction. At present, the only available one is sacubitril/valsartan.

If you are interested in learning how Sacubitril/valsartan works, here is some background information.

The first thing to understand is that the pathophysiology of heart failure involves an abnormal activation of the renin-angiotensin-aldosterone system (RAAS). This leads to vasoconstriction, hypertension, increased aldosterone levels, increased sympathetic tone, and eventually, cardiac remodelling, all of which worsen the disease over time. ACEIs or ARBs play a major role in reducing HF morbidity and mortality by blocking this abnormal activation

At the same time that the renin-angiotensin-aldosterone system is activated, the natriuretic peptide system is also activated, hence the elevated BNP and NT-pro BNP seen in heart failure. This compensatory mechanism leads to vasodilation, natriuresis, and diuresis. As a result, the natriuretic peptide system decreases blood pressure, lowers the sympathetic tone, and reduces aldosterone levels. The natriuretic peptide system functions antagonistically to the renin-angiotensin-aldosterone system and has favourable impact on heart failure. Natriuretic peptides are broken down by an enzyme called neprilysin.

Sacubitril/valsartan is a combination product. Sacubitril is a pro-drug that, upon activation, acts as a neprilysin inhibitor. So, it works by blocking the action of neprilysin, thus preventing the breakdown of natriuretic peptides, which leads to a prolonged duration of the favourable effects of these peptides.

However, because neprilysin also breaks down angiotensin II, inhibiting neprilysin will accumulate angiotensin II. For this reason, a neprilysin inhibitor cannot be used alone; it must always be combined with an ARB to block the effect of the excess angiotensin II. This is why Valsartan is used.

Another important substance broken down by neprilysin is bradykinin; neprilysin inhibition will also cause a build-up of bradykinin. Therefore, sacubitril cannot be used with an ACEI due to an increased risk of angioedema if both these drugs are combines or given in a short timeframe. And this is why when switching between ACEI and sacubitril/valsartan, the patient must undergo a 36-hour washout period to lower the risk of angioedema.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/i0L-Nv4bJzs

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through the NICE guideline on Chronic heart failure in adults: diagnosis and management [NG106], last updated in September 2025. Today’s episode focuses on the additional management of heart failure.

In previous episodes we covered the initial assessment and diagnosis and the drug management of the different subtypes of heart failure.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The NICE guideline on Chronic heart failure in adults: diagnosis and management [NG106] can be found here:

·      https://www.nice.org.uk/guidance/ng106

Additional information on ARNIs can be found here:

·      https://www.ncbi.nlm.nih.gov/books/NBK507904/#:~:text=Mechanism%20of%20Action,-The%20pathophysiology%20of&text=Valsartan%20is%20an%20angiotensin%20receptor,neprilysin%20will%20accumulate%20angiotensin%20II

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we are going to go through the NICE guideline on Chronic heart failure, which was last updated in September 2025.

Today’s episode focuses on the additional management of heart failure.

If you haven’t already, I recommend that you check the previous episodes where we covered heart failure diagnosis and the drug management of the different subtypes of heart failure.

Right, let’s jump into it.

And as we have just said, today we’re going to focus on the additional management of heart failure.

Now let’s start by looking at how to initiate and monitor medication use.

When tailoring treatment, we should use the person’s medical history, frailty status, and prognosis to decide which specific medicine combinations to use and how to introduce them.

In primary care, we should seek the advice from a heart failure specialist before starting someone on an angiotensin receptor–neprilysin inhibitor, that is, sacubitril/ valsartan.

Before prescribing an ACE inhibitor, ARB, angiotensin receptor-neprilysin inhibitor (ARNI), or mineralocorticoid receptor antagonist, we will measure renal function and electrolytes.

Once these drugs have been started, we should measure renal function and electrolytes:

• one to two weeks after starting treatment,
• one to two weeks after each dose increment,
• every three to six months once the maximum tolerated dose has been established,
• and at any time renal function may be compromised.

If the serum creatinine increases by more than 50%, or potassium rises above 5.5 millimoles per litre, we will follow local guidelines.

We will measure blood pressure, or ask the person to measure it themselves, before and after each dose increment. For people with symptoms of postural hypotension, we will measure blood pressure according to the NICE hypertension guideline, which essentially recommends ideally checking the initial blood pressure in the supine position, and then again after standing for at least 1 minute, in order to check for a drop in systolic blood pressure of 20 mmHg or more. Although checking the BP in a seated position can also be acceptable, we need to remember that measuring blood pressures from sitting to standing may miss some cases of postural hypotension, especially in older or frail people, and that measuring from lying to standing is more accurate for detecting a significant postural drop.

When prescribing beta-blockers, we should not withhold treatment solely because of age, or the presence of peripheral vascular disease, erectile dysfunction, diabetes, interstitial pulmonary disease, or COPD.

We will assess heart rhythm, heart rate, and conduction abnormalities using a 12-lead ECG before deciding whether to prescribe a beta-blocker.

We will not offer a beta-blocker to people with second-degree or third-degree heart block who do not have a pacemaker, or to those with bradycardia, that is, a heart rate below 50 beats per minute.

We will assess heart rate and clinical status after each betablocker dose increment, and for people with symptoms and bradycardia, we will consider repeating a 12-lead ECG after each dose increment.

For digoxin, we will not routinely monitor serum digoxin concentrations. But we should be aware that a digoxin level measured within 8 to 12 hours of the last dose may help confirm toxicity or non-adherence, but we must interpret results in the clinical context, since toxicity may occur even when the concentration is within the therapeutic range.

Now, let us move on to clinical review.

We will monitor all people with heart failure and provide:

·      a clinical general assessment including cardiac rhythm

·      a medication review checking for any necessary changes or side effects,

·      An assessment of renal function, and

·      Measurement of iron status and haemoglobin.

This is just the very minimum, Additionally, we should provide more detailed monitoring for people with significant comorbidities, co-prescribed medications, or recent deterioration. The frequency of monitoring will depend on the clinical situation and the stability of the patient’s condition.

If the clinical condition or medication has changed, we should monitor the patient more frequently — from days to every two weeks. For stable people with proven heart failure, we will monitor at least every six months.

For people under 75 years old with heart failure with reduced ejection fraction and normal renal function — that is, an eGFR greater than 60— we can consider measuring NT-proBNP levels to monitor and optimise treatment.

Now let’s look at other treatments and advice relevant to all types of heart failure.

We will use diuretics to relieve congestive symptoms and fluid retention, and we will titrate the dose up or down as needed, always using the lowest effective dose.

Amiodarone, should be started under specialist supervision and we will review the need to continue it every six months, and at each review, we will check liver and thyroid function tests and assess for side effects.

For people with heart failure and atrial fibrillation, we will follow the NICE recommendations on anticoagulation for stroke prevention. For people in sinus rhythm, we will consider anticoagulation if there is a history of thromboembolism, left ventricular aneurysm, or intracardiac thrombus.

We should offer annual influenza vaccination and a one-time pneumococcal vaccination to all people with heart failure.

For people of childbearing potential, we should discuss contraception and pregnancy. If pregnancy is being contemplated or occurs, we will seek specialist advice from both cardiology and obstetrics.

We will not routinely advise people with heart failure to restrict sodium or fluid intake. However, we should ask about salt and fluid consumption and provide advice when necessary, for example, by restricting fluids for dilutional hyponatraemia or by reducing intake for those with high salt or fluid consumption. Additionally, we will advise people to avoid salt substitutes that contain potassium in order to minimise the risk of hyperkalaemia.

In terms of air travel, we can advise that it will be possible for most people, depending on their clinical condition at the time.

Regarding driving, we will simply follow DVLA guidelines.

We should offer people with heart failure a personalised, exercise-based cardiac rehabilitation programme which should include psychological and educational components.

Finally, in terms of palliative care, we should not offer long-term home oxygen therapy solely for advanced heart failure. However, we should be aware that long-term oxygen may be offered for comorbidities such as COPD.

If symptoms are worsening despite optimal specialist treatment, we will refer to palliative care in discussion with the heart failure multidisciplinary team

So that is it, a review of the additional management of heart failure.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/UGD7-osSlv0

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through the NICE guideline on Chronic heart failure in adults: diagnosis and management [NG106], last updated in September 2025. Today’s episode focuses on the drug management of the different subtypes of heart failure.

The guidance on the remaining aspects of heart failure management will be covered in other episodes. In the previous episode we covered the initial assessment and diagnosis.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The NICE guideline on Chronic heart failure in adults: diagnosis and management [NG106] can be found here:

·      https://www.nice.org.uk/guidance/ng106

Additional information on ARNIs can be found here:

·      https://www.ncbi.nlm.nih.gov/books/NBK507904/#:~:text=Mechanism%20of%20Action,-The%20pathophysiology%20of&text=Valsartan%20is%20an%20angiotensin%20receptor,neprilysin%20will%20accumulate%20angiotensin%20II

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we are going to go through the NICE guideline on Chronic heart failure in adults, which was last updated in September 2025.

Today’s episode focuses on the drug management of the different subtypes of heart failure.

If you haven’t already, I recommend that you check the previous episode on heart failure diagnosis.

The guidance on the remaining aspects of heart failure management will be covered in the next episode, so stay tuned.

Right, let’s jump into it.

And as we have just said, today we’re going to focus on the specific drug treatment for heart failure.

Also, as we said in the previous episode, echocardiograms assess both systolic and diastolic function of the left ventricle.

Categorising cardiac function is crucial because the treatment of heart failure will be different depending on the ejection fraction.

We classify heart failure as follows:

• Heart failure with reduced ejection fraction, when the ejection fraction is 40% or below.
• Heart failure with mildly reduced ejection fraction, when it is between 41 and 49%.
• And Heart failure with preserved ejection fraction, when it is 50% or higher.

So let’s have look at the treatment of each of these subtypes

For people with heart failure with reduced ejection fraction, we will offer a combination of four medicines:

·      an ACE inhibitor,

·      a beta-blocker,

·      a mineralocorticoid receptor antagonist, and

·      an SGLT-2 inhibitor.

For people who are on the maximum tolerated dose of each of these four medicines but continue to have symptoms of heart failure, we should consider switching the ACE inhibitor to an angiotensin receptor–neprilysin inhibitor.

What are Angiotensin receptor–neprilysin inhibitors? They are a relatively new class of medications used specifically in the management of heart failure with reduced ejection fraction. At present, the only available one is sacubitril/valsartan, which combines two mechanisms of action:

Sacubitril, which inhibits neprilysin — an enzyme that breaks down beneficial natriuretic peptides. By blocking neprilysin, sacubitril helps with vasodilation, sodium excretion, and reduced cardiac remodelling.

And then we have Valsartan, an angiotensin II receptor blocker (ARB), which helps counteract the harmful effects of the renin–angiotensin–aldosterone system by reducing vasoconstriction, sodium retention, and aldosterone secretion.

Together, the combination of sacubitril and valsartan improves cardiac function, reduces hospitalisations, and lowers mortality in patients with heart failure with reduced ejection fraction.

OK, let’s go back to the general management of heart failure with reduced ejection fraction.

And we need to note that if certain medicines are not tolerated, there are alternative treatment combinations that we should consider.

For example, for people who have had angioedema after taking an ACE inhibitor, we will still offer a beta-blocker, a mineralocorticoid receptor antagonist, and an SGLT2 inhibitor, and we should also consider an angiotensin receptor blocker, or ARB instead of the ACEI. This is because the risk of angioedema is lower with ARBs than with ACE inhibitors, although it is not zero so we should use caution and monitor the patient accordingly. An important safety add-on is that we should not use sacubitril/valsartan in anyone with a history of angioedema, as this is listed as a contraindication.

People with heart failure with reduced ejection fraction who have symptoms of intolerance to ACE inhibitors, other than angioedema, should have a beta-blocker, an MRA, an SGLT2 inhibitor and sacubitril/valsartan. The initiation of sacubitril valsartan should be guided by a heart failure specialist

Additionally, in people with heart failure with reduced ejection fraction, we should assess iron status and check for anaemia using:

·      transferrin saturation (TSAT),

·      serum ferritin, and

·      haemoglobin.

For people with heart failure with reduced ejection fraction and haemoglobin less than 150 grams per litre, and iron deficiency, that is, a TSAT less than 20% or serum ferritin less than 100, we should offer intravenous iron therapy. This is because trial evidence shows that IV iron improves symptoms and quality of life and reduces HF hospitalizations in several settings, especially in patients with symptomatic heart failure with reduced ejection fraction.

If iron deficiency anaemia is identified, we should not assume it is related to the person’s heart failure, and we should consider investigating for alternative causes.

There are other drugs that can be initiated in a specialist setting. I will not cover them in detail, but specialist treatments options include ivabradine, hydralazine in combination with a nitrate, and digoxin.

Additionally, in heart failure with reduced ejection fraction we should avoid verapamil, diltiazem, and short-acting dihydropyridine calcium-channel blockers. The “why” boils down to hemodynamics and outcomes:

• Verapamil & diltiazem are negative inotropes and slow AV conduction. In heart failure with reduced ejection fraction that can worsen cardiac function and precipitate decompensation.
• Then Short-acting dihydropyridines (like immediate-release nifedipine) cause rapid vasodilation and reflex tachycardia and hypotension, which has been linked to increased mortality, so it is considered unsafe in HF

For people with heart failure with mildly reduced ejection fraction, we should also consider treatment with the same four drugs as the reduced ejection fraction subtype, that is, an ACE inhibitor, a beta-blocker, a mineralocorticoid receptor antagonist, and an SGLT2 inhibitor.

For those who have symptoms of intolerance to ACE inhibitors, we should consider an ARB, a beta-blocker, an MRA, and an SGLT2 inhibitor. But we need to note that an angiotensin receptor–neprilysin inhibitor, that is, sacubitril/valsartan, is not recommended in heart failure with mildly reduced ejection fraction. It is recommended only in heart failure with reduced ejection fraction.

SGLT2 inhibitors specifically recommended by NICE for heart failure with mildly reduced ejection fraction, are empagliflozin and dapagliflozin, for which we have specific NICE recommendations.

Finally, for people with heart failure with preserved ejection fraction, ACE inhibitors and betablockers are not specifically recommended, but we should consider a mineralocorticoid receptor antagonist and an SGLT2 inhibitor, again with specific guidance on empagliflozin and dapagliflozin as the preferred SGLT2 inhibitors in this subtype.

When treating heart failure in people with chronic kidney disease, if the eGFR is 45 or less, we should consider using lower starting doses and smaller dose increments for the medicine combinations already mentioned.

If the person’s eGFR is below 30, the advice of a renal physician should be sought.

So that is it, a review of the drug management of the different subtypes of heart failure.

In the next episode, I will cover additional details and further management recommendations.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/hjKE4JAQM6c

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through the NICE guideline on Chronic heart failure in adults: diagnosis and management [NG106], last updated in September 2025. Today’s episode focuses on the initial assessment and diagnosis.

The guidance on the remaining aspects of heart failure management will be covered in future episodes.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The NICE guideline on Chronic heart failure in adults: diagnosis and management [NG106] can be found here:

·      https://www.nice.org.uk/guidance/ng106

Additional information on ARNIs can be found here: 

·      https://www.ncbi.nlm.nih.gov/books/NBK507904/#:~:text=Mechanism%20of%20Action,-The%20pathophysiology%20of&text=Valsartan%20is%20an%20angiotensin%20receptor,neprilysin%20will%20accumulate%20angiotensin%20II

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we are going to go through the NICE guideline on Chronic heart failure in adults, which was last updated in September 2025.

Today’s episode focuses on the initial assessment and diagnosis.

The guidance on the remaining aspects of heart failure management will be covered over forthcoming episodes so stay tuned.

Right, let’s jump into it.

And as we have just said, today we’re going to focus on how we diagnose heart failure.

We will obviously begin by taking a thorough history, performing a clinical examination, and arranging appropriate tests to confirm the diagnosis.

And we should start by measuring N-terminal pro-B-type natriuretic peptide, or NT-proBNP, in anyone with suspected heart failure. Because very high levels of NT-proBNP carry a poor prognosis, we will refer people with suspected heart failure and an NT-proBNP level above 2,000 nanograms per litre — or 236 picomoles per litre — urgently, for specialist assessment and an echocardiogram within two weeks.

We should refer people with suspected heart failure and lower NT-proBNP levels, between 400 and 2,000 nanograms per litre — that’s 47 to 236 picomoles per litre — for specialist assessment and an echocardiogram but this time to be seen within six weeks.

We need to be aware that an NT-proBNP level below 400 nanograms per litre, or 47 picomoles per litre, in an untreated person makes a diagnosis of heart failure less likely. We also need to remember that the level of serum natriuretic peptide does not differentiate between heart failure with preserved, mildly reduced, or reduced ejection fraction.

When NT-proBNP levels are below 400 nanograms per litre, we should consider alternative causes for the symptoms. If there’s still concern that the symptoms might be related to heart failure, we should discuss the case with a heart failure specialist.

We also need to be aware that there are factors that can affect the NT-proBNP level. Examples of factors that can reduce the level are:

·      Obesity

·      African or African–Caribbean ethnic background, or

·      Treatment with certain medications. These include:

o  Diuretics,

o  Beta-blockers

o  Mineralocorticoid receptor antagonists

o  ACE inhibitors, ARBs and

o  Angiotensin receptor-neprilysin inhibitors. And let’s just quickly say that Angiotensin receptor–neprilysin inhibitors, or ARNIs, are a relatively new class of medications used in the management of heart failure with reduced ejection fraction. At present, the only available one is sacubitril/valsartan which combines two mechanisms of action:

§ Sacubitril, which inhibits neprilysin — an enzyme that breaks down beneficial natriuretic peptides. By blocking neprilysin, sacubitril helps with vasodilation, sodium excretion, and reduced cardiac remodelling.

§ And then we have Valsartan, an angiotensin II receptor blocker (ARB), which helps counteract the harmful effects of the renin–angiotensin–aldosterone system by reducing vasoconstriction, sodium retention, and aldosterone secretion. Together, this combination of sacubitril and valsartan improves outcomes in patients with heart failure with reduced ejection fraction.

Ok, going back to the factors that can affect NT-proBNP levels, we should remember that high levels can have causes other than heart failure — for example, pulmonary, renal, liver, or systemic disease, sepsis, COPD, diabetes, or liver cirrhosis.

As we can see, the main tools to diagnose heart failure are the NT-proBNP blood test followed by a transthoracic echocardiogram. The purpose for performing transthoracic echocardiography is to exclude important valve disease, detect intracardiac shunts and assess both systolic and diastolic function of the left ventricle.

Categorising cardiac function is important because the treatment of heart failure will be different depending on the ejection fraction.

We classify heart failure as follows:

• Heart failure with reduced ejection fraction, when the ejection fraction is 40% or below.
• Heart failure with mildly reduced ejection fraction, when it is between 41 and 49%.
• And Heart failure with preserved ejection fraction, when it is 50% or higher.

We will look at the specific drug treatment of each of these subtypes of heart failure in the next episode.

And going back to the diagnosis, although transthoracic echocardiography is our first-line imaging option, if image quality is poor, alternative imaging methods such as radionuclide angiography, cardiac MRI, or transoesophageal echocardiography should be considered.

Also, although NT-proBNP and echocardiography are the cornerstone of the diagnosis of heart failure, we should also consider further investigations to assess possible aggravating factors or alternative diagnoses. These include:

·      An ECG

·      A chest X-ray

·      Blood tests including renal, liver and thyroid function tests, a lipid profile, HbA1c, and a full blood count

·      And we will also do Urinalysis, and

·      Peak flow or spirometry.

We do this because we should always try to exclude other disorders that may present in a similar manner.

Once a diagnosis of heart failure has been made, we will assess its severity, causes, precipitating factors, type of cardiac dysfunction, and any correctable causes, and, in particular, for people with heart failure caused by valve disease, we will refer them for specialist assessment and advice.

We should also review patients with a historical diagnosis of heart failure, and manage them according to the NICE guideline only if the diagnosis has been confirmed with an echocardiogram. If heart failure is still suspected but no underlying cardiac abnormality has been identified on imaging, we will refer to a heart failure specialist.

So that is it, a review of the initial assessment and diagnosis of heart failure.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/qZPisPCp4eQ

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through new and updated recommendations published in September 2025 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The Full NICE News bulletin for September 2025 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2025-09-01&to=2025-09-30&ndt=Guidance&ndt=Quality+standard

The updated Clinical guideline CG57 on Atopic eczema in under 12s: diagnosis and management can be found here:

·      https://www.nice.org.uk/guidance/cg57

The updated NICE guideline on Chronic heart failure in adults: diagnosis and management NG106 can be found here:

·      https://www.nice.org.uk/guidance/ng106

The updated Quality standard on Chronic heart failure in adults QS9 can be found here:

·      https://www.nice.org.uk/guidance/qs9

The new NICE guideline on Pneumonia: diagnosis and management NG250 can be found here:

·      https://www.nice.org.uk/guidance/ng250

The updated Quality standard on Pneumonia: diagnosis and management QS110 can be found here:

·      https://www.nice.org.uk/guidance/qs110

The updated NICE guideline on Suspected acute respiratory infection in over 16s: assessment at first presentation and initial management NG237 can be found here:

·      https://www.nice.org.uk/guidance/ng237

The updated Clinical guideline on Bipolar disorder: assessment and management CG185 can be found here:

·      https://www.nice.org.uk/guidance/cg185

The updated technology appraisal guidance on Tirzepatide for treating type 2 diabetes TA924 can be found here:

·      https://www.nice.org.uk/guidance/ta924

The updated Technology appraisal guidance on Tirzepatide for managing overweight and obesity TA1026 can be found here:

·      https://www.nice.org.uk/guidance/ta1026

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we’ll look at the NICE updates published in September 2025, focusing on what is relevant in Primary Care only.

In recent months, there hasn’t been much in the way of updates that directly affect us in General Practice. But September is very different — there’s a lot we need to pay attention to. These updates cover eczema, respiratory infections, pneumonia, bipolar disorder, tirzepatide, and, importantly, a new updated guideline on chronic heart failure.

Right, let’s jump into it.

The updated NICE guideline on atopic eczema in children under 12 has revised the section on complementary therapies, washing, and clothing. The new wording makes it clear that children with atopic eczema may bathe or shower once daily. Bathing can help remove crusts and skin debris and improve comfort, but it should always be followed by emollient application to prevent the skin from drying out.

The update also clarifies that water softeners and silk garments do not improve eczema severity and therefore should not be recommended.

So, in summary: daily bathing is acceptable and can be beneficial if followed by emollient use, and water softeners or silk clothing should not be recommended because they provide no proven benefit.

The next section is on Chronic Heart failure. The updated NICE guideline has introduced substantial changes, particularly to how we treat and monitor different categories of heart failure. This is such an important area that I’ll only cover the highlights today, as I will cover it in more detail in a future episode.

The main focus of the update was the drug management of the three subtypes of heart failure, that is, heart failure with reduced ejection fraction, mildly reduced ejection fraction, and preserved ejection fraction.

For heart failure with reduced ejection fraction, that is, an ejection fraction 40% or less, the recommendations now reflect strong evidence for SGLT-2 inhibitors, which consistently reduce hospitalisations for heart failure and improve survival regardless of diabetes status. These drugs are now embedded alongside established treatments such as ACE inhibitors, beta-blockers, and mineralocorticoid receptor antagonists.

For heart failure with mildly reduced ejection fraction — that is, an ejection fraction between 41% and 49% — NICE issues new recommendations for the first time. This group used to be a bit of a grey area. The update highlights evidence that people with mildly reduced EF may benefit from SGLT-2 inhibitors in much the same way as those with reduced EF, and the guidance now advises considering them here too.

For heart failure with preserved ejection fraction, meaning an ejection fraction of 50% or more, NICE also makes new recommendations. In the past, management was mostly limited to controlling symptoms and comorbidities. Now, on the back of trial evidence, SGLT-2 inhibitors are also recommended here because they reduce hospitalisations for heart failure, even if mortality benefit is less certain.

In practice, this means SGLT-2 inhibitors will be used much more widely — not only in people with reduced EF, but also in those with mildly reduced or preserved EF.

An updated NICE Quality Standard on chronic heart failure has also been published, bringing it into line with these changes.

Next, there is a brand-new NICE guideline on pneumonia, which consolidates and replaces previous guidance, including antimicrobial prescribing guidelines.

The biggest change for us in primary care relates to children: the recommended course of antibiotics for non-severe community-acquired pneumonia without complications or underlying disease has been reduced from 5 days to 3 days. This is because evidence shows that shorter courses are just as effective at resolving symptoms, while reducing the risk of side effects and, most importantly, lowering the risk of antibiotic resistance.

Additionally, although more relevant to secondary care, there are new recommendations on corticosteroids in patients with high-severity community-acquired pneumonia when admitted to hospital. This reflects growing evidence that systemic steroids can improve outcomes in severe cases alongside standard antibiotic and supportive care. However, corticosteroids are not recommended for routine use in mild or moderate pneumonia, so it is something that we will not be doing routinely in Primary Care.

There is also an updated Quality Standard on pneumonia, aligned with the new guideline and reflecting the changes I’ve just mentioned.

Next, we have the updated NICE guideline on suspected acute respiratory infection which covers assessment at first presentation and initial management.

The main change here is that the section on the clinical diagnosis of community-acquired pneumonia in primary care has been removed, because that information is now fully covered by the new pneumonia guideline. In practical terms, pneumonia-specific recommendations move to the pneumonia guideline, while the guideline on respiratory infections continues to provide guidance on the assessment and initial management of these infections more broadly.

This guideline should also be read alongside NICE’s existing antimicrobial prescribing guidelines for acute cough, COPD exacerbations, sinusitis, and sore throat.

The latest update is on the clinical guideline on bipolar disorder, which focuses on recommendations around valproate use, following new safety advice from the MHRA.

The key change is that boys and men taking valproate must now be advised to use effective contraception throughout their treatment and for three months after stopping the drug. This means using condoms in addition to contraception used by a female sexual partner. Additionally, men who are planning a family within the next year should also discuss potential fertility risks and alternative treatment options.

Previously, recommendations were already strict around valproate use in females of childbearing potential. Valproate must not be initiated in anyone under 55 unless two specialists agree there are no other suitable alternatives or that the reproductive risks do not apply. For them, it can only be prescribed if other treatments are unsuitable and the Pregnancy Prevention Programme is in place.

The new update now extends this caution explicitly to male patients, confirming that valproate carries reproductive risks for both sexes.

Finally, there are updates to the NICE technology appraisals on tirzepatide — marketed as Mounjaro — covering both type 2 diabetes and the management of overweight and obesity.

The recommendations themselves remain unchanged. What has changed is that a commercial access agreement has now been added, together with updated pricing. This is intended to reduce the budget impact for the NHS and make implementation of the guidance more sustainable.

As a reminder, let’s remember that for type 2 diabetes, tirzepatide continues to be recommended when triple therapy with metformin and two other oral drugs is ineffective, not tolerated, or contraindicated, and when a GLP-1 receptor agonist would otherwise be considered. For obesity, it remains recommended in adults who meet the BMI and comorbidity thresholds specified in the original appraisal and following a gradual NHS roll out process.

So that is it, a review of the NICE updates relevant to primary care.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/AC3ncdm77Os

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through the draft NICE guideline on type 2 diabetes, which is open for public consultation until October 2025, and the final guidance being due in February 2026. Today’s episode is based on the NICE visual summary and the link to it is below.

