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Hi, my name is Navina. I'm one of the doctors working in um Nottingham Trust. Um I'm just going to teach about liver function tests how to interpret it. Um and hepatitis as well. And this is sort of more for the MSR exam. Um So hopefully by the end of this presentation, you'll be able to interpret the liver function test and the Hepatitis B screening bloods. So I think it's important that when we um to, to just categorize the liver function test. So first, when you look at the enzymes, you sort of need to conclude whether it's hepatic in nature. So the predominantly the at or the AST would be rise uh um cholestatic in nature. So the AP or the GGT would be raised all mixed. So you can't see if either the at or uh which one is more raised basically, then you're going to see the synthetic function and and this sort of comes down to what the liver does. So the liver produces clotting factor. So you look at things like platelet, you look at your promin time. So platelet production would be reduced, promin time would be raised and then you look at protein. So albumin and total protein would be reduced in someone who has got sort of chronic liver disease and bilirubin production would be increased as well. Um And then you also do the noninvasive liver screen, which includes the ultrasound scan. And then so someone who has deranged liver function test, it could be due to uh metabolic syndrome. So you do fasting lipid profile or HBA1C and then there's autoimmune conditions. So you do immunoglobulins, autoimmune screen and the celiac um screen and then there's infection. So you check hepatitis screen HIV screen and then things like hematochromatosis. Um So you check for ferritin, but ferritin is also an acute phase reactant. So it's not very reliable. So usually if ferritin is the range you go on to do iron studies and then you do ceruloplasmin or copper. However, ceruloplasmin or copper is usually used to diagnose Wilson's disease, but it's only it, it usually happens to any. So people who are under the age of 40 so people who are over the age of 40 wouldn't test cop plasmin or copper. So just breaking down the liver function test. If someone has predominantly raised ast more than the alt, then you think it's either alcohol related or it's an advanced fibrosis. If it's at, that's much higher than the AST, then it's hepatitis. If it's AP or GGT that's raised, it's cholestatic. So it's extrahepatic. So you think it's biliary in origin, it could be obstruction, infiltration or congestion. Um And then the antibodies I've just focused on the ones that have um repeated questions on. So, the antimitochondrial antibody would sort of make you think that it's primary biliary cirrhosis or the anti neutrophil cytoplasmic antibody that would make you think primary sclerosing cholangitis. And then you've got immunoglobulin. So you have got the IG M which you would think primary biliary cirrhosis iga a alcohol and I GG autoimmune diseases. So, here's the first question. So in this question, if you look at the blood test, you see the AST is raised as well as the alt, but the AST is much higher than the at and the um gamma glutamyl, um the GGT is raised as well. So you, you think alcoholic hepatitis. So in alcoholic hepatitis like mentioned before AST or T would be much higher than the A LT. Um And you manage alcoholic hepatitis with steroids. So the next question, OK. So for this one, so the patient has presented with vomiting, right, upper quadrant pain, jaundice. Um and that he admits to a relapse of alcohol misuse with an alcohol binge 24 hours prior. So the AST is um 260. His A LT is 100 and one. So you can see that predominantly the AST is raised and you know that his synthetic function is also deranged. So the inr and platelets are deranged and the albumin is low. So in this question, the answer is actually steroids. And so I get that it, um the Vitamin K could have thrown people off. But I if this, um thinking that it could be sort of an upper gi bleed, but if there was an upper gi bleed, um they would state that they would give the urea results so raised urea, they would also mention that patient has had um vomiting. They will mention about the content of the vomit, either a coffee ground or a bright red blood. Um So yeah, so that's why this is steroids because it's alcoholic hepatitis. So just a quick tip. So in the exam, I think the most difficult thing to sort of tackle is timing. So I would sort of recommend reading what the question wants first and then going and looking at the case vignette, at least you sort of know what you're looking for and not thrown off by any other information that's given. Ok. So, so for this one, so most of you got it right? It's ascending cholangitis. Um And I can understand why some people put pancreatitis. So I think obviously it could be a chronic pancreatitis. Um but this is a two month history and because they've got the