Primary Care Guidelines

Juan Fernando Florido Santana

A podcast intended for healthcare professionals wanting to keep up to date relevant information about clinical practice guidelines

  1. Podcast - Osteoporosis Treatment: When Bones Need Backup

    1 DAY AGO

    Podcast - Osteoporosis Treatment: When Bones Need Backup

    The video version of this podcast can be found here: ·      https://youtu.be/tdY5bOFmzbg This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE. NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country. This video refers to the clinical guideline by the National Osteoporosis Guideline Group. (details below). Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by them.   My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I review the treatment of osteoporosis, always focusing on what is relevant in Primary Care only. The information is based on the clinical guideline by the National Osteoporosis Guideline Group. The link to it is below. I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.     Disclaimer: The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions. In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido. Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release]  Music provided by Audio Library Plus Watch: https://youtu.be/aBGk6aJM3IU Free Download / Stream: https://alplus.io/halfway-through   There is a podcast version of this and other videos that you can access here:   Primary Care guidelines podcast:   ·      Redcircle: https://redcircle.com/shows/primary-care-guidelines ·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK ·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148 There is a YouTube version of this and other videos that you can access here:  The Practical GP YouTube Channel: https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk   The NICE clinical guideline on osteoporosis can be found here:   ·      https://www.nice.org.uk/guidance/cg146   The Clinical guideline for the prevention and treatment of osteoporosis by the National Osteoporosis Guideline Group can be found here:   ·      https://www.nogg.org.uk/sites/nogg/download/NOGG-Guideline-2024.pdf?v3   The NICE technology appraisal on Bisphosphonates for treating osteoporosis can be found here:   ·      https://www.nice.org.uk/guidance/ta464 Transcript If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description. Hello and welcome, I’m Fernando, a GP in the UK. Today we are going to review the treatment of osteoporosis, always focusing on what is relevant in Primary Care only. I have based this episode on the clinical guideline by the National Osteoporosis Guideline Group. The link to it is the episode description. Right, let’s jump into it. We will start by saying that we need a strategy to decide who gets treated, which is what we call “intervention thresholds.” We need to remember that the NICE guideline on assessing the risk of fragility fracture and Osteoporosis does not itself define fixed treatment thresholds. Instead, we are advised to follow local or national guidance when deciding when to treat. So, for the purpose of this video, I will explain the thresholds given by the National Osteoporosis Guideline Group. Here the intervention threshold (for people under 70) is set at a fracture risk equivalent to a same-age woman who has already had a fracture. As people age, the threshold for treatment rises, so at the age 70 years and above, fixed thresholds are applied. When FRAX is calculated we can get a result that shows low risk, intermediate risk, high risk and very high risk of a Major Osteoporotic Fracture. If the fracture risk is low, we will offer lifestyle advice. If a person’s calculated risk sits near that intervention threshold, then that is intermediate risk and we should consider a bone mineral density (BMD) measurement with DXA to refine the estimate. If after the bone mineral density result the risk is high, we move forward with treatment otherwise, we will reassess later. If the fracture risk meets or exceeds the intervention threshold, that person is considered high risk and eligible for treatment. If the risk is very high, for example if they have multiple risk factors — we may consider referral for more aggressive treatment. Let’s now focus on the non-drug measures recommended for preventing and managing osteoporosis. They should be recommended for everyone, whether or not we eventually use drugs. First — diet and nutrition, ensuring adequate calcium intake. Ideally this is achieved through food, but if needed, we can use supplements to reach recommended levels. We should also make sure vitamin D is addressed. For people at risk of low vitamin D — for example, those with limited sun exposure, people who are housebound, or living in care homes — we should offer vitamin D supplementation. Next —We should encourage regular weight-bearing and muscle-strengthening exercise, tailored to each person’s ability. This supports bone strength, maintains muscle mass, and helps prevent falls. Speaking of falls — for those with osteoporosis or fragility fractures, or at risk of fracture, we must assess their fall risk. For patients identified as at risk of falling, we should offer an exercise programme to improve balance and muscle strength. We must also address lifestyle factors. We should advise smoking cessation in smokers and recommend moderation of alcohol intake. For all patients we should also screen for and manage other medical conditions that may contribute to bone fragility, such as endocrine problems, malabsorption, chronic illness or immobility. Now let’s move on to the pharmacological treatment options for osteoporosis, based on the National Osteoporosis Guideline Group recommendations, and the NICE Technology Appraisal on Bisphosphonates for treating osteoporosis There are several effective drug treatments available, but for most patients, bisphosphonates remain the first-line option. These include oral alendronic acid, risedronate and ibandronate, as well as intravenous zoledronic acid and ibandronate if recommended by a specialist. How do bisphosphonates work? Bisphosphonates slow down the rate of bone breakdown by inhibiting osteoclast activity. This helps stabilise bone density and reduces the risk of fractures. What about risks and how do we minimise them? Common side effects include gastrointestinal irritation with oral bisphosphonates, and muscle or joint aches. Much rarer risks include atypical femoral fractures and osteonecrosis of the jaw. To minimise these, we ensure correct administration: oral tablets should be taken with a full glass of water on an empty stomach, with the patient remaining upright for at least 30 minutes. We also maintain good dental hygiene, have a dental check-up and complete major dental work before starting treatment where possible, and reassess the need for long-term therapy at appropriate intervals. Alongside bisphosphonates, denosumab is another established anti-resorptive option. If we use denosumab, we must plan from the start how we will eventually stop or switch treatment, because stopping it abruptly without follow-up therapy can lead to rebound bone loss and an increased risk of vertebral fractures. For patients at the highest fracture risk, we should seek specialist input. These patients may benefit from anabolic, or bone-forming treatments such as romosozumab, or other anabolic or sequential regimens. Now let’s look at how we manage osteoporosis treatment over time, that is, the long-term strategy. First: when we start a drug treatment for osteoporosis — for example a bisphosphonate or denosumab — we need a clear plan for how long that treatment should continue, how we’ll monitor it, and when we’ll reassess risk. For oral bisphosphonates, we generally treat for at least five years and for intravenous bisphosphonates, at least three years. In patients at higher risk — for instance people over 70, or those who’ve had hip or vertebral fractures, or patients on high-dose steroids — longer treatment might be needed. Also, if they sustain a further fragility fracture while on treatment, we will also keep going. In lower-risk patients, after five years of oral bisphosphonates (or three years of IV bisphosphonates), we may consider a treatment pause fo