The visual summary includes general guidance for all patient, and specific guidance for 7 different group of patients. In today’s episode we will cover 4 clinical groups and the remaining groups were covered in last week’s episode.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The NICE announcement on Type 2 diabetes management can be found here:

·      https://www.nice.org.uk/news/articles/biggest-shake-up-in-type-2-diabetes-care-in-a-decade-announced

The NICE draft guideline on Type 2 diabetes can be found here:

·      https://www.nice.org.uk/guidance/gid-ng10336/documents/450

The visual summary of the NICE draft guideline on type 2 diabetes can be found here:

·      https://www.nice.org.uk/guidance/GID-NG10336/documents/draft-guideline-2

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we are going to review the draft NICE guideline on type 2 diabetes, focusing on the main changes as applied to 7 specific groups of patients. In the previous episode we covered the first 3 groups so today we will cover the rest.

Right, let’s jump into it.

And, as you know, the draft guideline is open for consultation until October, and the final guidance is due in February 2026, so let’s not forget that it is only a draft, and we should not be making clinical decisions based on it yet.

Today’s episode is based on the visual summary created by NICE and the link to it is in the episode description.

The visual summary includes specific guidance for 7 different groups of patients:

1.   The group of patients with no relevant comorbidities, then

2.   Obesity

3.   Frailty

4.   CKD

5.   Heart failure

6.   Atherosclerotic cardiovascular disease and

7.   Early onset type 2 diabetes

And today we will look at the last 4 groups that we did not cover last time.

So let’s start with the CKD group.

For people with CKD, like for many of the other groups. the draft guideline recommends starting treatment with metformin plus an SGLT-2 inhibitor. Because of licensing reasons, we are advised to choose either empagliflozin or dapagliflozin in this group. If metformin is contraindicated or not tolerated, the SGLT-2 inhibitor can be offered on its own.

Treatment will also depend on kidney function, measured by eGFR. As we know, metformin in contraindicated if eGFR is less than 30, and, given that SGLT-2 efficacy decreases with advancing renal impairment, NICE recommends not using empagliflozin or dapagliflozin is eGFR is less than 20.

Therefore, the first line treatment on this basis is as follows:

• If eGFR is above 30 mL/min/1.73 m², in principle we will offer metformin plus dapagliflozin or empagliflozin, although, if metformin is not tolerated the SGLT-2 inhibitor can be given by itself.
• If eGFR is between 20 and 30, we will offer either dapagliflozin or empagliflozin alone.
• And, if eGFR is below 20, we will then go for a DPP-4 inhibitor in preference. If that is contraindicated or not tolerated, we will consider pioglitazone or insulin, given that sulfonylureas should not be given if the eGFR is below 30. This is because sulfonylureas accumulate in renal impairment and increase the hypoglycaemia risk.

If further glycaemic lowering is needed after first line treatment, we can use other options including DPP-4 inhibitors (if not already used), sulfonylureas or insulin depending on renal function and safety profile.

How does this differ from the previous guidance?

Like in other groups, the big change here is the earlier, more proactive use of SGLT-2 inhibitors specifically for renal protection, not just glucose lowering. Previously, SGLT-2 inhibitors were used after metformin for people with established albuminuria or heart failure. Now, the draft guidance recognises the trial evidence showing that, apart from the cardiovascular benefits, SGLT2 inhibitors also reduce progression of CKD, and this benefit occurs even in people with moderately reduced eGFR and independently of albuminuria. The slower progression of CKD is because SGLT2 inhibitors reduce albuminuria, intraglomerular pressure and protect against hyperfiltration.

Another nuance is that the draft now pushes dapagliflozin and empagliflozin explicitly into first-line therapy alongside metformin or alone if necessary, with thresholds set according to kidney function. And it also sets out a clear sequence for treatment as eGFR declines, including when to use DPP-4 inhibitors or move to insulin.

What this means in practice is that:

• We will need to check eGFR early and often, as it will determine the choice of treatment.
• Metformin + SGLT-2 inhibitor is the default down to eGFR 30; SGLT-2 inhibitor alone is preferred between 20 and 30, and below 20, we will switch to a DPP-4 inhibitor, and only after that will we consider pioglitazone or insulin if needed.
• And, practically, the bigger focus on protecting kidney function means that more patients will be started on dapagliflozin or empagliflozin earlier, so we will need to familiarise ourselves with renal thresholds and side effect monitoring.

Now, let’s move to the heart failure group.

For adults with type 2 diabetes and heart failure, NICE also recommends that the initial therapy should be metformin plus an SGLT-2 inhibitor. If metformin is contraindicated or not tolerated, then an SGLT-2 inhibitor alone is advised. If additional therapy is needed to help with weight management, then a GLP-1 receptor agonist (specifically subcutaneous semaglutide) can be considered provided there is no frailty and the patient has a preserved ejection fraction. After that, for further glycaemic lowering, we can add a sulfonylurea or insulin, remembering that pioglitazone is contraindicated in heart failure 

The difference with the old guideline is that the draft makes metformin + SGLT-2 inhibitor the standard, aiming to get heart failure-related benefits earlier. As we know, trial data show that SGLT2 inhibitors reduce hospitalization for heart failure, improve symptoms, slow progression, and improve cardiovascular mortality, independent of glycaemic control. So, using them early helps not just glucose but also cardiac outcomes.

But another big change is that the draft also acknowledges that weight loss (from GLP-1 RAs) can help reduce cardiac workload, reduce fluid overload, and improve quality of life in heart failure. Combining SGLT-2 inhibitors with semaglutide in patients for whom weight is an issue, is intended to deliver a dual benefit: cardiorenal protection and weight reduction. Previously, GLP-1 RAs were less likely to be used early in heart failure, and semaglutide had stricter criteria; now, semaglutide is explicitly considered earlier in heart failure when weight benefit is also a goal. Any limitations? Well, semaglutide will be limited to patients with obesity, preserved EF and no frailty. Frailty and ejection fraction matter because the benefits and risks of semaglutide vary (e.g. risk of dehydration and hypotension,) depending on heart function and overall general state.

What the changes mean in practice is that:

• We will start more patients on both metformin and an SGLT-2 inhibitor upfront. This also means that we will need to discuss SGLT-2 inhibitor side effects like the risk of genital infections, volume depletion, sick-day rules, and renal monitoring from the start.
• Patients will need assessment of heart failure subtype (especially ejection fraction) and frailty to decide who is eligible for early semaglutide.
• Monitoring will need to include not only HbA1c, but also cardiac function, kidney function, and watch for adverse events.
• And finally, when adding semaglutide, the expectation would be that it's for weight benefit, so obesity must be present.

Now, let’s look at the atherosclerotic cardiovascular disease group.

For them, we will offer triple therapy with metformin plus an SGLT-2 inhibitor and the GLP-1 receptor agonist, semaglutide, for additional risk reduction and weight benefit. And it is worth mentioning that we should also consider semaglutide for any other group if at any stage, ASCVD develops after treatment has already been started. If extra glycaemic lowering is needed, we will add a sulfonylurea, pioglitazone, or insulin. As we know, we should not combine a GLP1 receptor agonist and a DPP4 inhibitor, but if a GLP-1 RA isn’t appropriate, we will add a DPP-4 inhibitor instead and before considering the other options of a sulfonylurea, pioglitazone, or insulin.

This is different from the previous version because before GLP-1 RAs were not used for their cardiovascular benefit but their use was rather tied to glycaemic and BMI thresholds. The draft moves to routine early triple therapy with metformin, an SGLT-2 inhibitor, and semaglutide when ASCVD is present or develops, bringing GLP-1 therapy forward in the pathway.

This change is due to trial evidence showing that GLP-1 receptor agonists not only improve weight, blood pressure and post-prandial glycaemia, but they also reduce atherosclerotic cardiovascular events, with semaglutide having one of the strongest evidence for this reduction within the class. Combining semaglutide with metformin and an SGLT-2 inhibitor early is designed to achieve both cardio renal benefits as well as a lower atherothrombotic risk.

What it means in practice is that:

• We will treat ASCVD earlier with SGLT-2 inhibitors and semaglutide and, in principle, we will continue these therapies long term even if HbA1c or weight targets aren’t fully met.

Finally, let’s move to the early-onset type 2 diabetes group. For NICE this group refers to type 2 diabetes diagnosed in people under the age of 40.

First-line treatment here is metformin plus an SGLT-2 inhibitor like everybody else but, on top of that, the draft says that we should consider adding a GLP-1 receptor agonist early. If metformin is contraindicated or not tolerated, we will offer an SGLT-2 inhibitor and still consider adding a GLP-1 RA. If more glycaemic lowering is needed, the add-on choices are, again, a GLP 1 receptor agonist if not already prescribed, a sulfonylurea, pioglitazone, or insulin. If a GLP-1 RA isn’t appropriate we will add a DPP-4 inhibitor instead before considering a sulfonylurea, pioglitazone, or insulin.

This is different from the previous guidance because before early-onset type 2 diabetes did not have its own explicit guidance. NICE is changing this because it has been shown that early-onset type 2 diabetes carries disproportionately higher lifetime risk. In fact, large reviews show that early-onset T2D is linked to higher rates of complications and premature mortality at any given age compared with later-onset disease, due to the additional years exposed to hyperglycaemia, faster β-cell decline, and earlier cardio-renal and microvascular complications. So this is why NICE now favours earlier, multi-mechanism therapy in this group, including GLP-1 receptor agonists for their cardiovascular benefits.

What this means in practice is that we will start combination therapy sooner in the form of metformin + SGLT-2 inhibitor while, proactively considering a GLP-1 RA early, in many cases resulting in early triple therapy.

We will also need to assess tolerance and to monitor side effects as well as reviewing targets explicitly, while being aware that in early-onset T2D, continuing GLP-1 RAs may be appropriate even when targets aren’t met.

So that is it, an review of the draft NICE guideline on type 2 diabetes focusing on the visual summary.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/M0s2Vvlia70

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through the draft NICE guideline on type 2 diabetes, which is open for public consultation until October 2025, and the final guidance being due in February 2026. Today’s episode is based on the NICE visual summary and the link to it is below.

The visual summary includes general guidance for all patient, and specific guidance for 7 different group of patients. In today’s episode we will cover three clinical groups  and the remaining groups will be done in next week’s episode.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The NICE announcement on Type 2 diabetes management can be found here:

·      https://www.nice.org.uk/news/articles/biggest-shake-up-in-type-2-diabetes-care-in-a-decade-announced

The NICE draft guideline on Type 2 diabetes can be found here:

·      https://www.nice.org.uk/guidance/gid-ng10336/documents/450

The visual summary of the NICE draft guideline on type 2 diabetes can be found here:

·      https://www.nice.org.uk/guidance/GID-NG10336/documents/draft-guideline-2

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we are going to review the draft NICE guideline on type 2 diabetes, focusing on the main changes as applied to 7 specific groups of patients.

Right, let’s jump into it.

And, as you know, the draft guideline is open for consultation until October, and the final guidance is due in February 2026, so let’s not forget that it is only a draft, and we should not be making clinical decisions based on it yet.

Today’s episode is based on the visual summary created by NICE and the link to it is in the episode description.

The visual summary includes specific guidance for 7 different group of patients. In today’s episode we will cover three of the groups and we will finish the other groups in next week’s episode.

There are 7 groups:

1.   First, the group of patients with no relevant comorbidities, then

2.   Obesity

3.   Frailty

4.   CKD

5.   Heart failure

6.   Atherosclerotic cardiovascular disease and

7.   Early onset type 2 diabetes

So let’s start with the no relevant comorbidities group.

For adults with type 2 diabetes and no major comorbidities, the draft recommends metformin plus an SGLT-2 inhibitor from the outset. If metformin is contraindicated or not tolerated, then an SGLT-2 inhibitor alone should be offered. If further glycaemic lowering is required, the next step is to add a DPP-4 inhibitor and if this is not effective or tolerated, we can try a sulfonylurea, pioglitazone, or insulin.

This is very different from the previous guidance, which began with metformin monotherapy, and only added other agents if HbA1c targets were not met. SGLT-2 inhibitors and GLP-1 receptor agonists were generally reserved for people with established cardiovascular or renal disease, or later in the treatment pathway. The draft changes our thinking on everything by recommending dual therapy right at diagnosis for all, even in people without comorbidities.

Why is NICE changing the advice?

As we have already explained, evidence shows that SGLT-2 inhibitors consistently reduce heart failure admissions, slow CKD progression, and lower cardiovascular death. Trials have showed these effects in people without established CVD they are now recommended for all, not just for the high-risk subgroups.

What this means in practice is that now:

• The default first-line choice is now metformin + SGLT-2 inhibitor, not metformin alone.
• More people will start dual therapy earlier, meaning that we will need to discuss SGLT-2 inhibitor side effects like the risk of genital infections, volume depletion, sick-day rules, and renal monitoring from the start.
• In those who can’t tolerate metformin, an SGLT-2 inhibitor alone is acceptable. We also need to consider the fact that SGLT2 inhibitors will now be prescribed long term unless there are specific reasons to stop them.
• And, if further glucose control is needed, add-ons agents remain available but they now come after the SGLT-2 inhibitor, not before.

The next group is the obesity group:

For people with type 2 diabetes who also have obesity, the draft recommends also starting with metformin plus an SGLT-2 inhibitor. However, if further treatment is needed to reach glycaemic targets, we will add a GLP-1 receptor agonist if initial therapy started 3 months ago or more. This will usually mean adding subcutaneous semaglutide, provided there are no concerns about frailty and they have preserved ejection fraction (i.e., heart function is acceptable). If metformin is contraindicated or not tolerated, the pathway is to offer an SGLT-2 inhibitor plus semaglutide.

We are again reminded that GLP1 receptor agonists and DPP-4 inhibitors should not be combined. Therefore, if the patient is on a GLP-1 receptor agonist and further glycaemic control is needed, the next add-on therapies are sulfonylurea, pioglitazone, or insulin depending on the case.  However, if a GLP-1 receptor agonist is contraindicated, not tolerated, or not appropriate, we will add a DPP-4 inhibitor first before considering other agents such as a sulfonylurea, pioglitazone, or insulin, as all of these can lead to weight gain.

And let’s remember that previously, people with obesity were more likely to have a stepwise approach: metformin first, then add other agents and then move to GLP-1 RAs only if at last resort and if specific BMI thresholds were crossed.

The draft changes this: it brings semaglutide forward, in obesity and when weight reduction is a priority, also giving more flexibility in continuing GLP-1s if weight or glycaemic goals are lagging—as long as obesity remains a priority.

Why is NICE making this change?

• Primarily because there is strong trial evidence that GLP-1 receptor agonists produce sustained weight loss and
• additionally, evidence has accumulated around reduced major adverse cardiovascular events
• And finally, another justification is that many people with obesity carry a higher lifetime risk of cardiovascular disease so delaying GLP1 receptor agonists may mean a missed opportunity to reduce morbidity and mortality.

What does it mean in practice?

• Well, we will need to identify patients with both diabetes and obesity early, and discuss semaglutide sooner than before.
• Shared decision making must cover not only the benefits (weight loss, better cardiovascular risk, possibly better quality of life) but also the downsides like GI side-effects like nausea, and vomiting, injection route and monitoring requirements.
• We will also need to assess frailty and ejection fraction early and avoid semaglutide if there’s concern frailty might lead to harm (like e.g., unintentional weight loss, reduced reserves) or heart failure with reduced EF, which may be decompensated with GLP1 receptor agonist use.
• And, we will also need to monitor the effect on weight, glycaemia, heart and kidney function, being ready to stop the GLP1 receptor agonist if necessary.

And finally, the last group today, the frailty group.

The draft guidance states that if the person’s level of frailty increases the risk of adverse events from SGLT-2 inhibitors, we will consider metformin alone initially. If metformin is contraindicated or not tolerated, we will consider a DPP-4 inhibitor instead. After metformin, if further glycaemic lowering is needed, we will give a DPP-4 inhibitor (if not already used); and if a DPP-4 inhibitor is contraindicated, not tolerated, or already being taken, we will offer pioglitazone, a sulfonylurea, or insulin, explicitly taking into account hypoglycaemia and falls risk with sulfonylureas and insulin. Alongside this, the draft highlights the need for a medication review, aiming for the smallest effective number of drugs in frailty.

How does this differ from the previous guidance?

Earlier frailty modifiers were less explicit, whereas now, the draft makes frailty a front-door decision point: it deprioritises SGLT-2 inhibitors when volume depletion, hypotension, or acute illness risk is high; it elevates DPP-4 inhibitors as a low-burden alternative; and it puts structured deprescribing on the page. It also flags the hypoglycaemia risk with sulfonylureas and insulin in frail adults, which pushes us to choose agents which are safer in that respect.

NICE is making this change because frailty amplifies medication harms. For example, SGLT-2–related diuresis and BP lowering can precipitate dehydration, orthostatic symptoms, AKI, and falls; GLP-1 RAs can cause GI effects and anorexia that risk weight loss in the frail. By contrast, DPP-4 inhibitors are weight-neutral, have a low hypoglycaemia risk, minimal haemodynamic effects, and simple dosing. The emphasis on medication review reflects evidence that polypharmacy and hypoglycaemia are linked to falls, delirium, and hospitalisation in frail older adults.

What this means in practice is that we will need to:

• Assess frailty up front and let it shape drug choice and dosing.
• If frailty raises safety concerns with SGLT-2 inhibitors, we will start with metformin alone, or use a DPP-4 inhibitor when metformin isn’t suitable.
• We will prioritise low hypoglycaemia risk; being cautious with sulfonylureas and insulin, and use the lowest effective doses with clear sick-day rules.
• We will perform a formal medication review, deprescribing where possible, and aiming for the fewest drugs necessary.
• And we will keep focusing on symptoms, renal function, nutrition, and falls, not just HbA1c.

So that is it, an initial review of the new draft NICE guideline on type 2 diabetes focusing on the visual summary. In the next episode we will cover the remaining groups CKD, heart failure, atherosclerotic cardiovascular disease and early onset type 2 diabetes.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/xB8BStN4Owg

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through the draft NICE guideline on type 2 diabetes, which is open for public consultation until October 2025, and the final guidance being due in February 2026. Today’s episode is based on the NICE visual summary and the link to it is below.

The visual summary includes general guidance for all patient, and specific guidance for 7 different group of patients. In today’s episode we will review the general guidance and we will cover the various groups in future episodes.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The NICE announcement on Type 2 diabetes management can be found here:

·      https://www.nice.org.uk/news/articles/biggest-shake-up-in-type-2-diabetes-care-in-a-decade-announced

The NICE draft guideline on Type 2 diabetes can be found here:

·      https://www.nice.org.uk/guidance/gid-ng10336/documents/450

The visual summary of the NICE draft guideline on type 2 diabetes can be found here:

·      https://www.nice.org.uk/guidance/GID-NG10336/documents/draft-guideline-2

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we are going to review the draft NICE guideline on type 2 diabetes, focusing on the visual summary created by NICE. I will cover the information over several episodes, so stay tuned.

Right, let’s jump into it.

As you may know, the draft NICE guideline on type 2 diabetes is open for public consultation until October, and the final guidance is due in February 2026. It has attracted a lot of attention, but we need to remember that, for now, it is only a draft, which means it could still change. So, we should not be making clinical decisions based on it yet.

Today’s episode is based on the NICE visual summary and the link to it is in the episode description.

The visual summary includes general guidance for all patient, and specific guidance for 7 different group of patients. In today’s episode we will review the general guidance and we will cover the various groups in future episodes.

The first page of the draft visual summary sets out the general approach for all.

NICE begins by emphasising that diet and lifestyle are the foundation of management, and these need to be reinforced at every stage of the treatment pathway, pointing out that medicines should come on top of, and not instead of, these lifestyle measures.

When choosing drug therapy, the draft recommends discussing the benefits and risks of every option. That includes looking at each drug’s effectiveness for glycaemic control but also, and this is new compared with the previous guideline, weighing its impact on cardiovascular and renal outcomes.

The guideline also stresses that if a person has more than one comorbidity, for example obesity, cardiovascular disease or chronic kidney disease, we should make a shared decision with the patient about which comorbidity to prioritise in choosing treatment. This means that we move away from a purely HbA1c-driven model towards a model focused on complications and their prevention.

On reviewing medicines, the draft says that before changing therapy, we should first optimise the current regimen, bearing in mind that it may be appropriate to continue some treatment options, like SGLT-2 inhibitors or GLP-1 receptor agonists even if the effect on glycaemic control is not perfect. In fact, the draft advises continuing SGLT-2 inhibitors for their heart and kidney benefits even if they are not achieving glucose or weight targets.

For GLP-1 receptor agonists, the draft changes the stop rules: we will stop if they do not help the person achieve glycaemic or weight goals but only, and this is important, if the person does not have cardiovascular disease or early-onset type 2 diabetes, understood as type 2 diabetes diagnosed under the age of 40. This a huge change.  Previously, stopping criteria were more tightly linked to weight and HbA1c thresholds, for example, if the person had not lost at least 3% of body weight and dropped their HbA1c by 1% within six months. Now, because of the cardiovascular benefit of GLP-1 receptor agonists, it basically means that for people with atherosclerotic cardiovascular disease, it is continued long term, regardless of weight loss or HbA1c change. And a similar, more relaxed attitude also applies to people with early onset type 2 diabetes.

But, why this recommendation?

Well, this comes from trial evidence over the past decade. SGLT-2 inhibitors have consistently reduced hospitalisation for heart failure and slowed CKD progression, even when HbA1c effects were modest. Similarly, GLP-1 receptor agonists have reduced rates of major adverse cardiovascular events. Why these benefits? The pathophysiology is important here: SGLT-2 inhibitors reduce intraglomerular pressure, improve renal haemodynamics, induce diuresis, and reduce preload and afterload on the heart. On the other hand, GLP-1 receptor agonists improve weight, and have an effect on blood pressure and lipids. All these effects are the reason for the beneficial outcomes over and above glucose control

What this means in practice is that:

• The decision to start or continue medicines is now less about HbA1c in isolation, and more about long-term organ protection.
• SGLT-2 inhibitors should be maintained even if glycaemic targets aren’t achieved.
• GLP-1 receptor agonists should be stopped if they don’t achieve targets unless the person has early-onset diabetes or established cardiovascular disease in which case, their longer-term benefits justify continuation.

Finally, NICE advises against combining GLP-1 receptor agonists with DPP-4 inhibitors, as this combination offers no additional benefit.

Why is this? Let’s remember that DPP-4 inhibitors prevent breakdown of endogenous GLP-1, whereas GLP-1 receptor agonists directly activate GLP-1 receptors. Because the GLP-1 agonists already saturate the receptor and they are not affected by DPP-4 degradation, adding a DPP-4 inhibitor offers no additional glycemic or weight benefit. That’s why guidelines recommend using one or the other, but never both.

And before we end, let’s also quickly list the main current recommendations in the draft guideline, making reference to the recommendations that have been either deleted or changed in a major way.

1.   First, the recommendation to start metformin alone as first-line for most people without complications has gone. Now we will start dual Therapy with Metformin + SGLT-2 Inhibitor as Initial Therapy, the reason being the need to maximise the cardiorenal benefits of SGLT2 inhibitors.

2.   Second, the restrictive conditions to start GLP1 receptor agonists have also gone. Now there is Earlier and More Explicit Use of GLP-1 Receptor Agonists, Specifically Semaglutide, in order to maximise the weight and cardiovascular benefits of GLP1 receptor agonists. In particular, semaglutide is the preferred option because it has the most consistent and strong evidence as well as being the most cost-effective.

3.   Third, there is more weight on Stratification by Kidney Function and Frailty. As a result, the draft puts more weight on eGFR thresholds when deciding which medicines to use and it also identifies frailty as a modifier given that frailty increases treatment risks such as dehydration, side effects, hypoglycaemia, etc.

4.   Continuation Criteria and Stop Rules for GLP-1 receptor agonists are now different, meaning that if a person has cardiovascular disease or early onset diabetes, the recommendation is to continue GLP-1 even if glycaemic or weight targets are not fully met.

5.   The advice on how to introduce multiple medicines when initial therapy is combination therapy is also clearer. The draft specifies that medicines should be introduced one at a time. For example, first confirm tolerability of metformin, then of the SGLT-2 inhibitor, then if adding a GLP-1 RA, confirm tolerability of that in turn.

6.   Another change is that the draft is more explicit about reviewing medicines: checking effectiveness, and discontinuing medicines that are not effective unless there is an additional benefit like cardiovascular or renal protection.

7.   Then, insulin guidance has also had a major refresh. The new draft simplifies the advice into a more practical, class-based approach, giving more flexibility as to whether human or analogues insulins are recommended. This is pragmatic response to insulin product withdrawals and shortages. By focusing on broader insulin classes instead of individual types, the guidance is more flexible and easier to apply, even when supply issues arise.

8.   Another significant change is that GLP-1 receptor agonists can now be combined with insulin without the need for specialist approval, making access easier and quicker in primary care.

9.   The ordering and priority of Subsequent Therapy Options has also changed. The draft places DPP-4 inhibitors as the recommended option after Initial treatment. Sulfonylureas, pioglitazone, and insulin remain options but are considered after DPP4 inhibitors.

10. The recommendation against combining a GLP-1 receptor agonist with a DPP-4 inhibitor is repeated and is more strongly worded in the draft. The combinations does not add benefit so it should be avoided and removed if present.

11. The priority of additional therapies is also more dependent on the clinical group that the patient belongs to. This means that the draft makes the escalation pathway group-specific, and more prescriptive, with risks explicitly considered for each clinical category.

And to summarise and close, let’s review again how we think about treatment escalation from a general perspective. The general pathway looks like this:

• We will start most people on metformin plus an SGLT-2 inhibitor right from the beginning.
• For people with atherosclerotic cardiovascular disease, obesity and early onset type 2 diabetes we will consider semaglutide, early in the pathway, not as a late rescue option.
• If HbA1c isn’t controlled with first line treatment and more glucose lowering is needed, the first recommended add-on is a DPP-4 inhibitor, because these are well tolerated, weight neutral, and easy to use, but this only applies as long as the patient is not on a GLP1 receptor agonist.
• If a DPP4 inhibitor not suitable or not effective, then other options like sulfonylureas, pioglitazone, or insulin, can be introduced depending on the person’s needs.
• And finally, frailty will modify how we manage treatment escalation, prioritising safety and symptoms over artificial targets

The main message to remember is that the rationale of the draft guideline is to avoid the old problem of incremental, reactive prescribing, that is, waiting for one drug to fail before adding another, often leaving patients years without treatment that could protect their heart and kidneys.

So that is it, an initial review of the new draft NICE guideline on type 2 diabetes focusing on the visual summary. In the next episode we will cover the recommendations for specific clinical groups.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/mHyDaVHtb58

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through new and updated recommendations published in August 2025 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only. I also give an overview of the draft NICE guideline on type 2 diabetes open for consultation until October 2025 and due for publication in February 2026.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The Full NICE News bulletin for August 2025 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2025-08-01&to=2025-08-31&ndt=Guidance&ndt=Quality+standard

The updated quality standard Overweight and obesity management [QS212] can be found here:

·      https://www.nice.org.uk/guidance/qs212

The NICE announcement on Type 2 diabetes management can be found here:

·      https://www.nice.org.uk/news/articles/biggest-shake-up-in-type-2-diabetes-care-in-a-decade-announced

The NICE draft guideline on Type 2 diabetes can be found here:

·      https://www.nice.org.uk/guidance/gid-ng10336/documents/450

The visual summary of the NICE draft guideline on type 2 diabetes can be found here:

·      https://www.nice.org.uk/guidance/GID-NG10336/documents/draft-guideline-2

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we’ll look at the NICE updates published in August 2025, focusing on what is relevant in Primary Care only.

