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Good evening, everybody. Uh Once again, welcome to this me Primary Care Network event. It's great to have, gosh, over 100 of you already, over 100 and 50 almost 200. Gosh, the numbers keep climbing. It's great to see everybody. Uh My name is Tim Neal. I'm an F one doctor in Northern Ireland. I have the pleasure of sharing the uh the session tonight. Um We have a well known face back with us again tonight. Very excited to have Doctor Kevin Fernando. Um with us this evening again, he's a GP um with special interest in diabetes, cardiovascular renal metabolic medicine and also medical education. Um He's a fellow of the Royal College of GPS, Royal College of Physicians. He has so many accolades to his name, but his accolade tonight is to be our speaker, which is hopefully the biggest of all. Um, we're going to be chatting tonight about commonly abnormal blood tests in primary care, which I hope will be really useful for everybody. I'm certainly looking forward to it for, for some revision. Now, um, as usual, we will run for around 45 minutes to an hour, um for the presentation with some time for Q and A and we've been chatting beforehand. Kevin has sort of three distinct sections tonight. So we'll, uh, we'll pause for a little bit at the end of each section and do some questions and answers for each section and then anything that's coming through repeatedly. Um, I'll set off to the side and we'll address at the end. Um, keep an eye tonight. We do have some polls to keep things nice and interactive. So please engage with them and we can get some live feedback for Kevin as we go. Um, I just point out as, again, the Med All app is absolutely fantastic. Um, on there, you've got all your details, particularly the reference section, especially for tonight. You want to go in and look at LFT S or you want to go in and look at, er, abnormal, er, full blood pictures, things like that. It's fantastic for that. Um, looking at causes and referring you out to external reliable sources to tell patients about as well. So, um, be the first to hear about our events, get your certificates, give your feedback all from the Med All app. As you know, we have, um, the primary care events running almost every week and being on there means that you'll be the first to hear about what's coming up. But without any further ado from me, I'm going to hand over to Kevin. If I ask you, Kevin, you can pull up your slides again and we will get started this evening. Fantastic. I'll be here in the background, Kevin and uh enjoy everyone. Oh, you got a full screen slide there, got full screen slide and we're moving. Great. Excellent. All right, thanks. Yeah, thanks for that kind introduction, Tim. Good evening, ladies and gentlemen. Great to see you. So you on this evening, uh to join me much, much appreciated for those who haven't had the pleasure of uh meeting before. My name is Kevin Fernando, a GP partner in North Berwick Health Center. It's just a little town just east of uh Edinburgh. Longstanding interest as Tim said in all things, diabetes, cardiovascular renal, metabolic, and medical education. I also work for 11 day a week for Medscape, global uh producing global medical education content. So, in this session today we're gonna cover um it's a commonly abnormal blood tests in primary care. Uh It's something that causes a lot of bother for many of us in primary care. Certainly, my doc man inbox quickly fills up with a slightly abnormal blood tests. Never sure what to quite do with them. So, uh I've put together a series of presentations uh to, to make our lives a wee bit easier in primary care, but of course, ultimately to help improve the lives of our patients. So uh these are my disclosures, but this is a full independent session, not, not supported by any industry organization. So before we start with the main content, I just wanted to share some resources I've put together. II did this last time. I hope you found those previous resources helpful. These are some a abnormal blood test resources I've put together with my Medscape pattern. So this is hyponatremia in primary care, low sodium levels, very common in primary care. So I put together a one sheer, you can access it via the QR code. Cause a what is it? Of course causes investigations and two flow charts. Uh just to help investigate those low sodium levels. Ano another one on high and low calcium levels. Again, a very common finding in primary care and really uh the majority of people with hypercalcemia in primary care, we need to be aware of underlying conditions such as malignancy and primary hyperparathyroidism that accounts for around 90% of all cases of true persistent hypercalcemia. Another one on hypothyroidism, but particularly subclinical hypothyroidism. So where you have a normal free T four but elevated TSH. Again, very common finding in primary care and often over treated and not directly related to abnormal blood tests, but I do talk about high potassium levels. Um Some colleagues and I have put together resources on identifying C KD in primary care and intervening er for KD in primary care. Many of you will be aware there's been huge changes in how we manage chronic kidney disease in primary care. Uh focused around neurotherapy such as SGL T twos fen and now G LP ones. But part of these interventions, uh one sheet in particular is managing hyperkalemia in primary care. Another uh another particular challenge for us, isn't it? Especially when it gets phoned in late on a Friday afternoon and very quickly a couple of other resources you might find helpful. I think I mentioned last time my kids are mortified, but I have a youtube channel now with some patient facing content. They, as I said, they are absolutely mortified. They've all unfollowed me online. In fact, unfortunately, I think they followed unfollowed me in real life too. But I've got a series of, of videos on type two diabetes and lifestyle interventions. Um and also some uh videos on SGLT two inhibitors because they are the new standard of care for people living with type two diabetes. That's what I talked about on my previous medical uh webinar. So I've got 44 videos there that you might find helpful. So just a, a quick quick sign post concern resources. I hope you'll find helpful. So what we're gonna talk about today was Tim said we've got around about an hour or 45 minutes to an hour. And I want to cover three main uh blood tests that we commonly request in primary care. First of all abnormal liver, blood tests in primary care, the bane of my life, then we're gonna talk about abnormal iron studies in primary care and then finally, I'll talk about the appropriate use of inflammatory markers, specifically C RP and E sr in primary care. OK. And happy to take questions as we go along, we'll take a natural break after each section to talk about that to address any questions for that, that particular blood test, but any burning questions as we go along free field, feel free to type into the chat box and uh Tim, Tim can fire those questions at me. So as always helpful to have a patient to base our learning on. So this is ka one of my patients in North Berwick. She's 52 years old. She actually came to see me with some right upper quadrant pain worse after eating. So I thought she probably had perhaps some gall gall gallbladder disease. Uh So I referred her to assessment, referred her for some er for an ultrasound scan and that came back actually with a normal looking gallbladder. I think maybe a solitary gallstone, a normal co common bile duct caliber, but that hyper echoic appearance of her liver, that common finding often incidentally, isn't it of fatty liver on ultrasound? So I had also checked a few other bits and Bobs, her BP was 100 and 4892. She had quite marked dyslipidemia total cholesterol 6.3 triglycerides, 4.9 HDL was low at 0.8 and the lab were unable to calculate her LDL because of her high triglycerides ABM I recently recorded on vision was 33. A waist circumference is 88 and look at these bloods here. Those LFT S those mildly abnormal LFT S commonly found in our dot Man inbox II never really know what to do. So just click repeat four weeks and hope for the best. Slightly elevated. A