Primary Care Guidelines

The video version of this podcast can be found here: ·      https://youtu.be/xB8BStN4OwgThis 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 TranscriptIf 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 controlWhat 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 identifie

The video version of this podcast can be found here: ·      https://youtu.be/mHyDaVHtb58This 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+standardThe 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-2TranscriptIf 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.A

The video version of this podcast can be found here: ·      https://youtu.be/z7eZ1MLItGwThe previous episode on first line treatment of T2DM can be found here: ·      https://youtu.be/32Lf5UlyTOAThis 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=ecJGF5QCuMLQ6hrkThe NICE guideline on Type 2 diabetes in adults: management [NG28] can be found here:·      https://www.nice.org.uk/guidance/ng28 TranscriptIf 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 otherwiseIf 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, orHave 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 o

The video version of this podcast can be found here:·      https://youtu.be/32Lf5UlyTOAThis 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/id1608821148There is a YouTube version of this and other videos that you can access here: The Practical GP YouTube Channel: https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrkThe 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 inhibitorpioglitazonea sulfonylureaor 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 prescri

The video version of this podcast can be found here: ·      https://youtu.be/t8U8-isTieMThis 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/ng28TranscriptIf 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 orA Fasting plasma glucose level of 7.0 mmol/L or more orA 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 orEvery 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 profilestotal glycated haemoglobin estimation (if there are abnormal haemoglobins) orfructosamine. 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 andthen proceed to intensify drug treatment, generally by adding a second drug.These thresholds are heavily influenced by the results of clinical trials such as th

The video version of this podcast can be found here: ·      https://youtu.be/j5z0Qv35dWEThis 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+standardThe 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 TranscriptIf 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 thatThey 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 includeTotal cholesterolHDL cholesterol andTriglyceridesAnd that, from these, non-HDL and LDL cholesterol are calculatedLet’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 75Those with an eGFR betw

The video version of this podcast can be found here: ·      https://youtu.be/sUlAwcaUrB0The first episode can be found here: ·      https://youtu.be/nguVbiQc5WwThis 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-hypogonadismThe EAU pocket guideline can be found here:·      https://d56bochluxqnz.cloudfront.net/documents/pocket-guidelines/EAU-Pocket-on-Sexual-Reproductive-Health-2025.pdf TranscriptIf 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 erectionsLess frequent sexual activity or masturbation andDelayed ejaculationExamples of Physical Symptoms areReduced ability to perform vigorous activities Difficulty walking more than 1 kilometre Hot flushesLower energy levels andReduced physical strengthAnd finally, examples of Psychological Symptoms includeLow mood Loss of motivation General fatigueDifficulty concentrating andsleep disturbancesAs 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 hormoneHyperthyroidismLiver diseaseAgeingSmoking andHIV or AIDSA 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 steroidsHypothyroidismObesityCushing’s syndromeInsulin resistance, as seen in metabolic syndrome or type 2 diabetes andNon-alcoholic fatty liver disease (NAFLD) and related conditionsA 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 clin

