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Interpretation of Liver Function Tests

Aug 26 | 1:30 PM

Interpretation of LFT is crucial in diagnosing few conditions as well as in the understanding of body's overall metabolism. Let's go back to the residency days and brush up on basics of liver fuction test with Dr. Mahadev Desai

[Music] so for today's session on interpretation of liver function test we have sir is a very uh prominent physician practicing in ahmedabad and affiliated with fcg hospital he has over 35 years of teaching experience and ex-editor of the gujarat medical journal and a lecturer and he has been a part of numerous national conferences and we are really very fortunate to have him as one of our in-house doctors so let's start the session with dr mahadev desai and so uh yeah so before that let's start with the polls uh i will quickly uh start with the first poll and let's test your knowledge and see how much how much is it effective for you at the end of the session as well how much you have learned so let's start with first poll uh so the first poll is what is the test of choice for acute liver derangement and there are four options alt serum protein prothrombin time or alkaline phosphatase awesome awesome so we have around 25 percent people voting for serum protein can i make a comment yeah yeah good evening everyone welcome to this uh session on interpretation of the liver function test as i mentioned the liver function test in the command to introduce comma because what we are going to discuss is the overall test that we do for any diagnosis of any liver function derangement or liver diseases the first question i think we need to increase little time because if you read all the questions the 10 seconds are too short a time so it is possible to increase the time to it and we rerun the uh first question itself right maybe there will be some rethink yeah sure that's impossible i will read it or you can take the second question and but give little more time because 10 seconds too short a time uh for the reasons that you have to read these questions and select the options uh yes so so i will rerun the first poll again up for yeah yeah please or you try this timer only after you read out the questions right so 10 seconds are only to select all right or is it automatic i am not sure whether it's automatically called automatic so i will first read the question and then so the first question is what is the test of choice for acute liver derangement and you have four options uh alt serum protein prothrombin time and alkaline phosphatase so now i will be running the poll and uh let's let's run in okay run it again okay so please please uh select your answers yeah it's already increase the time that's good elc stands for the sgpt okay okay so this time we have got a 52 percent voted for alt sir sgp i would not give the answer right now because you'll know the answer yourself right and if we do the test again i'm sure the answer is going to change that much i can give you the second question sure so the second is what is the test of choice for chronic liver disease and we have four options first one is alt second one serum protein third one prothrombin time and fourth is alkaline phosphatase now i'll be running the poll and please uh give your select your answers so we have kept the four answers same for four different situations as you can make out yes so we have 37 percent the maximum voltage that's correct that's correct that's correct yeah awesome we have third question uh third poll is on what is the test of choice for polystatic jaundice and again the four options are same alt serum protein prothrombin time alkaline phosphatase so i will run the poll now right i'm glad that you know most of you know right so my job will be easier or maybe difficult i don't know that's it yeah go ahead the last one uh the last question is on what is the test of choice for acute liver injury and again we have the four uh options ald serum protein prothrombin time alkaline phosphatase i will run the pole [Music] okay so almost absolutely right yeah that's yeah again those who voted for realty in the first questions would now rethink if you rerun the post again because there's a difference between acute liver injury and acute liver function rearrangement that's what we will be discussing anyway i'm glad that more than 100 persons have already attended the poll right thank you so much and i hope we can start the session now right do i start the session monica yeah yes sir please go ahead yeah so good evening friends ah i am going to talk about the interpretation of liver function test and as i have said that i have put liver function test into the inverted comma what we mean by liver function test is this is how i am going to talk about my presentation first will have presentation then you will have question answer session and in between also if the computer feel that somebody has asked questions related to the topic that i am currently discussing we can discuss as well but please do not ask a question for which we are not discussed yet before that a disclaimer i am a general medicine or internal medicine specialist i am not a gastroenterologist i am not a hepatologist or i am not a pathologist so my discussion will be all around the clinical relevance of all these tests right and i will not be giving much of the statistics or the figures rest assured now as i said the first and very first important part is uh the what is the difference between liver biochemistry and liver functions when we ask liver function test it should be testing the liver functions but these are the liver functions liver has got synthetic function that means it produces so many compounds including the proteins and other things we'll be discussing metabolic functions right and the excretory function and the storage functions when we order the lever function place do we test all these things no and then whatever test we do are not always necessarily indicative of liver functions as you can see from the poles right we have got different functions we ask for now what are the functions of the liver that's very very important to understand the liver function is mainly liver is the only site in the body for the production of albumin and liver is also the important side for the production of plotting factors some of them are vitamin k dependent like the fitness factors like factor 2 factor 7 factor 9 and factor 10 are vitamin k dependent factors but there are also other clotting factors right from factor 1 factor 8 factor 7 all are produced or synthesized in a liver liver is also the site for cholesterol as well as the liver disposes of the ldl cholesterol too when it comes back from the circulations and hdl is called an uh scavenger and it helps in reducing the ldl from the circulation then we know liver is the site for storage of the glucose as well as production of the glucose glucose we don't have too much of the quota except probably only for that which lasts for two days and mainly the glucose is stored as glycogen and when your body needs glucose glucose is converted by the liver into gluconeogenesis or glycogenolysis then liver is an important organ for synthesis of thrombopoetin thrombopoietin is one which is responsible for the productions of the megakaryocytes which are the precursors for platelets of course thrombopoetin is not exclusively synthesized in liver like albumin we have other organs like kidney as well as bone marrow itself which is also helpful in the production of thromboprotein but liver is one of the important contributor to the production thermofitting and thereby the platelet productions not only platelet production but thrombopointing also helps