    8 min
  2. Podcast - Osteoporosis: Assessing Fracture Risk

    25 FEB

    Podcast - Osteoporosis: Assessing Fracture Risk

    The video version of this podcast can be found here: ·      https://youtu.be/GmCg9TskZNA This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE. NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country. This video refers to a number of medical articles on ADHD published by a number of organisations (details below). Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by any of them.   My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I cover ADHD increasing incidence, especially in adults, always focusing on what is relevant in Primary Care only. The information is based on a number of published medical articles. The links to them are below. I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.     Disclaimer: The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions. In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido. Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release]  Music provided by Audio Library Plus Watch: https://youtu.be/aBGk6aJM3IU Free Download / Stream: https://alplus.io/halfway-through   There is a podcast version of this and other videos that you can access here:   Primary Care guidelines podcast:   ·      Redcircle: https://redcircle.com/shows/primary-care-guidelines ·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK ·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148 There is a YouTube version of this and other videos that you can access here:  The Practical GP YouTube Channel: https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk   The NICE clinical guideline on osteoporosis can be found here:   ·      https://www.nice.org.uk/guidance/cg146 Transcript If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description. Hello and welcome, I’m Fernando, a GP in the UK. Today we are looking at the NICE guideline on osteoporosis, specifically how we diagnose it and how we assess the risk of fragility fractures, always focusing on what is relevant in Primary Care only. The links to the NICE guideline is the episode description. Right, let’s jump into it. Let’s start by saying that we should consider assessing fracture risk in all women aged 65 and over, and all men aged 75 and over. Additionally, we should also consider assessing fracture risk in women under 65 and men under 75 if they have risk factors. Examples of these risk factors include: • a previous fragility fracture, • current or frequent recent use of oral or systemic glucocorticoids, • a history of falls, • a family history of hip fracture, • a low BMI, below 18.5, • smoking, • drinking more than 14 units of alcohol per week • and any cause of secondary osteoporosis Causes of secondary osteoporosis can include endocrine conditions such as hypogonadism in either sex — including untreated premature menopause — and treatment with aromatase inhibitors or androgen-deprivation therapy. They also include hyperthyroidism, hyperparathyroidism, hyperprolactinaemia, Cushing’s disease, and diabetes. Other causes include gastrointestinal conditions such as coeliac disease, inflammatory bowel disease, chronic liver disease, chronic pancreatitis, and other causes of malabsorption. Then we have rheumatological conditions like rheumatoid arthritis and other inflammatory arthropathies as well as haematological diseases such as multiple myeloma, and haemoglobinopathies. And finally we have respiratory conditions like cystic fibrosis and COPD and other conditions like CKD and immobility due to neurological disease or injury. We should not routinely assess fracture risk in people under the age of 50 unless they have major risk factors — such as current or recent glucocorticoid use, untreated premature menopause, or a previous fragility fracture — because they are unlikely to be at high risk. Now, how should we actually assess the risk of fracture? We can use either FRAX — which we can use without a bone mineral density (BMD) value if a DXA scan hasn’t been done — or QFracture, to estimate the ten-year absolute risk. FRAX can be used for people aged 40 to 90, with or without a bone mineral density (BMD) value. QFracture can be used for people aged 30 to 84, but a bone mineral density (BMD) value cannot be added into that tool. If someone is older than the age range covered by these tools, we should assume they are at high risk. Additionally. we should interpret fracture-risk estimates with caution in people over 80, because a ten-year prediction may underestimate their short-term risk. We should not routinely measure bone mineral density with a DXA scan before doing a FRAX or QFracture assessment. These tools estimate a ten-year fracture risk using simple clinical information and help us decide whether a scan is actually needed. Skipping this step can lead to unnecessary DXA scans in people who are clearly low risk. It can also lead to missed scans in those whose risk is borderline, and it is therefore an inefficient use of resources. We only need to measure bone density when the FRAX or QFracture score is close to the intervention threshold, where a DXA result could change the treatment decision. So, the NICE guideline recommends using FRAX or QFracture first, and then requesting a DXA scan only if it is likely to influence management. If we do a DXA scan, once we have the bone mineral density result, we should recalculate the absolute risk using FRAX with the bone mineral density value included. The intervention threshold is the level of risk at which treatment is recommended. The NICE guideline does not define that threshold; instead, we, as clinicians, should follow local protocols or national guidance. I will cover this in a different episode on osteoporosis treatment. We should also consider measuring BMD before starting treatments that can rapidly reduce bone density, such as sex-hormone deprivation therapy for breast or prostate cancer. People under 40 should have BMD measured to assess fracture risk only if they have a major risk factor, such as multiple fragility fractures, a major osteoporotic fracture, or current or recent use of high-dose oral or systemic glucocorticoids — meaning more than 7.5 milligrams of prednisolone, or equivalent, per day for three months or longer. We should consider recalculating fracture risk in the future if the original risk was close to the intervention threshold and only after at least two years, or if the person’s risk factors change. Again, for intervention thresholds we will need to follow local protocols or national guidelines. We should also remember that risk-assessment tools can underestimate fracture risk in certain situations. This includes people with multiple fractures, previous vertebral fractures, high alcohol intake, high-dose glucocorticoid use, or other causes of secondary osteoporosis. As mentioned earlier, causes of secondary osteoporosis include endocrine, gastrointestinal, rheumatological, haematological, respiratory, metabolic, renal, and neurological conditions, as well as prolonged immobility. Finally, we should keep in mind that fracture risk can also be affected by factors not included in the risk tools — for example, living in a care home, or taking drugs that impair bone metabolism, such as anticonvulsants, SSRIs, thiazolidinediones, proton-pump inhibitors, and antiretroviral medications. So that is it, a review of the NICE guideline on osteoporosis. We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement. Thank you for listening and goodbye.