LT slightly elevated AST ALK four is OK. Gamma GT slightly elevated bilirubin is normal. Uh HBA1C is 45 millimoles per mole. So indicative of pre diabetes or I prefer the term at risk of type two diabetes. Her renal function is normal. She's not on any medications prescribed by myself. She doesn't take anything over the counter and she denies any illicit drug use. And in terms of her social history, she's a tattoo artist in Central Edinburgh. She's a nonsmoker and like most of my patients, she tells me she drinks alcohol within recommended limits. So, ladies and gentlemen, first question for you all. What do you think is the likely cause of her abnormal liver blood test? So I've got a touch unlikely cause and then I don't worry, I'm gonna take you through all the different types of liver tests. We might uh request and interpret primary care. But what are your thoughts here, ladies and gentlemen, what is the likely cause of a uh abnormal liver blood test? Do you think it might be a chronic HCV infection perhaps related to occupation? Is it muzzled the new terminology for NAFLD. I'll quickly tell you about that. Metabolic dysfunction, associated steatotic liver disease. A bit of a mouthful. But don't worry, I'll briefly tell you about that. Or is it MET A LD again? Some new terminology, metabolic alcohol related liver disease or are you worried? It's something a wee bit more sinister. A pa cellular carcinoma or something else. So, what are your thoughts here, ladies and gentlemen. Um, so, Tim, what have you got any? I can just pop the results of the pull up here now. Good stuff. Oh, yeah, I've got it there. So let's see. So lots, lots, two, lots going for, for mail. Yep, we've got 66% voting for 2 20% for three and then slightly lower for the others. Good stuff. And then the next question before we uh talk about liver tests is what do you do next? Then with respect to liver function tests, do you reinforce that all important lifestyle advice? Uh Talk about a weight, perhaps, refer her to a local weight loss uh management program revisit alcohol consumption or would you check a targeted liver screen or would you phone a friend, refer her to hepatology? Would you check a fib four? Um This is uh if you're not familiar with that, that's a, a AAA test. Uh It's a score that we can uh uh assess to, to look at her future risk of fibrotic liver disease. Or would you refer her for noninvasive liver imaging in the form of a fibro scan or would you try my usual dot man into strategy and repeat in another four weeks. What are your thoughts here? Ladies and gentlemen. So lots going for one here. I see Tim 14 is popular. I mean, in reality, many of us will do more than one option here. But yeah, lots for checking for fib four. I mean, we we want to be aware of a risk of progressive liver disease, fibrotic liver disease. So I think four is very sensible. Uh one absolutely sensible um as well. So, but AAA nice mixture of options there. Good stuff. Thanks. So let's go quickly talk about what mail is and then I'll focus on um abnormal liver blood tests. So NAFLD was just last year reed muzzled metabolic metabolic dysfunction associated steatotic liver disease. Now, I appreciate that's a bit of a mouthful, but it's really to tell us that NAFLD or mail is not primarily a liver disease, it's primarily a metabolic condition. So we now define Mail as individuals like my patient ka who has evidence of hepatic steatosis, that fatty uh liver appearance and at least one cardiometabolic risk factor from the usual range of cardiometabolic risk factors. BM I HBA1C BP lipids. So she actually has a full house, doesn't she? She's got a full house of cardiometabolic risk factors. And then mash is the new terminology for NASH A nash, nonalcoholic steatohepatitis is replaced by metabolic dysfunction, associated steatohepatitis. And Met. Ad I briefly mentioned is that combination of individuals who drink alcohol to excess and have metabolic liver disease. We all have patients like that, don't we? And why they are defined separately is our hepatology. Colleagues tell us these individuals are at particularly high risk of progressive liver disease, are particularly challenged to manage, challenging, to manage and that's why they're segmented differently. So really the one key take home message here about MASL. MASL is primarily a metabolic disease. It's the liver's manifestation of the metabolic syndrome. So a really useful take home message for us all working in primary care. So let's go back to basics though about abnormal liver blood test. Mil pardon me? Abnormal LFD is very common in primary care, aren't they? As we all know the degree of abnormality doesn't always correlate, does it with disease severity? Liver disease is often silent until quite advanced and we do make a rod for our own backs, don't we? We often tick that LFT box for unexplained or nonspecific symptoms. It's often ticked as a measure of wellbeing, isn't it? I'm always giving my GP trainees a hard time. Why have you ticked that LFT box? What question are you looking to answer? Because in reality, all of us here on this webinar tonight, one in five of us will have abnormal liver blood tests, but actually the majority of us will, will not have significantly a significant underlying liver disease. So to illustrate this a bit more detail, I found this really interesting study called a ballot study published over 10 years ago. Um It, it's a study set in Birmingham general practices. So very generalis to the patients you and me might see on a day to day basis, nearly 1300 people from primary care in Birmingham found to have abnormal LFT S but uh without known underlying liver disease. Ok. And what did they find in this score? Only 2.5% only 32 people with abnormal LFT S actually had an underlying specific disease of the liver. So it just shows how common abnormal LFT S are in primary care and actually how few people actually have underlying significant liver disease. But unsurprisingly 40% of that whole cohort had fatty liver appearance on ultrasound. So again, showing how common fatty liver disease is. Now, this is the reason we often tick that box, isn't it? We're worried about underlying primary or secondary malignancy. They found just eight malignancies in that cohort of nearly 1300 patients. Interestingly, in this study, they did do what I usually do with my LFD S. They repeated the LFD S every month for two years. And what did they find? They found that LFD S just remain persistently abnormal. So the authors of this study strongly concluded that instead of endlessly repeating LFD S, we need to be more proactive and undertake targeted liver screening test, other examination to try and elucidate the underlying cause of abnormal LFT S. They did find some useful things though they found that alt and alkaline phosphatase were most associated with significant underlying liver disease. So perhaps we should be paying more attention to those parameters and it mirrored what we already know about gamma GD. Largely a useless test, very high false positive rate and as we know, very sensitive to alcohol intake. So again, the office concluded liver disease is rare amongst those with abnormal LFT S in primary care. So I thought a really useful message for us all working in primary care. So it's worthwhile then, isn't it? Uh we as GPS nurses, pharmacists having a heuristic a rule of thumb flow chart at hand to try and identify patients with potentially modifiable liver disease. And that's why I wanted to take you through just now some key points um when considering requesting and indeed interpreting abnormal liver tests. Ok. So remember, first of all LFT S may be normal even in advanced liver disease. And conversely, as I've demonstrated already, um uh LFT S are frequently abnormal in the absence of liver disease. So um it very very challenging situation for us. OK. So that's why just interpreting FTS in isolation is not very helpful, often ineffective in diagnosing ruling in or ruling out liver disease. And that's why we need other targeted tests. And of course, history and examination. As always, we often check liver tests, don't we? To talk about to, to, to assess development of alcohol related liver disease? But again, the