in the maturations of the hematological stem cells into the megakaryocytes then the metabolic functions ah whatever that we eat whatever drugs we take are ultimately metabolized into the liver and an efficient liver takes care of all the junk food that we eat and luckily we don't get most of the problems in spite of all these stuff that we keep on taking whether it's medicines over the counter medicines or the food thanks to the ever efficient liver then there is also an important organ for excretion of the bile not only bile along with the bile there are bile salts bile acids that are also excreted and it's a way of excreting many of the other substances then liver is the important organ for the storage of vitamin d vitamin b12 iron glucose and many other these are just the bird's eye view of the functions of the liver there are many more but the important ones that i have mentioned now what we do when we say we have ordered liver function test ideally we should be lying liver biochemistry or liver profile but liver biochemistry when we write right or when we write lft right what we send or what we mean to the pathologist is that what we test is usually the alt ast alt stands for formally used to be called sgpt and sdot alt and ast are the transaminases and when you use alt is an alanine transfer rays when it is ast it is aspartic transferase when we use the word scpt in sjot they indicate the transaminases we'll be talking the next lines so that is one of the most important tests we order where we need to know about the liver pathology another important obviously serum bilirubin whenever we write serum bilubin we must mention not only serum bilirubin but we should mention cinnamon build with total direct and indirect we should also be asking for green analysis wherein we test bile salts and bile pigments like the bilirubin delivered in and bile salts then alkaline phosphate is known as alp is one of the important things to be done as we have said correctly that is for the cholestasis then is gamma glutamine transpect ideas there is also a very important test to be asked for growth hormone time it's a real real important test for the liver functions these last two are the real test that we test the function of the liver the synthetic function of the clotting factors and vitamin k dependent clotting factor so prothom in time is the first prevailing one which gives the idea about the liver functions the others are giving different aspects of the liver functions that we'll be discussing and the serum proteins again is a very important test for the knowing about the chronic liver disease again we'll be talking in little more detail about all these things but that's not enough in practice in fact when we are suspecting liver pathology or liver diseases we need to ask for many more tests these are the first round of tests or when we have clear cut evidence from the examination of the patient or patient has come with few of these reports we may go for the additional test at the first round but usually we ask for the additional test only hasn't been required that test may be the serological test for the different types of hepatitis viral infections or may be test for hemolysis or test for the autoimmune hepatitis or test for a rare disease like wilson disease all those things that will be again talking after we discuss the first round of the test that we order routinely so let's say why do we need liver biochemistry of the liver functions because that is the easiest way or the non-invasive way of screening for the presence of liver disease see the commonest liver disease is zero liver but you can't diagnose with hundred percent confidence cirrhosis of liver unless we do liver biopsy but in fact in practice we don't do liver biopsy i don't remember to have done liver biopsy last 20 years in any patients see liver biopsy can only confirm the presence of cirrhosis because the very worst cirrhosis indicates the histopathological picture of the liver disease diseased liver right but we don't do it unless that patient is plant for liver transplantation so that's why we need some test and this liver biopsy our liver biochemistry panel is good enough to suspect chronic liver is like cirrhosis and even manage only when we are thinking of subjecting the patient for transplantations then only we need to go for the liver biopsy such invasive test so it's a non-invasive test or screening test for presence of many liver diseases right it also gives idea about the efficacy of the treatment that we are giving whatever treatment we are giving for autoimmune hepatitis for hepatitis c or hepatitis b we can measure from the serial estimation of the liver function trace i would again emphasize that one isolated abnormal liver function or the test that we are does not mean anything we need to go for serial test right more than once to come to the conclusion of the possible reasons for that abnormal test then progression of the disease can be monitored by the this liver biochemistry and again it may reflect the severity of the disease right and as we know that there are two different kinds of classifications the child group classifications as well as the male score right that is model for end-stage liver disease these are all routinely used for before the liver transplantations right so this is why we need the liver function test now first and foremost we'll be talking about the commonest test that we asked in the liver biochemistry the alt and ast are the new names for scpt and sdot but still if you see the reports of the patients coming with reports they will either mention only scptn seot or may mention scpt into bracket although alt in bracket scpt so we have to keep mentioning as a pt and sdot because that's what is invoked in the with the pathologies or the technicians otherwise they may ask what is the test you ask for so always know scpt stands for serum glutamic pyruvic acid transaminase and surround glutamic oxidasity trans aminos when we write full form of sga protein as you can see pt they are the transaminases but when we say alt ast they actually indicate what this sgpt and seot are doing alt is the alanine transferase that means it's producing lne and exported by these enzymes and that is why we now talk of elt and ast rather than scpt and seot otherwise they indicate the same thing alt is the one which is commonly asked for if cost is a constraint only ask for alt because that's one which is very important gives idea of most of the liver problems right whether it's acute infections or injury so as for alt cost is a constraint and in very few situations we need to ask for both alt and a alt and asd right the normal values of alt is different in the males and females for males it is less than 50 units and females it is less than 35 and likewise ast also the normal values are different remember these values again vary from laboratory laboratory and the waste and the test or the kit that they use so it's better that you evaluate your reading or your patient's reading along with the normal values given by that particular laboratory they are very sensitive indicators of the hippie cell injury but they lack specificity right if you remember in our polls the last one that we asked the acute liver injury that held alt and ast are useful because these are the enzymes which are present in the hepatocytes within the hepatocytes they don't come out in the circulations unless the liver is damaged so alt and ast arrays only when the liver hepatocytes the basic cell unit of the liver is damaged and the alt and ast the alt is present only in the cytosol of the hepatocyte while ast is present in both cytosol and mitochondria again we don't want to go into details of that and