    7 min
  3. Podcast - Eos-in the Know: A Quick Guide to Eosinophilia

    18 FEB

    Podcast - Eos-in the Know: A Quick Guide to Eosinophilia

    The video version of this podcast can be found here: ·      https://youtu.be/V93jdGfnLIk This video refers to guidelines produced by a number of organisations (details below). Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by any of them.   My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I cover what to do if eosinophilia is found, always focusing on what is relevant in Primary Care only. The information is based on Haematological guidance by Camden CCG, Manchester Foundation Trust and King’s Health Partners. I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.     Disclaimer: The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions. In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.   Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release]  Music provided by Audio Library Plus Watch: https://youtu.be/aBGk6aJM3IU Free Download / Stream: https://alplus.io/halfway-through     There is a podcast version of this and other videos that you can access here:   Primary Care guidelines podcast:   ·      Redcircle: https://redcircle.com/shows/primary-care-guidelines ·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK ·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148 There is a YouTube version of this and other videos that you can access here:  The Practical GP YouTube Channel: https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk   My summary of the guidance consulted can be found here: ·      https://1drv.ms/b/s!AiVFJ_Uoigq0mQ4ZjYGRH1wkGBdc?e=Zuxx84 The resources consulted can be found here: ·      Camden CCG guidance: 1456246258-2f3891e610beaa6533f2c0ad7866e776.pdf(Review) - Adobe cloud storage ·      Manchester Adult anaemia guide: https://acrobat.adobe.com/id/urn:aaid:sc:EU:f96fe528-0a47-457c-b29a-a7efb87221e0 ·      Manchester Haematology GP guide: https://mft.nhs.uk/app/uploads/2021/02/MFT-Haematology-GP-Pathway-Guide-v4-11.2.21.pdf ·      King’s Health Partners: https://www.kingshealthpartners.org/assets/000/002/294/KCH_-_king_s_health_partners_-_quick_guide_to_haematology_original.pdf Transcript If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description. Hello and welcome, I’m Fernando, a GP in the UK. Today we are going to cover what to do when we encounter eosinophilia on a full blood count, always focusing on what is relevant in Primary Care only. I have based this episode on Haematological guidance by Camden CCG, Manchester Foundation Trust and King’s Health Partners. The links to them are in the episode description. Right, let’s jump into it. Eosinophilia refers to an increased number of eosinophils in the blood. Although thresholds may vary slightly between laboratories, eosinophilia is generally defined as an eosinophil count greater than 0.5 × 10⁹ per litre. Eosinophils are white blood cells involved in allergic responses, parasitic infections, and various inflammatory processes, so an elevated count can indicate a wide range of underlying conditions. Let’s have a look at some of the possible causes of eosinophilia. They include: • Asthma: particularly allergic asthma, which commonly has high eosinophil levels because of their role in airway inflammation and hypersensitivity reactions. • Then we have Skin disease such as eczema, atopic dermatitis, urticaria, and psoriasis: because these conditions involve allergic or immune-mediated inflammation, which often stimulates eosinophils. • Infections, especially those due to parasites, as well as fungal infections, tuberculosis and malaria. Parasitic infections are a very typical cause, but some fungal and bacterial infections can also trigger eosinophilia through chronic inflammation. • Another possible cause is Drugs, including penicillin, allopurinol, amitriptyline, and carbamazepine, although virtually any medication can be a possible trigger. Drug-induced eosinophilia often occurs as part of a hypersensitivity reaction. • Then we have Connective tissue diseases such as rheumatoid arthritis given that autoimmune and vasculitic conditions can increase eosinophils due to chronic inflammation. • We also have Solid malignancies, for example breast, renal, stomach, and lung cancer. This is because certain cancers release cytokines that stimulate eosinophil production. In some cases eosinophilia may be a paraneoplastic manifestation. • Then, Myeloproliferative disorders including leukaemia and lymphoma. Here eosinophilia can happen either because eosinophils are part of the malignant clone or due to cytokine-driven overproduction. • another cause, Respiratory diseases such as bronchiectasis and cystic fibrosis, again caused by the ongoing inflammatory response. • Then, Endocrine conditions such as Addison’s disease. This is because cortisol suppresses eosinophils and in Addison’s, the low cortisol will result in a high eosinophil count. • and finally we have Post-splenectomy. This is because the spleen normally helps regulate and remove eosinophils from circulation, so splenectomy will result in an increased eosinophil count. If the eosinophil count is greater than 2.5 × 10⁹/L, we will look for signs of organ damage. This is because very high eosinophil levels can lead to direct tissue injury. Activated eosinophils release toxic inflammatory mediators, and cytokines that can cause inflammation and fibrosis in virtually any organ. The heart, lungs, skin, gastrointestinal tract, and nervous system are particularly vulnerable. Damage can progress rapidly and we should consider urgent admission if there are red flags Red flags include: • Severe symptoms secondary to organ involvement, such as • difficulty breathing, • chest pain, • abdominal pain, or • neurological symptoms. • as well as other complications, including tissue damage, venous thromboembolism, or evidence of end-organ injury such as acute kidney injury or heart failure. Even in the absence of red flags, criteria for urgent referral to haematology are: • A leucoerythroblastic blood film, which suggests bone marrow infiltration, haematological malignancy or severe bone marrow stress. • And absolute eosinophil count greater than 5 × 10⁹/L, as this level significantly increases the risk of hypereosinophilic syndromes and progressive organ damage. If the urgent criteria are not met and the patient is clinically well, we will check the travel and drug history and assess for any evidence of atopy, such as asthma, eczema, or allergic rhinitis. We will then repeat the blood test within one to two weeks to confirm whether the eosinophilia is persistent and to look for possible underlying causes. Initial investigations will include: • As already mentioned, a repeat full blood count, to confirm that the eosinophilia is persistent and to check for other abnormalities which may suggest a bone marrow disorder. • A blood film, which can reveal abnormal cell morphology, blast cells, or features suggesting reactive versus clonal eosinophilia. • Inflammatory markers such as ESR and CRP, which help identify underlying infection, inflammation, or autoimmune disease. • Immunoglobulin E, as a high IgE is common in allergic disease, parasitic infections, and some hypereosinophilic syndromes. • An autoimmune profile, since eosinophilia can occur in connective tissue diseases and vasculitis. • Renal and liver function tests, because organ dysfunction can be both a cause and a consequence of eosinophilia. • A bone profile, as a high calcium may suggest granulomatous disease such as sarcoidosis or certain malignancies. This is because granulomatous conditions and some cancers increase the production of active vitamin D or stimulate bone breakdown, both of which increase calcium levels. • We will also check for LDH, which can be high in haematological malignancies and in high cell turnover. • Vitamin B12 and folate, since a raised B12 can be a clue to myeloproliferative disease, while a deficiency can contribute to abnormal blood counts. • A chest X-ray, particularly if tuberculosis, pulmonary eosinophilia, or sarcoidosis are suspected. • Stool culture and microscopy for ova, cysts, and parasites, as parasitic infections are a common and important cause of eosinophilia worldwide. • Serological antibodies for threadworm or other nematode infections, especially if there are suggestive symptoms. • and finally, Serological antibodies for schistosomiasis, depending on travel history and ideally after discussion with microbiology, as the timing can influence accuracy. Schistosomiasis is a parasitic infection acquired through contact with freshwater in endemic regions in Africa, the Middle East, South America, and parts of Asia, whi