The video version of this podcast can be found here: ·      https://youtu.be/OcxWFhMAbPQThis 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=ecJGF5QCuMLQ6hrkThe EAU sexual and reproductive health full guideline can be found here:·      https://uroweb.org/guidelines/sexual-and-reproductive-health/chapter/male-hypogonadismThe EAU pocket guideline can be found here:·      https://d56bochluxqnz.cloudfront.net/documents/pocket-guidelines/EAU-Pocket-on-Sexual-Reproductive-Health-2025.pdf TranscriptIf 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 commonOther chromosomal disorders, like Down syndromeAnd also, conditions like sickle cell disease, amongst othersAcquired causes of primary hypogonadism include:Drug-related like, for example, inChemotherapy drugs and Testosterone synthesis blockers like ketoconazoleDirect testicular damage, like, for example:Bilateral orchidectomy or testicular traumaRadiation to the testes andInfective or autoimmune orchitis And finally systemic diseases that affect the testes, like for example:Chronic illnessesCushing’s syndromeHIV andCancers like lymphoma or testicular cancerIn Secondary Hypogonadism we also have congenital and acquired causes.Congenital causes of secondary hypogonadism include:Haemochromatosis andOther genetic or idiopathic causes Acquired causes of secondary hypogonadism include:Drugs that suppress the hypothalamus or pituitary, like for example:Oestrogens and progestogensTestosterone or anabolic steroids Drugs that increase prolactin Opiates and CorticosteroidsLocal problems in the brain, like, for example:Head traumaTumours in the pituitary or hypothalamusSurgery or radiation to the pituitary gland andInfections or inflammation in the brainAnd finally systemic conditions that affect brain hormone control, such as, for example:Type 2 diabetes and metabolic syndromeChronic organ failureHIVRheumatoid arthritis and other chronic inflammatory diseasesCushing’s syndrome andEating disordersI 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 receptorsDrugs that interfere with testosterone functionHigh levels of SHBG (sex hormone-binding globulin), which reduces free testosterone andConditions like coeliac disease, which can also interfere with hormone actionLet’s now look in more detail into comorbidities associated with male hypogonadismAnd 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

The video version of this podcast can be found here: ·      https://youtu.be/nguVbiQc5WwThis 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 treatmentOffer 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 treatmentOffer 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-treatmentTranscriptIf 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 diseaseLet’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 a

The video version of this podcast can be found here: ·      https://youtu.be/GelDVWruIlAThe link to the video on updated migraine management can be found here:·      https://youtu.be/LumBxN-yFmIThis 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 TranscriptIf 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 feversudden‑onset headache reaching maximum intensity within 5 minutesnew‑onset neurological or cognitive dysfunctionhead trauma within the past 3 monthsheadache triggered by cough, sneeze or exercise or anorthostatic headache, that is, a headache that changes with postureAdditionally, we will consider further investigations or referral for people who present with new‑onset headache and:compromised immunity,a history of malignancy orvomiting 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 eyea swollen and or drooping eyelida constricted pupilnasal congestion or a runny noseand forehead and facial sweatingOn 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 reversibledevelop over at least 5 minutesand last 5 to 60 minutesHowever, 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 andChronic 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 headacheAnd 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 subc

The video version of this podcast can be found here: ·      https://youtu.be/LumBxN-yFmIThis 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+standardThe 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 TranscriptIf 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 ortriptans 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

The video version of this podcast can be found here: ·      https://youtu.be/HQnpwZFnedgThis 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.pdfThe 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.TranscriptIf 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 hirsutismWhen testosterone is significantly elevated, defined as greater than 5 nanomoles per litre or more than twice the upper limit of normal orAbnormal 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 amenorrhoeaLet’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, ino

The video version of this podcast can be found here: ·      https://youtu.be/pkP0aqNGqGIThis 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.pdfThe 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.TranscriptIf 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:Oligo- or anovulation.Clinical or biochemical signs of hyperandrogenism andPolycystic 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 testsProlactinLH, FSH, and oestradiol to exclude other causes of oligo- or amenorrhoeaTotal testosterone and SHBGAndrostenedione and DHEA-S or dehydroepiandrosterone if testosterone is raisedIf clinically suspected, 17-hydroxyprogesterone to rule out congenital adrenal hyperplasiaAnd finally, we should consider a transvaginal or transabdominal ultrasound to assess ovarian morphology and endometrial thicknessHow 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 ac