the alt has a longer half-life and that is why we prefer alt or ast in most of the routine situation as i repeat again if cost is a constraint it is better you go for only alp there are very few situations when you go for both in any given time if your alt or asd is more than 15 times of the upper limit suppose we consider 50 is an upper limit zone any values are over 750 or 800 we should think of two important conditions that is acute hepatitis or hepatotoxicity or liver ischemia right if we want to do both right then a few situations when we ask for alt and air ast or sdot scpt and we form find out the ratio of ast to alt sjot to scpt this is particularly required when we are thinking of alcoholic hepatitis if the patient gives history of alcoholic but the patient does not cure but we have some reasons to believe that the patient could have alcoholic hepatitis then we ask for the ratio of sgo2scpt if that ratio is more than two that means the ot is 200 and as if it is 100 or less though so ratio is more than two to one or along with that the gamma glutamic trans peptides which is something that will be talking down the line if that is increased by two times the upper limit of the normal u n is upper limit of the normal uln it should not be unl right so this is where you ask for azure in scpt both and look for or work out the ratio otherwise alt suffice then astlt ratio is also high in hepatitis c with cirrhosis and liver metastases whenever a patient is suffering from acute itc or chronic infections with hepatitis c est is more than the alt and in acute inflammations or cholesterol it is usually alt which is higher so maybe that is where it helps but again as i said only if the cost constraint you go for single otherwise you ask for both then these days we have got the epidemic of dengue language practically now pandemic or present throughout the perennially present in most of the countries in india most part of the india so particularly in dengue fever we always ask for the ast to begin with in the first test or first week itself if the ast is high then we have to watch out for that patience more closely because they are the ones who are likely to go into the complications of drinking like language hemorrhagic fever or wrong use syndrome importantly the normal ast values in the first week is a negative predictive elements i will be happy if the patient ast is less than normal or within normal range in the first week itself so it has a negative predictor to more than the positive predictive value that means if somebody's high and not that he will definitely develop the dengue hemorrhagic fever or dengue stock syndrome but he may stand the chance and that will observe that person more closely but if the ast value are less i means within normal range i'll be happy and will be more relaxed with that patient see these are the five common conditions that lead to elevated alt ast and you can see on the right panel the toxic or hepatic ischemic injury to the liver will have very high levels of sgpt or seot more than say 5 000 10 000 values we'll see only in these conditions in acute viral hepatitis generally we see anything from 500 to 3000 or thousands but in alcoholic hepatitis they are usually range around 100 to 500 but they don't cross usually more than 500 and in chronic hepatitis the values remain around 150 200 and in zeros is contrary to the belief even though liver is damaged but the values are never very high the reason is as i said earlier the tip this sdot and scpt or ltste are within the hepatocytes and in cirrhosis what we get is necrosis apoptosis but the cells are not damaged to that extent that will come into the circulation so this seo tscpt remains fairly uh just less than two or three times the upper limit of the normal in cirrhosis so this is something to remember when the values are very high we think of more hepatic injury or the toxic or ischemic induce the injury and we try to search from the history of the examinations whether the patient has been taking any drugs like the nsaids or the commonly used drugs some of the antibiotics like glybulinic acid amoxicillin combinations or statins or many such drugs that can cause hepatic injury anti-tb drugs right the next very important test that we asked for cerambilic as i said earlier serum bilirubin is asked for with total dielectric indirect but not that the laboratory people do all the three tests what they do is they do the total bilirubin and the direct bilirubin and the total minus direct bilirubin is indirect bilirubin indirect bilirubin is not tested separately in most of the laboratories even though these facilities are available with the laboratories with full satis uh sophistications the normal serum valuable levels the total is up to one milligram out of which the dialogue bilirubin is only 20 to 30 percent in fact if you see the believe in most of the people it should be less than the 5 to 10 percent so less than 0.5 0.05 to 1 milligram so direct bilirubin is the conjugated bilirubin the dielectric itself is a mixture of different types of fragments of bilirubin that is alpha bilirubin beta bilirubin gamma billion and a right we are not worried much about it there's a different source of the bilirubin that direct bilirubin means they are consecutive bilirubin or water soluble bilirubin bilirubin is we know the end product of catabolism of him and basically the when it is comes to the liver it is an unconjugated form and unless it is conjugated it is not water soluble and unless it is water similar it does not come to the body so whatever will be that comes to the bile right for the final disposal is always conjugated below in water soluble bilirubin right the indirect bilirubin is not bound to the it's bound to the protein it's not water soluble so it will not be excreted in the green whenever we get bilirubin in the urine it means it is a conjugated rupin keep that in mind right so indirect bilirubin is derived value as we said from the difference of the total between minus directly repeat the biller beam is very useful for the differential darkness of types of jaundice we know that basically there are three types of jaundice one is hemolytic jaundice second is hepatocellular jaundice and the third is cholestatic journeys out of which the hemolytic jaundice we get the unconsecutive european which is usually more than 1.2 milligram per deciliter and along with that there will be hardly any increase in the conjugate between if we are dealing with the patient of only hippo hematology hemolytic jaundice like say falsible malaria or maybe patients with g6 period efficiency or may be patient having hemoglobin operates like sickle or thalassemia like that right that is the these are the instances of hemorrhagic journeys there is one important condition we should keep in mind if patients say that he has zombies very frequently you can't have journalists frequently unless there is some probably a congenital disorder of the metabolism of the ruby so first person who is persistent or intermittent jaundice whenever he gets fewer whenever he takes drugs he may have bilirubin and that will have been unconscious bilirubin he has no symptoms of hepatitis or typical anorexia no surviving abdominal pain his enzymes levels lts they are all normal so this is a situation where think of an disorder of in her inborn error of metabolism that is gilbert syndrome gilbert syndrome there is conjugation is defective because of the for the font of the proteins which are required for conjugations right so that is what we should keep in mind it's not very common i hardly see one or two questions every year but they will keep on coming and you have to keep in mind that that person if he keeps coming