evidence suggests liver enzymes are a poor guide to the development of alcohol related liver disease. But actually what they can be helpful for or er, is promoting behavior change if someone, er, er, comes to see you because they feel they're drinking too much or if you manage to pick this up, check their bloods and the LFT S are up, actually, that can be useful in promoting behavior change. Ok. So uh that can be helpful, but don't think that uh alcohol related liver disease is limited to those who are, have alcohol dependence syndrome. The risk actually of liver disease doubles by any given alcohol intake. So even if you're drinking just seven units a day, if your BMI is over 30 five and you're drinking just seven units a day, your risk of liver disease doubles. Ok. So obesity a big risk factor for developing liver disease in the context of any alcohol intake. So I thought that was a very uh important message there as well. So when we're looking at liver tests, what sort of things do we look at? You'll all be familiar with this, we do with many blood tests. What we want to look is patterns, you know, pattern recognition is a big part of blood test interpretation. So, is the predominant pattern. A hepatocellular pattern. So your Ainas are up, I'll talk about at and ast just shortly or is it more an obstructive cholestatic picture where your gamma GT and your alkaline phosphatase are elevated? Or is it a mixed pattern, both hepatocellular and cholestatic? So look for the pattern, also look at the magnitude of any abnormality generally up to three times the upper limit of normal. We don't need to worry about too much in the context of statins, for example, and I'll talk about that shortly or is it 3 to 10 times the upper limit of normal? So that is a significant elevation or over 10 times the upper limit of normal. And these are situations where we may need to discuss with our hepatology colleagues. And of course, what's very helpful with any blood test is looking at the rate of change over time. Is it an acute deterioration in the liver test? We're seeing or has this been a more chronic deterioration? Ok. So when should we tick that LFT box, you know, rather than just ticking it indiscriminately, when should we tick it? Well, if you do have nonspecific s symptoms, suggestive of liver disease and probably the most sensitive symptoms here are anorexia or loss of appetite, fatigue or nausea. Or of course, if you've examined ka or your patient and you find evidence of chron chronic liver disease symptoms or signs of uh cirrhosis, for example, portal hypertension, liver ascites, peri peripheral edema spider nevi on the chest or hepatosplenomegaly as well, or maybe splinter hemorrhages. So, if you find signs of chronic liver disease, then of course, check, uh, consider checking LFD S or you might have a patient with, with, uh, uh, uh, uh, another long term condition that increases their risk of developing liver disease. So, does your patient have autoimmune thyroid disease? Then that increases his or her chance of developing autoimmune liver disease? Or does your patient have inflammatory bowel disease? Crohn's or ulcerative colitis? That individual has a 10% risk of developing ps E primary sclerosing cholangitis. Ok. And this is probably where we very commonly check by uh LFT S, don't we? The use of hepatotoxic drugs? So, dmards for rheumatological conditions, methotrexate azaTHIOprine terbinafine for fungal infections, fungal toenail infections and statins. LFT S are often checked for statins, aren't they? But actually the bottom line is statins do not cause liver disease. Ok. Statins cause a transient transaminitis which just settles with time. And in fact, we have increasing evidence that statins protect against liver disease and indeed reduce the risk of hepatocellular carcinoma. So next time you're starting a statin, all we need to do is check a baseline alt alone. And as that, as long as that's not three times the upper limit of normal, we can just start the statin. And indeed, there's no need to routinely recheck LFT S after a statin. So this is a guidance from America from a number of years ago to try and reduce LFT S checked in the context of statins and also reader some papers published in our BJ GP journal as well, which very much tell us we don't need to routinely check LFT S uh after starting a science. So that's had a huge impact on my practice. And that's been introduced in Edinburgh Guidance on, on our lab, lab request blood request screen. Um uh we just have a tick box now alt alone for statin initiation. So that's what I take. And again, as long as that's not three times upper limit of normal, I'll just start the atorvastatin or whichever statin. And I don't routinely recheck the LFT S if your patient has a family history of liver diseases, hemochromatosis is very common in Scotland, uh autosomal dominant. So then I might check LFT S and of course, a ferritin or Wilson's disease. I've never seen this in my, my career. I used to, I used to check and serial apartments regularly. How many cases of Wilson's disease I've ever picked up in my career. Zero. Last time I saw Wilson's disease was on an episode of, er, in the late nineties. So I'll talk about targeted liver screens shortly. Not everyone needs a full, full liver screen, alcohol misuse though we've discussed this already. It's, it's a poor guide. LFT S are a poor guide to the development of alcohol related liver disease but can motivate behavior change. And of course, if your patients have risk factors for viral hepatitis, um are they an IV drug user or like uh uh Kara, she works as a tattoo artist. So that also increases her risk. So let's talk about the specific liver blood test now in the last sort of 5, 10 minutes. So let's start with a LT alanine transaminase. So alt is predominantly a liver specific enzyme. Uh I remember that because there's an L an A LT and it's a sensitive marker of hepatocyte injury or death. So, viral hepatitis hep B hep C, paracetamol overdose or other drug induced hepatotoxicity. Ok. But like any blood test at does vary with a number of factors, age sex, ethnicity, BMI I illness and exercise. Ast on the other hand, is not as liver specific because it's present not just in the liver, it's in the cardiac muscle, smooth muscle and skeletal muscle. But actually AST is a much more sensitive marker of liver injury, particularly alcohol related liver injury. So if you have a very high ast or a high ast to alt ratio, that's strongly suggestive of alcohol related liver injury. Ok. Now, I don't check bloods in Children too often, particularly LFT S. But you can, you, you sometimes see an isolated rise in ast in Children in relation to underlying skeletal muscle disorders such as muscular dystrophy. Ok. So if you want to differentiate between uh an elevated asd due to a muscle disorder. Compared to a liver disorder, you can check a CK alongside to help determine the origin of that. ASD as I said, I rarely check bloods, particularly LFT S in Children. What about gamma GTE? Does it have a useful role? I've told you it's a largely useless test and it is difficult to interpret because it's present in multiple organs, the liver, the intestines, the kidneys, the pancreat and the prostate. Uh and it's raised by multiple factors. But importantly, it's not produced in the bone, which is why one of its most useful roles is establishing the likely origin of an elevated alkaline phosphatase is that alkaline phosphatase coming from the bone or the liver. And I'll tell you about that in just a minute. Other things that push up your gamma GT alcohol, as we discussed obesity and several drugs, um antibiotics, for example, they push your gamma GT on. So you can see it's a poorly specific uh blood test. But actually one of its other useful rules is actually the best predictor of mortality in people with established liver disease. So if you've got someone sadly with alcohol related liver disease, for example, with a very high gamma GT, that's a poor prognostic sign. But as I said, the best rule, the main role I use gamma GT for is to find out the likely origin of a high alkaline phosphatase. So what is al phos al phos another liver enzyme? But also found in the bone, the intestine, the