striate of um jaundice, right, upper quadrant pain and fever, you think it's it's um ascending cholangitis. It not many patients with pancreatitis would actually present with jaundice one. And secondly, if someone actually did have pancreatitis, the amylase would be much more elevated than this. So chalco stri ascending cholangitis, right, upper quadrant pain, jaundice and fever. Ok. So this next question. So in a 38 year old woman who's having pruritus and uh jaundice. So you see the bilirubin is deranged. So the synthetic function is deranged and you see that the ALP is much more higher than the alt and they've got positive antibodies and this would be primary bilary cirrhosis because primary biliary cirrhosis would have positive um antimitochondrial antibodies. So, just remember, um, so primary biliary cirrhosis tend to be in middle aged woman and they can present with pruritus jaundice and a PS mentioned before in that case, V and it can be related to um a few autoimmune conditions as well like rheumatoid, uh Sjogren's and celiacs disease. So they would typically have um antimitochondrial uh antimitochondrial antibodies. The M two subtype they'll have raised IgM. So when you test for the immunoglobulins, the IgM would be raised. Um and you treat them with um ursodeoxycholic acid. And what this does is it improves the progression of the disease. So it does, it, it, it slows the progression of the disease and it improves the patient's symptoms and then cholestyramine actually elevates the itching. So when patients have got a lot of pruritis, you can prescribe cholestyramine. Next question. OK. For this question, the answer is um Ursodeoxycholic acid. And the reason why I put this question is I think people tend to confuse between um, answering cholestyramine and um ursodeoxycholic acid. And it's just to make sure that, you know, which would be the management for the condition itself and which if they say what would be the most appropriate management for patients symptoms or to alleviate their symptoms, then you would put cholestyramine, but if it's to manage the disease itself, then it would be seen. Ok, next question. OK. So in this question, they're asking for diagnosis. So when you read the case v yet, it tells you that their alt is a bit high, but that's the only information that they've given, but they've given a list of medication and the patients BMI which tells you that the patient could have a metabolic syndrome going on. And, and if we look at the alcohol consumption, they are within sort of the recommended range of um alcohol consumption. So they have nonalcoholic uh liver disease, fatty liver disease. So with nonalcoholic fatty liver disease, it tends to happen in people who have metabolic syndrome. Um and they can have things like raised BMI, they can have raised triglyceride cholesterol. So they could be on medications like statins or they could have diabetes. So the first line to investigate this is to do an ultrasound. So because these patients can, their liver can basically progress um to have necrosis. So make sure that you do ultrasound and then you can also do a fibroscan to just make sure the extent of the fibrosis and biopsy if needed. Ok. Next question. Ok. So the answer for this question is Wilson's disease. So we read the question as a 23 year old person. So it's less than 40 they have unsteady gait, memory loss. Um, bit of neurological finding and also their liver function test is the range and they've got low copper level that should already tell you that it's Wilson's disease. Now, Wilson's disease means there's increased copper deposition and it usually tends to deposit in, it can deposit in liver causing hepatitis cirrhosis. It can deposit in the the basal ganglia causing dysarthria, dystonia or symptoms like Parkinson's and even in the kidneys. So things like Fanconi syndrome and some of the findings that you can find is the Kia flesher ring. So that is copper deposit in the membrane of the cornea. And you know, how do you test this? You check for the ceruloplasmin blood and copper levels in their blood and it will be reduced because they're being deposited in all these organs and how you treat it. You treat it with penicillAMINE and that is basically a shel uh medication. So it will remove copper. Ok. That's a question. So the answer for this is the anti neutrophil cytoplasmic antibody. So this patient, I think. So if you read the question and it says diagnosis, it's asking for diagnosis and then you see a history of ulcerative colitis um with jaundice and right upper quadrant pain, raised to bilirubin and alp. So you think um it's primary sclerosing cholangitis, which can have anchor. So usually primary sclerosing cholangitis has got an association with ulcerative colitis. They tend to happen in um in uh in a middle age man with um ulcerative colitis. Whereas primary biliary cirrhosis tends to be in middle aged woman. Um So these patients can have basically what