right we should know that he is a patient of gilbert syndrome it's an autosomal recessive disease we don't need any treatment except knowing that these are the patients who can have persistent jaundice which is an unconscious vitamin they will not have obviously any biosurvival in their urine because in unconscious between their enzymes levels will also be normal the hippie solar obstructive journeys both will have increased conjugated bilirubin and there comes the question or concept of delta bilirubin some of the laboratories give the breakup of the direct bilirubin into the conjugated bilirubin and delta bilirubin so what is delta b before that if you have a doubt between the obstructive jaundice and ebersolar jaundice we need to ask clinically some of the symptoms like whether the patient is having symptoms of because of the presence of bile salts into these substance tissues right these pruritus is one important symptom we keep in mind for obstacle jaundice the another symptom is the statoria isn't complaining of powell smelling wealthy voluminous tools which float in the commode that is typical of the male absorption because of the undigested fat so that is very important for symptom of obstructive jaundice where the patients will be having yellow urine and pale stones well hipper solar zone is there can be cholestasis because of the inflammations in the builder canaliculi but they usually they can have there is no question they do not have it but the other features will differentiate that will come together that alkaline phosphatase which will be the next line will be able to help us in differentiating the hepatocellular and obstructivity on this and of course we have other tests like sonography another test but what is delta between delta bilirubin is a type of direct bilirubin or a conjugated bilumin which is attached to the protein or albivin so this is one bilirubin which is attached to the protein that so it's a kind of bili protein when it is attached to the albumin it has a long half-life because the protein is long half life protein half life is anything from 14 to 20 days and that is why it stays in the circulations it remains into the liver or specifically in the biliric and alkali for a long time so that's where it's important is if you see a laboratory reading of somebody who has a bilirubin of five out of which four is delta bilirubin a rest testosterone and if the patient is otherwise improving so delta rubin delta bilirubin suggests that patient has cholestasis or it takes time for the bilirubin to clear but that patients urine bile salt bile pigments are absent that means they have no bilirubin urea but their bilirubin is high there's clearance yellow the patients and the relatives are worried that why this jaundice is not cleared when his appetite has improved his enzyme levels have cowed up so this is where it is helpful or that is where the importance of deltoid will be bilirubin is one which remains for a longer period right but otherwise uh you can know that the patients who have got a delta balloon but is otherwise improving rest assured convince the patient reassure them that you are going to be fine it's a delta milibean which is going to take time to clear then the next is yeah any questions monica yeah please shall we uh discuss there are a couple of questions related to sure sure sure yeah yeah sure sure so uh there is this one uh by satya narayan he asked about difference in alt and a asd see that's what i say that alt and ast but these are both the enzymes uh which are required for the conversion of alanine and aspartate to pyruvic acid and oxalic acid these are all different enzymes which are required for the crave cycles urea cycles ultimately they all produce the atp atp for the productions right so these are the different enzymes for the carrying out different functions but alt remains into the cytosol in the within the hepatocytes there are cytosols there are cytoplasm and there are mitochondria the ast is present in the mitochondria and again it's too much of detail but if somebody wants to know more details the mitochondrial ast and cytoplasmic cytosol astr again different right and that can be done by very specific test which is not required in most of the situation so alt that's why i said to begin with that if cost is a constraint or if you just want to give the screening test ask for only alt unless there are specific situation like alcoholic hepatitis or dengue fever or hepatitis c known as heat itc then only you ask for alt and asd both and go for the ratio right otherwise you don't need both tests because they both indicate the same thing that it is a injury to the hepatocytes which is more common in viral hepatitis which is more common in drug induced hepatitis and is more common in acute ischemic injury that means if the patient is shocked heart failure hypotensions right uh polytrauma they're all we expect the sapd to be very high seot to be very high you don't need to know about that we don't need to treat that you treat the parent conditions that is correct these chemo hypotensions and they will come down see in the phase of high scpt scot and bilirubin what we see the patient if the patient is improving and is the patient is a viral hepatitis s coming down will rubin matrix because of the delta will win if the scots apt are coming down even if the bilirubin is high but if the patients are improving i am happy in the phase of that if the prothermic damage is also high then there's the cause of connection right so we have to evaluate all the liver parameters and we don't give assign importance to only one parameter but routinely we don't ask for both i hope that satisfy or they can read questions right if you not answered to their satisfaction they can put another questions yeah anything else uh so so there is uh another question on asd aft ratio does it show fibrosis no i don't think that source fibrosis because the fibrosis is as i said the most often the fibrosis is the chronic labor disease that cirrhosis is the prototype of fibrotic disease and i don't think it's going to make any difference in that unless yes if it is a because of hepatitis c we expect est to be more than the alt so if it is because of the hepatitis c leading to cirrhosis ast will be higher than es alt yeah okay okay and then there is this question what about glycogen storage disease liver biopsy i don't think that we need to because we are talking of the interpretation of the liver function test glycogen storage disease they are usually not diagnosed by the blood case i suppose and as i am not an hepatologist or a gastroenterologist i must not have seen any personal gland they are usually present more in the childhood so pediatrics pediatricians are the one who deal with them or maybe if the patients who present later will have the organometal for hepatosplenomegaly and there may be will be able to pick up but the routine test i don't think that they would be picking up and maybe we need to go for the biopsy but i am not much aware about the arrangement of the liver function phase in relation to the glycogen storage disease but glycogen yeah is definitely one of the storage functions of the liver that much i can say okay fine so we go ahead with the next the third is after a ltast and bilobian we go for the alp that is alkaline phosphatase alkaline phosphate is in the serum can come from many sources in fact i forgot to tell that ast alt also come from the other tissues also even the muscles the kidneys and other structures also have the ast alt right in fact when i was a medical student or the resin doctors we did not have all the sophisticated tests for the microalpha infusion test today we do troponin but at that