kidneys and the white blood cells. Um generally alkaline phosphatase is also higher in Children. And we see elevated als in pregnancy because your placenta also produces uh alkaline phosphatase. And overall, we see alkaloid phosphatase elevated in a number of situations. Yes, chronic liver disease, cholestatic liver disease, bone disease, hepatic congestion due to right sided heart failure because of that back backflow of fluid. So if you do see a raised out force, then it is worth checking a gamma GT because if you have a high out force and a normal gamma GT, then think bone and go down the bone biochemistry route, check a calcium phosphate P th maybe. However, if you have a high gamma GT and a high out phos, then think liver and go down the liver route and do a targeted liver screen. Alternatively, some of you may have access to ap electrophoresis, quite an expensive test uh to check ap isoenzymes generally not something we do locally. Now, the one exception of caveat here, if you do have a persistently elevated out force, particularly over a hu a 200 of which you think is liver in origin, then it might be worth checking an AM E an anti mitochondrial antibody to exclude PBC primary biliary cirrhosis, relatively rare condition. Common in older women often presents with quite marked generalized itch in the absence of a rash. Ok. So just bear in mind that caveat. What about bilirubin? So, a question for you all, you can just type it into, uh, the chat box. What if you see an isolated elevated bilirubin? What, what are your thoughts there? What might that be? Any thoughts Gilbert someone to put? Absolutely Gilbert syndrome. So, if you're not familiar Gilbert syndrome is an isolated raised bilirubin, usually unconjugated and usually not above 70 in response to any physio log stress. So even a good bout of man flu can send your bilirubin up. It's very common in because it's autosomal dominant. So it affects one in every generation. Often noticed by a loved one who noticed their, their partner is mildly jaundiced when they become unwell, completely benign and just settles with time. So we can reassure our patients. However, just have at the back of your mind, sometimes we can see an isolated raised bilirubin in the context of hemolysis. So do inquire about any occult bleeding in the urine in the bowels, any bruising et cetera. And if there is a suggestion of hemolysis, you might want to consider a blood film reticulocyte count or an LDH. And I'll tell you about LDH in, in just a minute. Ok. So as I said in Gilbert syndrome, it's usually a non conjugated bilirubinemia. You sometimes see a conjugated bilirubin or bilirubinemia in obstructive uh uh jaundice, hepatobiliary obstruction of pancreatic tumors often or hepatitis from any cause HEP B HEP C or advanced cirrhosis as well. But the commonest thing we'll see in primary care is that unconjugated hyperbilirubinemia due to Gilbert Syndrome. Great albumin. Next, then albumin is a protein synthesized by the liver, as we all know, and it's actually a very sensitive marker of liver synthetic function. So, if you have a low albumin, that can be strongly suggestive of poor liver synthetic function. But of course, liver uh sorry albumin may be reduced in other clinical scenarios as well. Sepsis, systemic inflammation, nephrotic syndrome. So, I've been caught out by that before. If you see a persistently low albumin, no obvious cause dipstick the urine because if there's massive proteinuria, that's why they've got a low albumin. They're losing their album in their urine due to nephrotic syndrome. Heart failure can also cause a low albumin and any malabsorptive disorders or gi protein loss as well. Clotting factors. Next clotting factors synthesized in the liver. And um and they, if you've got abnormal clotting factors. So a prolonged prothrombin time or inr that's not good news. Is it that usually signifies significant liver damage. Usually you have over 70% hepatocyte loss. Uh if you've seen abnormal clotting factors, ok. But again, be aware that prolonged prothrombin time. I nr can also be caused by a Vitamin K deficiency in fat absorption and in chronic cholestasis as well. Similar situation with platelet induction, if you see low platelets, that's usually unfortunately an indicator of quite advanced liver disease as well. Usually due to splenic enlargement. So again, if you see low platelets, put a hand on the abdomen, examine the spleen, is it enlarged? Uh and then a adds to evidence of significant and advanced liver disease due to pre splenic enlargement secondary to portal hypertension. And then finally LDH, now er LDH was often recommended. My hospital colleagues, wasn't it? My oncology colleagues in in particular. So I never knew exactly why I was checking that LDH for them. But what LDH is it is a liver enzyme, but it's not specific to the liver. It's also produced in the heart and the muscle, muscle, but it is typically elevated as I put here liver diseases, but particularly liver diseases associated with hemolysis, solid tumors. Hence request by oncology, colleagues and lymphomas as well as viral hepatitis. So that's why we're sometimes asked to check LDH. I tend not to check LDH myself in primary care only when directed to by my secondary care colleagues. OK. So to finish up this section, then here's a really useful flow chart produced by the British Society of Gastroenterology, the B SG response to abnormal liver blood tests. So it really summarizes a lot of what I just said, uh nice pathways for the different patterns of abnormal liver blood tests. You might see this is really available online as a powerpoint slide. So I use this as a great teaching tool for my GP trainees, nurse trainees. So well worth having a look at this in your own time. I'll share my contact details at the end. Feel free to message me. I'm happy to share my, my whole slide deck if you wish, if you find, if you would find that uh uh find that helpful. OK. Great. And then the last resource I'll show you here is the muzzled resource. So I'm o obviously, you don't have time to talk about Mazz. Perhaps I can do that if I do another talk for med all. But I'll put together another one sheet on identification and management of people with Mazz and MSH in primary care. So do have a look at this if you have some time. OK, great. So Tim, I think we'll just stop there for the, the first section. It took slightly longer than planned, but the, the next two sections are much shorter. So don't worry, we'll, we'll finish on time. So any particular questions you want me to pick up on there? Just Yeah. Yeah, sure. Let me pull up. I've been selecting some out there from the, the chat as we went. So um SME has asked about how different in the difference between a raised alp due to low Vitamin D and or as opposed to the liver disease. Yeah. Yeah. So that I mentioned that that's where it's really useful to check the gamma GT. So if the gamma GT, uh if you've got a high out and a high gamma GT, then think liver, whereas if you've got a high uh gamma G, is there a high out forces and a normal gamma GT, then think bone. So that's where I would then check as she's alluded to calcium phosphate PTH Vitamin D So that the, the, the key is checking the gamma GT alongside the outs. Sure. And, and having the two together um in a similar way, I think we've already kind of covered this in regards to what levels of abnormal A should we discontinue statins? Yeah. So generally up to three times the upper limit of normal. I'm not worried at all. My hepatology colleagues are not worried at all. So just crack on atorvastatin 2040 up to three times the upper limit of normal. No worries. That's our cut off there. I added this question just as a little comment to see your thoughts, the names of these things getting ever more complicated. Ok. Uh The names of, of drugs. Oh, yeah, you're not kidding. All, all these new acronyms, I know it's a, it's a, I know sometimes it, it, it, it, it, it just feels like a headache, but actually I've gotta be honest, I do agree with the renaming of it just to hammer home that it's a metabolic disease and not indeed a, a AAA liver, primarily a liver disease. Yeah. Yeah. Sure thing. Um Again, I guess we kind of have covered this