Today there’s just one updated clinical area to cover, overweight and obesity. But I will also mention that the draft NICE guideline on type 2 diabetes has now been made public, so we will discuss that too.

Right, let’s jump into it.

And I know most of you will be keen to hear about the new diabetes guidance, and understandably so. But before we get to that, I would like to spend the first minute and a half on an area that’s often neglected: overweight and obesity. NICE has just released a new quality standard that replaces three separate guidelines, those on children, adults, and general clinical management, and brings them together into a single standard, reflecting new priorities and evidence.

There are eight quality statements on obesity.

In the first two statements, the focus is on better identification. For adults with long-term conditions, BMI should be recorded at least annually, and if BMI is under 35, waist-to-height ratio should also be measured. This represent a change from previous guidance where BMI alone was the main focus. Also, for children over the age of two, BMI should be recorded opportunistically. putting greater emphasis on early recognition.

Statements three, four, and five are all about improving access to services, including people with learning disabilities. Local authorities and commissioners need to maintain an up-to-date list of services to offer patients, which should reduce barriers and ensure equity of access.

Statements six, seven, and eight deal with clinical management. People prescribed weight management medicines should receive holistic care, covering diet, nutrition, and physical activity. Those who stop medicines or finish behavioural interventions should get long term follow up support, which recognises the importance of relapse prevention. And finally, adults discharged after bariatric surgery should be followed up at least annually within a shared-care model. This is also new because the need for ongoing shared care was not explicit before.

And that is it in respect of overweight and obesity. Now let’s move to the real headline, the draft new NICE guideline on type 2 diabetes. This is the one everyone’s been talking about. The draft is open for public consultation until October, and the final guidance is due in February 2026.

Today I’ll just give you a quick overview. But in a future episode, we’ll look at the proposed changes in slightly more detail, so stay tuned. Just remember, for now it’s only a draft, which means it could still change, and we should not be making clinical decisions based on it yet.

First, the biggest shift: Treatment no longer starts with just metformin. Instead, the new draft guideline recommends combination therapy from day one—metformin plus an SGLT-2 inhibitor for almost all adults with type 2 diabetes. This is a major departure from monotherapy and reflects the fact that type 2 diabetes is not only about sugar control. SGLT-2 inhibitors confer cardiac and renal protection, reducing cardiovascular events and slowing kidney disease progression, benefits that metformin alone can’t offer. NICE has been clear that SGLT2 inhibitors remain underutilised in practice. Why? In many cases, clinicians have stuck with the traditional stepwise model of adding medicines only when HbA1c goes up. Others may be concerned about cost, side effects, or uncertainty over who exactly should benefit. The new guideline cuts through that by saying: everyone with type 2 diabetes will benefit, so we need to make SGLT-2 inhibitors part of the standard starting treatment. The message is that we should be thinking beyond blood glucose from the very beginning, and treating cardiovascular and renal risk right from the start.

Second, we move away from risk-based prescribing. In the past, SGLT-2 inhibitors were reserved only for people with heart failure or at high cardiovascular risk, so their use was much more limited. As we have just said, the new draft guideline takes a completely different approach: now, SGLT-2 inhibitors are recommended for everyone with type 2 diabetes, regardless of their cardiovascular risk profile. The thinking here is simple — we know these drugs consistently reduce hospitalisations for heart failure and slow the progression of kidney disease, and those benefits apply across the board, not just in the highest-risk patients. On top of that, for people who already have established atherosclerotic cardiovascular disease, the guidance goes further by recommending that a GLP-1 receptor agonist, semaglutide, is added as well, creating a triple-therapy regimen right from the start. This combination gives comprehensive coverage: metformin for glucose control, SGLT-2 inhibitors for renal and heart protection, and GLP-1 agonists for both cardiovascular benefit and weight management. It’s simply a move towards using the right drug in the right place earlier, instead of holding them back as late-stage rescue therapies.

Third, let’s talk about GLP-1 receptor agonists a bit more, because this is another big change.

Previously, GLP-1 drugs were considered much later, often for people with obesity or those who hadn’t met glycaemic targets despite multiple therapies, and they were tied to strict BMI criteria. That’s no longer the case.

Now, semaglutide is recommended much earlier:

• It is recommended for people with type 2 diabetes and established atherosclerotic cardiovascular disease, it’s added on top of metformin and an SGLT-2 inhibitor as part of the initial treatment.
• And it is also recommended for people living with obesity or those with early-onset type 2 diabetes who still need extra glycaemic or weight management, so GLP-1 receptor agonists are also considered much sooner in the pathway for them.

And there’s another key change: continuation. In the old guideline, GLP-1 treatment was only continued if the person had lost at least 3% of body weight and dropped their HbA1c by 1% within six months. That rule is gone. Now, if semaglutide is prescribed for cardiovascular protection, it is continued long term, regardless of weight loss or HbA1c change. Only if it’s being used primarily for obesity or metabolic control do continuation decisions depend on whether agreed targets are met. In short, the focus has shifted from short-term numbers to long-term protection.

Fourth, insulin guidance has also had a major refresh.

The old guideline gave long, detailed lists of which insulin types to use in different scenarios. The new draft simplifies this into a more practical, class-based approach. Here’s what’s changed:

• We will start with basal insulin if needed. And what about short-acting and rapid-acting insulins? Well, if HbA1c remains high, then we will add short-acting insulin to basal insulin.

·      However, if someone’s HbA1c is very high, usually 75 mmol/mol or above, then basal plus short-acting insulin can be considered straight away. Rapid-acting insulin analogues are considered if someone’s lifestyle, eating patterns, or risk of hypoglycaemia makes them a better fit than human short-acting insulin. Pre-mixed short-acting analogues are also an option if appropriate. In practice, this means more flexibility while keeping the pathway simple.

• Additionally, the choice of basal insulin, whether human NPH or analogues, should be made through shared decision-making with the patient, taking into account the risk of hypoglycaemia, dosing convenience, and patient preference. If several options are suitable, we will choose the one with the lowest cost.

And this is important because these changes partly reflect a pragmatic response to insulin product withdrawals and shortages. By focusing on broader insulin classes instead of individual types, the guidance is more flexible and easier to apply, even when supply issues arise.

Importantly, GLP-1 receptor agonists can now be combined with insulin without the need for specialist approval, making access easier and quicker in primary care.

And finally, there has also been a change in how we think about escalation overall. Instead of relying on long lists of add-on options, the draft guideline now gives us a much clearer stepwise pathway. The idea is to simplify decision-making and the pathway looks like this:

• We will start most people on metformin plus an SGLT-2 inhibitor right from the beginning.
• If HbA1c isn’t controlled and more glucose lowering is needed, the first recommended add-on is a DPP-4 inhibitor, because these are well tolerated, weight neutral, and easy to use.
• If that’s not suitable or not effective, then other oral options like sulfonylureas or pioglitazone, or insulin, can be introduced depending on the person’s needs.
• For people with atherosclerotic cardiovascular disease, as we said earlier, we will add a GLP-1 receptor agonist, usually semaglutide, early in the pathway, not as a late rescue option.
• And insulin is no longer treated as a last resort — it can be integrated earlier and combined flexibly with GLP-1s when needed.

The rationale here is to avoid the old problem of incremental, reactive prescribing — waiting for one drug to fail before adding another, often leaving patients years without treatment that could protect their heart and kidneys.

So, in short: the new draft guideline is all about earlier combination therapy, universal access to SGLT-2 inhibitors, earlier and more consistent use of GLP-1 receptor agonists, a streamlined approach to insulin, simpler treatment pathways, always with a stronger focus on long-term cardiovascular and renal protection.

In the next episode, I will discuss how the draft guideline is envisaged to be used in specific groups of patients, so make sure not to miss it.

So that is it, a review of the NICE updates relevant to primary care, including an overview of the forthcoming draft guideline on Type 2 diabetes.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/z7eZ1MLItGw

The previous episode on first line treatment of T2DM can be found here:

·      https://youtu.be/32Lf5UlyTOA

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by them.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through the NICE recommendations on the drug treatment of type 2 diabetes, included in the NICE guideline NG28. The links to the NICE guideline can be found below.

In today’s episode, we are focusing on treatment options if further interventions are needed after first line treatment. If you haven’t already, I recommend that you check the previous episode on the first line drug management of type 2 diabetes.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The NICE guideline on Type 2 diabetes in adults: management [NG28] can be found here:

·      https://www.nice.org.uk/guidance/ng28

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In this episode, we’ll go through the NICE recommendations on the drug treatment of type 2 diabetes, included in the NICE guideline NG28. The link to it is in the episode description.

In today’s episode, we are focusing on glucose lowering treatment options if further interventions are needed after first line treatment.

If you haven’t already, I recommend that you check the previous episode on the first line drug management of type 2 diabetes.

Right, let’s jump into it.

So we are going to look at treatment options if further intervention is needed—basically, what to do after first-line treatment.

But first, let’s talk about reviewing drug treatments and when we will need to add an SGLT2 inhibitor at any point after starting first-line therapy.

For adults with type 2 diabetes, no matter where they are in their treatment journey, if they have or develop chronic heart failure, established atherosclerotic cardiovascular disease, or become high risk for cardiovascular disease, if they are not already on it, we should offer an SGLT2 inhibitor that has proven cardiovascular benefits. This can be added on to their current treatment or used to replace an existing medication.

And let’s remember that this is because there is strong evidence in large randomised controlled trials, that has shown that SGLT2 inhibitors not only improve blood glucose control but also reduce the risk of hospitalisation for heart failure, and in some cases lower cardiovascular mortality. These benefits are seen even in patients without diabetes, which highlights their role in protecting the cardiovascular system as well as the kidneys.

Right, now, before we look into how to intensify treatment, let’s quickly cover what NICE says about monitoring and targets.

Regarding diabetes monitoring, NICE recommends measuring HbA1c every 3 to 6 months until it’s stable on unchanging treatment. After that, once HbA1c is fully stable, measuring every 6 months is usually enough.

When it comes to HbA1c targets, we should discuss and agree on an individual goal with each patient. The aim is to help them reach and maintain that target—unless trying to do so causes problems like hypoglycaemia or lowers their quality of life.

Generally speaking, for those managing their diabetes with lifestyle changes or a single drug that doesn’t cause hypoglycaemia, the target is around 48 mmol/mol, or 6.5%. For patients on medications that do carry a risk of hypoglycaemia, the target is a bit higher, around 53 mmol/mol, or 7.0%.

If an adult’s HbA1c isn’t controlled by a single drug and rises to 58 mmol/mol, or 7.5%, or above, then we need to review and reinforce their current treatment and after that, we usually move to intensify drug treatment by adding a second medication.

Now let’s look at treatment options when further intervention is needed.

For adults with type 2 diabetes, if monotherapy isn’t enough to keep HbA1c below their individual target, we can consider adding one of the following:

·      a DPP-4 inhibitor,

·      pioglitazone,

·      a sulfonylurea,

·      or an SGLT2 inhibitor.

If dual therapy—usually metformin plus another oral drug—still isn’t controlling HbA1c below the agreed threshold, then we have two main options. We can either:

·      move to triple therapy by adding a DPP-4 inhibitor, pioglitazone, a sulfonylurea, or an SGLT2 inhibitor,

·      or we can consider starting insulin.

In adults with type 2 diabetes, if metformin is contraindicated or not tolerated, and dual therapy with two oral drugs still isn’t keeping HbA1c below the agreed threshold, then insulin should be considered. This essentially means that triple therapy is only recommended by NICE when one of those three drugs is metformin, not otherwise

If triple therapy with metformin and two other oral drugs isn’t effective, isn’t tolerated, or is contraindicated, we may consider switching one of those drugs for a GLP-1 mimetic—but according to NICE, this is only for adults who:

• Have a BMI of 35 or higher (with adjustments for people from Black, Asian, and other minority ethnic groups by reducing the BMI by 2.5 to 32.5) and who also have specific psychological or medical problems linked to obesity, or
• Have a BMI under 35 but for whom insulin would have significant occupational impacts, or where weight loss would help other serious obesity-related health issues.

GLP-1 mimetic therapy should only be continued if the patient shows a clear benefit, that is, a drop in HbA1c of at least 11 mmol/mol (or 1%) and a weight loss of at least 3% of their starting body weight within six months.

Also, we need to be aware that combining a GLP-1 mimetic with insulin should only be done under specialist care and advice.

So, as we’ve just seen, NICE recommends using GLP-1 mimetics mainly for people with type 2 diabetes who have a higher BMI or specific obesity-related problems. They also set clear criteria for continuing treatment, based on how well the patient responds metabolically and whether they lose enough weight.

Now, we should also point out that other guidelines, like those from the ADA and EASD, take a fairly different approach. They suggest considering GLP-1 receptor agonists earlier in the treatment journey—especially for patients who already have cardiovascular disease or are at high risk of developing it, no matter their BMI. These guidelines focus more on the cardiovascular benefits of GLP-1 therapies, in addition to blood sugar control.

So, while NICE tends to emphasize weight and BMI, the ADA and EASD put more weight on cardiovascular risk when they recommend GLP-1 receptor agonists.

This is because research has shown that GLP-1 receptor agonists can reduce the risk of major cardiovascular events in people with type 2 diabetes who either have established cardiovascular disease or are at high risk.

For example, the LEADER trial looked at liraglutide, and the SUSTAIN-6 trial studied semaglutide. Both showed significant reductions in cardiovascular events compared to placebo.

Next, let’s move on to insulin-based treatments for adults with type 2 diabetes.

When starting insulin therapy, we are likely to continue offering metformin—provided there are no contraindications or intolerance. At the same time, we should review whether other blood glucose-lowering medications are still needed.

For insulin options, we have several choices. The first line option for NICE is NPH insulin, which can be given once or twice daily, depending on the person’s needs.

A quick note about NPH insulin: it’s an intermediate-acting insulin with an onset of action around 1 to 2 hours after injection. Its peak effect usually occurs between 4 to 8 hours, and it lasts for about 12 to 16 hours. Because of this profile, it’s useful for covering blood sugar levels between meals and overnight.

We should consider starting both NPH and short‑acting insulin particularly if the person's HbA1c is 75 mmol/mol [9.0%] or higher. This can be administered either:

• separately or
• as a pre-mixed (or biphasic) human insulin preparation.

However, NICE also suggests we can consider using insulin detemir or insulin glargine as alternatives to NPH insulin in certain situations. For example:

• If the person needs help with injections,
• If they experience recurrent symptomatic hypoglycaemia, or
• If they would otherwise need twice-daily NPH insulin injections along with other medications.

And now a quick note on insulin detemir and glargine:

Insulin glargine is a long-acting basal insulin that provides a steady release over about 24 hours with no pronounced peak, which helps maintain more stable blood sugar levels throughout the day and night.

Insulin detemir is also a long-acting insulin but usually has a slightly shorter duration, lasting around 16 to 20 hours. It tends to have a mild peak and may require twice-daily dosing in some people to maintain adequate coverage.

Both glargine and detemir offer a more predictable action profile than NPH insulin, which can help reduce the risk of hypoglycaemia and improve blood glucose control.

When it comes to pre-mixed, or biphasic, insulin preparations, NICE recommends considering short-acting insulin analogues rather than short-acting human insulin—particularly if:

• The person prefers injecting insulin just before a meal,
• Hypoglycaemia is a concern, or
• Their blood glucose levels spike significantly after eating.

This is because short-acting analogue insulins are rapid-acting insulins designed to manage the blood sugar spikes that happen around meal times.

They start working fast—usually within 10 to 20 minutes—peak around 1 to 3 hours, and their effects last for about 3 to 5 hours. Because of this quick action and shorter duration, they can be injected right before or just after eating, offering more flexibility.

Common examples include insulin lispro, insulin aspart, and insulin glulisine.

One key advantage of these analogues over regular human insulin is a lower risk of hypoglycaemia, especially overnight or between meals. Their rapid onset and shorter duration mean insulin levels drop off sooner, reducing the chance of blood sugar dipping too low when it’s not needed.

Finally, if someone is already on NPH insulin, we should also consider switching from NPH insulin to a long-acting analogue like insulin detemir or insulin glargine if:

• They experience significant hypoglycaemia while using NPH insulin,
• They are unable to use the device required for NPH, or
• They need help with injections, and switching to a long-acting insulin analogue could reduce the number of daily injections needed.

We will need to monitor patients on a basal insulin regimen—whether that’s NPH, detemir, or glargine—for the possible need to add short-acting insulin before meals, or to switch to a pre-mixed, biphasic insulin preparation.

Similarly, adults on pre-mixed insulin should be regularly assessed to see if they need an additional injection of short-acting insulin before meals or if their blood glucose control would benefit from moving to a basal-bolus regimen with NPH, detemir, or glargine.

This ongoing review helps ensure insulin therapy is tailored to achieve the best possible blood sugar control for each patient.

So that is it, a review of the treatment options in type 2 diabetes if further interventions are needed after first line treatment.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/32Lf5UlyTOA

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by them.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through the NICE recommendations on the drug treatment of type 2 diabetes, included in the NICE guideline NG28. The links to the NICE guideline can be found below.

In today’s episode, we are focusing on the first line drug management. In the next episode, we will cover treatment options if further interventions are needed.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The NICE guideline on Type 2 diabetes in adults: management [NG28] can be found here:

·      https://www.nice.org.uk/guidance/ng28

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In this episode, we’ll go through the NICE recommendations on the drug treatment of type 2 diabetes, included in the NICE guideline NG28. The link to it is in the episode description.

In today’s episode, we are focusing on the first line glucose-lowering drugs. In the next episode, we will cover treatment options if further interventions are needed.

Right, let’s jump into it.

And before we look at regular glucose-lowering drugs, we first need to check whether rescue therapy is required, remembering that it can be necessary at any stage of treatment.

If the patient has symptoms of hyperglycaemia, we’ll consider starting insulin or a sulfonylurea, then review the treatment once blood glucose control is achieved. In symptomatic patients, the priority is to bring glucose levels down quickly to prevent complications and improve wellbeing. Because insulin and sulfonylureas lower blood glucose faster than most other diabetes medications, we’ll use these first, and once control is restored, switch to more suitable long-term treatment.

After that, we’ll move on to first-line regular drug treatment. The usual starting point is standard-release metformin. After starting a low dose, we will increase the dose gradually over several weeks to reduce the risk of gastrointestinal side effects, and if those occur, we can switch to a trial of modified-release metformin.

Metformin is recommended first because it’s been shown in large clinical trials to lower blood glucose with a low risk of hypoglycaemia, and it doesn’t promote weight gain. The UK Prospective Diabetes Study — or UKPDS — found that in people with type 2 diabetes who were overweight, metformin not only improved blood glucose control, but also reduced the risk of diabetes-related complications. Importantly, it also lowered their cardiovascular risk and overall mortality. These benefits, together with its long track record of safety, make metformin the preferred first-line treatment for most patients.

At the same time that we start metformin, we’ll assess the patient’s cardiovascular status and risk. The goal is to determine whether they have chronic heart failure, established atherosclerotic cardiovascular disease, or are at high risk of developing it.

We need to remember that established atherosclerotic cardiovascular disease includes conditions such as coronary heart disease, acute coronary syndrome, previous myocardial infarction, stable angina, ischaemic stroke or TIA, and peripheral arterial disease.

We also need to be aware that a high cardiovascular risk means a QRISK score above 10% in anyone aged 40 or over, or, for those under 40, having any one of these factors: hypertension, dyslipidaemia, smoking, obesity, or a family history in a first-degree relative of premature cardiovascular disease.

If the patient has chronic heart failure, established atherosclerotic cardiovascular disease, or is at high risk of developing cardiovascular disease, we’ll offer an SGLT2 inhibitor in addition to metformin — and we’ll do this regardless of their HbA1c level.

This approach is supported by strong evidence. Large randomised controlled trials, have shown that SGLT2 inhibitors not only improve blood glucose control but also reduce the risk of hospitalisation for heart failure, and in some cases lower cardiovascular mortality. These benefits are seen even in patients without diabetes, which highlights their role in protecting the cardiovascular system as well as the kidneys.

Now, when starting dual therapy with metformin and an SGLT2 inhibitor as first-line treatment, we’ll introduce the drugs sequentially. We will start with metformin first, then check tolerability, and then add the SGLT2 inhibitor as soon as metformin is confirmed to be well tolerated.

If metformin is contraindicated or not tolerated, our approach will also depend on the patient’s cardiovascular history and risk.

If they have chronic heart failure, established atherosclerotic cardiovascular disease, or are at high risk of developing it, we’ll offer an SGLT2 inhibitor as monotherapy. We do this because of the SGLT2 inhibitors cardiovascular benefits.

If the patient is not in any of these higher-risk groups, we can consider any other glucose-lowering treatments. Options include:

• a DPP-4 inhibitor
• pioglitazone
• a sulfonylurea
• or an SGLT2 inhibitor.

In order to make the right choice of drug, it may be a good idea here to give a comparative overview based on their effect on weight, hypoglycaemia risk etc.

And let’s start with weight. Although metformin was once thought to cause weight loss, NICE now describes it as weight neutral. DPP-4 inhibitors, or gliptins, are also generally weight neutral, meaning they usually don’t cause significant weight gain or loss. In contrast, SGLT2 inhibitors—also called flozins—tend to promote weight loss, which can be especially helpful for patients who are overweight or need to lower their cardiovascular risk. On the other hand, both Pioglitazone and Sulfonylureas are linked with weight gain, something to watch out for, particularly in patients where added weight could worsen insulin resistance or raise cardiovascular risk.

In terms of hypoglycaemia risk. Metformin, DPP-4 inhibitors, Pioglitazone, and SGLT2 inhibitors all carry a low risk of hypoglycaemia. However, Sulfonylureas stand out here with a much higher risk, especially in older adults or those with irregular meal patterns.

All these oral medications are contraindicated in diabetic ketoacidosis but SGLT2 inhibitors, in particular, carry a significant risk of ketoacidosis, including the unusual euglycemic form, so patients on these drugs need careful monitoring. Pioglitazone is also contraindicated in patients with current or past heart failure, as well as those with a history of bladder cancer or unexplained haematuria.

Renal function is another key factor. Most of these drugs need dose adjustments or close monitoring when kidney function is reduced. Metformin, for example, requires dose reduction or may need to be avoided depending on the patient’s eGFR. Most clinicians will reduce the dose of metformin to half if the eGFR is between 30 and 45 and metformin is stopped completely if eGFR falls below 30. Pioglitazone generally doesn’t require dose changes for kidney impairment, but it should still be used with caution.

Finally, liver impairment can affect how we prescribe these medications. Many require caution or should be avoided depending on the severity of liver disease. I won’t cover every detail here, but we should always consult the BNF before prescribing.

Because of what we said earlier about the increased risk of ketoacidosis, before starting someone on an SGLT2 inhibitor, we need to check if they might be at higher risk of diabetic ketoacidosis. This includes people who have had a previous episode of DKA, those who are currently unwell with an illness, or anyone following a very low carbohydrate or ketogenic diet.

And because of the risk that SGLT2 inhibitors carry in this respect, we will want to address any modifiable risks before starting them. For example, if someone is on a very low carb or ketogenic diet, they may need to delay treatment until they’ve stopped it. We will also advise them not to restart that kind of diet without talking to their healthcare team first, as they might need to stop the SGLT2 inhibitor if they do.

I will not go through all other possible side effects of SGLT2 inhibitors, but it’s important to know that SGLT2 inhibitors have been linked to a rare but serious infection called Fournier’s gangrene. This is a rapidly progressing infection of the genital and perineal area. It happens because SGLT2 inhibitors increase glucose in the urine, which can create an environment where bacteria grow more easily.

Patients at higher risk include those who are immunocompromised, have poor hygiene, or have other infections.

If Fournier’s gangrene develops, it can cause severe tissue damage and can quickly become life-threatening if not treated promptly. That’s why patients should be warned to look out for symptoms like redness, swelling, pain, or tenderness around the genital area, along with fever or feeling generally unwell.

If any of these symptoms appear, they should seek urgent medical care immediately, because early treatment is critical to prevent serious complications or the need for surgery.

And well, that brings us to the end of the first-line drug treatment section for type 2 diabetes.

There’s a separate part of the diabetes guideline that focuses on people with type 2 diabetes and chronic kidney disease, because they have some specific recommendations when it comes to SGLT2 inhibitors.

This section essentially says that, for patients with both CKD and type 2 diabetes, we start by giving an ACE inhibitor or an ARB, titrated up to the highest tolerated licensed dose if their albumin-to-creatinine ratio, or ACR, is 3 mg/mmol or higher.

Once they’re on this medication, we then add an SGLT2 inhibitor—on top of the ACEI or ARB—if their ACR is above 3 mg/mmol, especially if it’s over 30, and if they meet the appropriate eGFR thresholds for each particular SGLT2 inhibitor.

We also need to remember that not all SGLT2 inhibitors are licensed specifically for CKD. NICE has produced specific technology appraisals for dapagliflozin and empagliflozin for adults with chronic kidney disease. These two drugs can be given to CKD patients without type 2 diabetes specifically for their CKD management.

So that is it, a review of the first line drug management in type 2 diabetes. In the next episode, we will cover treatment options if further interventions are needed.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/t8U8-isTieM

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by them.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through recommendations on the diagnosis and monitoring of type 2 diabetes, which includes guidance by NICE. The links to the NICE guideline is in the episode description.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The NICE guideline on Type 2 diabetes in adults: management [NG28] can be found here:

·      https://www.nice.org.uk/guidance/ng28

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we’ll go through recommendations on the diagnosis and monitoring of type 2 diabetes using HbA1c, focusing on what is relevant in primary care only. This information includes guidance by NICE contained in the NICE guideline on Type 2 diabetes. The link to it is in the episode description.

Right, let’s jump into it.

Let’s start with the diabetic diagnostic thresholds. They could be:

• An HbA1c of 48 mmol/mol or 6.5% or more or
• A Fasting plasma glucose level of 7.0 mmol/L or more or
• A Random plasma glucose of 11.1 mmol/L or more in the presence of symptoms or signs of diabetes.

Why have these thresholds been chosen?

These thresholds are based on the evidence of glucose levels at which the risk of diabetes-related complications—particularly retinopathy—increases significantly.

They have been agreed in order to strike a balance between diagnostic accuracy and early intervention, helping to catch diabetes at a point where treatment can prevent progression and complications.

And let’s also remember that if the person has symptoms of diabetes, a single abnormal HbA1c or fasting plasma glucose level can be used, although repeat testing is always advisable to confirm the diagnosis.

However, If the person is asymptomatic, we should not diagnose diabetes on the basis of a single abnormal HbA1c or plasma glucose result. Instead, we should arrange repeat testing, preferably with the same test, to confirm the diagnosis. If the repeat test result is normal, we will monitor the person for the development of diabetes, and the frequency of such monitoring will depend on our clinical judgement.