time we were doing sdot and the test for screening case whether the patient could have multiple infections after ecg their test was as the ot but we don't do it anymore somebody would laugh at me if i said that seot for michael infractions so likewise alkaline phosphatase is also present in many other tissues or the other organs and it is found in liver bone kidney intestines placenta and but mainly it is present in the blood in a normal person's from coming from two sources the liver and the bone right there are different iso enzymes which can be tested by the different methods whether it is coming from the liver or whether it's come from the bone but we don't need to do it ordinarily we can interpret looking at the patients and the other test if the patient has raised alkaline phosphatase and also has the rays ggt which is our next it is to be discussed then obviously it is coming from the hepatic origin because the ggt will not be raised if the patient is alkaline phosphate is because of the bone moies if the patient has increased the bone turnover also there will be alkaline phosphatase if patient has pigeons disease alkaline phosphate is very high but then in that case a ggt will not be increased right and the normal values again are different for the males and females and different in the different situations when we were students the units were king angstrom units which were hardly from 0 to 30 units but now we use international units which is more standardized and there the normal values also differ for males it is forty five to one one five and female is thirty to hundred so raise alp and with rays gamma glutamine trans peptidase means it there is a lp is because of the hepatic origin liver alp is marginally raised coming to the liver pathology it is raised in liver and jelly like hepatitis but it will markedly raise when there is biliary obstruction either it is intra or extra tibetic options that means in hepatocellular jaundice with cholestasis and obstacle jaundice because of the stone in commonwealth the gallbladder disease or the pancreatic malignancy obstructing the common vita in that situations the alkaline phosphate will be market raised so that's an important feature to keep in mind and ask for it right next very important the alkaline phosphatase may be raised because what we do when we ask for serum alkaline phosphate is just the general alkaline phosphate is the generic alcohol and phosphorus you can see which may be raised if the patient happens to be a pregnant woman right that this alkaline phosphorus may be contributed by the placental alkaline phosphatase so it doesn't mean that patient has any liver pathology and incidentally curiously the patients with the blood group of o and b right when they consume the fatty meal there the intestinal alkaline phosphate is released and that may increase the alkaline phosphate levels and importantly the patients with diabetes even without any pathology any liver involvement can have raised alternate phosphates the significance of these things are not very clearly understood but this is very very important to evaluate whenever we get any one abnormal report out of the range without the parallel impairment or the other test are normal bilirubin is normal sc or tscpt are normal and only alkaline phosphate is raised look at the patient see the patient test again right look about the patients and drug history and all those things a patient is osteoporosis and he is now on treatment or stimulation on treatment obviously the alkaline phosphatase is indicative of the one turnover uh bone turnover so we are happy that it is increasing like that right the next is gamma glutamine trans peptides which is again from the hepatocytes and biliary epithelial cells but again it can also be there in kidney seminal vesicles pancreas spleen heart and brain so ggt the normal values are slightly higher in the males than the female right but the hepatic gt production is always increased we can say that ggtv always ask for when we are suspecting alcoholic liver disease whether it's alcoholic hepatitis right patient is denying but he has consumed the alcohol the last saturday and he has come with the vomiting nausea it could be just gastritis or it could be alcoholic hepatitis go for ggt go for seo tsgpt and ratio of it then we can make out so practically ggt we measure only in relation to the alcoholic hepatitis on relation to raise alkaline phosphates because alkaline phosphate like alkaline phosphatase ggt also may be increased in many other situations other than the liver pathology patients who are on drugs like anti-convulsion drug histamine receptor blockers right like running it in symmetrical pharmaceuticals or patients having diabetic nephropathy then it is not clear and that is why it is increased patients having hypertension obesities prosthetic disease everywhere ggt may be raised so ordinarily the gjt is not a part of the liver screening test or the liver biochemistry panels you are unnecessarily spending and confusing and the interpretation so don't go for ggt routinely only when we have a few things in mind then you go for it right serum proteins this is probably the first real liver function that we are as testing right so serum albumin as i said also in my opening remarks is exclusively synthesizing liver there is no other part of the body which produces or synthesizes albumin right so it is the indicator of liver functions provided we have ruled out protein area protein loss because of the protein area or malabsorption syndrome or poor nutritions patient is poor placenta is malnourished or cannot afford and doesn't take enough of proteins there are different situations otherwise in normal healthy persons if the albin levels are low we have ruled out the other causes of the hypo albino like protein urea nephrotic syndrome or male absorption then obviously it indicates the chronic liver disease why chronic liver this is why not acute because albumin is a long half-life as we discuss in the delta the bilirubin albumin half-life is anything from 15 to 20 days and that is why some insult today in albion is not going to be low right so second part there is an inbuilt reserve for the liver that the liver can increase their capacity increase the turnover of production of albumin twice its capacity right the normally the liver can produce around 15 grams of uh albumin daily right and there is a normal the turnover of around 300 to 400 grams of mean so it can increase double so that means 30 grams can be produced in a day right provided there is enough substrate obviously so you will not be able to see the chronic liver disease before at least three four weeks right so that is why the albumin serum albumin is now we have the answer for one of the questions asked in the poll that serum albumin is one of the test for because there are only four options given alt really the second was the albumin and the third was the alkaline phosphatase and the uh prothomine time so for a chronic liver disease probably the albumin is the answer for acute liver derangement the next that will be the pro-thermal time will be the answers of course what is more important to know right in relation to albumin if you have asked for the test for albumin it's very low right if the albumin is low patient is healthy percentage good uh history patient is from well uh means quite good family right his intake is good and he's not ill or he doesn't have edema to suspect hypoproteinaemia and his albin comes to two or two point five that is the decrease albin levels in acute setting right or patient may have a report of an uh the lever from about panel right before a week and then there will be news three point five or four and