as time has gone on but should all patients with abnormal LFT S be subject to ultrasound in the liver. No, absolutely not. No, no. I mean, we've got to use, I mean, I don't know about the colleagues on tonight but if I, if I was to request a routine ultrasound, that would be potentially up to six months anyway. Um, so, but no, not everyone with abnormal LFT S. Remember I started with a statistic, the majority of people with abnormal LFT S will not have underlying liver disease. So, absolutely, I'm not advocating requesting everyone but there's some basic investigations we can do targeted liver screens, other tests that will, you know, ee either help us diagnose any underlying cause or uh maybe push us towards requesting uh an ultrasound scan here. I'll ask a quick one here from Idris as well. Um I think we may have touched on low albumin and low clotting factors, but at what level should be, we worried about low liver function rather than raised. A lot of what we focused on has been sort of raised. You know, I suppose it's the synthetic function. So the the albumin is the main one. If I go back to that, the albumin is a way if you've got a persistently low albumin, um then you know that, that, that is worrying that might be a uh an indicator of poor liver synthetic function. Uh again, rule out those other conditions, but I in terms of low test, you know, low LA LT, we're not worried about low A. If I go back to the beginning ones, no alt, low ast, low gamma GT, we don't need to worry about um, similar with fo and bilirubin. It's really the, the, the synthetic function, the albumin and the platelets. If they are low, these are signs of potentially advanced liver disease. Sure. In the interest of time, Kevin, I'm gonna, I'm gonna take two more quick fire ones and then we'll, we'll let get on to the next side. So we chatted about statins. But what about Metformin? Putting liver function tests off? Uh Metfor? No. So Metformin is not typically associated with uh abnormal LFT S. So, and in fact, Metformin can be helpful in, in NASL or NAFLD because of that insulin resistance. So, um uh AAA again, I would use that same rule of thumb if the LFT S are even up to three times the lipo normal, just crack on with the Metformin. If the LFT S are over three times the normal, that individual needs further investigation. Sure. And lastly from far, the, is there a specific test for Gilbert? We know it's genetically inherited but is there anything we can do to? Yeah. II, I'm not sure if there's a genetic, I'm sure there must be a genetic test but you can check for, you know, conjugated or unconjugated bilirubinemia. If you are not sure if this is Gilbert, maybe you want to exclude, you know, hemolysis or, or well, not hemolysis, hepato biliary obstruction. And then you can actually, you can do conjugated or unconjugated, uh, tests, uh, urine tests. Yes. Brilliant. Fantastic. I think Kevin, the interest of time, I'll keep the other questions that I had on there, but I will, we can move on. Ok. Good stuff. So, we've got Hugh. Next, Hugh is 72 years old. He came to see me in surgery because he had not been feeling quite himself around three weeks now, headache and pain in his left knee. And this was on the background of generalized moderate osteoarthritis predominantly affecting his back and his both of his knees. No sy uh no, nothing on systemic inquiry. Fairly cursory examination, to be honest, was unremarkable. So I checked his bloods, his FBC, his LFD S despite I've just what I've just told you, I ticked the LFD volts. His S were all normal and I checked his inflammatories markers. His E sr was 35 and his C RP came back at less than one. So, ladies and gentlemen, what do you do next? And a number of options here? And Tim will pull up in a pool in a minute. Do you look up, raised D DSR on GP notebook before realizing you've used up your, your financials pages nightmare when that happens or more seriously? Would you check a myeloma screen? He's 72. He's got nonspecific symptoms or are you wondering whether this might be possible, polymyalgia, rheumatica. Would you try the steroid? So, oh, are you worried about possible GCA a giant cell arteritis, temporal arteritis. Would you refer urgently to rheumatology for a temporal artery biopsy or would you arrange an abdominal ultrasound to exclude renal carcinoma? Or you're not so worried about that? Esr and would you just wait and see if he develops any symptoms? So, what are your thoughts here? Ladies and gentlemen. So lots going for six. I see Tim, which is great. Yep. About 63% 68% ever rise and six seems to be your most popular out. Good stuff. So let's talk, ladies and gentlemen, this is a, a quick section here on use of E SR and C RP in primary care because these are over requested as well in primary care. You can see here over the last 15 years. E Sr and C RP requesting have gone up like that because they're commonly requested, aren't they in primary care for diagnosing and monitoring of inflammatory conditions such as polymyalgia, giant cell arteritis infections, autoimmune conditions and also to rule out cancers. Ok? And, and often both, pardon me, often, both E Sr and C RP are checked and this just generates more workload for us, doesn't it in primary care? Because sometimes you get results like we've just seen for you a higher E SR or a normal C RP or a vice versa. You also see lots of false positives with inflammatory markers leading to more appointments, repeat tests and referrals. So let's start with which is better E SR or C RP. I'm surprisingly there's little evidence comparing E SR head to head to C RP. But and there's always that principle is guiding principle is treat the person not the number. So let's start with E sr. So someone's already pointed out in the chat box, the rule of thumb for upper limit of normal of the E sr and this is what I used as a medical student all those years ago, for women is age plus 10, divided by two and for men, it's age divided by two. So he is 72. So actually the upper limit for normal for him is 36. So actually 35 may well be normal for him. OK? And again, as someone's just pointed out in the chat box, E sr is affected by a number of other conditions. So we've mentioned gender and age pregnancy, temperature, certain drugs, aspirin, anticoagulants, smoking status, plasma protein concentration and red blood cell concentration as well. Now E sr in contrast to C RP rises relatively slowly over 24 to 48 hours and then decreases even more slowly taking weeks and weeks to normalize. So we need to be aware of that when interpreting results, we need to be aware in particular of an E SR over 100. If you see an E sr over 100 there's a over 97% positive predictive value for underlying significant illness. So that means if you see an E sr over 100 there's a 97% chance that individual has a significant underlying disorder. And the three key conditions to rule out are myeloma renal cancer and giant cell arteritis. Ok. So in the past, I often checked E sr for suspected myeloma as I've just, you know, told you. But actually when you drill down into the evidence, evidence suggests, yes, E sr is better for myeloma, particularly over 100. But if we suspect myeloma, the best test is protein, electrophoresis or urinary Ben Jones protein or indeed both. So that's definitely changed my practice. If I suspect myeloma, I'm not checking any sr I'm checking the protein electrophoresis and urinary Ben Jones protein rheumatoid arthritis. Another condition I often check E SR and or C RP. But the nice rheumatoid arthritis guideline clearly tells us if we clinically suspect rheumatoid arthritis, bilateral small joint arthritis, evidence of sinusitis, we should be referring urgently even with normal inflammatory markers. Ok. Because early dmard therapy is pivotal, isn't it to prevent the progression and the development of complications of rheumatoid arthritis? Ok. What about C RP then? So in contrast to ES RCR P rises much more quickly in a response to any infection or inflammation often within 12 hours and the half life of C RP is 12 to 24 hours. So, roughly you would expect your C RP to half every day and eventually normalize after 3 to 7 days. And an advantage of C RP, it's not affected by the