happens is they have fibrosis of the intra and extrahepatic ducts. So on E RCP and M RCP, see beating because one area would be fibrosis and the other area would be dilated basically. Um So yeah, they would have Bianca positive. OK. So try this question and then I'll explain the hepatitis bloods, tran's previous hepatitis infection. Um I'll explain how to interpret it, then we can go through a few other questions and it probably makes sense. So with the hepatitis screening blood. So first you look whether a patient has got surface antigen positive. So if they've got surface antigen positive, then you, it's either they have an, so if it's positive, then they have an infection or if it's negative, then they don't have an infection. So let's see if, let's say they've got surface antigen positive. OK. So they have surface antigen. Then you think about the IG M and the I GG forget about the surface and the core at the moment when they have positive surface antigen, if they have immunoglobulin. So I GM is an acute immunoglobulin and I GG is a chronic immunoglobulin. So it's ob race in sort of chronic conditions. So if someone's got I GM positive and I GG negative, that will tell you that they've got an acute infection. Ok. If they have I GM negative and IG G positive, then they have a chronic infection, which means the antigen is still present, but the acute, the acute phase has lapsed and now the body is being able to produce this chronic uh um immunoglobulin to be able to fight the infection. Ok. So if surface antigen is negative, then you think it's either the person has had a previous um infection that there's no more surface antigen, but there might be some antibodies uh or the person has been immunized before. So now you bring in the factors of whether it is surface or core. So if you think about it, if you think of it as two consent, if you think of the virus as two concentric circles, the core and the surface, the virus has to get through the surface, to get into the core and replicate. So if the antibody against the surface is present and the one against the core is present, that means it's a previous infection. So the virus has gone through the surface and the core and and the body has been able to sort of produce immunoglobulins against this, therefore, a previous infection. And OK. And then if let's say the surface immunoglobulin antibody is positive but the core is negative, then you think immunization because the an the um vaccine that we get is for the antibody for the surface. Um I GG that's what we get. So if you think about it is so that basically is to avoid, you give a vaccine and that will produce the immunoglobulin to avoid the virus from getting into the surface through the surface to the cause. So you will have the positive um surface antibody. So now we'll try this question. So for this one, OK, if we break it down, so it's asking for diagnosis. So this person has got a core antibody but the surface antigen is negative. So we go, we go step by step. So if the surface antigen is negative, it could either mean that they are immunized or they've had a previous infection. But the immunization is only against the surface one and it's not against the core. So if your core one is positive, therefore, it is a previous Hepatitis B infection that is now cleared. OK. So the next one, OK. So if we go through this step by step again, so the antigen is negative, which could mean two things previous infection or they've had immunization and then if you look at their antibody, so the antibody for the surface antigen is positive, but they don't have any against the co antigen. So it's not really breached um into the cell to replicate and then produce antibodies. Therefore, this person has been immunized. All right. So today I thought we just a quick quiz adopter of the nice guidelines of how we manage type two diabetics. And what order of medications we use? Thinking about the contraindication side effects as well as the HBA1C targets we should go for. So, just to kick things off, I think to keep it interactive, we'll just start with a question. So you investigate a 67 year old gentleman who's complaining of polyurea and polydipsia, his random blood sugar is 11.6. What's the most likely diagnosis from the options below? Ok. And I think pretty much everyone's got the right response. That's correct. So the answer is a, he's type two diabetic. Um The reason why he's doesn't have impaired glucose tolerance is if your random BM is greater than 11, then you've definitely got um a in the type two diabetic range prediabetes is based on um an HBA1C threshold and likewise impaired fasting glucose. We've got a random BM here. So he's not had a fasting glucose test. And why has he not got modi maturity onset diabetes of the young? Because this is quite a rare thing. Type two diabetics is very common. I'm sure you see a lot of this on the ward and um there tends to be a strong genetic history in MDI. So