This guidance to not diagnose diabetes in an asymptomatic person based on a single abnormal result is based on principles of biological variability, and the importance of avoiding misdiagnosis.

This is because Glucose levels and HbA1c can fluctuate due to a variety of reasons and a single abnormal result may not reflect the person's usual glycaemic status. Repeating the test helps rule out false positives due to possible transient factors or a lab artefact or error.

Can we use HbA1c and plasma glucose interchangeably to diagnose type 2 diabetes?

Well, in general, yes, but there are times when HbA1c should not be used to diagnose diabetes. This is the case for:

• Children and young people under the age of 18. 
• Pregnant women or women within 2 months postpartum. 
• People with symptoms of diabetes for less than 2 months. 
• People at high diabetes risk who are acutely ill.
• People taking medication that may cause hyperglycaemia (for example, long-term corticosteroids). 
• People with acute pancreatic damage, including pancreatic surgery.
• And People with end-stage renal disease (ESRD).

Additionally, HbA1c should be interpreted with caution in people with abnormal red blood cell turnover or abnormal haemoglobin type, like: 

• Abnormal haemoglobin, such as haemoglobinopathy, including sickle cell trait.
• Severe anaemia (of any cause).
• Altered red cell lifespan (for example, in post-splenectomy). 
• And a recent blood transfusion.

Why do we need caution in these situations?

Well, HbA1c reflects the percentage of haemoglobin that has glucose attached to it—essentially giving us an average of blood glucose over the past 2 to 3 months, which is the typical lifespan of a red blood cell. However, anything that alters red blood cell turnover or haemoglobin structure can affect the accuracy of this measurement. For example:

• In conditions like haemoglobinopathies (e.g. sickle cell trait or thalassaemia), the structure of haemoglobin is different, which can interfere with how HbA1c is measured or how glycation occurs.
• In severe anaemia or increased red cell turnover, red blood cells are cleared from the circulation more quickly, so there’s less time for glucose to attach—leading to falsely low HbA1c.
• Conversely, if red cells live longer than normal (such as after splenectomy), HbA1c may be falsely high because glucose has more time to accumulate.
• And finally, after a recent blood transfusion, the donor’s red blood cells—often with a different glycaemic history—can distort the result.

So, in these cases, HbA1c may not accurately reflect the patient’s glycaemic control, and alternative measures like fasting glucose or an oral glucose tolerance test may be more reliable.

What about diabetic monitoring?

NICE recommends that we should measure HbA1c levels in adults with type 2 diabetes:

• Every 3 to 6 months until HbA1c is stable on unchanging therapy or
• Every 6 months once the HbA1c and diabetic therapy are stable. 

If HbA1c monitoring is invalid because of disturbed erythrocyte turnover or abnormal haemoglobin type, we will need to estimate trends in blood glucose control using one of the following:

• quality-controlled plasma glucose profiles
• total glycated haemoglobin estimation (if there are abnormal haemoglobins) or
• fructosamine. 

What do these alternative forms of monitoring involve?

Well:

• Quality-controlled plasma glucose profiles involve measuring fasting and postprandial glucose at regular intervals, giving a day-to-day picture of control, although they don’t reflect long-term trends as well as HbA1c.
• Total glycated haemoglobin measures all forms of glycated haemoglobin (not just HbA1c), and may be more accurate when variant haemoglobins interfere with standard HbA1c assays.
• And finally, fructosamine reflects glycation of serum proteins (mainly albumin) rather than haemoglobin, giving an average of blood glucose over the past 2–3 weeks. As we have said, it's useful in cases where red blood cell lifespan is abnormal, but also in pregnancy, or when rapid changes in glucose control are occurring.

Each of these methods has limitations, but they can give a more reliable picture than HbA1c when red cell-related interference is present.

What about HbA1c targets?

NICE advises that we should discuss and agree an individual HbA1c target with patients, encouraging them to reach and maintain it, unless any resulting adverse effects (including hypoglycaemia), or their efforts to achieve their target impair their quality of life.

However, from a general perspective, for those managed either by lifestyle and diet alone, or combined with a single drug not associated with hypoglycaemia, we should aim for an HbA1c target of 48 mmol/mol (6.5%). For those on a drug associated with hypoglycaemia, we will aim for an HbA1c target of 53 mmol/mol (7.0%). 

In adults, if HbA1c levels are not adequately controlled by a single drug and rise to 58 mmol/mol (7.5%) or higher:

• we will review and reinforce their current treatment and
• then proceed to intensify drug treatment, generally by adding a second drug.

These thresholds are heavily influenced by the results of clinical trials such as the UKPDS (or United Kingdom Prospective Diabetes Study), which is still one of the most influential long-term RCTs on glycaemic control in type 2 diabetes.

It showed that intensive blood glucose control (targeting HbA1c around 53 or ~7.0%) significantly reduced:

• Microvascular complications (like retinopathy, nephropathy, and neuropathy).
• And additionally, long-term benefits for macrovascular outcomes emerged in extended follow-up giving rise to the so-called “legacy effect”

What is exactly the legacy effect?

Well, it describes the fact that participants in the UKPDS randomised controlled trial were followed for 10 years after the trial ended. Although the differences in HbA1c between intensive and conventional groups disappeared within a year, the intensive group still had significantly lower rates of both micro and macrovascular complications as well as all-cause mortality. In a way, this showed that early good control leaves a "metabolic imprint" that protects patients long term, even if later control becomes less strict.

However, although tight control can be beneficial, we will consider relaxing the target HbA1c on a case-by-case, with particular consideration for people who are older or frailer, if:

• they are unlikely to achieve longer-term risk-reduction benefits, for example, people with a reduced life expectancy
• if tight blood glucose control would put them at high risk if they developed hypoglycaemia, for example, if they are at risk of falling, they have impaired hypoglycaemia awareness, or they drive or operate machinery as part of their job
• or if intensive management would not be appropriate, for example if they have significant comorbidities. 

This is because there is strong evidence that in older or frail adults, sometimes the risks of hypoglycaemia may outweigh the benefits of strict control. In particular, the ACCORD Trial found that intensive glucose lowering (with a target HbA1c of less than <6.0%) increased all-cause mortality in people with type 2 diabetes at high cardiovascular risk. In fact, the trial had to be stopped early due to this excess mortality. Our take home message is that tight control is not always safe, especially in older, comorbid populations.

On the other hand, if the HbA1c level is lower than their target and they are not experiencing hypoglycaemia, we will encourage them to maintain it, being aware that there are other possible reasons for a low HbA1c level, for example deteriorating renal function or sudden weight loss. 

So that is it, a review of the diagnosis and monitoring of type 2 diabetes.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/j5z0Qv35dWE

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through new and updated recommendations published in July 2025 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The Full NICE News bulletin for July 2025 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2025-07-01&to=2025-07-31&ndt=Guidance&ndt=Quality+standard

The updated quality standard Cardiovascular risk assessment and lipid modification [QS100]  can be found here:

·      https://www.nice.org.uk/guidance/qs100

The new technology appraisal Dapagliflozin for treating chronic kidney disease [TA1075] can be found here:

·      https://www.nice.org.uk/guidance/ta1075

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we’ll look at the NICE updates published in July 2025, focusing on what is relevant in Primary Care only.

Today we just have two clinical areas to discuss, the updated quality standard on cardiovascular risk assessment and a new technology appraisal on Dapagliflozin for CKD.

Right, let’s jump into it.

There are only 5 updated quality standard on cardiovascular risk assessment and lipid modification, so let’s have a look at them:  

Quality statement 1 refers to the identification of adults who are likely to be at high CV risk.

What does the new statement say?

It says that General practices should systematically search their patient records to identify people who are likely to be at high risk of CVD. Using routinely collected data, practices can estimate someone's 10-year risk of CVD ideally using the QRISK3 tool.

What’s different from the old guideline?

Previously, the guidance said that If a person between 25–84 was flagged as having an increased CVD risk, we would offer them a formal QRISK3 assessment.

Now, the focus is to use a proactive, structured search of patient records to find those likely to be at risk. So instead of waiting for risk to be flagged, we now go looking for it.

However, we have to be cautious and use clinical judgment, especially in groups which may have missing or incomplete data in their records, which can lead to their risk being underestimated.

Let’s now look at Quality Statement 2, which covers Diet and lifestyle advice for primary prevention.

What does the new guideline say?

Someone with a CVD risk of 10% or more, should be given lifestyle advice and this should happen within 3 months of their risk score being recorded.

What’s different from the older guidelines?

The previous (now obsolete) standards said that:

• People should be assessed for secondary causes before being offered statins and that
• They should get lifestyle advice before being offered statins.

So, this update simplifies and strengthens this advice. Everyone with a ≥10% CVD risk should get lifestyle advice within 3 months. It's no longer just a “before statins” step. It’s a core part of primary prevention.

Let’s move on to Quality Statement 3, on Lipid-lowering treatment for primary prevention.

What does the new guideline say?

People with a 10-year CVD risk of 10% or more should be prescribed a high-intensity statin unless it's not suitable for them. If they can’t tolerate statins or have a medical reason not to take them, then an alternative lipid-lowering treatment should be offered.

The recommended statin here is atorvastatin 20 mg, which is proven to be effective.

What’s different?

Under the obsolete standards we were first advised to try lifestyle changes, and only if those changes were ineffective or unsuitable, would a discussion about statin therapy take place

Now, the emphasis is on timely treatment. If a person has a 10-year CVD risk of 10% or more, and they choose to start treatment, they should be prescribed a high-intensity statin straightaway, usually atorvastatin 20 mg. There is no longer a requirement to try lifestyle changes first. While lifestyle advice remains important, it’s not a prerequisite to offering statins. This change reflects stronger evidence that earlier intervention with statins in high-risk people can significantly reduce the risk of CVD events.

But let’s remember other key considerations:

• For those close to the 10% threshold, we will need to use our clinical judgement.
• For Trans people we need to be aware that QRISK3 needs the biological sex, which may not reflect an individual’s gender identity, so adjustment may be necessary.
• And for people aged 85 and over: Atorvastatin 20 mg may still be appropriate, but we should consider factors like frailty, comorbidities, polypharmacy, etc.

Quality statement 4 refers to Assessing response to lipid-lowering treatment. This one focuses on how we monitor people after starting or changing lipid-lowering treatment, such as statins.

The obsolete guidance recommended that adults on a high-intensity statin should have a repeat lipid profile and liver transaminase levels measured after 2 to 3 months.

What’s changed?

The new quality statement broadens this. It now applies to all adults starting or changing any lipid-lowering treatment, not just those on high-intensity statins.

This change recognises that monitoring response and safety is important for everyone, not just high-intensity statin users.

And let’s remember that Fasting is not required for a full lipid profile, which should include

• Total cholesterol
• HDL cholesterol and
• Triglycerides
• And that, from these, non-HDL and LDL cholesterol are calculated

Let’s now look at the final quality statement, Quality statement 5 which focuses on Secondary prevention of cardiovascular disease

The previous (now obsolete) guidance said that people newly diagnosed with CVD should be offered atorvastatin 80 mg and that, if someone developed side effects, they should be offered a lower dose or a different statin.

What’s changed?

The new guidance shifts the focus from prescribing a specific drug or dose to achieving a specific cholesterol target. It says that people with CVD should have either:

• An LDL cholesterol which is 2 or below (≤ 2.0 mmol/L),
• Or a non-HDL cholesterol which is 2.6 or below (≤ 2.6 mmol/L)

This is a move toward outcome-focused care, rather than just prescribing a medication and assuming it's effective.

So, instead of asking:

"Did we prescribe atorvastatin 80 mg?"

We now ask:

"Has this person’s cholesterol actually reached a level that protects them?"

Besides, using non-HDL cholesterol as an alternative to LDL is helpful when LDL hasn't been specifically measured or calculated. Let’s remember that, for example,  LDL may not be calculated in people with very high triglycerides.

Let’s now take a few minutes to go through the updated NICE guidance on dapagliflozin for chronic kidney disease. This updated recommendation replaces earlier guidance and reflects both new evidence and a broader treatment scope for patients with CKD.

So, what’s changed?

Under the previous guidance dapagliflozin was only recommended for people with CKD, with or without type 2 diabetes, but only if their eGFR was between 25 and 75.

This meant that certain patients were excluded — for example:

• Those with mild CKD and an eGFR above 75
• Those with an eGFR between 25 and 45 with normal levels of albumin in their urine
• And notably, those without diabetes and without significant proteinuria

At the time, these restrictions were based mostly on the inclusion criteria of the DAPA-CKD trial, and also concerns that the size of the eligible population might have been overestimated.

Now, with this update, things have shifted significantly.

The new guidance states that dapagliflozin can be used more widely, in people with an eGFR between 20 and 90 as long as certain conditions are met.

For people with an eGFR between 20 and 45, no additional criteria are required.

But for those with an eGFR between 45 and 90, they must also either:

• Have type 2 diabetes, or
• Have a urine albumin-to-creatinine ratio or ACR of 22.6 milligrams per millimole or more

So, this new recommendation includes a much broader group of patients, especially those with early-stage CKD and diabetes, or those with elevated proteinuria but better preserved kidney function.

Why has it changed?

The change is due to new evidence, including meta-analyses and indirect treatment comparisons between dapagliflozin and empagliflozin. While the two haven’t been directly compared in a clinical trial, the available data suggest that they are similarly effective and safe for people with CKD.

Also, the costs of dapagliflozin and empagliflozin are comparable, so there’s no financial reason to prefer one over the other.

As a result, NICE has aligned the eligible population for dapagliflozin with that of empagliflozin creating a consistent and flexible approach to SGLT2 inhibitor use in CKD.

It also reflects a more inclusive and practical approach, one that gives patients better access to effective treatment and gives clinicians greater flexibility when choosing between dapagliflozin and empagliflozin.

So that is it, a review of the NICE updates relevant to primary care.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/sUlAwcaUrB0

The first episode can be found here:

·      https://youtu.be/nguVbiQc5Ww

This episode makes reference to guidelines produced by the European Association of Urology. The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by them.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through the recommendations by the European Association of Urology (EAU) on male hypogonadism, focusing on what is relevant in Primary Care only. The links to the guideline is in the episode description.

Today’s episode covers the clinical presentation, interpretation of test results, and a brief overview of the management.

The previous episode focused on the definition, classification, causes, and clinical associations of male hypogonadism.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The EAU sexual and reproductive health full guideline can be found here:

·      https://uroweb.org/guidelines/sexual-and-reproductive-health/chapter/male-hypogonadism

The EAU pocket guideline can be found here:

·      https://d56bochluxqnz.cloudfront.net/documents/pocket-guidelines/EAU-Pocket-on-Sexual-Reproductive-Health-2025.pdf

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we’ll I go through the recommendations by the European Association of Urology (or EAU) on male hypogonadism, focusing on what is relevant in Primary Care only. The link to the guideline is in the episode description.

In today’s episode, we’ll focus on late-onset hypogonadism, its presentation, interpretation of test results, and a brief overview of the general management.

If you haven’t already, I recommend that you check the previous episode where we cover the definition, classification, causes, and clinical associations of male hypogonadism.

Right, let’s jump into it.

The diagnosis of functional hypogonadism is based on the exclusion of an organic or structural cause. The main causes suggested for functional hypogonadism are obesity, comorbidities and ageing, with the first two accounting for most cases. This is because the evidence shows that chronic comorbidities can interfere with the HP testicular axis leading to functional hypogonadism. In fact, the role of ageing in hypogonadism up to age 80 years seems relatively small.

Late onset hypogonadism is a term that is used, frequently incorrectly to describe the declining testosterone production due to ageing or simply the detection of hypogonadism in adults.

However, the truth is that late onset hypogonadism is in fact a broad clinical entity including adult-onset forms which can have an organic or functional origin and can be primary or secondary. Late onset hypogonadism is frequently diagnosed in the absence of an identifiable organic cause, and it becomes more prevalent with age. By definition LOH must comprise both persistent specific symptoms and biochemical evidence of testosterone deficiency.

The mainstay of LOH diagnosis includes signs and symptoms consistent with hypogonadism coupled with biochemical evidence of low morning total testosterone levels on two or more occasions, measured in fasting conditions.

In the history, we will take note of specific symptoms associated with hypogonadism. Symptoms can be grouped into three main categories: sexual, physical, and psychological.

Examples of sexual Symptoms include:

• Reduced libido
• Erectile dysfunction
• Fewer spontaneous erections
• Less frequent sexual activity or masturbation and
• Delayed ejaculation

Examples of Physical Symptoms are

• Reduced ability to perform vigorous activities
• Difficulty walking more than 1 kilometre
• Hot flushes
• Lower energy levels and
• Reduced physical strength

And finally, examples of Psychological Symptoms include

• Low mood
• Loss of motivation
• General fatigue
• Difficulty concentrating and
• sleep disturbances

As we can see, some of these symptoms are non-specific and need to be taken in context with the clinical and biochemical state. Also, headache and/or visual disturbance may indicate a pituitary related disorder.

As part of the physical examination, BMI and the measurement of waist circumference are strongly recommended for everyone. This is because of the strong association between hypogonadism and obesity. Testicular and penile size, as well the presence of sexual secondary characteristics can also provide useful information regarding the overall androgen status. Finally, digital rectal examination (DRE) should be performed before testosterone therapy or to support suspicion of hypogonadism where we would normally expect reduced prostatic volume.

How should we investigate male hypogonadism? The main initial test is obviously serum testosterone.

Testosterone levels are produced in a circadian variation, which may persist in ageing men. Testosterone levels are also potentially influenced by food intake therefore, serum total testosterone should be measured in fasting conditions and in the morning, usually between 07.00 and 11.00 o’clock. A confirmatory measurement should always be undertaken in the case of an abnormal value.

A testosterone of 12 nmol/L should be considered as a possible threshold for starting testosterone therapy in the presence of typical symptoms.

If abnormal total testosterone levels are found, we should check LH and FSH along with prolactin (PRL) in order to investigate possible underlying conditions and exclude possible organic causes. Let’s look at these tests individually:

FSH and LH levels can help differentiate between the diagnosis of primary or secondary hypogonadism. In primary hypogonadism, testosterone will be low and gonadotropins will be high, In secondary hypogonadism, testosterone will be low and gonadotropins will be low or inappropriately normal.

Due to its negative influence on libido, PRL should also be considered as a first-line screening test in patients with reduced sexual desire.

In addition, contrast-enhanced pituitary MRI scanning, as well as other pituitary hormone evaluations, is required in the presence of specific symptoms such as visual disturbances, headache and when hyperprolactinemia is confirmed.

We also need to be aware that total testosterone values may change as a function of circulating SHBG levels.

Let’s now look at the factors that may affect SHBG concentrations:

Common Conditions That Increase SHBG include:

• Certain drugs, like anticonvulsants, oestrogens, and thyroid hormone
• Hyperthyroidism
• Liver disease
• Ageing
• Smoking and
• HIV or AIDS

A high SHBG can lead to lower free testosterone, even if total testosterone looks normal.

Conversely, and although not connected to hypogonadism, Conditions That Decrease SHBG levels include:

• Drugs like glucocorticoids, testosterone, or anabolic steroids
• Hypothyroidism
• Obesity
• Cushing’s syndrome
• Insulin resistance, as seen in metabolic syndrome or type 2 diabetes and
• Non-alcoholic fatty liver disease (NAFLD) and related conditions

A low SHBG can lead to higher free testosterone, and it may be a sign of underlying metabolic issues.

Therefore, Understanding SHBG levels is important because it helps us interpret total testosterone results more accurately, especially in men with metabolic or endocrine disorders.

In clinical conditions that may affect SHBG levels, checking free testosterone can be considered. However, there is currently no consensus on threshold values, so this remains an area of uncertainty.

Having considered all this, let’s look at a Step-by-Step Approach to Evaluating Male Hypogonadism.

Firstly, we will Start with a clinical suspicion, so if a man presents with symptoms like fatigue, low libido, erectile dysfunction, or reduced muscle mass, we should consider hypogonadism.

As initial lab test for hypogonadism, we will check total testosterone, ideally in a morning fasting sample (between 7–11 AM).

If the result:

• Is low or borderline, we will repeat the testosterone to confirm it and add LH, FSH, prolactin and possibly SHBG and free testosterone depending on our clinical judgement.
• However, if the result Is normal, then hypogonadism is unlikely. However, if symptoms are strong and highly suspicious, we could consider repeating the test and checking other tests, including free testosterone.

If the repeat sample confirms low testosterone then we will need to differentiate the type of hypogonadism by looking at the gonadotropins:

• If testosterone is low and LH/FSH is high, we are looking at Primary hypogonadism (which in principle would be a testicular problem)
• However, if testosterone is low and LH / FSH is low or normal, then we are looking at Secondary hypogonadism (which would refer to a hypothalamic or pituitary problem)

Depending on the type, we will take the following Next steps:

• For primary hypogonadism:
• We can consider karyotyping (like e.g. Klinefelter syndrome) and
• We will refer to Urology to fully assess testicular function
• For secondary hypogonadism:
• We should consider referral and further imaging such as a pituitary MRI scan to exclude pituitary tumours and
• We should also assess for chronic illness, obesity, metabolic disorders and medications that could interfere with the hypothalamic pituitary axis

Additionally, if SHBG is abnormal (e.g. in obesity, ageing, or liver disease), we could also consider, if not already done, checking free testosterone, as this may give a better diagnostic clarity.

In terms of management, I will not say much because the treatment will be guided by secondary care. I will just mention that, generally, Patients with symptomatic hypogonadism (usually with a total testosterone < 12 nmol/L) without specific contraindications are given testosterone therapy.

Absolute contraindications for testosterone therapy are untreated breast and prostate cancer (PCa) and conditions such as cardiovascular events, a Haematocrit ≥ 54% and poorly controlled congestive heart failure.

There are a range of relative contraindications and cautions, which will need to be considered by secondary care.

Finally, we will need to Check the patient’s fertility needs. If the patient wants to maintain fertility, we should avoid testosterone therapy in secondary hypogonadism and consider alternatives like gonadotropins instead. This is because Testosterone therapy suppresses gonadotropin and endogenous testosterone secretion as well as spermatogenesis, reducing fertility as a result.

So that is it, a review of late-onset hypogonadism, its presentation, interpretation of test results, and a brief overview of management.

Remember to check the previous episode where we covered the definition, classification, causes, and clinical associations of male hypogonadism.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/OcxWFhMAbPQ

This episode makes reference to guidelines produced by the European Association of Urology. The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by them.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through the recommendations by the European Association of Urology (EAU) on male hypogonadism, focusing on what is relevant in Primary Care only. The links to the guideline is in the episode description.

Today’s episode covers the definition, classification, causes, and clinical associations of male hypogonadism.

The next episode will focus on the clinical presentation, interpretation of test results, and a brief overview of the management.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:  

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The EAU sexual and reproductive health full guideline can be found here:

·      https://uroweb.org/guidelines/sexual-and-reproductive-health/chapter/male-hypogonadism

The EAU pocket guideline can be found here:

·      https://d56bochluxqnz.cloudfront.net/documents/pocket-guidelines/EAU-Pocket-on-Sexual-Reproductive-Health-2025.pdf

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we’ll I go through the recommendations by the European Association of Urology (or EAU) on male hypogonadism, focusing on what is relevant in Primary Care only. The link to the guideline is in the episode description.

In today’s episode, we’ll cover the definition, classification, causes, and clinical associations of male hypogonadism.

In the next episode, we’ll focus on the clinical presentation, interpretation of test results, and a brief overview of the management.

Right, let’s jump into it.

Male hypogonadism is a clinical condition characterised by symptoms (with or without physical signs) and confirmed by low testosterone levels. Hypogonadism is linked to reduced testicular function, leading to decreased production of androgens (such as testosterone) and/or impaired sperm production.

This may result from a primary problem within the testes (that is, primary hypogonadism) or from insufficient stimulation by the hypothalamic–pituitary axis (or secondary hypogonadism). In rare cases, it may be due to reduced cellular response to testosterone.

Hypogonadism can negatively affect various organ systems and overall quality of life. This episode focuses on the management of adult male hypogonadism, also known as late-onset hypogonadism (LOH), although it may include some comments on congenital or pre-pubertal forms of the condition.

The prevalence of LOH increases with age, with the major causes being obesity, other co-morbidities (e.g., diabetes) and overall poor health. Ageing accounts for a low percentage of hypogonadism, as there is only a small gradual decline in testosterone, up to the age of 80 years, in healthy ageing men.

There is a high prevalence of LOH within specific populations, including patients with obesity, type 2 diabetes (T2DM), metabolic syndrome (MetS), cardiovascular disease (CVD), chronic obstructive pulmonary disease (COPD), renal disease and cancer. In particular low testosterone levels are relatively common in men with T2DM and in those with metabolic abnormalities.

Klinefelter syndrome, a trisomy associated with a 47,XXY karyotype, is the most prevalent genetic cause of primary hypogonadism, with a global prevalence of 1/500-1,000 live male births. However, < 50% of individuals with Klinefelter syndrome are diagnosed during their lifetime.

Male hypogonadism can be classified according to the cause into primary hypogonadism or secondary hypogonadism. A compensated or subclinical form of hypogonadism, characterised by normal testosterone and a high LH, has also been reported but the clinical significance of this condition is unclear.

The classification of hypogonadism has also been divided into two broad categories: ‘Classical or Organic’ and ‘Functional’.

Classical hypogonadism includes: congenital or acquired diseases causing structural and/or irreversible impairment of the pituitary and/or testes.

Functional hypogonadism is diagnosed in the absence of any recognised organic abnormality and it is mainly a consequence of co-morbidities. It should be treated first by improving the underlying condition (e.g., anorexia in a younger male).

Late onset hypogonadism represents an even broader clinical entity including adult-onset forms which can have an organic or functional origin and can be primary or secondary. Late onset hypogonadism is in the majority of cases diagnosed in the absence of an identifiable organic cause. By definition LOH must comprise both persistent specific symptoms and biochemical evidence of testosterone deficiency.

Finally, as we said earlier, in rare cases, it may be due to reduced cellular response to testosterone and its metabolites.

The European association of urology guideline maintains a classification of Primary and Secondary Hypogonadism, with special reference to LOH.

Classifying hypogonadism by its underlying cause will also help guide treatment options. For example, in secondary hypogonadism, both fertility and testosterone levels can potentially be restored with proper therapy. In contrast, primary hypogonadism usually requires testosterone replacement, which can impair fertility by suppressing the hypothalamic–pituitary–testicular (HPT) axis.

We need to remember that when hypogonadism develops after puberty—especially as men age—its symptoms may be mild and often mistaken for normal ageing.

Let’s now look at some common causes for the three main categories of male hypogonadism. Please note that this list is not exhaustive.

In Primary Hypogonadism we can have congenital and acquired causes.

Common congenital causes of primary hypogonadism include:

• Klinefelter syndrome – the most common
• Other chromosomal disorders, like Down syndrome
• And also, conditions like sickle cell disease, amongst others

Acquired causes of primary hypogonadism include:

• Drug-related like, for example, in
• Chemotherapy drugs and
• Testosterone synthesis blockers like ketoconazole
• Direct testicular damage, like, for example:
• Bilateral orchidectomy or testicular trauma
• Radiation to the testes and
• Infective or autoimmune orchitis
• And finally systemic diseases that affect the testes, like for example:
• Chronic illnesses
• Cushing’s syndrome
• HIV and
• Cancers like lymphoma or testicular cancer

In Secondary Hypogonadism we also have congenital and acquired causes.