multiple factors. I've just told you gender age pregnancy, et cetera. And another useful role of C RP is to check if a ferritin is truly elevated and I'll be coming on to iron studies in the last section. So it can be uh worth checking ACR P alongside ferritin. Ok. So let's talk about some of the evidence of checking E SR and C RP in primary care and whether it adds value to our ongoing management. Ok. And spoiler alert, the answer is no. So these were recent papers published in the BJ GP just in 2019. So just about four years ago, two large observational studies comparing the accuracy of C RP versus the diagnostic accuracy of E SR. And also importantly, observing whether checking both C RP and E SR together improved that diagnostic accuracy and in a nutshell, what did they find? There was little difference in the accuracy of C RP versus E SR. They found perhaps that C RP had slightly superior diagnostic accuracy for infections but was equivalent for autoimmune conditions and cancers. And generally, the authors of these studies concluded they felt CRP should be first line test. Uh If we are gonna use an inflammatory marker. And what about checking both together? Did that help us in primary care? No, testing multiple inflammatories simultaneously. Both ESR and CRP did not increase our ability to rule out disease. Unsurprisingly checking both together resulted in more abnormal and discordant results of one high, 11, low one and more costs because of more tests. And interestingly and quantitatively, they found that the negative predictive value of a single test or either E SR or C RP was similar to the negative predictive value of doing both tests together. So no clear advantage of doing uh both together. So that's definitely changed. Me and my colleagues practice, we never checked both together and to be honest, we are checking much, much less er inflammatory markers in primary care. So overall, the authors concluded inflammatory markers have a low accuracy for disease outcomes. With the notable exception of polymyalgia, rheumatica. Ok. And inflammatory markers overall have poor sensitivity and we should not use them as a rule out test. We need to potentially use them alongside our clinical acumen our history and also our examination findings too. And if that's not enough, look at these figures for every 1000 inflammatory marker tests performed in primary care, anticipate 236 false positive results, generating an additional 710 GP appointments, 229 phlebotomy appointments and 24 referrals in the next six months. So, II did this mini presentation for my colleagues in North Berwick and it really hammered home that a lot of us were over requesting inflammatory market tests and it was having a bigger impact on workload but also on resources too. So well worth having a look at that in your own time. Ok, great. So to finish this exam, some key take home messages. Normal inflammatory markers are useful really in ruling out a few specific conditions, polymyalgia, giant cell arteritis, myeloma and interestingly, infection of hip revisions. Ok. Raised inflammatory markers are very common in primary care. And of course, they do increase the probability of a condition being present, present. But we need further investigation from history and examination. And overall in family markers are just too nonspecific to be a useful tool for diagnosing serious underlying disease. So if we do find reason, the markers incidentally like I did for you and no obvious clues from the history or examination, absolutely. Take a wait and see approach that said if you see an E sr over 100 that's persistent. The likelihood is of an underlying condition is much higher, 97% positive predictive value and we should take a focused history examination and further investigations as required. So really the key message of these studies, we should not use inflammatory markers to blindly fish or reassure ourselves. This is just gonna create work, false, false reassurance and over investigation. Ok. So what happened to you? So I saw those bloods, I phoned you to discuss his results. His headache had largely settled actually, but he was still feeling just not quite himself but certainly nothing new on history. No new red or yellow flags. So we just took a watch and wait approach. I checked in him again on a couple of weeks and actually he continued to improve over the subsequent two weeks without any further treatment or further investigations. And I did not repeat his bloods. So I'll finish with a, a lovely quote from Voltaire, er, very relevant to you. The art of medicine consists in amusing the patient while nature cures the disease. Great over to you, Tim for some quick questions and comments there before I finish off with iron studies. Fantastic. Kevin gosh. That saying from Volta just kind of hammers at home, doesn't it? It really does. Right. Let me pull up another couple of questions more to do with the C RP. So, um Abigail has asked, let me just get down to it. What way is, er, affected by the red blood cell count? Yeah. So if you have an elevated red blood cell that can artificially elevate your E sr it can because it increases the viscosity of the blood. Yeah. Sure. So it's just a case of keeping an eye on that. Um Vij has said about esr potentially being elevated in obesity alone. Have you heard of that? Or any thought obesity raises a number like you get a persistent neutrophilia as well. Um, with obesity as well, you get elevated neutrophil count. So, obesity can cause a number of blood abnormalities and rightly to point out including e sr sure we'll take two more. Um, Jessica before we had kind of concluded on what actually happened with you was saying about with the nonspecific back pain with a myeloma screen. Have been a reasonable, I think it wouldn't have been reasoning if we go back to Hughes case study. I suppose it's all in the history and clinical examination. I mean, when I uh sort of assessed him and as I said, it was a fairly cursory examination, my gut feeling just didn't say say myeloma to me, but he is 72. Myeloma often does pre present very non specifically. So, no. Absolutely. I think checking a urinary Ben Jones protein and or protein electrophoresis would have been quite justified. Absolutely. Yeah. And I think looking back to the uh to the poll, I think uh to be fair, Jessica, the second most popular answer was that um myeloma screen. Um So, and last one for this section Soni has said about using ASR to monitor treatment response for polymyalgia. Yeah, it's a great question and I should have mentioned that earlier on. So actually, a big change in my Edinburgh guidance is we no longer use E sr to monitor polymyalgia. We use C RP. So II, I'll, I'll uh you know, so I'll start start steroids, prednisoLONE, 20 mg, you know, titrate that down down to 10 and then every 4 to 6 weeks. I'll check ACR P to see what level of inflammation there is for the polymyalgia. So that's what I use. And certainly everyone in Edinburgh uses to monitor uh um polymyalgia. Uh C RP. Not E sr Fantastic. Ok. We will pause the Q and A there and let you go on to the last section. Gavin. Great. So it's 825 Tim. So, unfortunately, I think I'm gonna, I'm gonna run over just by about fine, fine. I I'm sure people will not be annoyed just with those questions. Ok. So Oscar is my last patient. Uh another one of my patients in North be he's 53 years old. Um He came to see me because of a three month history of fatigue, lethargy, joint pain and what was bothering him most was loss of libido as well. Ok. Just no desire um to, to have sex with his partner. He's been living notably with type two diabetes for three years. Um I checked a few other parameters. His BM I is 31. His BP is 100 and 4987 blood pulse, 72. Again, a fairly cursory examination. I was running pretty late to him. So, but nothing, nothing of note on examination. So I just checked a stack of blood for him and his FBC, his UF U NE LF DST FT S were all normal. I did a lipid profile. His LDL was 3.5. His HBA one C was 55 millimoles per mole. And I also checked a ferritin because as I mentioned already, hemochromatosis is more common in Scotland. And those presenting features did make me think could this be possibly hemochromatosis with the