    9 min
  4. Podcast - NICE News - January 2026

    11 FEB

    Podcast - NICE News - January 2026

    The video version of this podcast can be found here: ·      https://youtu.be/us-qmMn8gsk This episode makes reference to guidelines produced by the "National Institute for Health and Care Excellence" in the UK, also referred to as "NICE". The content on this channel reflects my professional interpretation/summary of the guidance and I am in no way affiliated with, employed by or funded/sponsored by NICE. NICE stands for "National Institute for Health and Care Excellence" and is an independent organization within the UK healthcare system that produces evidence-based guidelines and recommendations to help healthcare professionals deliver the best possible care to patients, particularly within the NHS (National Health Service) by assessing new health technologies and treatments and determining their cost-effectiveness; essentially guiding best practices for patient care across the country. My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I go through new and updated recommendations published in January 2026 by the National Institute for Health and Care Excellence (NICE), focusing on those that are relevant to Primary Care only.   I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.     Disclaimer: The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions. In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.   Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release]  Music provided by Audio Library Plus Watch: https://youtu.be/aBGk6aJM3IU Free Download / Stream: https://alplus.io/halfway-through   There is a podcast version of this and other videos that you can access here:   Primary Care guidelines podcast:   ·      Redcircle: https://redcircle.com/shows/primary-care-guidelines ·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK ·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148 There is a YouTube version of this and other videos that you can access here:  The Practical GP YouTube Channel: https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk The Full NICE News bulletin for January 2026 can be found here:   ·      https://www.nice.org.uk/guidance/published?from=2026-01-01&to=2026-01-31&ndt=Guidance&ndt=Quality+standard   The updated guideline on Suspected cancer: recognition and referral [NG12] can be found here: ·      https://www.nice.org.uk/guidance/ng12 The updated guideline on Overweight and obesity management [NG246] can be found here: ·      https://www.nice.org.uk/guidance/ng246 Transcript If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description. Hello and welcome! I’m Fernando, a GP in the UK. In today’s episode, we’ll look at the NICE updates published in January 2026, focusing on what is relevant in Primary Care only. And this time we have two updated guidelines relevant to us in General Practice: the guidelines on Suspected cancer and on Overweight and obesity management. The changes are minimal so today we have a very short episode. Right, let’s jump into it. And let’s start with the guideline on obesity and overweight management. The update is narrow and specific and clarifies that height-to-weight ratios should only be used to classify the degree of central adiposity in children and young people aged 5 years and over. Before this amendment, the guideline included height-to-weight ratios for children, but it did not explicitly state that these ratios should not be used in under 5s. This is because height-to-weight ratios in younger children, may not be validated or appropriate. In fact, in children under 5 years: ·      Body proportions change very rapidly as part of normal growth and development ·      There is wide normal variation in body shape and fat distribution and ·      Height to weight ratios do not accurately reflect central adiposity in this age group and therefore using these ratios risks overestimating or underestimating adiposity However, in children aged 5 years and over: ·      Body proportions become more stable ·      Patterns of central fat distribution are more consistent ·      And the available evidence supports height to weight ratios in this age group as they are more likely to reflect true central adiposity No other recommendations, were changed. Everything else remains as it was in the previous published guideline. Now let’s move to the guideline on suspected cancer. In January 2026 the update information for the NICE guideline on suspected cancer states that NICE has removed an incorrect recommendation related to blood tests for suspected myeloma. However, when you look at the guideline as it stands, things appear a little confusing, so it is worth looking at this in more detail. Originally, the guideline listed a broad panel of blood tests for suspected myeloma in primary care. This included serum protein electrophoresis and serum free light chain testing, alongside a full blood count, calcium, and plasma viscosity or ESR. Bence Jones urine testing was suggested as an alternative if serum free light chain testing was not available. These tests were recommended for people with features such as persistent bone pain or an unexplained fracture. Subsequently, NICE amended the wording of this section to place greater emphasis on serum protein electrophoresis and serum free light chain testing as the key initial investigations. So the obvious question is this. Has NICE really now removed the recommendation to offer blood tests for suspected myeloma altogether? At face value this looks like guidance that is moving backwards and forwards. The confusion is increased by the fact that if you look at the recommendations organised by site of cancer, under haematological cancers, the guideline still clearly lists blood tests for suspected myeloma. So what is actually happening here? In theory, the update information reflects the official and authoritative change to the guideline. It may be that parts of the published recommendations text have not yet been fully revised or synchronised on the NICE website. However, I have also reviewed other sections of the NICE website, including committee discussions and rationale documents, and I have not been able to find any explanation for this change. That also raises the possibility that the update statement itself may be an error. In practical terms, my view is that we should probably continue to request blood tests for suspected myeloma until the guideline text has been fully updated and this discrepancy is clarified. That is, we should request a full blood count, calcium, plasma viscosity or ESR, paraprotein, using serum protein electrophoresis and serum free light chains. If serum free light chain testing is not available, we can use a Bence–Jones test to check for free light chains contained in urine. I have raised a query directly with NICE, and we should have further clarification soon. For now, this is very much a case of watching this space. So that is it, a review of the NICE updates relevant to primary care. We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement. Thank you for listening and goodbye.