Congenital causes of secondary hypogonadism include:

• Haemochromatosis and
• Other genetic or idiopathic causes

Acquired causes of secondary hypogonadism include:

• Drugs that suppress the hypothalamus or pituitary, like for example:
• Oestrogens and progestogens
• Testosterone or anabolic steroids
• Drugs that increase prolactin
• Opiates and
• Corticosteroids
• Local problems in the brain, like, for example:
• Head trauma
• Tumours in the pituitary or hypothalamus
• Surgery or radiation to the pituitary gland and
• Infections or inflammation in the brain
• And finally systemic conditions that affect brain hormone control, such as, for example:
• Type 2 diabetes and metabolic syndrome
• Chronic organ failure
• HIV
• Rheumatoid arthritis and other chronic inflammatory diseases
• Cushing’s syndrome and
• Eating disorders

I will only touch briefly on the Androgen Resistance or Reduced Testosterone Activity type, where testosterone levels may be normal, but the body can't respond properly to it.

Causes include:

• Genetic conditions affecting androgen receptors
• Drugs that interfere with testosterone function
• High levels of SHBG (sex hormone-binding globulin), which reduces free testosterone and
• Conditions like coeliac disease, which can also interfere with hormone action

Let’s now look in more detail into comorbidities associated with male hypogonadism

And the first one is obesity. Low testosterone levels are common in obese men. Male hypogonadism is associated with a greater percentage of fat mass and low testosterone levels are strongly associated with increased visceral adiposity, lipid deposition in the liver and muscle and atherosclerosis.

The second one is Metabolic Syndrome (MetS) and Type 2 Diabetes (T2DM), given that male hypogonadism is commonly associated with Metabolic Syndrome and its individual components, including:

• Central obesity
• Hyperglycaemia
• Insulin resistance
• Dyslipidaemia and
• hypertension

Additionally, several randomised controlled trials (RCTs) have shown that testosterone therapy can:

• Improve insulin resistance
• Reduce blood glucose levels
• Lower total cholesterol and LDL cholesterol

Some studies suggest that testosterone therapy in men with MetS and low testosterone may be associated with reduced mortality compared to those who are untreated, although the results are not conclusive.

Erectile dysfunction is very common in men with MetS and T2DM. Additionally, although ED is multifactorial, up to 30% of men with ED also have testosterone deficiency. This means that

• Men presenting with ED should be screened for Metabolic Syndrome and diabetes but also that
• Those with ED should also have their testosterone levels measured to screen for possible hypogonadism, especially if they have diabetes or metabolic syndrome.

I will also just finally mention that data suggest that low testosterone levels are more frequently associated with worse clinical outcomes in men with COVID-19 although the link and the exact implications are still under investigation.

So that is it, a review of the definition, causes and clinical associations of male hypogonadism.

Remember that in the next episode I will cover late onset hypogonadism in more detail including the clinical presentation, laboratory testing and its interpretation and a brief overview of the general management.  

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/nguVbiQc5Ww

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE" and Public Health England. The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by them.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through the recommendations on H Pylori testing and treatment, focusing on what is relevant in Primary Care only. It is based on the NICE guideline on Gastro-oesophageal reflux disease and dyspepsia in adults (CG184) and the quick reference guide on the subject by Public Health England. The links to them are in the episode description.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

Eradication regimens:

First-line treatment

Offer people who test positive for H pylori a 7‑day, twice-daily course of treatment with:

·      a PPI and

·      amoxicillin and

·      either clarithromycin or metronidazole.

Choose the treatment regimen with the lowest acquisition cost, and take into account previous exposure to clarithromycin or metronidazole. 

Offer people who are allergic to penicillin a 7‑day, twice-daily course of treatment with:

·      a PPI and

·      clarithromycin and

·      metronidazole. 

Offer people who are allergic to penicillin and who have had previous exposure to clarithromycin a 7‑day course of treatment with:

·      a PPI and

·      bismuth and

·      metronidazole and

·      tetracycline.

Second-line treatment

Offer people who still have symptoms after first-line eradication treatment a 7‑day, twice-daily course of treatment with:

·      a PPI and

·      amoxicillin and

·      either clarithromycin or metronidazole (whichever was not used first line). 

Offer people who have had previous exposure to clarithromycin and metronidazole a 7‑day course of treatment with:

·      a PPI and

·      amoxicillin and

·      tetracycline (or, if a tetracycline cannot be used, levofloxacin).

Offer people who are allergic to penicillin (and who have not had previous exposure to a fluoroquinolone antibiotic) a 7‑day, twice-daily course of treatment with:

·      a PPI and

·      metronidazole and

·      levofloxacin.

Offer people who are allergic to penicillin and who have had previous exposure to a fluoroquinolone antibiotic a 7‑day course of:

·      a PPI and

·      bismuth and

·      metronidazole and

·      tetracycline.

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The NICE clinical guideline on Gastro-oesophageal reflux disease and dyspepsia in adults (CG184) can be found here:

·      https://www.nice.org.uk/guidance/cg184

The NICE recommendations organised by site of cancer on the guideline Suspected cancer: recognition and referral can be found here:

·      https://www.nice.org.uk/guidance/ng12/chapter/Recommendations-organised-by-site-of-cancer#upper-gastrointestinal-tract-cancers

The Public Health quick reference guide on Helicobacter pylori in dyspepsia: test and treat can be found here:

·      https://www.gov.uk/government/publications/helicobacter-pylori-diagnosis-and-treatment

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we’ll I go through the recommendations on H Pylori testing and treatment, focusing on what is relevant in Primary Care only. It is based on the NICE guideline on Gastro-oesophageal reflux disease and dyspepsia and the quick reference guide on the subject by Public Health England. The links to them are in the episode description.

Right, let’s jump into it.

What is helicobacter pylori and why is it relevant?

Helicobacter pylori (also commonly referred to as simply H. pylori) is a gram-negative bacterium that colonises the human gastric mucosa. It’s usually acquired in childhood and persists unless treated.

Now, in terms of prevalence, we see big differences between developed and developing countries:

·      In developing countries, prevalence can exceed 70–80% in adults, largely due to poor sanitation, crowded living conditions, and limited access to clean water.

·      In contrast, in developed countries, the prevalence is much lower—usually around 20–40%—and continues to decline. Better hygiene, sanitation, and widespread antibiotic use are key reasons for this.

Overall, socioeconomic status, living conditions, and age are the main factors influencing prevalence.

So why is H. pylori important?

H Pylori plays a key role in the development of chronic gastritis and peptic ulcer disease and is a major risk factor for gastric adenocarcinoma and MALT lymphoma.

Here’s how it works: H. pylori infection reduces mucosal defences and increases gastric acid secretion, which together lead to ulcer formation, particularly in the stomach and duodenum. On top of that, the ongoing presence of the bacteria triggers a chronic inflammatory response that causes chronic gastritis. Chronic gastritis, over time, can progress to atrophic gastritis, then intestinal metaplasia, then dysplasia—and eventually, adenocarcinoma.

Now, let’s look at MALT lymphoma—MALT stands for mucosa-associated lymphoid tissue—H. pylori infection stimulates the development of this tissue in the stomach, which isn’t normally there. The chronic stimulation by the bacteria drives B-cell proliferation and can eventually lead to malignant transformation into low-grade B-cell lymphoma. Interestingly, in early-stage MALT lymphoma, H. pylori eradication alone can lead to regression of the lymphoma. That really highlights how central the bacterium is in the disease process.

So, how do we test for H. pylori?

The main options are the urea breath test and stool antigen test. There's also serology, though we are advised against using that routinely.

The urea breath test is the most accurate, but it needs a prescription and staff time to carry out—so it’s not always practical in primary care. In most cases, we’ll use a stool antigen test instead.

We need to remember that recent or ongoing PPI use can reduce the bacterial load and increase the chance of a false-negative result—particularly with breath and stool tests. So, if the patient has been on a PPI, we should stop it and leave a two-week washout period before testing.

The H Pylori serology test has a low cost but also a lower accuracy so it is not recommended for most patients, and positive results should be confirmed by a second test such as a Urea Breath Test, or biopsy. H Pylori serology has very good negative predictive value in low prevalence developed countries and it is most useful in patients with acute gastrointestinal bleed, to confirm a negative urea breath test or stool antigen test when there is a possibility that blood and PPI use would make those test results unreliable. Serology testing detects IgG antibodies, so it does not differentiate active from past infection. Near patient H Pylori serology testing is not recommended and only locally validated laboratory-based serology are acceptable. Additionally, Public Health England states that we should not use serology testing post eradication therapy or in children and the elderly.

What does NICE say about when to test?

H. pylori testing is addressed in two areas of the NICE guideline:

– Uninvestigated and functional dyspepsia and

– Peptic ulcer disease

Let’s look at dyspepsia first.

And to clarify, the term dyspepsia is used broadly in primary care—it includes recurrent epigastric pain, heartburn or acid reflux, with or without bloating, nausea, or vomiting.

For these patients—if there are no alarm symptoms—we follow a ‘test and treat’ approach for H. pylori.

But before we go further, let’s remind ourselves of the alarm symptoms and what to do if they’re present.

If someone presents with significant acute GI bleeding, we will refer them immediately to A&E.

We will also refer under the suspected cancer pathway to exclude oesophageal or stomach cancer if they have:

– Dysphagia,

– Or if they’re aged 55 or over, have weight loss, and also have either upper abdominal pain, reflux, dyspepsia, or a mass suggesting stomach cancer.

We should also consider direct access upper GI endoscopy in:

People of any age with a history of haematemesis or

In people aged 55 and over with:

– Treatment-resistant dyspepsia or

– Upper abdominal pain with low haemoglobin or

– Raised platelets with any upper GI symptoms, like nausea, vomiting, weight loss, reflux, dyspepsia or upper abdominal pain or

– Or nausea or vomiting with either weight loss, reflux, dyspepsia or upper abdominal pain

Now, let’s go back to dyspepsia without alarm features.

In these cases, we’ll test for H. pylori. If the patient has already been prescribed a PPI, we’ll stop it and wait at least two weeks before testing, because—as we have already said—PPIs can interfere with the test result.

Once testing is done, we will offer a four-week course of a full-dose PPI for dyspepsia. If H. pylori is detected and eradication treatment given, we will not routinely re-test in cases of functional dyspepsia. This is because 64% of patients with functional dyspepsia will have persistent recurrent symptoms, so re-testing after eradication is not recommended.

However, things are different in peptic ulcer disease.

Here, we test for H. pylori and, if positive, we will treat it. But unlike with functional dyspepsia, we will re-test after eradication therapy—usually 6 to 8 weeks after starting treatment, depending on the size of the lesion.

And while we usually do the initial test with a stool antigen test, when it comes to re-testing, we should use the urea breath test instead. That’s because there isn’t enough evidence to support using the stool test to confirm successful eradication.

So, in summary, NICE recommends testing for H Pylori in uninvestigated dyspepsia and in peptic ulcer disease. Additionally, Public Health England adds that we could also test in other scenarios, like patients before taking NSAIDs, if they have a prior history of gastro-duodenal ulcers/bleeds, as well as patient with unexplained iron-deficiency anaemia, after negative endoscopic investigation has excluded gastric and colonic malignancy, and investigations have excluded all other potential causes.

Now that we know when to test for H Pylori, are there cases where we shouldn’t routinely test?

And the answer is yes. NICE doesn’t recommend routine H. pylori testing in patients with proven oesophagitis or with predominant symptoms of gastro-oesophageal reflux disease. Public Health also advises against testing children with functional dyspepsia. In these cases, if further assessment is needed, we should refer them to secondary care.

So, what do we do with the test results?

If the result is negative, we can reassure the patient. The negative predictive value of all tests is over 95%, especially in low-prevalence settings like the UK.

If the result is positive, we will offer eradication therapy. That means a 7-day, twice-daily course of a PPI plus two antibiotics.

NICE recommends the following PPI doses twice a day for eradication therapy:

– Esomeprazole or rabeprazole: 20 mg

– Omeprazole: 20 or 40 mg

– Lansoprazole: 30 mg

– Pantoprazole: 40 mg

For first-line treatment, we combine the PPI with amoxicillin and either clarithromycin or metronidazole. If the patient is allergic to penicillin, we will use both clarithromycin and metronidazole.

There are other regimens depending on whether the patient has had previous exposure to clarithromycin or metronidazole, whether they have penicillin allergy or not and whether we are looking at first line or second line treatment. I will not go through all the different possible regimens, as you can look at all the different possibilities in the NICE guideline on dyspepsia. I have also put all the recommended regimens in the episode description.

If eradication therapy is not successful with second-line treatment we will seek advice from a gastroenterologist. 

So that is it, a review of the assessment and management of cluster headache.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/GelDVWruIlA

The link to the video on updated migraine management can be found here:

·      https://youtu.be/LumBxN-yFmI

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through the updated NICE recommendations on the diagnosis and management of cluster headaches, focusing on those that are relevant to Primary Care only. It is based on the clinical guideline on headaches in over 12s: diagnosis and management [CG150].

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The updated clinical guideline Headaches in over 12s: diagnosis and management [CG150] can be found here:

·      https://www.nice.org.uk/guidance/cg150

The MHRA advice on the use of topiramate can be found here:

·      https://www.gov.uk/drug-safety-update/topiramate-topamax-introduction-of-new-safety-measures-including-a-pregnancy-prevention-programme

The NICE recommendations organised by site of cancer on the guideline Suspected cancer: recognition and referral can be found here:

·      https://www.nice.org.uk/guidance/ng12/chapter/Recommendations-organised-by-site-of-cancer#brain-and-central-nervous-system-cancers 

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we’ll I go through the updated NICE recommendations on the diagnosis and management of cluster headache, focusing on what is relevant in Primary Care only. It is based on the NICE guideline on headaches or CG150 and the link to it is in the episode description.

Right, let’s jump into it.

Cluster headaches are a primary headache disorder. Let’s remember that we classify headache disorders as either primary or secondary. The cause of primary headaches isn’t well understood, so we group them by clinical pattern. The most common primary headache disorders are tension-type headache, migraine, and cluster headache.

By the way, if you are interested in the updated management of migraines, check the corresponding episode on this channel. The link to it is in the episode description.

Secondary headaches are due to underlying disorders including medication overuse headache, giant cell arteritis, raised intracranial pressure, and infection.

Headaches are very common and there’s often concern about possible underlying causes from both patients and healthcare professionals.

So, firstly, let’s look at when we need to consider further investigations or referral.

The NICE cancer guideline says that we should suspect a brain or a central nervous system malignancy in

·      adults if there is progressive, sub‑acute loss of central neurological function. We will refer them urgently for direct access, MRI scan of the brain to be done within 2 weeks. Alternatively, we can refer for a CT scan if MRI is contraindicated

·      In children and young people with newly abnormal central neurological function, we will arrange instead a very urgent specialist referral, that is, an appointment within 48 hours. 

There are some headache features that should also instigate further investigations or referral. The list is long and it includes symptoms such as:

• worsening headache with fever
• sudden‑onset headache reaching maximum intensity within 5 minutes
• new‑onset neurological or cognitive dysfunction
• head trauma within the past 3 months
• headache triggered by cough, sneeze or exercise or an
• orthostatic headache, that is, a headache that changes with posture

Additionally, we will consider further investigations or referral for people who present with new‑onset headache and:

• compromised immunity,
• a history of malignancy or
• vomiting without other obvious cause.

Once secondary causes of headaches have been excluded, then we’ll know that we are dealing with a primary headache. But, how do we differentiate cluster headache from other primary headaches such as migraine or tension-type headache?

Well, we will diagnose it according to the headache clinical features. So, let’s have a look at these features, and compare them with what we would expect in migraine and tension-type headache.

Let’s look at the pain location first. In cluster headache the pain location is unilateral, usually around the eye, above the eye and along the side of the head or face. In migraine it can be unilateral or bilateral and in tension-type headache it is usually bilateral.

The pain quality in cluster headache is variable. It can be sharp, boring, burning, throbbing or tightening. In migraine the pain is usually pulsating, although in young people it can also be throbbing or banging and in tension-type headache it is pressing or tightening and generally non‑pulsating.

The pain intensity in cluster headache is severe or very severe whereas in migraine it is moderate or severe and in tension-type headache it is mild or moderate.

When it comes to the effect on activities, there is restlessness or agitation in cluster headache. In migraine it is aggravated by, or causes avoidance of, routine daily activities whereas tension type headache is not normally aggravated by routine activities.

And finally, the duration of cluster headache is usually 15 minutes to 3 hours whereas in migraine it is usually 4 to 72 hours in adults, but sometimes shorter, from about 1 hour in young people. In tension-type headache it is usually anything from 30 minutes to continuous.

Cluster headache also usually presents with associated symptoms and we can consider them to help with the diagnosis.

For example, in cluster headache, on the same side as the headache we can find:

• a red or watery eye
• a swollen and or drooping eyelid
• a constricted pupil
• nasal congestion or a runny nose
• and forehead and facial sweating

On the other hand, common associated symptoms in migraine are unusual sensitivity to light or sound as well as nausea and vomiting. Additional, migraine can also have symptoms of aura, which can occur with or without headache.

Typical aura symptoms include speech disturbance, visual symptoms such as flickering lights, spots or lines and partial loss of vision; and also, sensory symptoms such as numbness or pins and needles.

 Generally, aura symptoms:

• are fully reversible
• develop over at least 5 minutes
• and last 5 to 60 minutes

However, we need to remember that tension type headache usually does not have any other associated symptoms.

If we look at the frequency of the headache, we can classify cluster headache in either episodic or chronic.

Episodic cluster headache has a frequency from once every other day to 8 times a day with a pain-free period of more than 1 month and

Chronic cluster headache is the same, that is, from once every other day to 8 times a day but with a continuous pain-free period of less than 1 month in a 12-month period.

And let’s remember that both migraine and tension-type headache can also be episodic when it happens fewer than 15 days per month or chronic when it is 15 or more days per month for more than 3 months.

Let’s now look at the management of cluster headache

And first of all, for people with a first bout of cluster headache we should consider neuroimaging, discussing with or referring to a specialist if necessary.

As the actual treatment for acute cluster headache, we will offer oxygen and/or a subcutaneous or nasal triptan. Currently, nasal triptans are unlicensed for this and the subcutaneous route is also unlicensed in under 18s.

When using oxygen for the acute treatment of cluster headache:

• we will use 100% oxygen at a flow rate of at least 12 litres per minute with a non‑rebreathing mask and a reservoir bag and
• we will arrange provision of home and ambulatory oxygen. 

When using a subcutaneous or nasal triptan, we will prescribe a sufficient number of doses, bearing in mind that the attacks may be multiple and frequent, so the quantity needed may also be significant.

We will not offer paracetamol, anti-inflammatory painkillers, opioids, ergots or oral triptans for the acute treatment of cluster headache.

What is the position in respect of prophylactic treatment for cluster headache?

NICE does not actually specify exactly when prophylactic treatment should be initiated. But in general, we should consider prophylaxis if:

• The patient has chronic cluster headache
• If attacks are frequent, severe, or disabling
• If there’s a need to reduce acute medication use
• And sometimes in episodic cluster headache, we can initiate prophylaxis early in a cluster period, ideally at the onset of symptoms, because, even if the bout is expected to last only a few weeks, prophylaxis can reduce frequency, severity, and duration of the attacks.

NICE recommends verapamil as the only option for prophylactic treatment during a bout of cluster headache. This is at the moment an off-label use of verapamil and, if we are unfamiliar with its use for cluster headache, we should seek specialist advice, including advice on ECG monitoring. The BNF actually says that it should be initiated under specialist supervision.

For cluster headache that does not respond to verapamil or during pregnancy, we should refer to a specialist

So that is it, a review of the assessment and management of cluster headache.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/LumBxN-yFmI

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through new and updated recommendations published in June 2025 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The Full NICE News bulletin for June 2025 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2025-06-01&to=2025-06-30&ndt=Guidance&ndt=Quality+standard

The updated clinical guideline Headaches in over 12s: diagnosis and management  [CG150] can be found here:

·      https://www.nice.org.uk/guidance/cg150

The MHRA advice on the use of topiramate can be found here:

·      https://www.gov.uk/drug-safety-update/topiramate-topamax-introduction-of-new-safety-measures-including-a-pregnancy-prevention-programme

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we’ll look at the NICE updates published in June 2025, focusing on what is relevant in Primary Care only.

We’ve got another short episode today, as there is just one updated clinical guideline relevant to us, the guideline on headaches in people over 12.

Right, let’s jump into it.

The update to the guideline makes only a very small change. NICE has changed the strength of recommendations on migraine prevention. Now, topiramate and propranolol are ‘consider’ options, alongside amitriptyline, whereas previously, only amitriptyline was a ‘consider’ option, and the other two were actively ‘offered’. This change better reflects the balance between benefits and harms with these three medicines.

And that is it. Given how straightforward this update is, let’s take the opportunity to review the overall management of migraine.

And we will start by saying that Headaches are among the most common neurological problems seen by GPs. They’re debilitating, and a major cause of time off work or school. They also represent a substantial burden on society.

We classify headache disorders as either primary or secondary. The cause of primary headaches isn’t well understood, so we group them by clinical pattern. The most common primary headache disorders are tension-type headache, migraine, and cluster headache.

Secondary headaches are due to underlying disorders. Examples include medication overuse headache, giant cell arteritis, raised intracranial pressure, and infection. Medication overuse headache often occurs in people already taking medication for a primary headache disorder.

The greatest health and social burden of headaches is caused by primary headaches and medication overuse headache.

Many people with headache don’t have an accurate diagnosis. Diagnosis can be difficult, and there’s often concern about possible underlying causes from both patients and healthcare professionals. By improving recognition of primary headache disorders, we’ll manage headaches better, improve quality of life, and reduce unnecessary investigations.

Now, let’s review the acute treatment of migraine with or without aura.

For this, we should offer combination therapy with an oral triptan and an NSAID, or an oral triptan and paracetamol depending on our clinical judgement.

For young people aged 12 to 17, we’ll consider a nasal triptan instead of an oral one. Currently, this is off-label in under-18s, except for nasal sumatriptan.

If someone prefers to take only one medicine, we’ll consider monotherapy with an oral triptan, NSAID, aspirin at 900 mg, or paracetamol, depending on their circumstances. And again, for 12 to 17-year-olds, we’ll consider a nasal triptan.

Because of the link with Reye’s syndrome, we should not offer aspirin to under-16s.

When prescribing a triptan, we’ll start with the lowest-cost option, and try alternatives if it’s not effective.

We should consider using an antiemetic alongside other acute migraine treatments, even if the person doesn’t have nausea or vomiting.

If oral preparations, or nasal preparations in young people, are ineffective or not tolerated, we’ll consider non-oral metoclopramide or prochlorperazine. If we do use one of these, and a non-oral NSAID or triptan hasn’t been tried, we’ll consider adding one.

We need to be aware of special warnings and precautions for metoclopramide and prochlorperazine as per the BNF, and we should discuss the benefits and risks with the patient.

At present, only buccal prochlorperazine is licensed for migraine. Other preparations are only licensed for nausea and vomiting.

Rimegepant (an oral calcitonin gene-related peptide [CGRP] inhibitor placed on or under the tongue) is recommended as an option for the acute treatment of migraine with or without aura in adults, only if:

• at least 2 triptans were tried and they did not work well enough or
• triptans were contraindicated or not tolerated, and NSAIDs and paracetamol were tried but did not work well enough.

We should not offer ergots or opioids for acute migraine treatment.

Now let’s turn to prophylactic treatment.

We will consider propranolol, topiramate, or amitriptyline to prevent migraine. This decision should follow a full discussion of benefits, risks, and suitability.

We will take into account the following factors:

• People with depression and migraine could be at an increased risk of using propranolol for self-harm so we should use caution when prescribing it.

·      We’ll follow MHRA guidance on topiramate: it should not be used for migraine prophylaxis in pregnancy or in women of childbearing potential unless the Pregnancy Prevention Programme conditions are fulfilled. That includes using highly effective contraception. The link to the MHRA advice is in the episode description.

·      For amitriptyline, we need to follow guidance on the prescribing of antidepressants and the management of medicines associated with dependence or withdrawal symptoms.

·      Currently, topiramate and amitriptyline are unlicensed for migraine in children and young people.

If the first prophylactic treatment doesn’t work or isn’t tolerated, we should discuss trying another. If necessary, we move on to the third option, unless there are safety concerns.

We will not offer gabapentin for migraine prevention.

If all three options, propranolol, topiramate, and amitriptyline, are ineffective, not tolerated, or unsuitable, we’ll consider a course of up to ten acupuncture sessions over five to eight weeks.

We can advise that the food supplement riboflavin 400 mg daily may help reduce migraine frequency and intensity for some people.

Calcitonin gene-related peptide (CGRP) inhibitors are recommended for preventing episodic or chronic migraine in adults with at least four migraine days per month, but only if at least three other preventive medicines haven’t worked, aren’t tolerated, or are unsuitable due to safety concerns. Of these agents, only atogepant is oral—the others are injectables.

Rimegepant is another Calcitonin gene-related peptide (CGRP) inhibitor which is placed on the tongue or under the tongue and which is recommended for preventing episodic migraine in adults who have between four and fourteen migraine attacks per month, but only if at least three preventive treatments haven’t worked or are unsuitable. It’s not recommended for chronic migraine.

Let’s remember that episodic migraine means fewer than 15 headache days per month, and chronic migraine means 15 or more headache days per month for more than 3 months.

And in summary, atogepant can be used as prophylaxis for both episodic and chronic migraine, whereas Rimegepant only for episodic migraine

Once prophylaxis has been given, we’ll review the need for ongoing treatment three to six months after starting it.

We’ll stop CGRP inhibitors after twelve weeks if the number of migraines hasn’t reduced by at least 50% in episodic migraine—or 30% in chronic migraine.

We need to remember that we will not offer combined hormonal contraception to women and girls with migraine with aura and, for predictable menstrual-related migraine that doesn’t respond to standard acute treatment, we’ll consider frovatriptan 2.5 mg twice daily or zolmitriptan 2.5 mg twice or three times daily, on days when migraine is expected. These are currently off-label uses.

During pregnancy, we’ll offer paracetamol for acute migraine. We can consider a triptan or NSAID, but only after discussing the need and the associated risks.

If prophylaxis is needed in pregnancy, we will seek specialist advice.

So that is it, a review of the NICE updates relevant to primary care, including a review of the treatment of migraines

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/HQnpwZFnedg

This channel may make reference to guidelines produced by a number of NHS organisations. The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by them.

My name is Fernando Florido (also known as Juan Fernando Florido Santana), a GP in the UK. In this episode, I will go through the diagnosis and primary care management of polycystic ovarian syndrome (PCOS), focusing on what is relevant in Primary Care only. For this advice I have looked at the published advice on the NHS Health website, North East London ICB and Health Improvement Scotland. The links to this guidance can be found below.