joint pain loss of libido sexual function? Ok. And his ferritin came back at 612. Normal range in my lab is 20 to 300. He's on his Metformin and atorvastatin though he did admit to me, he does take them somewhat sporadically. He works in construction recruitment. He's a nonsmoker. And in contrast to Ka, he did freely admit to me that he drinks regular and liberal amounts of alcohol at probably at least 40 units a week. So last two questions for you, ladies and gentlemen, what do you do next with respect to Oscar's blood? Particularly that ferritin value? Would you check fasting iron studies? Would you check C RP? Would you check a full liver screen or a couple of you have typed that in already? Do you suspect hemochromatosis? Would you go on and do a genetic mutation screen or would you explore the sexual dysfunction? Check his gonadotrophins, LH FSH and testosterone in view of his loss of libido. So, should we stick that pull up there? Fantastic. So what do you all think? So, I see a few of you have typed in your answers already, which is great, but some of you wanna answer the pool as well. So we've got uh yeah, some people are already put in polycythemia. So, oh, that might be the previous. Sorry. Yeah, hemochromatosis. So, and check for gene good. Um Three check for liver screen fasting iron studies. So, a real mixed of answers, isn't there? Tim? Yeah, a very, very, very mixed slightly out in front of the hemochromatosis. Great. And that, that reflects real life. We'd all do things a wee bit differently. Wouldn't be in primary cares. GP nurses and pharmacists. So here's the $64,000 question. Then what do you think is going on then with Oscar? Do you think this is liver disease? Is it muzzled? We've already talked about, is it alcohol related liver disease? He is putting away at least 40 units a week or is it related to his type two diabetes and his metabolic derangement or is it hemochromatosis as some of you have suggested? Or do you think there is something uh hypothalamic going on? Is this hypogonadotrophic hypogonadism? So, what are your thoughts here, ladies and gentlemen. So a few of you have already said hemochromatosis. So that's great. Anyone think it could be one of the other conditions? So, hemochromatosis coming in highest with alcohol related liver disease in second place. Good stuff. Ok. So now in the last seven or eight minutes, I'm gonna talk about interpreting iron studies in primary care and I'll focus on those high ferritin levels that Oscar has. So we've had a number of papers published in the BMJ actually, over the last seven or eight years, really helpful. And again, another test we commonly take in primary care uh to investigate iron deficiency, the possibility of iron overload and also to screen for hemochromatosis. So let's start with what iron studies are. So, first of all, we have ferritin. Now, ferritin is your intra storage form of iron and it's your best investigation for iron deficient anemia. So remember, a low hemoglobin, a low M CV is not diagnostic of an iron deficient anemia, but a low ferritin is diagnostic of an iron deficient anemia. That said as we all, I'm sure are aware, ferritin is an acute phase reactant. So it goes up in any sort of an infection or inflammation. So we'll talk about how we manage that uh in in in the context of ferritin levels in the context of infection just shortly transin. On the other hand, is the main transport iron that control levels of free iron. So if you've got lots of iron in the body iron overload, then you need less transferrin don't need because you need to shift less iron around the body. Whereas if you are iron deficient, your transferrin levels go up because you need to transport more iron around the body. Serum iron is simply the amount of circulating iron bound to transferrin. However, this is a poorly uh it's not a very useful test, highly variable it, serum iron varies on what you've eaten or drink for drunk, for breakfast or particularly things like orange juice. It, it's affected by infection and inflammation too. Transferrin, unsaturation. On the hand is a very helpful test because it is the proportion of iron binding sites of transferrin that are occupied by iron. So it's actually our best test for iron overload. So if we are looking to exclude hemochromatosis, which most of us are, that was the first test, I would look at what is oscar's transparent saturation. If it's over around about 40 to 50% that's suggestive of true iron overload. OK. So some tips on requesting iron studies. Now this is something that I was only aware of about four or five years ago. Iron studies should be measured only on a fasting morning sample. So this came into our ice request system just a couple of years ago when I take iron studies, a reminder comes up to tell me fasting morning sample required. OK. And that's because as I mentioned already what we eat or drink can affect serum iron. And secondly, like many blood tests, iron studies should not be tested during acute illness because in acute illness, you normally get consumption of iron by cells. So iron levels may fall. So similar with thyroid. OK. So do not check iron studies during any sort of acute illness. Some on the top tips here and I've mentioned this one already. Do not assume all microcytic anemias are iron deficient anemias. You need to check a ferritin. Ok. And if you do find a low ferritin, then that is indeed diagnostic of an iron deficient anemia. However, as I've said already, if you have a normal or high ferritin, that does not exclude iron deficient anemia because as I've said, ferritin is an acute phase reactant if you have any infection or inflammation that will send your uh ferritin up. So, what do we do in this situation? Well, if you do have a microcytic anemia, but a normal or high ferritin, then check iron studies and also ACR P. So if you have a low serum iron and a higher transferrin, then that is diagnostic of an iron deficient anemia. Ok. And as I said, useful to check the CRP as well if you have a high ferritin because um if you have a normal ferritin, um uh sorry, a normal that excludes any significant infection or inflammation, doesn't it? So, just some top tips there on interpreting iron studies. So I did that for Oscar. I checked his iron studies, his fasting iron studies and his serum iron came back at 30 his transferrin came back at three, his trans saturation came back at 30% and his C RP came back at less than one. So, what are your thoughts? Ladies and gentlemen, on his iron studies, on the basis of what I've just talked you through abnormal normal. Don't know, normal. Alistair said normal. Absolutely. He's got normal sight in particular. I wanna see his transferring saturation because we were all worried, weren't we about hemochromatosis? But his transferring saturation is 30%. So, completely normal CRP is also normal. So that means his ferritin is a truly elevated ferritin, isn't it? It's ferritin was 600 plus. So what does that ferritin mean? And that's what I'm gonna take you out, uh take you through just now. So this is a little table I put together and don't worry, I've got a resource I'll share with you in just a second. Um That guides us through what we might see in various conditions of iron deficiency or iron overload. OK. So in iron overload, which we all suspected you would expect a normal or high M CVA high ferritin, which Oscar does have high serum ferritin, low transferrin and a high transferrin saturation. But he, as we discussed, have got normal uh uh study. So what is causing that? High? Um ferritin and a lot of you have already put down some really sensible suggestions, acute illness. Um uh I know I said it's likely metabolic. I think I'm with you there. I think it's likely it's type two diabetes, metabolic dysfunction. But let's talk about that in a bit more detail. Now, so once again, a normal fasting transferrin saturation usually excludes iron overload. It has indeed for Oscar, hasn't it? However, if it transparent saturation was up then. Absolutely, we should consider primary iron overload or hereditary hemochromatosis. So generally, we should consider a genetic mutation screen if your ferritin level is up and your transferrin saturation is above around about 