suddenly it has come to albany of two 2.5 right or three that is probably the decrease albumin because of the trauma or inflammatory conditions this is called a negative phase reactant in the kovid time we have learnt about the acute phase reactance reactants fairytales increase ldh is increasing c-reactive proteins are increased they are all increased as an acute phase reactant but there are also acute negative phase reactants acute phase reactants which are negative that means they are reduced the tumor necrosis factor the interleukin they suppress the albumin synthesis temporarily so albumin is a negative acute phase reactant we have to keep in mind so that we don't get the knee jerk reaction of prescribing the albumin infusions because albumin is right as something very expensive and it's going to work for only three or four weeks right to the patient and it's costly very costly one albumin infusion will be around 10 000 rupees and even if without albumin infusion if the patient's acute condition is over uh believe me these are being returned to normal if it is a part of acute negative phase reaction so please do not over interpret the albumin in the acute setting if the clinically does not fit with the hypoalbunemia or hypoprotein that's very very important and if there is suggestion of chronic liver disease because of the other features obviously low albumin alone or low almond increased globulin or the reversal of albino globin ratio will definitely point towards the chronic liver disease then prothomy time another important hepatic synthetic functions we know prothomine is the indicator of the liver the coagulations liver is a site for production of the plotting factors we have got 12 clotting factors right out of each there are many factors which are vitamin k dependent there are many factors which are not k dependent but all are produced in the liver factor 8 is also produced elsewhere but liver is one of the cheap site for the production of clotting factors along with other albumins proteins right so whenever there is a liver function derangement the prothomine time will be elevated or increase prothoming time is always correlated or compared with the normal from the control all laboratories will give the pay proton time two readings will get it or you will get inr that is international normalized ratio where they are standardized because different laboratories use different thermoplastic required for the prothomine assessment now if you use different thermoplastin you will have got different normal values so that is why you always use the control for that controls sample as well as for the patient samples if you just do an inr that is the ratio of normal for the patient's proton time to that of the control you get a value which is fairly standardized so always look for the inr and that inr is a marker of the status of the coagulations and there is a marker of the liver functions but believe me proton can be raised in other situation like patient has thrombocytopenia of the passengers other patient is on anticoagulants like warfarin obviously will go for the prothoming time measurement because it affects the vitamin k dependent plotting factor so growth from mean time though it's a very important marker of acute hepatic function abnormality you have to see whether it is not abnormal because of other situations like patients obviously bleeding more patient has thrombotic situations based on the deep information based on anticoagulants all the situations also fulfillment time may be raised again prothumb in time like the serum proteins and the other test bilirubin are important part of the parameters for childhood and mbld that is the model for the insect liberties course which are required for the classification and for selection of the patience for liver transplantations but proton time may be abnormal in other situations even in the phase of the abnormal protein term in presence of jaundice it could be elevated because of the obstacle jaundice in obstructive journeys the bile salts don't treat the intestines so they vitamin k dependent plotting factors and the other factors vitamin k depend uh the fat dependent vitamin k and the others you know adeka the fat soluble vitamins so if there are no fat absorbed no vitamin k is absorbed so the patient will abnormal protein time but in that case even one single injection of vitamin k will reverse the proton tank so that's the important thing even in the phase of cholesterol generis or obstacle changes if the prothomine time is prolonged we can make out whether it is because of the involvement of the liver parenchyma or because of the simple malabsorption of the vitamin k in that situations they tell me a pro-theming time will be corrected after injection of vitamin c it's very very important to know right next is the other tree so this finishes the part one that is the normal test we ask for the again i repeat alt-a-s-t or s-p-t-s-e-o-t serum bilirubin total direct indirect then alkaline phosphatase serum proteins especially the albumin and the ratio of albumin to globulin and the alkaline phosphatase and prothoming time these are the basic tests of based on this basic test and after having seen the patients or examine the patients and taken the histories right and we are sure that it is not because of the either drug toxicity or the right we come to conclusions that probably the patient has either acute hepatitis then we go for the to confirm whether it's acute viral hepatitis because of hepatitis a b c or e we ask for the theological markers for hepatitis a and e you ask for the antihepatitis aigm right nt hav igm is the test we ask for for markers of phi beta it is a and e igm is always increase immediately the first to respond in any acute infections right igg indicates the chronic infections or it may be a neutralizing antibodies if you get igg against hepatitis b that means the patient has been infected earlier and probably now he is immune to that hepatitis b so for hepatitis b we ask for the test hbsag or what we used to be called hepatitis b surface antigen or australian antigen that we used to be called the knee of the hbc so for hepatitis b we asked for a hepatitis b surface antigen hb is a g particularly by allies at test if you do it by latex it may be falsely positive but if you ask for analyzer test for hbsag if the patient has hepatitis b active infections will be able to pick up patient might have present little latent hbsig is clear but still patient has the jaundice and we want to make sure that it is hepatitis b infections then we go for another it is called nt hbc igm that is igm against the core antigen that will be present only if the patient has been having the active infections it will not be present if the patient has been given hepatitis b vaccines right if the patient is in turn hepatitis b vaccine the anti-hbc igm will not be present right so ask for anti-hpc igm in a window period when the patient has hpse is clear and igg antibodies have not come up still so that is for a betaines b for hepatitis c infections usual hepatitis doesn't give an acute hepatitis it's an incidental uh detection whenever the patient has raised alt right and no other symptoms but patient has issued blood transfusion cell blood products you go for this screening for hepatitis c in the form of anti-hcv antibodies if nthc antibodies are present your strong suspicion you ask for hcv viral load hepatitis c viral load is asked for we can ask for the hpv viral load also if hbs is positive and for hepatitis c like hepatitis a you only ask for i n t h a v n t h a e i g m e beta is e n t n t h e v i g m right or if the patient has the symptoms suggestion pre-coma hepatic encephalopathy epsilon is