In the previous episode, I covered the initial assessment and investigations of PCOS.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The link to the PCOS information on the NHS Health website can be found here:

·      https://www.nhs.uk/conditions/polycystic-ovary-syndrome-pcos/

The link to the PCOS guideline by Primary Care North East London ICB can be found here:

·      https://primarycare.northeastlondon.icb.nhs.uk/wp-content/uploads/2025/01/Pathway-Polycystic-Ovary-Syndrome-10_2024.pdf

The link to the PCOS information by Right Decisions for Health and Care - Healthcare improvement Scotland can be found here:

·      https://rightdecisions.scot.nhs.uk/ggc-clinical-guidelines/gynaecology/gynaecology-guidelines/guidelines-a-z-all-gynaecology-guidelines/polycystic-ovarian-syndrome-622/

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I am Fernando, a GP in the UK. Today, we will go through the primary care management of polycystic ovarian syndrome (PCOS), focusing on what is relevant in Primary Care only. For this advice I have looked at the published advice on the NHS website, North East London ICB and Health Improvement Scotland. The links to them are in the episode description.

If you haven’t already, I recommend that you watch the previous episode where I cover the initial assessment and diagnosis.

Right, let’s jump into it.

And let’s start by reminding ourselves of the referral recommendations.

We should consider endocrinology referral if:

• There are severe symptoms such as signs of virilisation or rapidly progressing hirsutism
• When testosterone is significantly elevated, defined as greater than 5 nanomoles per litre or more than twice the upper limit of normal or
• Abnormal levels of DHEA or dehydroepiandrosterone, androstenedione, or 17-hydroxyprogesterone, which could indicate the possibility of alternative diagnoses such as congenital adrenal hyperplasia, Cushing’s syndrome, or androgen-secreting tumours.

Otherwise, the Management of PCOS is symptom-driven, so we should identify the patient's main concern, whether it's menstrual irregularity, hirsutism, fertility, or metabolic risk.

Also, we should not neglect psychological wellbeing given that many women with PCOS are at increased risk of anxiety, depression, and body image issues. We should therefore screen for symptoms of anxiety and depression as well as other mental health conditions, and offer appropriate management if indicated.

For all patients, lifestyle modification is the first-line of treatment, especially in those who are overweight. A weight reduction of even 5 percent can restore ovulation, reduce androgen levels, and improve insulin sensitivity. Women should be counselled that although PCOS is associated with weight gain, it does not inherently make weight loss more difficult. Referral to local weight management services may be appropriate and could be advised.

Cardiovascular disease risk should be assessed by assessing individual risk factors and we should counsel patients on possible long-term complications including T2DM, hypertension, hyperlipidaemia, CVD, obstructive sleep apnoea and endometrial cancer. Screening for type 2 diabetes is recommended, especially if they have a BMI over 25 or additional risk factors such as age over 40, gestational diabetes, or a family history of diabetes.

Although HbA1c is usually preferred for the diagnosis of diabetes for practical reasons, the North East London Primary care guideline recommend testing with OGTT instead.

Let’s stop here for a moment and ask ourselves, why would OGTT be preferred in PCOS?

There are two main reasons:

Firstly, because HbA1c can miss impaired glucose tolerance given that postprandial glucose spikes may occur early in the disease process, even before fasting glucose or HbA1c becomes abnormal.

Also, HbA1c Can Miss Early Glucose Dysregulation, especially in younger women and those with mild or intermittent abnormal glycaemia. So this is why an OGTT may be preferred over HbA1c in these situations.

But let’s go back to the general management. And, as we said earlier, the treatment should be symptoms driven. So, let’s now look at the treatment in specific clinical scenarios.

From a practical perspective, we should check whether the patient is pregnant or trying to get pregnant. If they are, we should:

·      Stop any hormonal treatment

·      Offer preconception counselling (including high dose folic acid 5mg if obese)

·      Refer them to fertility or obstetric services depending on the situation and

·      If pregnant, we should also organise an OGTT

Fertility treatment in secondary care may include ovulation induction with drugs such as clomiphene or letrozole. If these fail, gonadotrophins or laparoscopic ovarian drilling may be considered.

But, if the patient is not pregnant and not planning to get pregnant, we will check which symptom they are most concerned about and treat each patient holistically according to their concerns. This could be:

·      Acne

·      Hirsutism or

·      Oligo or amenorrhoea

Let’s have a look at the management of acne first.

For this we can offer:

·      The combined hormonal contraceptive if appropriate,

·      Any other acne treatment as per dermatology guidelines or

·      We could prescribe spironolactone checking baseline U&Es and considering ongoing monitoring if clinically indicated, for example, if they are >45 or have other relevant comorbidities. Although this is an unlicensed use, the North East Primary care guidelines advocate their use in general practice.

But spironolactone is a potassium sparing diuretic. Why does it work in acne?

There are two ways. By blocking androgen receptors and by reducing androgen production in the ovaries and adrenal glands. Since androgens stimulate oil production in the sebaceous glands, blocking their action leads to less sebum, which reduces the clogged pores and the inflammation that cause acne.

Let’s now look at the treatment options for hirsutism. They are:

·      Hair removal methods e.g. shaving, waxing, and laser

·      The combined hormonal contraceptive, considering dianette, which is a combination of Cyproterone acetate and Ethinylestradiol, a synthetic estrogen

·      Metformin, which should be considered over inositol for hirsutism and central adiposity

·      And finally the BNF also states that, for hirsutism, topically applied eflornithine (Vaniqa®) is of some benefit in reducing facial hair growth and should be used for 3 months prior to referral for laser treatment of hirsutism.

What do we need to know about eflornithine or Vaniqa?

Eflornithine inhibits specific hair follicle enzymes slowing down the rate of hair growth, making facial hair appear finer, lighter, and less noticeable over time.

Key points that we need to about it is that:

• It does not remove existing hair but reduces regrowth speed.
• Effects may take 8 weeks or more to become noticeable.
• It’s often used alongside other hair removal methods like plucking or laser.
• And once treatment is stopped, hair growth usually returns to baseline.

Eflornithine is particularly useful for women with mild-to-moderate facial hirsutism who prefer a non-hormonal, non-systemic option.

But we have also just said that Metformin should be considered over inositol for hirsutism and central adiposity.

But, why? And what are inositols? And how do we prescribe them?

Well, in the UK, inositol is not available as a licensed prescription medicine in the BNF and it is considered a dietary supplement.

Some international PCOS management guidelines note that inositol could be considered for metabolic improvements (like insulin resistance), but evidence for reproductive benefits (such as ovulation or hirsutism) is still limited, and no specific dose or form is recommended. Some private or fertility specialists may support its use given its good safety profile and occasional anecdotal success but it cannot be formally prescribed.

So, if it cannot be prescribed, how are people accessing it in the UK?

At the moment, it can be obtained from Supplement retailers or speciality health stores.

The North East Primary Care guideline does recommend inositols for some aspects of PCOS management, but obviously, it is a grey area where your individual clinical judgement will be the deciding factor.

How does inositol actually work?

Inositols are naturally occurring sugar alcohols that act as second messengers for insulin at intracellular level, improving insulin sensitivity and decreasing androgens.

Why is metformin better than inositol for hirsutism?

There are various reasons.

1. Firstly, there is evidence that metformin reduces central adiposity and insulin resistance more consistently than inositol.

2. Then metformin has a greater effect on Hirsutism. We need to remember that hirsutism is largely driven by hyperandrogenism and that Metformin indirectly lowers androgens by improving insulin sensitivity (which in turn reduces ovarian androgen production). Inositols may reduce androgens too, but the effect is milder and less predictable.

When Might Inositol Still Be Considered? We can recommend them:

• If the patient cannot tolerate metformin.
• In mild PCOS symptoms without central obesity or significant insulin resistance
• If there is a patient preference for over-the-counter non-pharmacological treatments or
• As an adjunct to other therapies.

If the main concern is oligomenorrhoea or amenorrhoea we need to remember that oligo- or amenorrhoea is a risk factor for endometrial hyperplasia and carcinoma and we should aim for a minimum of 4 periods per year to protect the endometrium.

So, in this situation, we should organise a TVUSS to assess endometrial thickness if there has been prolonged amenorrhoea or abnormal vaginal bleeding. An endometrial thickness < 7mm makes hyperplasia unlikely. Referral for biopsy and possible hysteroscopy should be considered if the endometrial thickness is raised.

The treatment options for oligo- or amenorrhoea are:

·      A cyclical progestogen e.g. medroxyprogesterone 10 mg OD for 14/7 every 2-3 months

·      The combined hormonal contraceptive

·      The Levonorgestrel Intrauterine System

·      Metformin, which may be most beneficial in high metabolic risk groups. We need to be aware that Metformin is not licensed for treating PCOS in the UK, but it can be used "off-label" if clinically appropriate. However, The BNF states that Treatment with insulin-sensitising drugs, such as metformin, should NOT be prescribed routinely as first-line therapy and it should only be initiated by a specialist. There is evidence that Metformin improves short-term insulin sensitivity and also reduces androgen concentrations, but there is limited supporting evidence on the long-term benefits in PCOS. So, this is why it should only be prescribed in the context of a specialist endocrine clinic

·      And finally, other options for oligo or amenorrhoea include

o  A Progesterone Only Pill such as Drosperinone for their antiandrogenic effect and

o  Inositol although the evidence is limited.

Before ending, let’s look at COC in a little bit more detail. One of the known benefits of combined hormonal contraception is that it increases SHBG. So, combined oral contraceptives are commonly used in PCOS for the treatment of acne, hirsutism, and menstrual irregularity but again this is an unlicensed indication.

But, why does CHC increase SHBG?

The main reason is the oestrogen component of CHC (normally ethinylestradiol), which has a hepatic effect by increasing synthesis of several proteins, including SHBG. Then, the higher circulating SHBG levels bind to free testosterone, reducing the free androgen index. This leads to reduced clinical signs of hyperandrogenism (e.g., acne, hirsutism, or alopecia).

However, we also have to bear in mind the progesterone side of CHC. Not all progestogens are equal. Some CHCs contain anti-androgenic progestogens (e.g., drospirenone, or cyproterone), whereas others do not. So we should choose the contraceptive wisely.

So that is it, a review of the management of polycystic ovary syndrome.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/pkP0aqNGqGI

This channel may make reference to guidelines produced by a number of NHS organisations. The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by them.

My name is Fernando Florido (also known as Juan Fernando Florido Santana), a GP in the UK. In this episode, I will go through the initial assessment and diagnosis of polycystic ovarian syndrome (PCOS), focusing on what is relevant in Primary Care only. For this advice I have looked at the published advice on the NHS Health website, North East London ICB and Health Improvement Scotland. The links to this guidance can be found below.

In the next episode, I will go through the primary care management of PCOS.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The link to the PCOS information on the NHS Health website can be found here:

·      https://www.nhs.uk/conditions/polycystic-ovary-syndrome-pcos/

The link to the PCOS guideline by Primary Care North East London ICB can be found here:

·      https://primarycare.northeastlondon.icb.nhs.uk/wp-content/uploads/2025/01/Pathway-Polycystic-Ovary-Syndrome-10_2024.pdf

The link to the PCOS information by Right Decisions for Health and Care - Healthcare improvement Scotland can be found here:

·      https://rightdecisions.scot.nhs.uk/ggc-clinical-guidelines/gynaecology/gynaecology-guidelines/guidelines-a-z-all-gynaecology-guidelines/polycystic-ovarian-syndrome-622/

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I am Fernando, a GP in the UK. Today, we will go through the initial assessment and diagnosis of polycystic ovarian syndrome (PCOS), focusing on what is relevant in Primary Care only. For this advice I have looked at the published advice on the NHS website, North East London ICB and Health Improvement Scotland. The links to them are in the episode description.

In the next episode, I will go through the primary care management, so stay tuned for that.

Right, let’s jump into it.

Polycystic Ovary Syndrome is a common endocrine disorder affecting approximately 6 to 10 percent of the female population in the UK. It is a heterogeneous condition, presenting with a spectrum of clinical features and long-term health implications.

The main clinical features are:

·      Hyperandrogenism (including hirsutism, acne, and male-pattern hair loss)

·      Menstrual irregularity with associated anovulatory infertility.

·      overweight in 40-50% of cases and

·      Insulin resistance in 10-15% of slim and 20-40% of obese women but all women with PCOS are at an increased risk of developing type 2 diabetes.

What causes polycystic ovary syndrome (PCOS)?

The exact cause of PCOS is unknown, but it often runs in families.

We know that it's related to abnormal hormone levels in the body, including high levels of insulin secondary to insulin resistance and an increased production and activity of hormones like testosterone.

But what is the exact pathophysiology of PCOS?

Well, it’s a complex condition with several interconnected mechanisms.

First, there’s disruption in the hypothalamic-pituitary-ovarian axis. The brain increases the frequency of gonadotropin pulses, which leads to more stimulation of LH than FSH. This imbalance, often with a higher LH to FSH ratio, stimulates the ovaries’ theca cells to produce excess androgens. These androgens are responsible for many of the clinical features, like hirsutism, acne, and male-pattern hair loss.

Low FSH also means the follicles in the ovary don’t develop properly. They tend to grow to around six or seven millimetres, but they don’t ovulate. These small, underdeveloped follicles build up around the edge of the ovaries, creating a classic appearance on ultrasound.

To make matters worse, those high androgen levels further disrupt follicle development, reinforcing the cycle of anovulation. And when ovulation doesn’t happen, periods become irregular or stop altogether, which increases the risk of endometrial hyperplasia due to unopposed oestrogen.

Another major part of the pathophysiology is insulin resistance. Many women with PCOS, even those who aren’t overweight, have insulin resistance. The exact reason isn’t fully understood, but it’s thought to involve a defect in insulin signalling inside muscle and fat cells.

This hyperinsulinemia together with LH stimulate even more androgen production by the ovaries and it also lowers the liver’s production of sex hormone-binding globulin, which raises the amount of free testosterone.

And to add to all this, those excess androgens go on to worsen insulin resistance at the tissue level, creating a vicious cycle of more insulin, more androgens, more resistance, and more insulin again.

How is it diagnosed?

PCOS can be diagnosed when two out of the following three Rotterdam criteria are met. These are:

1. Oligo- or anovulation.
2. Clinical or biochemical signs of hyperandrogenism and
3. Polycystic ovarian morphology on ultrasound.

But this is always after excluding other causes such as thyroid dysfunction, Cushing’s syndrome, hyperprolactinaemia, late-onset congenital adrenal hyperplasia, and androgen-secreting tumours.

There is no consensus on the criteria needed to diagnose PCOS in adolescents. This is because diagnosing PCOS in adolescents is harder as the diagnostic features used in adults e.g. oligomenorrhoea, acne and PCO morphology on USS can be normal pubertal physiological events that are transient. We should not diagnose it in under 18 unless both clinical hyperandrogenism and irregular cycles persist for more than two years post-menarche. Some like the American Academy of Family Physicians argue that, for this age group, all three Rotterdam criteria be met before the diagnosis is made.

As we can see, the clinical features of PCOS are varied. So let’s have a look at some definitions in the Rotterdam criteria:

Firstly, we have oligo or anovulation. Oligomenorrhea is defined as cycles more than 35 days apart but less than 6 months apart and amenorrhea as the absence of menstruation for 6 to 12 months after a previously established cyclic pattern.

Secondly, we have hyperandrogenism. This could be diagnosed either clinically, by the presence of excessive acne, androgenic alopecia, or hirsutism, or chemically, by high serum levels of total, or free testosterone 

And finally, we have Polycystic Ovary features on Ultrasound. A single ovary showing these features is sufficient for the diagnosis of polycystic ovaries. However, we need to be aware that USS is not necessary if the first two criteria are present. USS is only necessary if we need it to rule out a tumour or the patient has met only one of the other Rotterdam criteria. This is because Polycystic ovaries features can be found in as many as 62% of patients with normal ovulation, with prevalence declining with age.

A thorough history and examination are essential. We should ask about cycle regularity, acne, hirsutism, and family history. We should also record BMI and blood pressure, given that these patients are at higher cardiometabolic risk.

Baseline investigations should include:

• Thyroid function tests
• Prolactin
• LH, FSH, and oestradiol to exclude other causes of oligo- or amenorrhoea
• Total testosterone and SHBG
• Androstenedione and DHEA-S or dehydroepiandrosterone if testosterone is raised
• If clinically suspected, 17-hydroxyprogesterone to rule out congenital adrenal hyperplasia
• And finally, we should consider a transvaginal or transabdominal ultrasound to assess ovarian morphology and endometrial thickness

How should we interpret these results?

Well, SHBG is usually normal or low in PCOS and provides a measurement of the degree of hyperinsulinaemia."

This is because Insulin suppresses the production of SHBG (sex hormone-binding globulin) in the liver, so in PCOS where insulin resistance is common, SHBG levels are often low or at the lower end of the normal range; as a result, low SHBG can serve as a useful surrogate marker for insulin resistance. Low SHBG means more free active testosterone, contributing to symptoms like acne and hirsutism.

We also have that LH, oestradiol and free androgen index, are usually normal or elevated in PCOS.

The reason for the high free androgen index is that SHBG is used to estimate it. So, if SHBG is low then the free androgen index may still be high even when total testosterone is normal, suggesting true biochemical hyperandrogenism.

LH is often elevated, especially in slim women with PCOS, due to increased gonadotrophin pulsatility. A raised LH:FSH ratio (e.g., >2:1) is typical, but not required for diagnosis.

And then, oestradiol is usually normal or mildly elevated in PCOS due to continuous oestrogen production from the ovaries and peripheral conversion in adipose tissue, despite anovulation.

FSH, prolactin and TSH are usually normal and these tests are done to rule out other causes of oligo/amenorrhoea.

FSH is usually normal in PCOS. If elevated, we should consider premature ovarian insufficiency.

Equally, prolactin is usually normal. If elevated, we should consider prolactinoma or drug-induced hyperprolactinaemia.

TSH is done to exclude hypothyroidism, which can also cause menstrual irregularity.

So, these are exclusion tests. They are checked to avoid misdiagnosing PCOS when another endocrine disorder is responsible.

And finally, we have that total testosterone is normal or high in PCOS. However, if it is significantly elevated, generally > than 5 nmol/l or more than 2 x upper limit of normal range, we will need to check DHEA, or dehydroepiandrosterone, androstenedione and 17-hydroxyprogesterone to rule out congenital adrenal hyperplasia, Cushing’s syndrome, and androgen-secreting tumours."

The reason for this is that in PCOS, total testosterone is often normal to mildly elevated, but significant elevations raise red flags and need further investigations.

DHEA-S or dehydroepiandrosterone increases in adrenal disorders. Androstenedione is produced also by the ovary and adrenal glands and finally, 17-hydroxyprogesterone which is elevated in non-classic congenital adrenal hyperplasia

Additionally, we should also consider Cushing’s syndrome or androgen-secreting tumours if the clinical picture is severe (e.g., when there is rapid virilisation) even if the total number is not very high.

And let’s end with some referral recommendations.

When should we refer women with PCOS to endocrinology?

We should consider endocrinology referral if:

• There are severe symptoms such as signs of virilisation or rapidly progressing hirsutism
• When testosterone is significantly elevated, defined as greater than 5 nanomoles per litre or more than twice the upper limit of normal or
• Abnormal levels of DHEA or dehydroepiandrosterone, androstenedione, or 17-hydroxyprogesterone, which could indicate the possibility of alternative diagnoses

So that is it, a review of the assessment and diagnosis of polycystic ovary syndrome.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/58WdoYFUUjU

This channel may make reference to guidelines produced by a number of NHS organisations. The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by them.

My name is Fernando Florido (also known as Juan Fernando Florido Santana), a GP in the UK. In this episode, I will go through the assessment and management of hypomagnasemia, focusing on what is relevant in Primary Care only. For this advice I have looked at the published guidance by NHS Dorset, NHS Kent and Medway, NHS Lanarkshire, Gloucestershire Hospitals NHS Trust, and Royal Cornwall Hospitals NHS Trust. The links to this guidance can be found below.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:  

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The link to the guideline by NHS Dorset can be found here:

·      https://nhsdorset.nhs.uk/Downloads/aboutus/medicines-management/Other%20Guidelines/Management%20of%20hypomagnesaemia%20in%20primary%20care%20Jan%2023%20-%20Copy.pdf?boxtype=pdf&g=false&s=true&s2=false&r=wide

The link to the guideline by NHS Kent and Medway can be found here:

·      https://www.dgsdvhformulary.nhs.uk/media/1168/hypomagnesaemia-in-adults-primary-care-guide.pdf

The link to the guideline by NHS Lanarkshire can be found here:

·      https://rightdecisions.scot.nhs.uk/media/1539/hypomagnesaemia-in-primary-or-secondary-care.pdf

The link to the guideline by Gloucestershire Hospitals NHS Trust can be found here:

·      https://www.gloshospitals.nhs.uk/media/documents/Hypomagnesaemia_jcPg0oV.pdf

The link to the guideline by Royal Cornwall Hospitals NHS Trust can be found here:

·      https://doclibrary-rcht.cornwall.nhs.uk/DocumentsLibrary/RoyalCornwallHospitalsTrust/Clinical/Pharmacy/TreatmentOfHypomagnesaemiaInAdultsClinicalGuideline.pdf

The link to the guideline by Worcestershire Acute Hospitals NHS Trust can be found here:

·      https://apps.worcsacute.nhs.uk/KeyDocumentPortal/Home/DownloadFile/1559

The link to the MHRA advice on hypomagnesaemia associated to long term PPI use can be found here:

·      https://www.gov.uk/drug-safety-update/proton-pump-inhibitors-in-long-term-use-reports-of-hypomagnesaemia

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I am Fernando, a GP in the UK. Today, we will go through the assessment and management of hypomagnesemia, focusing on what is relevant in Primary Care only. For this advice I have looked at the published guidance by a number of NHS organisations in the UK including Dorset, Lanarkshire, Gloucestershire, Cornwall and Kent and Medway. The links to them are in the episode description.

Right, let’s jump into it.

Hypomagnesaemia is defined as a serum magnesium concentration below 0.7 mmol/L. The normal reference range for serum magnesium is between 0.7 and 1.0 or 1.05 mmol/L, depending on the guideline used.

Magnesium is the second most abundant intracellular electrolyte after potassium, and is an essential cofactor in numerous enzyme systems. It also regulates the transport of calcium and potassium across cell membranes, contributing to neuromuscular conduction, muscle contraction, and cardiac rhythm.

The majority of total body magnesium is stored in bone and soft tissue and only around 1% is in extracellular fluid. Therefore, serum levels may not accurately reflect total body stores. It is possible to see a normal serum level when there is a total body magnesium deficit like in a chronic magnesium deficiency secondary to inadequate dietary magnesium. The reverse, that is, a low serum level and normal total body magnesium, is also possible and is usually seen with drugs which increase excretion of magnesium. Additionally, approximately 25% of plasma magnesium is bound to albumin, so high or low albumin states can also affect the magnesium levels.

Changes in magnesium levels usually occur gradually over months or years and symptoms are often absent, particularly when serum levels are only mildly reduced. They become more common when concentrations fall below 0.5 mmol/L, but there are times when they may also occur in the 0.5–0.7 mmol/L range.

The most common symptoms are:

Muscular and mobility symptoms, including muscle weakness, tremors, ataxia, spasms, fasciculations.

Neurological symptoms, including dizziness, paraesthesia, hallucinations, delirium, seizures, depression, confusion, and coma.

Cardiovascular symptoms, including ECG abnormalities, arrhythmias, and increased sensitivity to digoxin.

Metabolic effects including altered glucose homeostasis, and associations with hypocalcaemia and hypokalaemia.

And finally, other symptoms such as anorexia, nausea, vomiting, and fatigue,

But let’s go back for a moment and ask, why is low magnesium associated with hypocalcaemia and hypokalaemia?

Low magnesium can lead to hypocalcaemia because magnesium is required for the release of PTH. When magnesium is very low, PTH secretion decreases, which leads to reduced calcium reabsorption in the kidneys and reduced calcium release from bone, resulting in low calcium levels.

And what about hypokalaemia? Here the mechanism is connected cellular pumps that regulate intra and extracellular potassium homeostasis which leads to increased renal potassium loss, causing potassium levels to decrease.

Both the hypocalcaemia and hypokalaemia may be refractory to treatment until magnesium is corrected

Let’s now look at the causes and risk factors of hypomagnesemia.

The first cause is Reduced Intake, reduced Absorption or increased gut losses like in:

• Malabsorption (including coeliac disease, Crohn’s disease, and short bowel syndrome)
• Malnutrition and anorexia nervosa
• Chronic diarrhoea
• And excess alcohol intake

Increased Renal Loss like in:

• Renal tubular disorders
• Diabetes and diabetic ketoacidosis
• Hyperaldosteronism
• Hyperthyroidism
• And vitamin D deficiency

Drug-Induced like for example with the use of:

• Proton pump inhibitors (PPIs)
• Both loop and thiazide Diuretics
• Theophylline
• Some chemotherapy agents
• And Digoxin, also bearing in mind that low magnesium may increase digoxin toxicity

And finally Miscellaneous causes such as

·      Acute pancreatitis

·      and excessive lactation

We should prioritise the monitoring of magnesium in patients taking multiple risk drugs or with two or more risk factors.

But let’s pause for a moment. Did we just say that vit D deficiency also causes hypomagnesaemia? And why is that?

Well, in fact, the relationship between magnesium and vitamin D is bidirectional, that is, each influences the metabolism and availability of the other. For example, vitamin D deficiency can cause or worsen hypomagnesaemia by reducing magnesium intestinal absorption and indirectly increasing its renal loss. Conversely, magnesium is a cofactor in the enzymatic steps that convert vitamin D to its active form and, as a result, magnesium deficiency can impair vitamin D activation and function.

Therefore, both deficiencies often coexist, especially in patients with malabsorption, chronic disease, or poor nutrition, and they may exacerbate each other.

Also, of all the drugs mentioned before, PPIs are probably the most commonly and widely prescribed. Because of reported cases of severe hypomagnesaemia associated with prolonged PPI use, normally after 1 year but sometimes as early as 3 months, the MHRA has published a drug safety alert advising healthcare professionals to:

• Consider baseline magnesium measurement before starting PPIs and to
• Monitor magnesium periodically during prolonged treatment, particularly in patients on diuretics or digoxin

We also need to reiterate that for patients on PPIs, symptoms may develop insidiously and be overlooked. PPI related hypomagnesaemia generally resolves upon magnesium replacement and discontinuation of the PPI.

PPIs can also be obtained over-the-counter but patients are advised not to take them for more than 4 weeks without consulting a doctor.

Hypomagnesemia can be graded as:

• Mild: when the levels are below 0.7 but above 0.50 (i.e. 0.51–0.69 mmol/L)
• Moderate: when the levels are 0.50 or below but above 0.40 (i.e. 0.41–0.50 mmol/L)
• And Severe: when the levels are 0.40 mmol/L or below. Here, urgent referral is advised, especially if symptomatic or with concurrent low potassium or calcium.

Let’s now look at the General Principles of management. We will:

• Treat underlying causes
• Discontinue offending drugs where possible (seeking advice if not feasible)
• Consider switching PPIs to H2 antagonists (e.g. famotidine, or nizatidine)
• And we will bear in mind that oral replacement is preferred for asymptomatic mild or moderate deficiencies whereas IV magnesium is required for severe deficiency, symptomatic moderate deficiency or if oral supplements are not tolerated

For Oral Replacement, we will look at the BNF, being aware that magnesium preparations may not be interchangeable due to differences in bioavailability, therefore we should exercise caution when switching between them.