    5 min
  5. Podcast - Cut to the Clot: Raised HCT Explained

    4 FEB

    Podcast - Cut to the Clot: Raised HCT Explained

    The video version of this podcast can be found here: ·      https://youtu.be/4NysH3aEPMM This video refers to guidelines produced by a number of organisations (details below). Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by any of them.   My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I neutropenia always focusing on what is relevant in Primary Care only. The information is based on Haematological guidance by Camden CCG, Manchester Foundation Trust and King’s Health Partners. I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.     Disclaimer: The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions. In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.   Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release]  Music provided by Audio Library Plus Watch: https://youtu.be/aBGk6aJM3IU Free Download / Stream: https://alplus.io/halfway-through   There is a podcast version of this and other videos that you can access here:   Primary Care guidelines podcast:   ·      Redcircle: https://redcircle.com/shows/primary-care-guidelines ·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK ·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148 There is a YouTube version of this and other videos that you can access here:  The Practical GP YouTube Channel: https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk   My summary of the guidance consulted can be found here: ·      https://1drv.ms/b/s!AiVFJ_Uoigq0mQ4ZjYGRH1wkGBdc?e=Zuxx84 The resources consulted can be found here: ·      Camden CCG guidance: 1456246258-2f3891e610beaa6533f2c0ad7866e776.pdf(Review) - Adobe cloud storage ·      Manchester Adult anaemia guide: https://acrobat.adobe.com/id/urn:aaid:sc:EU:f96fe528-0a47-457c-b29a-a7efb87221e0 ·      Manchester Haematology GP guide: https://mft.nhs.uk/app/uploads/2021/02/MFT-Haematology-GP-Pathway-Guide-v4-11.2.21.pdf ·      King’s Health Partners: https://www.kingshealthpartners.org/assets/000/002/294/KCH_-_king_s_health_partners_-_quick_guide_to_haematology_original.pdf Transcript If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description. Hello and welcome, I’m Fernando, a GP in the UK. Today we are going to cover what to do when we encounter a high haematocrit, including initial assessment, follow up and management, always focusing on what is relevant in Primary Care only. I have based this episode on Haematological guidance by Camden CCG, Manchester Foundation Trust and King’s Health Partners. The links to them are in the episode description. Right, let’s jump into it. And we will start by saying that haematocrit measures the proportion of blood volume taken up by red blood cells. It can be expressed either as a percentage—from 0 to 100 or as a decimal proportion, from 0 to 1. Because it reflects the relative volumes of red cells and plasma, the haematocrit is influenced not only by the absolute number of red blood cells but also by the amount of circulating plasma. Any change in either component will affect the final value. A high haematocrit raises the possibility of polycythaemia. Polycythaemia can be diagnosed when the haematocrit is greater than 0.52 in men and greater than 0.48 in women. These thresholds help identify affected people, but they do not, by themselves, tell us the cause. Polycythaemia is sometimes referred to as erythrocytosis, but this is not entirely accurate. Erythrocytosis specifically refers to an increased number of red blood cells in the circulation. Polycythaemia, on the other hand, is defined by a raised haematocrit, not by a direct count of red blood cells. As a result, it is possible to have a high haematocrit without true erythrocytosis. This distinction matters because there are two types of polycythaemia. The first is absolute polycythaemia, where an increased red cell mass is genuinely present, that is, true erythrocytosis. The second is relative or apparent polycythaemia, where the haematocrit is high not because there are more red cells, but because the plasma volume is reduced. Dehydration, diuretics, or plasma loss can all create this picture, leading to a raised haematocrit despite a normal red cell mass. It is also common in obese men, and it is also associated with smoking, alcohol, hypertension and stress. Despite the potentially reversible causes of relative or apparent polycythaemia, these patients are also at risk of occlusive vascular episodes. On the other hand, we have absolute polycythaemia, which reflects a true increase in red cell mass. This can be divided into primary and secondary causes. The primary cause is Polycythaemia Vera (PV). Well over 90% of patients with PV have an acquired mutation in the JAK2 gene, which plays an important role in regulating erythropoiesis. Because of this mutation, the bone marrow becomes hypersensitive to growth signals and produces red blood cells even when erythropoietin levels are low. In other words, these patients do not need as much erythropoietin to drive red cell production. The main features of Polycythaemia Vera are therefore: • a positive JAK2 mutation test, • a low serum erythropoietin level. Polycythaemia Vera is also commonly associated with low ferritin, because the accelerated and unregulated production of red cells consumes large amounts of iron. Being a myeloproliferative disorder, Polycythaemia Vera may also show raised white blood cells and/or platelets, reflecting the involvement of the bone marrow. Secondary polycythaemia, on the other hand, results from a physiological increase in erythropoietin production. The kidneys release more erythropoietin in response to reduced oxygen levels, so secondary polycythaemia can be an appropriate response to chronic hypoxia, as seen in COPD, congenital or acquired heart disease, and in smokers. It can also be an inappropriate response when erythropoietin is produced by tumours, such as certain renal or liver tumours, or even uterine fibroids, which can secrete erythropoietin autonomously. Other possible causes of secondary polycythaemia include anabolic steroids and testosterone therapy, as androgens stimulate erythropoietin production through hormonal pathways. In cases of secondary polycythaemia, the pattern is different: • the JAK2 mutation is negative, • erythropoietin levels are high, and • ferritin, white blood cells and platelets are normal. So what do we do when we receive a high haematocrit result? Well, Criteria for urgent referral are a haematocrit greater than 0.60 in men or greater than 0.56 in women. We should also refer urgently if the patient has had a recent thrombosis, shows any abnormal bleeding, or reports neurological or visual symptoms. These features raise concern for hyperviscosity or an underlying myeloproliferative disorder, both of which require immediate specialist assessment. If the criteria for urgent referral are not met, the next step is to confirm the result by repeating the blood test. In order to differentiate between apparent and absolute polycythaemia, the blood sample should be taken without a tourniquet, and we should ensure that the patient has not been fasting, is well hydrated, and has been advised about alcohol intake and smoking, as these factors can artificially raise the haematocrit. In this repeat blood test, we should request: • A repeat full blood count, to confirm whether the raised haematocrit is persistent and to check for associated abnormalities in white cells or platelets. • A blood film, which can reveal morphological clues to myeloproliferative disease or other haematological disorders. • We should screen for diabetes, hyperlipidaemia and hypertension, as these cardiovascular risk factors often coexist with secondary causes of polycythaemia and may contribute to vascular complications. • As mentioned earlier, we should also check Ferritin, to assess iron stores, which may be depleted in Polycythaemia Vera due to increased red cell production. • and finally renal and liver function tests, since kidney or liver disease may contribute to secondary polycythaemia or influence erythropoietin production. Additionally, if we suspect absolute polycythaemia, the following tests should be done: • Genetic testing for the JAK2 mutation, which is positive in the great majority of patients with Polycythaemia Vera. • And erythropoietin levels, which help distinguish primary from secondary causes, being low in PV and elevated in secondary polycythaemia. However, in the UK, JAK2 mutation testing and serum erythropoietin levels are not routinely available in primary care. In most areas, these investigations are carried out by haematology teams, as they form part of the specialist work-up for m