drowsy patience is a known placement of sterosis we want to make sure that this could be hepatic and cellulopathy or even in the presence of acute hepatitis patient has some symptoms suggest you of your degenerative go for serum ammonia serum ammonia is one of the important things to know that patient has hepatic and cellulopathy right so that's the test we ask for ldh is also considered to be one of the tests for the liver panel but basically it's a very insensitive case compared to ltsc it's a very insensitive test but it is useful when we are suspecting hemolysis or we are suspecting ischemic injury in these situations the ldh will rise parallel to the eltast is chemical injury especially so ischemic injury ldh is important otherwise in hemolysis it is important otherwise it's not important in the other so we don't ask routinely for lth alpha phytoprotein we ask for whenever we are suspecting liver cancers right the alpha entity tips in again we don't transfer routinely we ask for it when we are suspecting alpha and trypsin deficiency which we suspect when the patient has got cirrhosis without the definite history of alcohol definite history of any of the infections or when patient has both emphysema and the liver diseases cirrhosis of liver and young age then we look for alpha and antibodies right g6pd comb stays uh we asked for whenever patient does hemolytic jaundice or anemia and five nucleotides we don't ask for because it's imperative probably same as that of the ggt so we don't ask for we have never asked for i don't know whether it's done routinely in the laboratories most of the laboratories so basically the additional tests are this the second line of the additional tests are for more uncommon diseases like primary biliary cirrhosis which is now called primary biliary cholangitis so where you ask for anti-mitochondrial antibodies this test we do right only when we are suspecting primary biliary cirrhosis the female patients they were symptoms of holy stasis and the enzymes are not their alts they are not mercedes bilirubin is high so when we go for the anti-mitochondrial antibodies they are exclusively increasing pbc that is primary biliary colenditis we ask for test for autoimmune hepatitis right like anti-smooth muscle antibodies ana dst and anchor anti-nuclear antibodies double-stranded dna or anti-neutrophilic cytoplasmin can be what is we ask for when you are suspecting autoimmune hepatitis that is anti-liver kidney microsomal antibodies these are very selective we don't need for most of the patients like that if you are suspecting wilson disease because the patient has neurological symptoms placentas on ophthalmic examination k surfacer ring then we go for the uh serum celluloplasmins or urinary copper levels we know wilson disease is the store at the increased copper because the copper is not metabolized so copper is stored in the liver and some of the tissues in the brain the iron when we suspect hemochromatosis we also ask for the test we don't ask for routinely but we may ask for sonography of the abdomen right or we may ask for fibroscan or biopsy which is routinely not as for because most of them the diagnosis is made now another important thing is if the patient happens to be a pregnant woman and the liver function test or liver biochemistry is abnormal this is a very tricky situations and we know there are many benign and very life-threatening situations are there any questions monika yes uh there are many questions yeah when you appear i think there are questions so we can go for it because rest of the things are different totally different yeah yeah sir so uh there is a question by dr preetham he has asked normal bilirubin level but if we see markedly high alp and ggt levels so what may be the interpretation increase uh increase alp and ggt yeah in alcoholic hepatitis you may have increased the enzymes ltst bilirubin may not be increased because the c bilirubin the liver has capacity to clear the ability to be 10 times its normal right but if the there is hepatitis there is an inflammations the alt ast will rise the ggt will rise but the bilirubin because the liver has the capacity and the liver functions are even if the liver is normal concerning hepatocytes will clear the velar beans so billy bill will not rise so i will think of the patients with alcoholic hepatitis right and the bilirubin the clinical jaundice will come only when the middle ear crosses to milligram but actually the direct bilirubin when it is more than 0.3 itself suggest that the bilirubin started accumulating in the blood okay and so there is this question uh by dr tarini she is which is more important marker for att induced liver injury whether it is trans amines or bilirubin well i did not get att means antituberculosis treatment aptt induced liver injury yeah that's a very i think that's a one full session to be discussed the drug-induced liver injury out of which the tuberculosis anti-tuberculosis drugs are definitely very very important because it's a drug-induced injury the most important marker are the enzymes right rupeed and depends see which particular drug we are thinking of see all the nttp drugs especially the first line of drugs the ins the pharmaceutical and pyrexes number these three are the ones which are hypnotoxy but contrary to the belief repampisin is the least hypertoxic the most important hypotoxic amongst the three are the inh and second is the pyrisinamide again the type of injury because of these compounds are different some of them produce cholestasis some of them produce the direct injury to the liver somehow produce the obstructions so some of these idiosyncratic reactions so there is it's a very very different topic but generally we go for the enzymes levels and when the enzymes levels are high whatever is the reason even if the patient has no clinical journeys or high bilirubin we have got to stop the all nttv drugs and then when we have to introduce we introduce the drugs one by one and there too in a smaller positions because we don't know whether it's a radio synchronic reactions or a hypertoxic injury because of the direct toxic effect of the drugs so we always introduce the drug separately but the moment the enzymes levels are high more than the fight times the upper limit of normal we have to stop whatever drug we are giving right so just the last one we will be taking is abnormal pt inr interpretation and correction how to uh right as i said right see i have already made my point that prothome in time in the phase of chronic liver disease is a different than proton time in a normal person's right if the patient has no has no liver disease and the proton time is abnormal what i mean is the all other liver parameters they have to ask for lts ctba sdot proteins i mean alkaline for they are all normal that means probably the prothoming times abnormal because of the non-liver pathology in that situations we have to go for the cause suppose it's because of the patient taking the drugs like warfarin if the warfarin is the responsible cause for the proteomic time you go if the inr is very high stop warfarin only for two days and the protherm will come down or if the patient is bleeding in phase of the patient on warfarin you give vitamin k and that will correct the vitamin so whether the prothoming time is corrected after the vitamin k is important and if the patient has no liver disease or patient a small absorption patient is releasing too many antibiotics and that produce the fat the mild absorption that produces the all fat soluble vitamin deficiencies in which one of them is vitamin k again in that phase also you give it i mean k and the protherm will be corrected so all that you have to take the drug history