Usually the first-line treatment is with:

• Magnesium aspartate (or Magnaspartate®) which comes in sachets and is preferred for all ages above 2 years

Second-line options include:

• Magnesium glycerophosphate tablets and
• Magnesium citrate

Another oral option includes:

• Magnesium glycerophosphate in liquid form, which is unlicensed but is sometimes used when there are tolerability issues.

Additionally,

• Magnesium sulphate can be administered in secondary care by intravenous infusion, or by intramuscular injection

And let’s remember that IV Replacement is required:

• In severe hypomagnesemia, when Serum magnesium is 0.4 mmol/L o r below
• In symptomatic Moderate hypomagnesaemia, that is, when magnesium is between 0.4 and 0.5 and there are symptoms and also
• Any low level in a patient on digoxin with symptoms

Possible Adverse Effects of oral magnesium include diarrhoea, so we should recommend having it with meals to reduce gastrointestinal irritation.

We should also bear in mind that oral magnesium reduces the absorption of:

• Bisphosphonates
• Tetracyclines and
• Quinolone antibiotics

In terms of monitoring and Follow-Up we should obviously:

• Monitor serum magnesium during and after replacement
• Then continue rechecking at regular intervals in patients with ongoing risk factors
• But also monitor for symptoms of hypermagnesaemia, particularly in renal impairment. Possible symptoms of hypermagnesaemia or high magnesium levels include Respiratory depression, loss of reflexes, confusion, vomiting, cardiac arrhythmias, and coma. Cardiac arrest may occur at levels above 6 mmol/L.

And let’s finish with a quick overview of recommended Patient Education. Patients who are at risk of hypomagnesemia, particularly those on long term PPIs, should be advised to

• Report symptoms such as tremor, vomiting, tiredness, muscle cramps, loss of appetite and fatigue
• They should also increase magnesium-rich foods including green vegetables, wholemeal grains, nuts, pulses, and seafood
• We should also advise them that “Hard” water also contains magnesium salts
• And advise OTC magnesium supplements if there are no clinical concerns such as, for example, severe renal impairment, heart block, bradycardia, or myasthenia gravis.

So that is it, a review of the guidance on the assessment and management of hypomagnesaemia.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/Y3POCL-rh_Y

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through new and updated recommendations published in May 2025 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only.  

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.   

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido. 

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:  

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The Full NICE News bulletin for May 2025 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2025-05-01&to=2025-05-31&ndt=Guidance&ndt=Quality+standard

The update on Suspected cancer: recognition and referral [NG12] can be found here:

·      https://www.nice.org.uk/guidance/ng12

·      https://www.nice.org.uk/guidance/ng12/chapter/Recommendations-organised-by-site-of-cancer#upper-gastrointestinal-tract-cancers

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we’ll be looking at the NICE updates published in May 2025, focusing on what is relevant to Primary Care only.

We’ve got another short episode today, as there is only one clinical area to discuss: new advice on the cancer recognition guideline.

Right, let’s jump into it.

And this update refers to the early detection of upper gastrointestinal cancers. It only touches on the recommendations for oesophageal and stomach cancers, and it will not really change our practice very much, given that it affects the referral process only. The difference is that before, when someone developed red flag symptoms, we were advised refer them for an urgent direct access upper GI endoscopy (to be performed within 2 weeks), whereas now, the advice is to refer them using a suspected cancer pathway referral.

Is there a real difference? Well, in fact, there is. Let’s have a look at it:

The main difference between lies in who triages the referral, the urgency and coordination of care.

For example, in an urgent Direct Access Upper GI Endoscopy (done within 2 weeks)

• The GP directly refers the patient to the endoscopy service, who triages the referral without specialist review.
• Also, although urgent direct access endoscopy is expected within 2 weeks, it's not formally tracked like a cancer pathway.
• And finally, there is no coordinated follow-up if something is found. The GP will receive the report and must then arrange further care.

On the other hand, a Suspected Cancer Pathway Referral means that

• The hospital’s cancer referral team triages the referral and coordinates and tracks the process. This often means that the patient is seen or tested within 2 weeks, but the formal definition of a Suspected Cancer Pathway Referral is that the patient has the diagnosis of cancer either confirmed or ruled out within 28 days of the original referral.
• The advantage of this model is that if a cancer is found, follow-up is already embedded in the system.

So that is really the only change. Since today’s episode is so short, let’s take the opportunity to review re recommendation on upper GI cancers.

For Oesophageal and stomach cancers, we will refer them on a suspected cancer pathway if they:

• have dysphagia or
• are aged 55 and over, with weight loss, and they have any of the following:
• upper abdominal pain
• reflux or
• dyspepsia

We will consider non-urgent, direct access upper gastrointestinal endoscopy in people with haematemesis and in people aged 55 or over with:

• treatment‑resistant dyspepsia or
• upper abdominal pain with low haemoglobin levels or
• raised platelet count with any of the following:
• nausea
• vomiting
• weight loss
• reflux
• dyspepsia and
• upper abdominal pain or
• nausea or vomiting with any of the following:
• weight loss
• reflux
• dyspepsia and
• upper abdominal pain.

In terms of pancreatic cancer, we will refer if they are aged 40 and over and have jaundice. And we will also consider an urgent, direct access CT scan (to be done within 2 weeks), or an urgent ultrasound scan if CT is not available, in people aged 60 and over with weight loss and any of the following:

• diarrhoea
• back or abdominal pain
• nausea or vomiting
• constipation or
• new‑onset diabetes.

And finally, in terms of Gall bladder cancer or liver cancer

We will consider an urgent, direct access ultrasound scan (to be done within 2 weeks) in people with an upper abdominal mass consistent with either an enlarged gall bladder or an enlarged liver.

So that is it, a review of the NICE updates relevant to primary care.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/mq658X-teEc

This channel may make reference to guidelines produced by the British Society for Haematology. The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by them.

My name is Fernando Florido (also known as Juan Fernando Florido Santana), a GP in the UK. In this episode, I will go through the guideline by the British Society for Haematology on thrombophilia testing, focusing on what is relevant in Primary Care only.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The link to the guideline by the British Society for Haematology on thrombophilia testing can be found here:

·      https://onlinelibrary.wiley.com/doi/10.1111/bjh.18239

The link for the British Society for Haematology website can be found here

·      https://b-s-h.org.uk/

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I am Fernando, a GP in the UK. Today, we will go through the guideline by the British Society for Haematology on thrombophilia testing, focusing on what is relevant in Primary Care only. A link to it is in the episode description. We’ll go through the main tests included in a thrombophilia screen, explain why they matter, and go over when screening is recommended in specific clinical situations.

Right, let’s jump into it.

Thrombophilia is a condition where the blood has an increased tendency to clot. This increases the risk thrombosis and may be inherited, acquired, or a mix of both.

However, thrombophilia screening focuses only on factors identifiable through laboratory testing. Broader contributors like cancer, inflammation, and obesity, although linked to thrombosis, cannot be assessed with this panel and we are not going to address them today.

A thrombophilia screen includes a number of tests which we are going to group by their pathophysiological mechanism:

First, we assess for deficiency of natural anticoagulants like Antithrombin, Protein C and Protein S. Deficiencies in any of these increase the clotting risk. A simple way to remember them is with the mnemonic: C, S, A — Coagulation Suppressors Absent.

Second, we look for genetic mutations that make clotting factors resistant to natural anticoagulants. These include, Factor V Leiden and Prothrombin Gene Mutation. These mutations lead to excess clotting either by preventing anticoagulation or by increasing clotting factor levels.

Third, we consider acquired autoantibodies that interfere with the body's anticoagulant mechanisms or activate endothelial cells. These include Lupus anticoagulant, Anti-cardiolipin antibodies and Anti-β2-glycoprotein I antibodies. These markers are typically associated with antiphospholipid syndrome.

I hope that grouping the thrombophilia screen this way will make it easier to understand and remember.

We can classify thrombophilias between hereditary and acquired thrombophilias. The most clearly defined genetic thrombophilias are the factor V Leiden variant, the prothrombin gene mutation, protein C deficiency, protein S deficiency, and antithrombin deficiency. 

On the other hand, important acquired thrombophilias include antiphospholipid syndrome, paroxysmal nocturnal haemoglobinuria, myeloproliferative neoplasms and the presence of a JAK2 mutation. Pregnancy is a hypercoagulable state due partly to physiological changes.

Both heritable and acquired thrombophilias can interact to further increase the risk of thrombosis, for example during pregnancy and the postpartum period.

So now, let’s consider the actual laboratory testing. And the first issue to look at is, should we screen the general population for thrombophilia?

And although Elevated levels of procoagulant factors may increase the risk of thrombosis, the relationship is not straightforward. Why is this?

1. Firstly, there is a Multifactorial Risk. Thrombosis isn’t caused by one factor alone. Other conditions like obesity, inflammation, or immobility may coexist with elevated procoagulant factors, confounding the interpretation.
2. Then there is the Dual Roles of Coagulation Proteins. That is, some factors have both procoagulant and anticoagulant roles, which makes the overall effect more difficult to assess.
3. And then there is the issue of Limited Predictive Value. Measuring elevated levels of these factors (like Factor VIII, fibrinogen, etc.) may show associations with thrombosis risk in population studies, but it doesn’t consistently predict individual risk.

So, in summary, the guideline does not recommend routine screening of procoagulant factors because it would not change the management for the majority of people. Instead, it supports individualised decision-making.

Now, let’s look and the significance of testing in each category of test.

The first category refers to natural anticoagulants. What about testing for their Deficiency?

The associations of Protein C, Protein S and Antithrombin deficiencies with increased risks of VTE are well-established. The degree of deficiency is variable but in general thrombosis risk rises as soon the levels of protein C, S or Antithrombin fall below the normal range.

These deficiencies also interact with acquired risks. It has been found that a transient provoking factor is present in approximately 50% of episodes of thrombosis in genetically predisposed people. 

Another consideration is that, when testing for deficiencies of physiological anticoagulants, this should be performed only after 3 months of anticoagulation for acute thrombosis, given that the result would not change the initial acute management and there is uncertainty over the validity of earlier results.

The next category of tests includes Factor V Leiden and prothrombin gene mutation.

These two cases are the most common genetic variants predisposing to thrombosis. Their prevalence varies in populations of different ethnicity, being more common in people of European descent and being rare or absent in other ethnicities.

There are a large number of other genetic variants but the only ones that are included in thrombophilia panels at present are these two, factor V Leiden and prothrombin gene mutation because the clinical relevance of other genetic types is not well established.

The last two categories of tests make reference to cases acquired thrombophilia. They can be genetic and non-genetic.

Let’s look at the non- genetic causes first and the main one is Antiphospholipid syndrome

The diagnosis of antiphospholipid syndrome is dependent on the presence of at least one clinical feature (either thrombosis or pregnancy morbidity) and at least one laboratory feature of antiphospholipid antibodies which include lupus anticoagulant , anticardiolipin antibodies or anti-β2-glycoprotein-I (anti-β2GPI) antibodies. The antiphospholipid antibodies need to be persistent, that is, present on two or more occasions at least 12 weeks apart.

There is uncertainty in the thrombotic risks of these patients depending on whether the thrombosis was provoked or unprovoked.

Therefore, the advice is that:

• Screening for antiphospholipid antibodies is recommended following thromboembolic disease which is either unprovoked or provoked by a minor risk factor.
• And, as antiphospholipid syndrome is an acquired thrombophilia, screening for antiphospholipid antibodies is not recommended in family members.

I will just mention that catastrophic antiphospholipid syndrome is a rare, but a potentially fatal variant characterised by extensive microvascular thrombosis leading to multiorgan failure.

And finally, the last category of tests refers to the genetic causes of acquired thrombophilia.

Here, I will just mention that Paroxysmal nocturnal haemoglobinuria (PNH) and myeloproliferative neoplasms (MPN) are acquired genetic traits that have clonal stem cell abnormalities. Myeloproliferative neoplasms include polycythaemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). The JAK2 mutation is strongly associated with an increased thrombophilia risk too.

Here the advice is that we should test for these conditions in patients with thrombosis at unusual sites and FBC abnormalities.

Now let’s look at the General advice on the role of thrombophilia testing in certain clinical scenarios

We have said that general screening is not recommended but, for patients with a strong personal and/or family history of unprovoked thrombosis, further genetic analysis is recommended.

The major hereditary thrombophilic traits follow Mendelian inheritance although with variable penetrance. Overall, the recurrence risk is determined by the clinical situation (e.g., whether the thrombosis was provoked or unprovoked) along with non-Mendelian risk factors (e.g., body mass index and age) rather than the inherited thrombophilia itself. Therefore, selective testing of first-degree relatives may be advisable only when this will alter their management choices, for example, in women of childbearing age.

What about Ischaemic stroke?

Well, excluding cerebral venous sinus thrombosis, this area remains controversial and the Recommendations after a stroke are that

• In general, testing for thrombophilia is not recommended.
• But testing for antiphospholipid antibodies should be considered in patients <50 years of age in the absence of identifiable risk factors for cardiovascular disease
• Additionally, in patients with stroke, an abnormal full blood count should prompt consideration for testing Paroxysmal nocturnal haemoglobinuria and myeloproliferative neoplasms

And to end, let’s look at the recommendations for Thrombophilia testing in relation to pregnancy

Pregnancy is an acquired hypercoagulable state. The incidence of thrombosis in pregnancy is a 5- to 10-fold increase in relation to non-pregnant females, rising further in the first 6 weeks postpartum to a 20- to 80-fold increase in risk.

Additionally, women who have had previous adverse outcomes—such as recurrent first-trimester pregnancy loss or stillbirth—should be screened but this screening should be limited to testing for antiphospholipid antibodies.

So the guideline recommends that:

• Testing for antithrombin deficiency may be considered in pregnant women with a known family history of this deficiency.
• In women with a history of unprovoked thrombosis or with recurrent or late pregnancy loss, testing for antiphospholipid antibodies should be performed
• And that Antiphospholipid antibody testing should be done outside pregnancy as the results may not be reliable during pregnancy.

So that is it, a review of the guideline on thrombophilia testing.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/qNboajtlrrs

This channel may make reference to guidelines produced by the British Society for Haematology. The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by them.

My name is Fernando Florido (also known as Juan Fernando Florido Santana), a GP in the UK. In this episode, I will go through the guideline by the British Society for Haematology on the investigation and management of a raised serum ferritin, focusing on what is relevant in Primary Care only.

In the last two episodes I covered the guideline on iron deficiency and functional iron deficiency.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The link to the guideline by the British Society for Haematology on the investigation and management of a raised serum ferritin can be found here:

·      https://doi.org/10.1111/bjh.15166

The link for the British Society for Haematology website can be found here

·      https://b-s-h.org.uk/

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I am Fernando, a GP in the UK. Today, we will go through the guideline by the British Society for Haematology on the investigation and management of a raised serum ferritin, focusing on what is relevant in Primary Care only. A link to it is in the episode description.

If you haven’t already, I recommend that you check out the last two episodes where we covered the laboratory diagnosis of both iron deficiency and functional iron deficiency

Right, let’s jump into it.

Serum ferritin level is one of the most commonly requested investigations in both primary and secondary care. Whilst low serum ferritin levels invariably indicate reduced iron stores, raised serum ferritin levels can be due to multiple different causes, including iron overload, inflammation, liver or renal disease, malignancy, and metabolic syndrome.

Reduced ferritin levels are only found in patients with reduced body iron stores. However, in some circumstances, for example in patients with co-existent inflammatory disorders, ferritin may be within the normal or elevated range even when iron stores are reduced and anaemia is due to iron deficiency.

On the other hand, the clinical and laboratory management of patients with raised ferritin values is not that well recognised and this is why we are covering it here.

Levels in serum can be raised because of inflammation, tissue damage as well as by any condition or treatment that leads to a genuine increase in iron stores (e.g. blood transfusion or iron infusion).

Most UK path labs simply report 300–400 μg/l as the upper limit of normal for ferritin in adult males and 150–200 μg/l as the upper limit of normal for adult females. There is however considerable variation in response to age, ethnic origin and sex. Mean ferritin values in neonates are high (around 200 μg/l) and remain so for about 2 months.

Mean ferritin values are higher at all ages in adult black males. In black females, higher ferritin values are only seen after the menopause. In multi-ethnic population studies in the USA it was found that elevated ferritin values are found more frequently in Afro-Caribbean and Asian subjects than in the white or Hispanic population. Indeed, very high ferritin levels >1000 μg/l are 2–3 times more common in black and Asian volunteers despite not having a true iron overload problem so it is argued that the normal ranges should take into account the variation due to age, gender and possibly ethnic origin

Serum ferritin is the most frequently requested haematinic assay in the UK and some 50% of ferritin requests are made from primary care.

The commonest causes of a high ferritin without iron overload relate to inflammatory disorders, malignancy, chronic alcohol consumption, liver disease or metabolic abnormalities.

For the majority of persons with a raised ferritin, chronic inflammatory or infective causes as well as liver disease, alcohol and malignancies will be the more likely conditions seen in practice, and if clinically apparent, further investigations of the causes of the high ferritin may not be necessary. Let’s look at the different causes individually:

In the Liver: Elevated ferritin is seen in almost any cause of liver injury, including alcoholic and non-alcoholic steatohepatitis (NASH), and viral hepatitis

In the Kidneys: Ferritin is not a useful marker of iron stores in patients with chronic kidney disease (CKD), and is elevated in almost half of all patients on maintenance haemodialysis but the raised ferritin does not represent iron that is available for erythropoiesis. For CKD patients on treatment with erythropoietic stimulating agents (ESA), iron supplementation should routinely be offered unless their ferritin is >800 μg/l.

In Malignancy: ferritin  is frequently elevated, and cancer has been the most frequent association in some studies of the causes of a high ferritin.

In Inflammatory and infective disorders: ferritin levels may correlate with disease activity, for example in systemic lupus erythematosus (SLE) and rheumatoid arthritis. Other inflammatory conditions and acute or chronic infections will also produce elevations in ferritin, usually with elevated CRP, but normal Tsat.

Mention should be made of anaemia of chronic disease (ACD), also termed anaemia of inflammation, the pathogenesis of which includes a state of functional iron deficiency, which we discussed in the last episode

A more recently described cause of raised ferritin is the metabolic syndrome, sometimes referred to as dysmetabolic hyperferritinaemia: patients typically demonstrate elevated ferritin levels with normal Tsat

Then we have Haematological causes and: A variety of red cell disorders, characterised by ineffective erythropoiesis or haemolysis, are associated with increased ferritin; these include thalassaemic disorders, hereditary spherocytosis and inherited or acquired sideroblastic anaemias. Prolonged or chronic transfusion therapy, for example in patients with major haemoglobinopathies, myelodysplastic syndromes, or during treatment for haematological malignancies, will also cause transfusional iron overload.

So in summary, reactive causes of raised serum ferritin levels, including malignancy, inflammatory disorders, renal failure, liver disease and metabolic syndrome, are all considerably more common than true iron overload.

There are other genetic causes of an elevated serum ferritin including hemochromatosis, Still disease, and other rare disorders

How do we investigate raised serum ferritin?

When ferritin is raised, the most crucial questions to ask are

(i)            is it secondary to a known clinical condition, and

(ii)          (ii) is it associated with iron overload?.

A clinical history and examination, together with a few simple investigations, will often reveal the probable underlying cause. In particular, patients should be questioned about alcohol intake and other risk factors for liver disease, transfusion history or oral iron supplementation, family history of iron overload and the presence or absence of diabetes mellitus, obesity and hypertension, history of early cataracts, as well as for symptoms and signs that may point to an underlying inflammatory or malignant disorder. Initial investigations should include a full blood count, repeat ferritin, Tsat, renal function tests and LFTs (with viral hepatitis serology if LFTs are abnormal) and inflammatory markers, such as CRP and ESR. Glycosylated haemoglobin levels may indicate impaired glucose tolerance, and raised serum lipids, body mass index and hypertension may point to underlying metabolic syndrome. Abdominal ultrasonography may demonstrate an echogenic liver suggesting alcohol- or non-alcohol-related fatty liver disease.

Iron overload is more likely to be present if the ferritin has risen progressively or the ferritin is >1000 μg/l.

It is worth noting that acute infections, menstrual bleeding and recent blood donation can temporarily reduce Tsat to within the normal range in patients with iron overload indicating that normal Tsat does not completely exclude iron overload. In the setting of persistent borderline results, genotyping for haemochromatosis should be performed.

Males with ferritin > 300 μg/l and Tsat >50% and females with ferritin > 200 μg/l and Tsat > 40% will usually have iron overload. We will leave this here as we are not looking into the diagnosis or management of haemochromatosis here today.

How do we manage a raised ferritin without elevated transferrin saturation?

In otherwise well patients with unexplained elevated ferritin and Tsat <40% (female) or <50% (male), a period of observation may be informative: stable, moderately increased levels may not require further investigation, whereas fluctuating levels are typically seen in hepatic steatosis or alcohol excess. Persistent unexplained high levels, especially at levels >1000 μg/l, merits consideration of onward referral to a specialist, usually a hepatologist.

In most cases of a high ferritin secondary to inflammatory or other conditions, management of the underlying condition will lead to reduction in ferritin levels. For example, alcohol abstinence will usually lead to improvement in ferritin within weeks to months; and weight loss and improved control of diabetes and blood pressure will usually lead to lowering of levels in patients with metabolic syndrome.

There is no evidence to support venesection therapy in patients with increased ferritin associated with liver disease other than heamochromatosis

In Conclusion

The finding of a raised serum ferritin is a common conundrum in modern day clinical practice, both in primary and secondary care. Iron overload is a relatively uncommon cause of this picture and can be excluded by the finding of a normal transferrin saturation, so consideration of the many reactive causes like hepatic, malignant, renal, haematological and metabolic causes is important: many cases will not require further investigation if a few simple investigations are performed. Rarer causes will require specialist molecular genetics for diagnosis.

So that is it, a review of the laboratory investigations of a raised serum ferritin.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/Ugo6U9QI2xY

This channel may make reference to guidelines produced by the British Society for Haematology. The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by them.

My name is Fernando Florido (also known as Juan Fernando Florido Santana), a GP in the UK. In this episode, I will go through the guideline by the British Society for Haematology on the laboratory diagnosis of functional iron deficiency, focusing on what is relevant in Primary Care only.

In the last episode I covered:

·      The guideline by the British Society for Haematology on the laboratory diagnosis of iron deficiency

In the next episode, I will cover:

·      The assessment of raised ferritin

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The link to the new guideline by the British Society for Haematology on the laboratory diagnosis of functional iron deficiency can be found here:

·      https://onlinelibrary.wiley.com/doi/10.1111/bjh.12311

The link for the British Society for Haematology website can be found here

·      https://b-s-h.org.uk/

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I am Fernando, a GP in the UK. Today, we will go through the guideline by the British Society for Haematology on the laboratory diagnosis of functional iron deficiency, focusing on what is relevant in Primary Care only. A link to it is in the episode description.

If you haven’t already, I recommend that you check out the last episode where I covered the laboratory diagnosis of iron deficiency

And in the next episode, I will cover the assessment of raised ferritin. So, stay tuned for that!

Right, let’s jump into it.

Whilst the concept of functional iron deficiency—or FID—is both important and very relevant to us in Primary Care, reading the full guideline can be overwhelming. It’s full of detailed considerations more relevant to specialists and secondary care. So, instead of summarising that in its entirety, I’m just going to give you a general overview. I’ll take you through the relevant investigations, explaining each one in plain terms, and linking it back to what we need to know and do in general practice.

And first of all, what is Functional Iron Deficiency (FID)?

Functional Iron Deficiency happens when the body has enough iron stored, but can’t get it to where it’s needed — particularly, the bone marrow where red blood cells are made. This is different from true iron deficiency, but the effect is similar: not enough haemoglobin is made, leading to anaemia.

Why Does This Happen?

FID is common in long-term illnesses, like:

• Chronic inflammation (e.g. rheumatoid arthritis)
• Infections
• Cancer and
• Chronic kidney disease (CKD)

In these situations:

• The liver produces hepcidin, a hormone that blocks iron release from stores and reduces absorption from the gut.
• So, even if ferritin looks normal or high, the bone marrow can’t access the iron, so red cell production is reduced.

What Should GPs Know about functional iron deficiency?

Let’s look at a very simplified version of the Pathophysiology. And that is that

• Chronic Inflammation leads to→ ↑a rise in Hepcidin → ↓which reduces Iron transport → which in turn leads iron not reaching the Bone.
• This results in anaemia of chronic disease.
• FID can also happen when bone marrow is overstimulated (e.g., from treatment with ESA in CKD), using iron faster than it can be delivered.

When should we Suspect FID? We should suspect it clinically if there is anaemia in chronic disease (especially if it is not improving with oral iron). We should also suspect it depending on test results. And let’s now look at the list of possible tests that can be requested for functional iron deficiency, starting with the ones that we can order in Primary Care:

·      Firstly, we have MCV or Mean cell Volume and MCH or Mean Cell Haemoglobin. They tell us the average size of red blood cells and the average amount of haemoglobin in each red cell respectively.

They are useful at the time of diagnosis and for tracking trends over weeks or months. However, they don’t change quickly, so they not suitable for identifying rapid changes.

·      Then we have serum Ferritin. This one we all know well. It reflects the amount of stored iron in the body. If it’s under 15 micrograms per litre, that strongly indicates true iron deficiency. Ferritin is an acute phase reactant—it rises in inflammation and chronic disease. So, a high ferritin doesn’t exclude FID. In CKD patients, a ferritin under 100, or sometimes even 200 increases the likelihood of requiring further iron treatment. In CKD, values as high as 1200 may still be consistent with iron-restricted anaemia. But we should not use ferritin alone to guide treatment but consider it in the context of other tests too.

·      Then we have Transferrin Saturation – or TSAT which shows the percentage of transferrin that is actually carrying iron. Alone, it’s not a reliable guide for iron therapy in CKD patients but combined with ferritin and other tests it can help diagnose FID or monitor treatment. Transferrin saturation can also be influenced by inflammation, so it’s not a standalone tool.

·      Now let’s move onto more specialist markers of iron status, especially for functional iron deficiency, like %HRC – Percentage of Hypochromic Red Cells, which measures the proportion of red cells that contain less haemoglobin than they should. It’s actually the best-established lab test for detecting FID.

·      Then we have CHr – Reticulocyte Haemoglobin Content, which measures how much haemoglobin is in reticulocytes. It’s the second most established marker for FID and a value of less than 29 picograms suggests functional iron deficiency.

·      There are other truly specialist tests, which are:

o  Zinc Protoporphyrin

o  Bone Marrow Examination

o  sTfR – Soluble Transferrin Receptor

o  Serum Erythropoietin and

o  Hepcidin, which we mentioned earlier and which plays a role in the pathophysiology of functional iron deficiency

What is the typical picture of anaemia in FID?

Well, haemoglobin is usually low or normal, often showing a normocytic normochromic picture.

Ferritin will be normal or high Because being an acute-phase reactant, it’s falsely elevated in inflammation

Transferrin saturation is usually low <20% despite the high ferritin. Transferrin saturation is reduced because of iron being unavailable.