    11 min
  6. Podcast - Platelet Down: A Quick Look at Thrombocytopenia

    28 JAN

    Podcast - Platelet Down: A Quick Look at Thrombocytopenia

    The video version of this podcast can be found here: ·      https://youtu.be/TQB5tJvM0VM This video refers to guidelines produced by a number of organisations (details below). Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by any of them.   My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I cover what to do if thrombocytopenia is found, always focusing on what is relevant in Primary Care only. The information is based on Haematological guidance by Camden CCG, Manchester Foundation Trust and King’s Health Partners. I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.     Disclaimer: The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions. In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.   Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release]  Music provided by Audio Library Plus Watch: https://youtu.be/aBGk6aJM3IU Free Download / Stream: https://alplus.io/halfway-through   There is a podcast version of this and other videos that you can access here:   Primary Care guidelines podcast:   ·      Redcircle: https://redcircle.com/shows/primary-care-guidelines ·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK ·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148 There is a YouTube version of this and other videos that you can access here:  The Practical GP YouTube Channel: https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk   My summary of the guidance consulted can be found here: ·      https://1drv.ms/b/s!AiVFJ_Uoigq0mQ4ZjYGRH1wkGBdc?e=Zuxx84 The resources consulted can be found here: ·      Camden CCG guidance: 1456246258-2f3891e610beaa6533f2c0ad7866e776.pdf(Review) - Adobe cloud storage ·      Manchester Adult anaemia guide: https://acrobat.adobe.com/id/urn:aaid:sc:EU:f96fe528-0a47-457c-b29a-a7efb87221e0 ·      Manchester Haematology GP guide: https://mft.nhs.uk/app/uploads/2021/02/MFT-Haematology-GP-Pathway-Guide-v4-11.2.21.pdf ·      King’s Health Partners: https://www.kingshealthpartners.org/assets/000/002/294/KCH_-_king_s_health_partners_-_quick_guide_to_haematology_original.pdf Transcript If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description. Hello and welcome, I’m Fernando, a GP in the UK. Today we are going to cover what to do when we encounter thrombocytopenia on a full blood count, always focusing on what is relevant in Primary Care only. I have based this episode on Haematological guidance by Camden CCG, Manchester Foundation Trust and King’s Health Partners. The links to them are in the episode description. Right, let’s jump into it. Thrombocytopenia is the platelet count is low, which is defined as a platelet count below 150 × 10⁹ per litre. But before we assume a true low platelet count, we need to remember that thrombocytopenia can often be an artefact. This happens when platelets clump together in the EDTA sample tube, giving a falsely low automated count. So, the first step is always to confirm the result with a repeat full blood count and a blood film. The blood film not only rules out platelet clumping but can also provide important clues about the underlying cause. There are many potential causes of thrombocytopenia so, let’s have a look at them: First, we have alcohol excess. Chronic alcohol use can directly suppress bone marrow production and shorten platelet lifespan. It is also frequently associated with chronic liver disease, where the spleen often becomes enlarged due to portal hypertension destroying more platelets than usual — a process known as hypersplenism. Then we have recreational drugs, which can also impair platelet production or trigger immune-mediated destruction. Then, travel history is also very important. Malaria, for example, often presents with thrombocytopenia, sometimes even before fever or parasitaemia becomes obvious. Tuberculosis can also cause thrombocytopenia, either through bone marrow involvement or immune-mediated mechanisms. Then we should consider liver and renal disease. In chronic liver disease we have already explained that hypersplenism is the most common cause of thrombocytopenia in liver disease. In renal disease, platelet lifespan is reduced because uraemia makes platelets more fragile, causing them to break down more quickly. In addition, bone marrow suppression may also occur. Then we have medications as another common culprit. NSAIDs, heparin, digoxin, quinine, anti-epileptics, antipsychotics and proton pump inhibitors are all recognised causes. Most drug-induced thrombocytopenia is caused by either: • immune-mediated platelet destruction, or • direct suppression of platelet production in the bone marrow. Heparin is the main exception because it causes thrombocytopenia through a unique immune reaction that activates platelets, leading to their consumption and a fall in the platelet count. Another possible cause are nutritional deficiencies, especially vitamin B12 and folate deficiency, which can impair bone marrow production and lead to thrombocytopenia, often alongside other cytopenias. We also need to consider viral causes. For example, Epstein–Barr virus frequently causes a temporary drop in platelets, which typically resolves within a few weeks. HIV and hepatitis B or C can cause persistent thrombocytopenia either through direct bone marrow suppression, immune-mediated destruction, or associated splenomegaly. Then, malignancy is also on the list, because both haematological cancers and solid tumours can infiltrate or suppress the bone marrow. Then we have bone marrow failure syndromes, such as aplastic anaemia, which will often present with thrombocytopenia together with anaemia and neutropenia. Another cause is immune thrombocytopenic purpura, or ITP, which is an autoimmune condition that destroys platelets. In adults, ITP can be acute or chronic, and the platelet count can fall to very low levels even when the patient looks otherwise well. Finally, autoimmune conditions such as SLE can present with thrombocytopenia as part of a broader immunological process. Now that we have had a look at the causes, how should we manage these patients? We have already mentioned that we should confirm thrombocytopenia with a repeat FBC and blood film. If the thrombocytopenia is confirmed, we will need to check if there are urgent criteria. First of all, we should arrange urgent same-day hospital assessment when the platelet count is below 20 × 10⁹ per litre and any concerning clinical features are present. These include: • Active bleeding, even if minor, because bleeding risk rises sharply at very low platelet levels. • An abnormal blood film, such as the presence of blasts suggesting acute leukaemia, or red cell fragments suggesting microangiopathic haemolysis, as these findings indicate potentially life-threatening conditions. • And finally an altered consciousness or confusion, which may point to serious systemic illness, intracranial bleeding, severe infection, or thrombotic microangiopathy. We should make an urgent outpatient haematology referral if the platelet count is below 50 × 10⁹ per litre, even without symptoms. This is because at this level, the risk of spontaneous bleeding increases, and many underlying causes — such as ITP, bone marrow failure, or haematological malignancy — require urgent assessment. Additionally, when the platelet count is below 50, it is unsafe to continue antiplatelet agents or anticoagulants, so these should be stopped unless a specialist advises otherwise. We should also make an urgent outpatient haematology referral when the platelet count is between 50 and 100 and certain concerning features are present. These include splenomegaly, lymphadenopathy, other cytopenias, pregnancy, or planned surgery. This is because all of these situations increase the risk of serious underlying disease or increase the risk of bleeding. However, if the platelet count is above 50 and none of the urgent referral criteria are present, we should then arrange the following baseline investigations: Firstly, we begin with a repeat full blood count and a blood film to confirm the thrombocytopenia, rules out platelet clumping, and look for abnormal cell morphology. Then we will check Vitamin B12 and folate levels to rule out deficiency. Ferritin and iron studies are also helpful, given that iron deficiency can occasionally contribute to low platelets. Inflammatory markers, such as ESR and CRP, which can suggest infection, inflammation, or an underlying autoimmune process. An autoimmune profile to exclude autoimmune-mediated platelet destruction. Renal, liver and thyroid function tests to identify chronic liver disease, renal failure and thyroid disease given that both h