45%. That will vary from lab to lab. But also don't forget about secondary iron overload. Has also had a recent blood transfusion. Has he had a recent IV iron infusion? Is he taking over the counter iron supplements or indeed, are you prescribing him iron supplements or has he got rarer conditions like a chronic hemolytic anemia or that medical school diagnosis? Porphyria, cutanea, tardia, never seen that or heard of that since medical school. So, uh the bottom line though is for people like Oscar, 90% of those with high ferritin levels will not have iron overload. Most are reactive high levels secondary to as your colleague very correctly said metabolic dysfunction or type two diabetes can also be reactive to liver disease. So, fatty liver disease, he probably has males as well, doesn't he alcohol excess, which he also has has thyrotoxicosis, any sort of acute and chronic inflammation, malignancy, renal failure or any acute cardiac event as well. So you can see a number of causes of this high, potentially high ferritin. Our hematology colleagues though are quite clear, we should consider hematology referral for further investigation if he has an unexplained serum ferritin, that's persistently above 1000. Ok. So do have that uh in the back of your mind because if you have a persistently unexplained ferritin over 1000 higher risk of underlying malignancy. So, to finish off, then, ladies and gentlemen, what happened with Oscar? Well, his iron studies were normal, so I've ruled out iron overload. So I didn't do a hemochromatosis gene assay. As I said, I felt his ferritin was lightly reactive to alcohol, uh and his type two diabetes and metabolic derangement. So I reinforced all all important lifestyle advice and I'm gonna hone in on his type two diabetes and alcohol er excess. And I'm gonna just simply repeat that ferritin perhaps a few other liver tests, hepatitis serology, et cetera, 3 to 4 months later. So a quality improvement activity for us all, a couple of them. First of all is serum ferritin used routinely in your practice as an investigation for iron deficient anemia. Remember a low M CV microcytic anemia is not diagnostic of iron deficient anemia, but a low ferritin is indeed uh diagnostic of an iron deficient anem. And secondly, if we are prescribing iron, and I think I mentioned this last time. Big change in practice for all of us. No need to prescribe iron three times a day. Our patients never took it anyway, one tablet daily or indeed one tablet every other day is more than sufficient when prescribing iron therapy. This has been a hugely positive change to my team's clinical practice and indeed our patient's compliance with iron. Um and that's because if you take even more than one tablet of iron a day, your liver produces something called hepcidin. And what hepcidin, then it actually prevents further uh gastric absorption of iron. So it's your body's way of preventing iron overload. So, my hematology colleagues are quite clear one tablet daily of iron or indeed one every other day. Ok. So I put together one sheer on this too, interpreting iron studies in primary care, er that table I showed you interpreting iron studies and also um the flow chart for managing these serum ferritin levels in primary care. Ok. So I think that pretty much brings me to the end. I did notice someone made a lovely comment about uh my, my GP notebook podcast. II moved on from GP Notebook, but you'll be glad to know, I think you'll be glad to know. I have launched a new Pod for, for Medscape. It's a global podcast. Um I just launched it about a couple of months ago and II just had a new episode go live a few, few days ago on non visible hematuria. Uh the the Prints of the Urology Wall, what we previously called microscopic hematuria, how we manage that in primary care but not done a number of general uh GP topics. So please do do have a listen, it's available on the Medscape website and also on Spotify as well. It's called Medical Mental Great Tim. So that brings me today I'm sorry, I just ran over by eight or nine minutes there. I thanks everyone for, for listening. Hear my contact details. Happy to share my slides as a PDF if you want to email me or if you have any other questions or comments. So I'll hand back to any questions on that last bit on iron Studies. Everybody by the I do not think there's a single person in the worried about it. Everybody to have that so much as II have to say, can I put two quick questions to you about the iron? I'm happy to stay on as long as you need me to. Um an interesting question just from Claire about a persistently raised mean cell volume but normal iron studies b12 and foliate that macrocytic anemia. Could it be alcohol? I was just teaching, I don't know if any of you were at the pulse conference in Birmingham earlier this week, I was presenting there on the full blood count. Uh and yeah, ma and macrocytosis. So, er yeah, so the blood definitely do a blood film uh because uh blood film, I suppose if you've ruled out all the usual causes and you've done all the right tests, there could be alcohol but rarely it can, can be a bone marrow disorder, particularly in an older person. So I would definitely check a blood film uh to rule out any uh particular abnormalities. Um and, and, and some of the other certain nutritional. It can also be drug induced as well. So, I'd be interested to see what their regular medications are. A number of commonly prescribed drugs that can cause a, a macrocytosis as well. Sure thing. And, and the last question we'll take, I think for this evening, just from Ahmad. Um, how long? It's a great question. I think everybody's advice is different. But how long should we be prescribing iron for there? Personally? Doing sort of 3 to 4 months then recheck. And does that seem reasonable? Yeah, that seems reasonable. I put on my iron resource here. There's the red box in the bottom left management of iron deficiency. So I talk about what nice says, but we can be here normally, you know, it takes at least a couple of months to be back, replete in iron again and then I would normally sort of recheck it if we're back in the, er, the right direction or near the normal target range. Absolutely. I think it's reasonable to continue it for another couple of months. Reinforce that with dietary advice and then, and then stop the iron therapy. But I, I've definitely found now that I'm prescribing it once a day is much, much better, less constipation, of course, as well. Um, so I'm seeing much quicker improvements, to be honest in ferritin and full blood count. I am so ready to change my practice. Obviously being an F one, I'm still working in hospital and I'm looking forward to going in and cutting all the cards down to. It's very, you know, I know we're very good at starting medications in primary care. But absolutely, what's more satisfying is stopping medications? Absolutely. Um, folks, I, on behalf of everybody, all 380 that there were at one point. Absolutely remarkable. Kevin extended absolutely huge. Thank you once again for such an interesting, um, in, in every single way Interactive. Absolutely loved it. Really, really great. Um I'm going, I'm going to let Kevin's contact details, stay on the screen there. A couple of links earlier on in the chat, I popped one into Kevin's youtube channel. Um I popped one in for a couple of other things, so please check those out as well. Um I come in to you again about the, the metal app. You can fill out your feedback form on there and get your certificate for um tonight's event and we take that feedback. Believe you me, we listen to it. I've been reading through feedback trying to plan for future middle primary care and I certainly hope Kevin we will have you back again in the future. Everybody loves to see you as do we really appreciate your help. We will get the slides up. Um Kevin has said he's more than happy for us to share his slides and the resources there and the recording from tonight, we will get up over the next couple of days as well. So, um without any further going along, we will close down tonight's session and say another massive thanks to Kevin. Kevin. Really appreciate it. Thanks very much. Thanks everyone for joining me. Much appreciated. Fantastic.