it's part of a cohort of patients who have specific genetic mutations that interrupt their insulin secretion. And the vignette normally is the patient's a lot younger. We've got a 67 year old gentleman in this question. So he's not quite as sprightly young gentleman anymore. And normally you'll have also, um, phrases such as a strong family, history of diabetes and they tend to be and their investigations to abnormal ketones, ketones aren't mentioned in this, um, questions them. But remember, common things are common. So if you're trying to decide between it, I mean, it couldn't not be moldy but because common things are common, the most likely answer here is type two diabetes. Ok. So how do we diagnose type two diabetes? Um This is relatively, very straightforward but just a quick through um two criteria or two thresholds, you can either of the patients present symptomatic. So these are symptoms, they could have such as weight loss, fatigue, recurrent uti s and they are also and to have abdominal blood sugar levels of which there are three different tests. Um, the most reliable and the most common one and the easiest to remember is probably HBA1C and it needs to be greater than 48 to be considered. If the patient is also symptomatic to have type two diabetes. The thresholds for fasting BM and random BM are a little bit harder to remember. But one thing I remember if any of you guys have been to Asia, there's a lot of 7-Eleven corner shops around. So if you enjoy snacking, you have a lot of snacks. And thus, if you're more like if you have a fasting BM of greater than seven or a random BM of greater than 11, you're more likely to reach the threshold of having type two diabetes. If you're also symptomatic, of course, there's also the idea of impaired fasting glucose and impaired glucose tolerance. These aren't necessarily required to um, give a type two diabetic uh diagnosis, but they are just threshold. Remember. So I think don't focus on remembering these exact numbers, but focusing on fasting BM needs to be greater than seven and and BM needs to be greater than 11. So fasting BM is close to seven but not quite seven. They probably got impaired fasting glucose. And if the oral glucose tolerance test, which is basically the patient fasts and then they have two hours after being given the glucose challenge, it's between seven to and 11, they probably have impaired glucose tolerance and then just going back um for patients the others criteria, if you're not symptomatic, for instance, if you're having a wellbeing test or maybe a patient has a strong family history of diabetes or maybe you're talking looking at gestational diabetes, if the patient is um asymptomatic but have deranged investigations, you need two tests, two samples, sorry. And it need to be of the same test to confirm persistent hyperglycemia and a formal diagnosis of type two diabetes. Um So HBA1C levels. The main thing is greater than 48 you're type two diabetic. But if you are between 42 to 47 you're considered prediabetic nowadays. And this is typically managed in primary care by education, lifestyle advice. And for patients who um are being continuously monitored um yearly with their HBA1C not improving, these patients can be started on Metformin treatment. So you might see patients in real life and possibly in the VT. But realistically, the questions you're going to have in the M SRA are going to be a lot simpler where the um a patient who has H VC less than 40 might be on Metformin. Um But just another thing to bear in mind, HBA1C is not suitable for all age groups. So, um again, that might be a question and be like, what test would you use for a patient with sickle cell disease? Um So such as the hemoglobinopathies, you wouldn't want to test HBA1C to confirm diabetes. So in these groups, you might use um a impaired fasting glucose level or impaired glucose tolerance. Um ok, so moving on the initial management, actually, protective diabetes is always conservative. The classic stepwise ladder we use in medicine. So from conservative to medical to surgical, which isn't as relevant, but the same idea. So we want patient education and some people can just control their type two diabetes without any medication such as changing their diet and exercising more. And nowadays that them Desmond is a structured education program we can use for patients to optimize the type two diabetes. And we also want to ensure there's individualized care. Ok. So next question, a 58 year old female was presented with three months of fatigue and four episodes of UTI in the past six months, her fasting glucose was 8.1. She was convinced on 500 mg of Metformin BD. What would her target HBA1C be fantastic. So I think the majority of you guys have got the correct answer. So our target H A1C will be 48. Firstly, um there is no target HBA1C of 42. But between the ranges of 42 to 47 you would be considered prediabetic. Um So this patient is symptomatic and she