    9 min
  7. Podcast - Chole-Stuck: Cholestatic LFTs explained

    21 JAN

    Podcast - Chole-Stuck: Cholestatic LFTs explained

    The video version of this podcast can be found here: ·      https://youtu.be/lhtciu3O8tc The video on raised bilirubin pattern can be found here: ·      https://youtu.be/ndAus37PfsE The video on hepatitic pattern abnormal LFTs can be found here: ·      https://youtu.be/rIX46swVSfg This episode refers to guidelines on the management of abnormal liver function tests by the British Society of Gastroenterology. Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by them.   My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I cover what to do when we encounter abnormal LFTs with a cholestatic pattern, always focusing on what is relevant in Primary Care only.    I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.     Disclaimer: The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions. In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.   Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release]  Music provided by Audio Library Plus Watch: https://youtu.be/aBGk6aJM3IU Free Download / Stream: https://alplus.io/halfway-through   There is a podcast version of this and other videos that you can access here:   Primary Care guidelines podcast:   ·      Redcircle: https://redcircle.com/shows/primary-care-guidelines ·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK ·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148 There is a YouTube version of this and other videos that you can access here:  The Practical GP YouTube Channel: https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk   My summary guide can be downloaded here: ·      https://1drv.ms/b/s!AiVFJ_Uoigq0mQ8MRxaNYnA1_pzh?e=H2U7rS   The resources consulted can be found here: BSG- British Society of Gastroenterology: ·      bsg.org.uk/clinical-resource/guidelines-on-abnormal-liver-blood-tests ·      Guidelines on the management of abnormal liver blood tests (bsg.org.uk) o  First published on: o  BMJ article: o  Guidelines on the management of abnormal liver blood tests | Gut (bmj.com)   Transcript If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description.   Hello and welcome, I’m Fernando, a GP in the UK. Today we are going to cover what to do when we encounter abnormal LFTs with a cholestatic pattern, always focusing on what is relevant in Primary Care only.   This episode is based on the British Society of Gastroenterology guidelines on abnormal Liver function tests. A link to it is in the episode description.   Right, let’s jump into it. And let’s start by remembering that there are three common patterns of abnormal liver function tests or LFTs: A cholestatic pattern, normally showing a high ALP and GGT, which is what we will concentrate on today. An isolated raised bilirubin with otherwise normal liver tests.And a hepatitic pattern, with a raised ALT and AST indicating hepatocellular injury. By the way, if you are interested in finding out more about the last two types, make sure to watch the corresponding episodes on this channel. The links are in the episode description.As we have said, LFTs showing a cholestatic pattern normally present with a high ALP and GGT. Alkaline phosphatase, or ALP, is produced mainly in the liver but is also found in bone, intestines, kidneys and the placenta. Levels are physiologically higher in childhood because of rapid bone growth, and in pregnancy due to placental production. Raised ALP can come from either hepatic or non-hepatic sources. The main source of non-hepatic ALP is bone. ALP increases in bone disease because it is produced by osteoblasts, the cells responsible for forming new bone. Any condition that increases osteoblast activity or bone turnover—such as healing fractures, Paget’s disease, bone metastases, or vitamin D deficiency—causes osteoblasts to increase their activity, releasing more ALP into the circulation. We should remember that the most common cause of an asymptomatic, non-hepatic raised ALP is vitamin D deficiency. And let’s remember that vitamin D deficiency increases bone turnover because low vitamin D reduces calcium absorption from the gut. To maintain normal calcium levels, parathyroid hormone rises and stimulates bone breakdown to release calcium. This increase in bone remodelling activates osteoblasts leading to a rise in ALP. But as we are focusing on liver function tests, what is the source of a raised hepatic ALP? From a pathophysiological perspective, hepatic ALP rises when bile flow is impaired, also known as cholestasis. And, why does cholestasis cause a rise in ALP? It happens because alkaline phosphatase is found in high concentration in the cells lining the bile ducts. When bile flow is impaired, pressure builds up in the biliary system and the bile duct epithelium becomes irritated. This stimulates these cells to produce and release more ALP into the bloodstream. This is the reason why ALP rises in, for example, gallstone disease, strictures, or cholangitis. On the other hand, γ-glutamyltransferase, or GGT, is found in the liver but not in bone. Therefore, when ALP is raised, measuring GGT helps determine whether the source is hepatic or non-hepatic. A raised ALP with a normal GGT suggests a bone-related cause, whereas a raised ALP with a raised GGT supports a hepatic origin and should prompt further assessment of cholestatic liver disease. GGT rises in cholestasis because it is also highly concentrated in the cells lining the bile ducts. When pressure builds up in the biliary system, these cells release more GGT into the bloodstream. In addition, cholestasis causes oxidative stress because retained bile acids are toxic to liver cells. In response, the liver increases GGT production, as GGT is involved in antioxidant and detoxification pathways, leading to the characteristic rise in cholestatic liver disease. A high GGT can also be due to obesity, excess alcohol, or medications. In obesity and NAFLD, fat accumulation within the liver creates oxidative stress, so the liver up-regulates GGT to protect hepatocytes from free radical damage. In this context, an elevated GGT reflects metabolic stress rather than structural cholestasis. In alcohol use, ethanol metabolism produces toxic intermediates that also generate oxidative stress, which further stimulates GGT production as part of the liver’s detoxification response. We will not go into detail on how to proceed with an isolated raised ALP, that is, with a normal GGT, as today we are focusing on cases where there is clear hepatic involvement, meaning that both ALP and GGT are high in a true cholestatic pattern. How should we investigate and manage these patients? When we manage patients with any abnormal liver function tests, we must begin by recognising red flags that require urgent action. According to the British Society of Gastroenterology guidelines, if there are signs of synthetic liver failure – such as unexplained clinical jaundice, a low albumin, or a raised INR – or if there is a suspicion of malignancy, for example unexplained weight loss or marked cholestasis, then the patient should be urgently referred or admitted for specialist assessment. If the pattern is cholestatic, we will proceed with a full liver screen. This is because cholestatic abnormalities are often related to structural biliary disease, autoimmune cholestatic conditions, or infiltrative disorders, and these require a broader diagnostic approach than simple repeat testing. What tests should be done in a full liver screen? A full liver screen should include an ultrasound scan of the liver and biliary tree, which is the first-line imaging test. Ultrasound helps identify biliary dilatation, gallstones, strictures, masses, or features of chronic liver disease. In addition to imaging, blood tests should include hepatitis B and C screening, an autoantibody screen, serum immunoglobulins, ferritin and transferrin saturation, and, often and where clinically appropriate, a coeliac screen, alpha-1 antitrypsin levels, and caeruloplasmin. These tests collectively help detect autoimmune cholestatic diseases such as primary biliary cholangitis, metabolic conditions such as haemochromatosis or Wilson’s disease, and chronic viral hepatitis. It is also worth emphasising that this full liver screen is recommended not only for cholestatic abnormalities but also for patients who present with a hepatitic pattern, as the BSG guideline advises a comprehensive assessment irrespective of the pattern or the degree of derangement once initial red flags have been excluded. The management in primary care is fairly simple, because the British Society of Gastroenterology recommends that once initial investigations have been completed, these patie