The video version of this podcast can be found here: ·      https://youtu.be/58WdoYFUUjUThis 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=wideThe 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.pdfThe link to the guideline by NHS Lanarkshire can be found here:·      https://rightdecisions.scot.nhs.uk/media/1539/hypomagnesaemia-in-primary-or-secondary-care.pdfThe link to the guideline by Gloucestershire Hospitals NHS Trust can be found here:·      https://www.gloshospitals.nhs.uk/media/documents/Hypomagnesaemia_jcPg0oV.pdfThe 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.pdfThe link to the guideline by Worcestershire Acute Hospitals NHS Trust can be found here:·      https://apps.worcsacute.nhs.uk/KeyDocumentPortal/Home/DownloadFile/1559The 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-hypomagnesaemiaDisclaimer: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.TranscriptIf 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 correctedLet’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 nervosaChronic diarrhoea And excess alcohol intake Increased Renal Loss like in:Renal tubular disordersDiabetes and diabetic ketoacidosisHyperaldosteronismHyperthyroidismAnd vitamin D deficiencyDrug-Induced like for example with the use of:Proton pump inhibitors (PPIs)Both loop and thiazide DiureticsTheophylline Some chemotherapy agentsAnd Digoxin, also bearing in mind that low magnesium may increase digoxin toxicityAnd finally Miscellaneous causes such as ·      Acute pancreatitis ·      and excessive lactationWe 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 toMonitor magnesium periodically during prolonged treatment, particularly in patients on diuretics or digoxinWe 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 ar

The video version of this podcast can be found here: ·      https://youtu.be/Y3POCL-rh_YThis 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+standardThe 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 TranscriptIf 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 thatThe 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 orare aged 55 and over, with weight loss, and they have any of the following:upper abdominal painreflux ordyspepsiaWe will consider non-urgent, direct access upper gastrointestinal endoscopy in people with haematemesis and in people aged 55 or over with:treatment‑resistant dyspepsia orupper abdominal pain with low haemoglobin levels orraised platelet count with any of the following:nauseavomitingweight lossrefluxdyspepsia andupper abdominal pain ornausea or vomiting with any of the following:weight lossrefluxdyspepsia andupper 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:diarrhoeaback or abdominal painnausea or vomitingconstipation ornew‑onset diabetes. And finally, in terms of Gall bladder cancer or liver cancerWe 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.

The video version of this podcast can be found here: ·      https://youtu.be/mq658X-teEcThis 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.TranscriptIf 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?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.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.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 syndromeThe 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 wi

The video version of this podcast can be found here: ·      https://youtu.be/qNboajtlrrsThis 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.15166The 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.TranscriptIf 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 deficiencyRight, 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 episodeA 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 TsatThen 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 indic

The video version of this podcast can be found here: ·      https://youtu.be/Ugo6U9QI2xYThis 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.12311The 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. TranscriptIf 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)InfectionsCancer andChronic 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 thatChronic 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 Protoporphyrino  Bone Marrow Examinationo  sTfR – Soluble Transferrin Receptoro  Serum Erythropoietin ando  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 inflammationTransferrin 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 deficiencyESR or CRP tend to be high in functional iron deficiency reflecting underlying inflammation and finally functional iron deficiency also show thatReticulocyte Hb content is low and percentage of hypochromic cells are highWhen 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 comorbiditiesAnd 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 lowTo exclude other causes, for example bleeding, B12/folate deficiency, chronic kidney disease etc.To manage oral iron therapy and initial assessment remembering thatWe 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

The video version of this podcast can be found here: ·      https://youtu.be/ZdHSs-QBtacThis 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. TranscriptIf 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 diagnosticSo, 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 anaemiaFerritin is borderline or normal but there's suspicion of iron deficiency e.g., in chronic inflammation orThere'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 aTSAT <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

The video version of this podcast can be found here: ·      https://youtu.be/aB6Z7tASKrcThis 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 TranscriptIf 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 calciumeither plasma viscosity or ESRparaprotein, using serum protein electrophoresis andSerum 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 oraged 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 thatHave 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 anda 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 includeAn overall review of the patient looking at things like:Cognition and mood.Diet, and weight loss.Hearing and visual impairments.Dizziness.Functional ability.Urinary continenceGait, 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 drugs2- 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.