has got a fasting glucose of greater than seven. So between those two criteria, she's got diagnosed as type two diabetes and she's already commenced on medication. So if conservative measure fails, how do we manage type two diabetes? We'll discuss on that. But the 3 HBA1C targets we need to know is if a patient is confirmed type two diabetic, the um first starting HBA1C target is 48 millimoles per um And this is the target if the patient at these just managed conservatively on lifestyle measures or they're on single non hypoglycemic drugs such as medicine, uh Metformin, sorry, which is what this lady has. But if they are started on two or more diabetic medications or they started on drugs that causes a drop in your blood sugar, which in this case would be classic would be glipiZIDE. Their target HBA1C is increased to 53. And if medications isn't improving and there may be, they're on triple therapy drugs which we'll touch upon. Next. Their H B1 C targets increases further to 58 millimoles. So there's not a few, not a lot of numbers. Do you remember for type two diabetic management? Just 4853 and 58. Okie Dokes. Our next question. A for 87 year old woman has commenced on Metformin for type two diabetes. So quite similar to the previous question. After two weeks, she complains she's unable to tolerate Metformin due to diarrhea. What would you do next? So I think most of people have got the correct response. So the answer is see to the next question. So we've got a 60 year old female with a past medical history of emphysema and congestive cardiac failure who is complaining of feeling tired all the time. HBA1C of 56 with an EG fr of 56. What management would you give for this patient? The majority have got the right answer. The answer is E OK. So I've created a step wise lider ladder of how to think about type two diabetes, drug management. If conservative measure fails, the first thing we give is always give Metformin unless they've got really impaired renal function but normally you start with um uh reduced dose if they've got reduced E fr and you gradually titrate that up. Of course, the classic side effects are gi upset. So if they're having diarrhea and gi discomfort, you titrate them to modify release Metformin. But the nice guidelines nowadays says for patients who have are at risk or have established cardio um cardiovascular disease, you should also start an SGL T two inhibitor. Once they're established a Metformin treatment. Hence, that previous patient who has a history of um cardiac failure, they will also be started on Metformin plus the Gliflozin. Next. After that, your HBA1C is still greater than 48. Our initial HBA1C target. Despite being on Metformin, you need to increase the treatment and there's very options you can pick and which we can pick. We'll discuss a later. You need to balance the end of the plan of the patient with the pros and cons of each medication. And if their HBA1C target now is greater than 58 millimoles cause you're giving them two or more diabetic drugs. Um then although your HBA1C target at this point would be 53 you need to start them on triple therapy or insulin therapy and if that isn't working, so they're on triple therapy and their H B1 C target is at the higher threshold. Now, 58 what do you do? So you can then start them on what is quite trendy nowadays, one of the G LP one mimetics. So anything in sending glutide? So lerot semaglutide, G LP one mimetics are very much second or in this case, third line drugs, it's not your first option of choice. They act very similar to DPP four inhibitors. They act in the same pathway but just at different points. So if you do start them on a GLP agonist, remember to stop any um DPP four inhibitors you've put them on. And these patients that benefit are the ones who are, have a large BMI. So metabolic syndrome or weight loss would actually benefit general comorbidity such as other things you think about maybe high precision hypertension or hyperlipidemia. And also maybe for those who insulin treatment is not just for such as drivers where D val A have specific guidelines to minimize hypoglycemia causing driving accidents and you would maintain them on G LP one receptors. So these glutide, if you're shown to effectively reduce the weight loss and also improve the HBA1C levels, remember if you're on the fourth tier, now your HBA1C target will remain at 58. So I've just as quickly summarize the nice guidelines. So, and what as I mentioned before, patients who are on Metformin, um That's basically first line for everyone unless they're not tolerating it. And these patients who have a cardiovascular risk. If they're not tolerating Metformin, the first option choice, you use the Gliflozin. If they are able to tolerate Metformin, you do Metformin plus gliflozin. So who are these patients at cardiovascular risk? There's um there's two groups. So those who are established cardiovascular disease or they are established heart