    9 min
  8. Podcast - Platelet Points: Making Sense of Thrombocytosis

    14 JAN

    Podcast - Platelet Points: Making Sense of Thrombocytosis

    The video version of this podcast can be found here: ·      https://youtu.be/3QL2R2IV83o This video refers to guidelines produced by a number of organisations (details below). Please note that the content on this channel reflects my professional interpretation/summary of the guidance and that I am in no way affiliated with, employed by or funded/sponsored by any of them.   My name is Fernando Florido and I am a General Practitioner in the United Kingdom. In this episode I cover what to do if thrombocytosis is found, always focusing on what is relevant in Primary Care only. The information is based on Haematological guidance by Camden CCG, Manchester Foundation Trust and King’s Health Partners. I am not giving medical advice; this video is intended for health care professionals, it is only my summary and my interpretation of the guidelines and you must use your clinical judgement.     Disclaimer: The Video Content on this channel is for educational purposes and not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or seen on this YouTube channel. The statements made throughout this video are not to be used or relied on to diagnose, treat, cure or prevent health conditions. In addition, transmission of this Content is not intended to create, and receipt by you does not constitute, a physician-patient relationship with Dr Fernando Florido, his employees, agents, independent contractors, or anyone acting on behalf of Dr Fernando Florido.   Intro / outro music: Track: Halfway Through — Broke In Summer [Audio Library Release]  Music provided by Audio Library Plus Watch: https://youtu.be/aBGk6aJM3IU Free Download / Stream: https://alplus.io/halfway-through   There is a podcast version of this and other videos that you can access here:   Primary Care guidelines podcast:   ·      Redcircle: https://redcircle.com/shows/primary-care-guidelines ·      Spotify: https://open.spotify.com/show/5BmqS0Ol16oQ7Kr1WYzupK ·      Apple podcasts: https://podcasts.apple.com/gb/podcast/primary-care-guidelines/id1608821148 There is a YouTube version of this and other videos that you can access here:  The Practical GP YouTube Channel: https://youtube.com/@practicalgp?si=ecJGF5QCuMLQ6hrk   My summary of the guidance consulted can be found here: ·      https://1drv.ms/b/s!AiVFJ_Uoigq0mQ4ZjYGRH1wkGBdc?e=Zuxx84 The resources consulted can be found here: ·      Camden CCG guidance: 1456246258-2f3891e610beaa6533f2c0ad7866e776.pdf(Review) - Adobe cloud storage ·      Manchester Adult anaemia guide: https://acrobat.adobe.com/id/urn:aaid:sc:EU:f96fe528-0a47-457c-b29a-a7efb87221e0 ·      Manchester Haematology GP guide: https://mft.nhs.uk/app/uploads/2021/02/MFT-Haematology-GP-Pathway-Guide-v4-11.2.21.pdf ·      King’s Health Partners: https://www.kingshealthpartners.org/assets/000/002/294/KCH_-_king_s_health_partners_-_quick_guide_to_haematology_original.pdf Transcript If you are listening to this podcast on YouTube, for a better experience, switch to the video version. The link is in the top right corner of the video and in the episode description. Hello and welcome, I’m Fernando, a GP in the UK. Today we are going to cover what to do when we encounter thrombocytosis on a full blood count, always focusing on what is relevant in Primary Care only. I have based this episode on Haematological guidance by Camden CCG, Manchester Foundation Trust and King’s Health Partners. The links to them are in the episode description. Right, let’s jump into it. Thrombocytosis is when the number of platelets is high, which is usually defined as a raised platelet count above 450 × 10⁹/L. But before moving on, let’s clarify the terminology: should we call it thrombocytosis or thrombocythemia? There is an important difference. Thrombocytosis is much more common and arises as a secondary response to another condition, which is why it is also known as reactive thrombocytosis. In contrast, thrombocythemia, also called primary or essential thrombocythemia, is far less common and represents a myeloproliferative disorder in which the bone marrow produces platelets in an uncontrolled, abnormal way. Another important distinction is that patients with reactive thrombocytosis have normal platelets, so their risk of thrombosis and bleeding is relatively low. On the other hand, patients with thrombocythemia have abnormal platelets, which increases their risk of both blood clots and bleeding complications. From a clinical perspective, thrombocythemia often presents with splenomegaly and a platelet count greater than 1000 × 10⁹/L. So, let’s have a look at the possible causes. Causes of thrombocytosis include: • Iron Deficiency Anaemia: which is one of the most common causes of reactive thrombocytosis. When iron levels are low, the bone marrow increases its overall activity in an attempt to compensate for the anaemia. Although iron deficiency limits the production of red blood cells, platelet production is not restricted in the same way. As a result, the bone marrow produces more platelets. In addition, inflammatory signals associated with chronic iron deficiency can further stimulate thrombopoietin pathways, increasing platelet numbers even more. This is why thrombocytosis often resolves once the iron deficiency is corrected. • Another cause is Malignancy, because some tumours release inflammatory cytokines that eventually increase platelet formation. This reactive response is common in several solid cancers, particularly the “LEGO” cancers, that is: • Lung • Endometrium • Gastric • and Oesophageal cancer • Another cause is general Inflammation, where cytokines stimulate excessive platelet production. • Also Infection, which can cause transient reactive thrombocytosis. • Post-splenectomy and hyposplenism, such as in coeliac disease, since the spleen normally helps remove circulating platelets. • Post-operative states, where inflammation and stress responses increase platelet counts. • And finally, a primary myeloproliferative disorder, such as essential thrombocythemia. How should we respond to thrombocytosis? The criteria for urgent haematology referral are: • A platelet count exceeding 1000 × 10⁹/L, which raises concern for a myeloproliferative disorder and a significant risk of thrombosis. • Splenomegaly, which may indicate a primary haematological process such as essential thrombocythemia or myelofibrosis. • A recent history of thromboembolism, as thrombocytosis can contribute to recurrent clotting events. • A platelet count above 600 × 10⁹/L in a patient at high risk of thromboembolism or cardiovascular disease, since the combination significantly increases clinical risk. • Neurological symptoms, which may reflect microvascular complications associated with very high platelet counts. • Any signs of malignancy, given that multiple cancers can cause reactive thrombocytosis. • any other significant abnormal full blood count indices, which may suggest a bone marrow disorder rather than a reactive process. • And finally, if there is Abnormal bleeding. And let’s stop here for a moment and discuss how it is possible that thrombocytosis can be associated to a high risk of both thrombosis and bleeding. On one hand, thrombosis risk in thrombocytosis is due to the high number of circulating platelets, which makes clots more likely. In addition, inflammation causing reactive thrombocytosis can also create a prothrombotic environment. Together, these factors increase the thrombosis risk. On the other hand, bleeding risk in thrombocytosis can occur for two main reasons. First, in primary or essential thrombocythemia, the platelets produced by the bone marrow are structurally and functionally abnormal and these abnormal platelets do not work effectively, so clot formation is impaired. Secondly, thrombocytosis may affect the von Willebrand factor. Von Willebrand factor is a protein that helps platelets stick to damaged blood vessels and to each other, making it essential for the first steps of clot formation. However, when platelet counts become very high, the excess platelets bind and remove the most active forms of von Willebrand factor from the circulation. This leads to a functional depletion known as acquired von Willebrand syndrome. It explains the paradoxical situation in which a patient can have thrombocytosis and yet be at increased risk of bleeding. If none of the urgent referral criteria are present, we will investigate for underlying causes by arranging the following initial tests: • A repeat full blood count, to confirm that the thrombocytosis is persistent. • A blood film, which may reveal abnormal platelet morphology or other features suggestive of a myeloproliferative process. • Inflammatory markers such as ESR and CRP, since inflammation is a common cause of reactive thrombocytosis. • Ferritin and iron studies, as iron deficiency frequently elevates platelet counts. • And we will consider a coeliac screen, because coeliac disease can lead to hyposplenism or iron deficiency, both of which are associated with thrombocytosis. If the patient is asymptomatic and no obvious cause is identified, we will repeat the full blood count 4 to 6 weeks later. If the thrombocytosis persists above 450 × 10⁹/L, we will refer to haematology routinely for further assessment. So that is it, a review of the assessment and management of thrombocytosis. We have come to the end of this episode. Remember that this is not medical advice but only my summary and my interpretation of the guidelines. You must always use your clinical judgement. Thank

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