Serum iron is low, both in true iron deficiency and functional iron deficiency. However, TIBC is normal or low, whereas it would be high in true iron deficiency

ESR or CRP tend to be high in functional iron deficiency reflecting underlying inflammation and finally functional iron deficiency also show that

Reticulocyte Hb content is low and percentage of hypochromic cells are high

When should we refer to Secondary Care?

We should consider referral if:

·      There is persistent or unexplained anaemia, and we suspect FID and when oral iron hasn’t worked.

·      If The patient is on (or might need) IV iron or erythropoiesis-stimulating agents (ESAs) which are managed in secondary care.

·      If There is diagnostic uncertainty like for example mixed deficiencies, or a high ferritin but the picture still points to iron deficiency anaemia or

·      If there is anaemia in CKD stages 4–5, active cancer, or complex comorbidities

And to end, let’s remember that our role in Primary Care is:

• To Recognise the FID pattern: that is, chronic disease + anaemia + and a ferritin which is not low
• To exclude other causes, for example bleeding, B12/folate deficiency, chronic kidney disease etc.
• To manage oral iron therapy and initial assessment remembering that
• We should not overlook anaemia in patients with chronic disease. FID is treatable but IV iron and ESA are specialist decisions.

So that is it, a review of the laboratory investigations of functional iron deficiency.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/ZdHSs-QBtac

This channel may make reference to guidelines produced by the British Society for Haematology. The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by them.

My name is Fernando Florido (also known as Juan Fernando Florido Santana), a GP in the UK. In this episode, I will go through the guideline by the British Society for Haematology on the laboratory diagnosis of iron deficiency in adults (excluding pregnancy) and children, focusing on what is relevant in Primary Care only.

In the coming episodes, I will also cover the recommendations by the British Society for haematology on:

·      The assessment of raised ferritin

·      The concept of functional iron deficiency

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The link to the new guideline by the British Society for Haematology on the laboratory diagnosis of iron deficiency can be found here:

·      https://onlinelibrary.wiley.com/doi/full/10.1111/bjh.17900

The link for the British Society for Haematology website can be found here

·      https://b-s-h.org.uk/

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I am Fernando, a GP in the UK. Today, we will go through the guideline by the British Society for Haematology on the laboratory diagnosis of iron deficiency, focusing on what is relevant in Primary Care only.

In the coming episodes, I will also cover their recommendations on:

·      The assessment of raised ferritin

·      The concept of functional iron deficiency

So, stay tuned for those!

Right, let’s jump into it.

The British Society for Haematology produces Good Practice Papers to recommend good practice in areas where there is limited evidence but where a degree of consensus is likely to be beneficial to patient care.

The laboratory diagnosis of iron deficiency is difficult, because iron homeostasis is dynamic and no single test can provide an accurate assessment of iron absorption, transport, storage, and utilisation.

Iron metabolism in adults and children can be considered equivalent, and these recommendations are applicable to both paediatric and adult practice, but it does not include pregnancy.

Let’s start by saying that iron deficiency is the most common cause of anaemia worldwide. In the UK, the prevalence of iron deficiency anaemia can go up to 6% depending on age and sex, with higher rates in certain groups like menstruating women and those aged over 85 years.

The prevalence of iron deficiency without anaemia, however, is not well documented.

In this episode we are just focusing on the laboratory assessment of iron status and not the full guidance on iron deficiency anaemia which requires a detailed history, clinical examination and the review of, for example, national gastrointestinal and gynaecology guidelines as well as other local pathways.

The British Society for Haematology has suggested an algorithm for the laboratory investigation of iron deficiency anaemia which we will review at the end. But first, let’s look at the different laboratory parameters that we will need to consider.

As you may already be aware, the main diagnostic tests in iron deficiency anaemia are a full blood count and ferritin.

So let’s now start with the red cell parameters in a full blood count. Anaemia will be confirmed if haemoglobin or Hb is below the reference range. But Hb alone does not indicate iron status and at population level, there’s considerable overlap in Hb levels between iron-replete and iron-deficient people.

Iron deficiency is typically associated with microcytic hypochromic anaemia.

But low MCV, MCH, or MCHC can also appear in other conditions, especially the thalassaemias.

Interestingly, MCV can be normal in up to 40% of iron-deficient patients, and also in cases of mixed haematinic deficiency.

There are other advanced parameters like percentage of hypochromic cells (%HRC) and reticulocyte mean Hb content which can help evaluate iron availability further.

Given that Erythrocytes contain about half of the body’s iron at any one time,

a high percentage of hypochromic cells or low reticulocyte Hb content — without thalassaemia — suggests that iron is not adequately reaching newly formed red cells, which could be due to iron deficiency or iron restriction.

Morphological changes appear in iron deficiency and generally, anisocytosis precedes hypochromia and microcytosis but blood cell morphology is not diagnostic

So, in summary, in respect of full blood counts, it is recommended that:

• If thalassaemia is not present, any of MCV, MCH, or MCHC result which is below normal could suggest iron deficiency,
• On the other hand, normal red cell indices do not exclude iron deficiency as a cause of anaemia. Further investigation may still be required if there is high clinical suspicion.
• Mean reticulocyte Hb content of <29 pg can support the diagnosis of iron deficiency if initial tests are inconclusive and finally, although not diagnostic,
• Inspection of a peripheral blood film should be performed when the diagnosis is unclear.

Let’s now move onto ferritin.

Ferritin reflects iron stores and levels <15 µg/L strongly suggest iron deficiency.

Levels up to 30 µg/L can still be consistent with deficiency but are less specific.

Ferritin acts as an acute phase protein, meaning it rises with inflammation, kidney disease, liver disease, and malignancy and, because of this, interpreting ferritin in inflammatory states can be challenging.

Formulas to correct ferritin with CRP or ESR have been proposed, but the evidence isn’t robust enough for clinical use.

So, in summary, the recommendations are that:

• In children over 5 and adults a ferritin <15 µg/L is indicative of iron deficiency.
• For children under 5 the threshold is a ferritin <12 µg/L. However,
• A ferritin level within the normal range does not exclude iron deficiency if there’s inflammation or chronic disease and further investigation is often needed.

And this is where iron studies come into play. They should not be done routinely but they should be considered when:

• FBC shows microcytic or hypochromic anaemia
• Ferritin is borderline or normal but there's suspicion of iron deficiency e.g., in chronic inflammation or
• There's a need to differentiate iron deficiency from other causes of anaemia (like thalassaemia)

Iron studies include primarily: serum iron, total iron binding capacity (TIBC) and transferrin saturation (TSAT).

Let’s break this down.

Serum Iron only measures ferric iron bound to transferrin, not the iron in haemoglobin. Someone with iron deficiency will usually exhibit a low concentration of serum iron, but it is a dynamic parameter with well-established day-to-day variability. Consequently, measuring serum iron in isolation is not helpful but its measurement is required to allow calculation of percentage TSAT.

ON the other hand, TIBC and Transferrin rise in iron deficiency. Transferrin is a negative acute phase protein so its concentration may be reduced in inflammation. Although TIBC and transferrin have less variability than serum iron, their specificity remains poor so they are not really that useful for diagnostic purposes.

Finally, transferrin Saturation (TSAT) is calculated as the ratio of serum iron to TIBC or transferrin.

It reflects how much transferrin is carrying iron, but like serum iron, it’s variable and diurnal fluctuations can be up to 70%. Also conditions like malnutrition and chronic illness affect its accuracy.

A diagnostic threshold for TSAT has not been well established, but it has been suggested a target of <16% as a screening threshold.

So, in summary,

• Serum iron, TIBC and transferrin should not be used alone in diagnosing iron deficiency but a
• TSAT <16% can support the diagnosis if other tests are inconclusive.

As promised, let’s look at the algorithm proposed in this paper by the British Society for Haematology.

The first line tests for the investigation of iron deficiency anaemia are a FBC, ferritin and CRP. Based on the results, we have three main scenarios.

The simplest one is when haemoglobin is normal and no anaemia is identified.

In these cases, if ferritin is below 15, we should still suspect iron deficiency and investigations into the cause of the iron deficiency may still be required.

The other two scenarios is when there is anaemia.

And according to WHO criteria, anaemia is when Haemoglobin is:

Below 130 in adult males

Below 120 in non-pregnant females or

Below their age and gender specific reference range in children

So, if there is anaemia but no signs of inflammation, that is, CRP is normal,

But ferritin is below 15

Then this is a case of iron deficiency anaemia

However, if ferritin is 15 or higher,

Then iron deficiency is unlikely and we should consider other causes of anaemia

If there is anaemia but also signs of acute or chronic inflammation, that is, when the CRP is high

If ferritin is below 15

We should also regard this as iron deficiency anaemia.

If ferritin is higher than 150,

Then iron deficiency is also unlikely and we should consider other causes of anaemia

But if ferritin is between 15 and 150 in the context of a high CRP

Then further tests will be required, including a blood film and iron studies.

Blood film morphology will help us exclude alternative diagnoses and

We are likely to consider a diagnosis or iron deficiency anaemia if TSAT is <16% or mean reticulocyte haemoglobin content is less than 29 pg

In summary, we have summarised the current investigations for iron deficiency but this should be used alongside clinical guidelines, for example like in suspected gastrointestinal bleeding.

So that is it, a review of the laboratory investigations of iron deficiency.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/aB6Z7tASKrc

This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country.

My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through new and updated recommendations published in April  2025 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The Full NICE News bulletin for April 2025 can be found here:

·      https://www.nice.org.uk/guidance/published?from=2025-04-01&to=2025-04-30&ndt=Guidance&ndt=Quality+standard

The links to the guidance covered in this episode can be found here:

The NICE guideline on Falls: assessment and prevention in older people and in people 50 and over at higher risk [NG249] can be found here:

·      https://www.nice.org.uk/guidance/ng249

The update on Suspected cancer: recognition and referral [NG12] can be found here:

·      https://www.nice.org.uk/guidance/ng12

·      https://www.nice.org.uk/guidance/ng12/chapter/Recommendations-organised-by-site-of-cancer#myeloma

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we’ll be looking at the NICE updates published in April 2025, focusing on what is relevant to Primary Care only.

We’ve got another short and snappy episode today, as there are only two clinical areas to discuss: the brand-new national guideline on fall prevention and new advice on cancer recognition and early detection.

Right, let’s jump into it.

And let us start with the update on the cancer recognition guideline, which affects the recommendations on blood tests for myeloma. These recommendations have been amended in response to a series of reviews to improve earlier diagnosis. So now those with an unexplained fracture or persistent bone pain, particularly back pain, and especially if they are aged 60 or over, should be investigated for myeloma, although we can consider it for people under 60 too. For this assessment we will request the following blood tests:

• a full blood count 
• serum calcium
• either plasma viscosity or ESR
• paraprotein, using serum protein electrophoresis and
• Serum free light chains. If the serum test is not available, we can use a Bence–Jones test to check for free light chains in the urine. 

The change means that we should now include serum protein electrophoresis and serum free light chain testing in the initial diagnostic blood tests and this testing should be offered instead of the traditional urine test for Bence–Jones protein. 

The second section refers to a brand-new guideline on falls assessment and prevention. These recommendations are for people who are:

• aged 65 or over or
• aged 50 to 64 with 1 or more factors that could increase their risk of falls. These factors include long-term conditions such as arthritis, dementia, diabetes or Parkinson's disease, having had a stroke and having a learning disability.

The guideline recommends a comprehensive assessment and management plan for these patients. But, who should we prioritise?

Well, we should offer comprehensive falls assessment and management to people who have fallen in the last year and who:

• Are frail.
• Were injured in a fall.
• Have experienced a loss of consciousness related to a fall.
• Have been unable to get up independently after a fall or that
• Have had 2 or more falls in the last year.

For people who have fallen in the last year and who do not have any of these criteria we should assess their gait and balance

And if they have a gait or balance impairment:

• We will simply offer a falls prevention exercise programme and
• a home hazard assessment.

But let’s go back to the people in the first group, those at highest risk and the ones that need a Comprehensive falls assessment. What should this assessment include? Well, we should check for:

• Alcohol misuse.
• Perform a Neurological and Cardiovascular examination including a lying and standing BP.
• We will do an Osteoporosis risk assessment including the risk of fragility fractures.
• A review of medication and long-term medical conditions and also include
• An overall review of the patient looking at things like:
• Cognition and mood.
• Diet, and weight loss.
• Hearing and visual impairments.
• Dizziness.
• Functional ability.
• Urinary continence
• Gait, balance, mobility, etc 

And once we have done this assessment, what does the comprehensive falls management entail? Well, apart from addressing obvious issues identified in the assessment, this management plan should include: 

1- A structured medication review and, for those on psychotropic drugs, we will discuss their increased risk of falls, considering stopping these medications, liaising with specialist services if necessary. Psychotropic medicines include antipsychotics, antidepressants, anxiolytics, mood stabilising agents, and antiepileptic drugs

2- we will refer to occupational therapy and any other appropriate service for a home hazard assessment and a fall prevention exercise programme

3- We will consider the need for surgical interventions, such as cataract surgery or a pacemaker, if these problems have played a role in their falls, and finally, 

2- Although there is insufficient evidence to support taking vitamin D supplements specifically to lower the risk of falls, we will encourage people to follow NHS advice on taking vitamin D to maintain bone and muscle health. For adults and children over 4 years old this advice is that they should consider taking a daily supplement containing 10 micrograms or 400 IU of vitamin D during the autumn and winter months, generally from early October to the end of March, and this includes pregnant and breastfeeding women. Between early April to the end of September, most people can make all the vitamin D they need through sunlight and from a balanced diet, so they may choose not to take a vitamin D supplement during these months. However, people at risk of vitamin D deficiency, including the frail and the housebound and also those with darker skin, for example those of African, African-Caribbean or south Asian background should take 10 micrograms or 400 IU of vitamin D throughout the year. The advice for infants and children under 4 is slightly different and it is not covered here.

So that is it, a review of the NICE updates relevant to primary care.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/474v7gUrz38

This channel may make reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

My name is Fernando Florido (also known as Juan Fernando Florido Santana), a GP in the UK. In this episode, I will go through the new NICE guideline on coeliac disease: assessment and management, NG20, focusing on what is relevant in Primary Care only.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The link to the NICE guideline on coeliac disease can be found here:

·      https://www.nice.org.uk/guidance/ng20/chapter/recommendations

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I am Fernando, a GP in the UK. Today, we will go through the new NICE guideline on coeliac disease: assessment and management, or NG20, focusing on what is relevant in Primary Care only.

Right, let’s jump into it.

And before we start on the guideline itself, what is coeliac disease exactly?

Coeliac disease is a genetic, immune-mediated enteropathy triggered by gluten in some people. It primarily affects the small intestine, leading to villous atrophy, crypt hyperplasia, and malabsorption.

Why does it happen? Well, the pathophysiology is as follows:

Gluten (specifically gliadin) is found in wheat, barley, and rye. An enzyme called tissue transglutaminase (tTG) modifies gluten peptides. In genetically predisposed people, these modified peptides are presented to T-cells, triggering an inappropriate immune response. This leads to inflammation and damage to the small intestinal mucosa, particularly in the proximal small bowel.

We should suspect coeliac disease and offer serological testing if there is:

• persistent unexplained abdominal or gastrointestinal symptoms
• fatigue or weight loss
• mouth ulcers
• unexplained iron, vitamin B12 or folate deficiency
• first‑degree relatives affected.
• conditions such as type 1 diabetes, autoimmune thyroid disease, and irritable bowel syndrome (in adults) and we should also consider testing in a number of other conditions, for example:

·      reduced bone mineral density,

·      unexplained neurological symptoms (like peripheral neuropathy or ataxia)

·      persistently raised liver enzymes and

·      Down's and Turner syndromes

However, before arranging any investigations we will need to explain that any test is accurate only if a gluten‑containing diet is eaten during the entire diagnostic process. This also means that they should not start a gluten‑free diet until diagnosis is confirmed by a specialist, even if the results of a serological test are positive.

Additionally, people following a normal diet should be advised to eat some gluten in more than 1 meal every day for at least 6 weeks before testing.

If they have already restricted their gluten intake and they are unable to re‑introduce it, we will refer them to gastroenterology explaining that it may be difficult to confirm their diagnosis even by intestinal biopsy.

People who have tested negative for coeliac disease should be retested if new suggestive symptoms arise or persist, particularly if they have type 1 diabetes or a family history.

What serological testing should we do for coeliac disease?

NICE recommends that the first choice of test should be IgA tissue transglutaminase antibodies (tTG) together with total immunoglobulin A (IgA) to exclude deficiency. But why is this?

Let’s remember that everyone has the tissue transglutaminase enzyme (tTG). However, in people with coeliac disease, the immune system produces autoantibodies against this enzyme — particularly IgA autoantibodies.

This autoantibody response is:

• Highly specific to coeliac disease
• Triggered by gluten exposure in genetically susceptible people and
• Correlate with intestinal damage (i.e. the higher the autoantibodies, the more likely there is villous atrophy)

This is why serum IgA tissue transglutaminase antibodies are the first-line screening test — it’s convenient, non-invasive, and has high sensitivity and specificity, especially in untreated people.

Additionally in adults the lab should test for IgA endomysial antibodies (EMA) if IgA tissue transglutaminase antibodies are weakly positive and consider additional tests if IgA levels are low. Then the Lab should clearly communicate the interpretation of the results as well as the recommended action.

We should then refer anybody with positive serological test results to a gastrointestinal specialist for further assessment, which for adults will most likely include endoscopic intestinal biopsy.

We should also refer those with negative serological test results if coeliac disease is still clinically suspected.

People diagnosed with coeliac disease should have an annual review in order to:

• measure weight and height
• review symptoms and diet
• and consider the need for specialist dietetic advice.

For those who have persistent symptoms despite gluten exclusion we should:

• review the certainty of the original diagnosis
• refer them to a specialist dietitian to investigate continued exposure to gluten
• and investigate potential complications or coexisting conditions such as irritable bowel syndrome, lactose intolerance, bacterial overgrowth, or colitis.

If no other cause is found we would call it refractory coeliac disease and we will need to refer them and consider prednisolone while waiting for specialist advice.

We should give people with coeliac disease sources of information on the disease, including, for example:

·      Specialist groups and dietitians

• how to manage social situations, like eating out and travelling
• avoiding cross contamination at home and
• immunisation against pneumococcus, all of this
• Being aware that people with coeliac disease may experience anxiety and depression.

In terms of dietary management, they should seek advice before taking over‑the‑counter vitamin or mineral supplements, explaining that they may need to take specific supplements such as calcium or vitamin D if their dietary intake is insufficient.

We can also explain that:

• they can choose to include gluten‑free oats in their diet at any stage and
• continuing them will depend on their response.

So that is it, a review of the NICE guideline on coeliac disease.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/JP5EvxGd8g4

This channel may make reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

My name is Fernando Florido (also known as Juan Fernando Florido Santana), a GP in the UK. In this episode, I will go through the new NICE guideline on acute asthma, NG244, focusing on what is relevant in Primary Care only. Given how extensive the guidance is, in this episode I will just focus on lessons from asthma deaths and near-fatal asthma as well as reviewing the concept of difficult asthma.

In the last four episodes I covered the initial assessment and treatment in both adults and children.

Just like the NICE guideline on the management of chronic asthma, which was updated in November 2024, the NICE guideline on acute asthma is also a collaborative initiative developed by NICE, the British Thoracic Society (BTS), and the Scottish Intercollegiate Guidelines Network (SIGN). It replaces previous guidance, and you can find a link to it in the episode description.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through 

There is a podcast version of this and other videos that you can access here:

Primary Care guidelines podcast:

·      Redcircle: https://redcircle.com/shows/primary-care-guidelines

·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK

·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148

There is a YouTube version of this and other videos that you can access here: 

• The Practical GP YouTube Channel: 

https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk

The link to the new NICE guideline on acute asthma can be found here:

·      https://www.nice.org.uk/guidance/ng244/chapter/Managing-acute-asthma

Based on recommendations on managing acute asthma in the BTS/SIGN British guideline on the management of asthma:

·      https://rightdecisions.scot.nhs.uk/bts-nice-and-sign-asthma-pathway/managing-acute-asthma/

Disclaimer:

The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions.

In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.

Transcript

If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.

Hello and welcome, I am Fernando, a GP in the UK. Today, we will go through the new NICE guideline on acute asthma, or NG244, focusing on what is relevant in Primary Care only. Just like in chronic asthma, the NICE guideline on acute asthma is a joint effort by NICE, BTS and SIGN and a link to it is in the episode description.

In this episode I will just focus on lessons from asthma deaths and the concept of difficult asthma.

In the last four episodes I covered the initial assessment and treatment in both adults and children and, if you have not already, I recommend that you check them out.

Right, let’s jump into it.

Confidential inquiries into over 200 asthma deaths in the UK have identified that most asthma deaths occurred before the patient reached hospital and that there are three main contributing factors: the disease itself, medical management, and patient behaviour or psychosocial issues..

And let’s start by looking at Disease Factors:

Although, In a minority the fatal attack occurred suddenly in a patient with mild or moderately severe asthma, the majority of patients who died from asthma had chronically severe disease.

In terms of Medical Management:

Many deaths were linked to inadequate treatment with inhaled corticosteroids (ICS) or oral steroids, as well as poor monitoring of asthma severity. Follow-up care was often insufficient, and some patients should have been referred to specialists sooner. The use of written management plans was notably underutilised.

A key finding from the National Review of Asthma Deaths report, published in 2014 by the Royal College of Physicians, highlighted the link between heavy or increasing use of short-acting beta agonists (or SABAs) and asthma deaths. Prescribing more than 12 SABA inhalers per year should prompt a thorough review of the patient’s management.

Asthma deaths have also been reported after inappropriate prescriptions of beta blockers and non-steroidal anti-inflammatory drugs, so All asthma patients should be asked about any previous reactions to these medications.

Sedation should be avoided during acute asthma attacks unless it is necessary for anaesthetic or intensive care procedures.

The National Review of Asthma Deaths report also revealed an increased risk of death within one month of hospital discharge following an acute attack, underscoring the need for close follow-up in primary care.

Let’s now look at Adverse Psychosocial and Behavioural Factors:

And These factors are important because they were present in most patients who died of asthma. Key risk factors include poor adherence to treatment, failure to attend appointments, and psychiatric conditions. So we, as Healthcare professionals, must recognise that patients with severe asthma combined with psychosocial vulnerabilities are at greater risk of death.

So, who are these patients? Patients at Risk of Near-Fatal or Fatal Asthma are usually those who have severe asthma along with one or more of the following:

• A history of near-fatal asthma, including previous ventilation or respiratory acidosis.
• Previous hospital admission for asthma, especially within the past year.
• The need for three or more classes of asthma medication.
• Frequent or heavy use of β2 agonists. and
• Multiple emergency department visits, particularly in the last year.

AND additionally, adverse Psychosocial and behavioural factors, including:

• Non-adherence to treatment or monitoring.
• Missing appointments
• fewer GP contacts.
• Frequent home visits
• self-discharge from hospital.
• Mental health conditions such as psychosis, depression, or self-harm.
• Current or recent use of major tranquillisers.
• Denial of the severity of their condition.
• Substance or alcohol misuse.
• Obesity.
• Learning difficulties.
• Financial or employment problems.
• Social isolation.
• Childhood abuse. As well as
• Severe domestic, marital, or legal stress.

Patients admitted with a severe asthma attack should be followed by a respiratory specialist for at least a year post-admission.

For patients who have experienced near-fatal asthma, it’s advisable to involve a close relative when discussing future management plans and They should remain under specialist supervision indefinitely.

Let’s now touch on the concept of Difficult Asthma:

Difficult asthma refers to cases where asthma-like symptoms and attacks persist despite high-dose asthma therapy. There is no universally agreed definition, but it typically applies to patients with ongoing symptoms or frequent attacks despite maximum treatment.

In this context, difficult asthma is defined by:

·      persistent symptoms and/or frequent asthma attacks despite the following treatments:

o  in adults:

§ the use of high-dose ICS plus one other agent such as a LABA or LTRA or

§ The use of medium-dose ICS plus two other asthma agents such as a LABA and LTRA or any other appropriate additional therapy

o   However, in children this concept applies to those on:

§ medium-dose ICS plus one other agent such as a LABA or LTRA; or

§ low-dose ICS plus two other asthma agents such as a LABA and LTRA or any other appropriate additional therapy or

• those taking oral steroids Frequently or continuously.

Patients with difficult asthma require a thorough evaluation, including:

• Confirming the asthma diagnosis.
• Identifying the cause of persistent symptoms. and
• Assessing adherence to treatment.

This should be done by a multidisciplinary asthma service with expertise in managing complex cases.

The Factors Contributing to Difficult Asthma are:

• Poor Adherence and managing it is beneficial improve asthma control and there is some evidence that it can improve lung function and quality of life. Objective monitoring of adherence is more reliable than self-assessment.
• Then Given that difficult asthma is frequently linked to adverse psychosocial factors. We should routinely assess for coexisting psychological co-morbidity and, In children, this should include a psychosocial family assessment.
• Then Patients with difficult asthma have been found to have high rates of dysfunctional breathing, which can mimic asthma or coexist with asthma,
• Also, Given that Acute asthma can be associated with IgE-dependent sensitisation to indoor allergens, patients with difficult asthma and recurrent hospital admissions, should be tested for mould allergies.
• And finally patients with difficult asthma, could have induced sputum eosinophil counts to guide steroid treatment.

And what is this induced sputum eosinophil count?

Although this isn’t done routinely in primary care, let’s quickly explain what it involves.

Before starting, we will check spirometry or peak flow to get a baseline.

Then, in order to prevent bronchospasms, we will give the patient a short-acting β2-agonist (like salbutamol) before starting the test.

Then, For Sputum Induction, the patient inhales a mist of hypertonic saline (usually 3% to 5%) using a nebuliser. If their FEV₁ drops by 20% or more, we will stop the procedure immediately.

After Sputum Collection, the lab will provide the percentage of eosinophils seen. A result of >3% suggests eosinophilic inflammation, which can help guide asthma treatment decisions, such as oral steroids.

So that is it, a review of lessons from asthma deaths and the concept of difficult asthma.

We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement.

Thank you for listening and goodbye.

·      https://youtu.be/LxlmAeHzjsg

This channel may make reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE.

My name is Fernando Florido (also known as Juan Fernando Florido Santana), a GP in the UK. In this episode, I will go through the new NICE guideline on acute asthma, NG244, focusing on what is relevant in Primary Care only. Given how extensive the guidance is, in this episode I will just focus on the treatment of acute asthma in children.

In the last three episodes I covered the initial assessment in adults and children and the treatment in adults and in the next episode, I will cover:

·      Lessons from asthma deaths and near-fatal asthma as well as reviewing the concept of difficult asthma

Just like the NICE guideline on the management of chronic asthma, which was updated in November 2024, the NICE guideline on acute asthma is also a collaborative initiative developed by NICE, the British Thoracic Society (BTS), and the Scottish Intercollegiate Guidelines Network (SIGN). It replaces previous guidance, and you can find a link to it in the episode description.

I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.  

Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release] 

• Music provided by Audio Library Plus 
• Watch: https://youtu.be/aBGk6aJM3IU 
• Free Download / Stream: https://alplus.io/halfway-through