failure or they have a high cure risk score of greater than 10%. And these patients with those who want to put them on a statin as well. And obviously, they have established cardiovascular disease, whether um ac A or heart failure, you put them on a higher dose of atorvastatin. Another thing to consider is patients who are diabetic with impaired renal function. So reduced E fr or they have protein urea, you also put them on glia in to improve um their outcomes from a cardiovascular perspective as well. Um And you also of course, put them on an ace inhibitor to minimize protein urea for patients with kidney function disease as well as I just put it aside for lipid modification, any type one diabetics, regardless of the cure risk score, if they're diabetic for more than 10 years or they're bother than 40 years of age and they have the established renal function disease as well. So, diabetic neuropathy. So you got to raise that women to creatin AAC, you also put them on a statin as well. Um So just as a quick summary, I've put drugs, these are the drugs not insulin treatment that patients would be on. So what I've done is summarized it is that on the right hand side are drugs that are known to improve or reduce your weight loss and they're not to cause hypoglycemia. So the classic options are your gliflozin, like we mentioned are good for patients with cardiovascular disease, either at risk or established or you want to reduce their weight because it will actually help with their other comorbidities. Your first option are normally the DPP four inhibitors which are gliptin. So you have to base on the same pathways in the GLP one agonist I mentioned right at the end, but this is sort of a later line option. So firstly, you try them with the gliptin, they work on the same pathways. So the incretin effect especially, especially what happens is when you eat oral glucose um activates incretins being infested in your small intestine which increases insulin cri secretion. So you get that blood sugar in your blood being hoovered in size, you have reduced hyperglycemia. So the DPP um inhibitors basically um stop DPP four enzymes breaking down. So they produce, maintain more incretins and effect. Whereas the G LP one mimetics mimic the incretin effect to artificially produce more incretin. While CBP four inhibitors naturally prevent incretin breakdown. So two drugs that are increasing weight are the sulfurea, the gliclazide and the thiazines. Um So these drugs um are not as popular because increasing weight will be per for your other diabetic comorbidities and self diarrheas is the only one to cause an increased risk of hypoglycemia. So, all again, caution in patients who are D VL E licensing such as HTV drivers because you want to minimize um hypoglycemia as well. Um Sulfon, um thiadiazines increase weight gain by water retention. So, not ideal for patients who also have known heart failure. And there's a risk that's classically in M CQ of patients with bladder cancer. You want to avoid giving these um P pioglitazone et cetera to these patients. And another thing is um microscopic hematuria is a red flag for bladder cancer. So you want to avoid giving these um medications as a second or third line drug to these patients. So you've got a 60 year old with type two diabetes um managed with Metformin dapagliflozin. So he's on two drugs already, but this is actually the first line treatment um because he's got a past medical history of heart failure. So his HB AC is beyond 48. The target that we want is 61 despite good, good compliance. What drugs do you want to give next? Ok. So the answer is B and I can see why people went for Leo but the reason we have not is firstly, we can discount A and C any um anything in that. So th um Thia letta, like we mentioned um is bad in heart failure. So ignore our A and C. Um So then we're left with BC and E. So we've got a right, a large patient. His BM I is 33. So we don't want to cause any more weight gain and sulfonylurea increased weight gain. So we grow at D. So we're left with B and E and like I said, G LP one mimetics or anything in eye, um These are more lateral line options. So we want to go for the DPP four inhibitors first because that's more higher up in a nice slider. And if they're not responding well to B PP four inhibitors as part of triple therapy, we can then consider GLP one mimetics. Thank you very much for your time and likewise, so we want to thank our sponsors um based on your feedback that you really like practice questions, we've been hosting these webinars. So revise Mr Sra offers a 48 hour free trial for those that would like to access their website and pass meds if you scan a QR called how now it's become a beta tester. You can always still get three weeks of free access to any question bank of your choice. And this includes the M Sra. Thank you guys and thank you for joining for that. Goodbye and thank you, Nana as well. Thank you. Take care. Bye bye.