and also see whether that proteomic time is corrected by giving the vitamin k right in patients with liver disease again it's very very important to see that whether the patient has cholestasis or of that is all obstacle jaundice or just in a terminal phase of cirrhosis where vitamin even after giving term in k it will not be corrected because it's a deficiency of plotting factors itself all factors over and above the vitamin c event factors in that case these are if you take the child or male co score they will definitely say that is probably child ceo the male score is very high and these are the candidates for liver transplantation so we have to see the patient right that is what in fact going to be one of the slides that never interpret any of the liver functions isolated we have got to see the piece and see the other test also okay right yeah can we go ahead yeah lever function assessment your asses meaning is very very important very tricky and it's very very difficult also at times right because there are many benign conditions like intra hepatic cholesterol pregnancy where you don't need to do much prevalent symptomatic treatment as against the acute fatty liver of the pregnancy with a very serious condition so there are liver abnormal functions which we divide into there are specific situations of syndromes which are specific to pregnancy right the pregnant lady has come i am always concerned whether the patient has abnormal liver functions because of the disease which are unique to pregnancy like acute fatty liver of the pregnancy or in tripeptic cholesterol or there are diseases which have a systemic manifestation along with liver involvement like the eclipse or pregnancy or health syndrome health is stands for the acronym stands for the hemolysis with elevated liver enzymes and low platelet counts potentially a very life threatening situations for the mother as well as the fetus and whether it is the acute fatty liver or ecclesia or help sometimes the only treatment or the first treatment is terminus of the pregnancy no matter what is the justices only thing that you can wait for may be for correcting the mother's hematological picture that she should not bleed when we are terminating the pregnancy that's for mother's interest and maybe we can correct with some of the drugs like the steroids for fetal maturity if the child is not the fetus is not mature these are the only decisions we look for or there may be the situations where because of the pregnancy some of the disease underlying disease are exacerbated be a woman with cholesterol disease or with the vascular disease like birth child syndrome which is a thrombotic conditions basically pregnancy is a pro-traumatic situations right and that is nature protection against the severe leading postpartum right no bleeding should occur so that the mother would not develop the severe enemy or there may be placental insufficiency so basically the pregnancy there is always a balance of anticoagulants and propellant factors and body tries to adjust but certain diseases like butchers know maybe more if there is a more prothrombotic factors are more and see incidentally patient has viral hepatitis b with other family members also having the viral hepatitis but if the patient happens to be pregnant that hepatitis infection carries more risk so that we have to keep in mind so my point is the liver function test how to be interpreted more carefully more follow-up and with the situations whether the patient the first trimester of pregnancy second times of the pregnancy in first trimester most of the pregnant woman would have the vomiting which is a morning sickness but which may be a gravity like hyperemesis gravidarum that can also be with the altered function so point is that don't interpret liver function trees in pregnancy like routine non-pregnant situations you have to be also in constant touch with the obstetricians and maybe require the question to logistics and another part because of the presence of pregnancy some of the markers also change say there may be serum albumin is less because there is marked increase in the plasma the blood volume is increased that may produce chemo dilution and the normal serum albin level will go down and because of the placental alkaline phosphatase the alkaline phosphatase will be high so if the alkaline phosphate is come very high you don't get worried about some serious diseases like cholestasis or because of some bone tone or its may be just an alkaline phosphate is because of the placenta because of the pregnancy so that's not to be worried about so point is don't interpret liver function taste in pregnancy like in the non-pregnant state in the remain the next is the limitless of the liver function test or the liver biochemistry the american gastroenterologist had prudently wisely said that you must have a very rational approach to the interpretation of the liver parameters always always interpret liver parameters in context of the situations look at the patients whether the patient is symptomatic take the history look at the patients right and also ask in the history about the drugs drugs not only our allopathic drugs but there are many homeopathic drugs the ayurvedic drugs many homemade situa drugs that the patient might be taking which no all drugs and food are metabolized in the liver and that can alter the liver functions so always always ask about the history examine the patient and then only interpret because the abnormal liver test may not be related to liver pathology as we have said that that's maybe some severe hypoxia severe hypotensions may alter the liver function test liver is temporarily not functioning because of the hypoxia but that doesn't mean the liver is disease and waste ltst does not require any treatment for the liver you need to treat the primary conditions like hypotension shock hypoxia and the second part patient has the cirrhosis or some serious liver functions abnormality but the levers are not raised alts t may not be raised right for a very long time so always interpret with caution and this is the last part very important part that there can be falsely elevated el touristy because of many other situations say if you have not collected the blood properly that is the pathologist or the laboratory will do it automatically but they do not know you do not know we do not know when we interpret the report that there is a pre analytical error that means the blood sample correction is the proper see if somebody has received the injections sjo tspt will rise because they are part of the muscles so seo tscpt alone may be rise but normally they do not rise more than two times or three times the upper limit of the normal so when patient has received inter muscle injections or patients phlebotomy was not clear their patient is obese or more fat or the patient is fussy or the technician is not is very new then maybe it has taken the blood after multiple punctures or the blood has not reached to the laboratory in time or the patient has that the prolonged predicate applications all this may alter the alt asd because they are part of the system then there may be situations which are other than the sampling right uh alt may be low if the patient is consumed caffeine we don't know the significance that is what the literature says then alt not alt may be raised in renal failure because of the handling of the kidneys with all these enzymes then falsely increase in both astin health is possible with certain drugs like erythromycin frozemite which is a diuretic can alter the this so this is very very important and in crohn's disease which is an inflammatory bowel disease again there may be lower lt levels again we don't know the significance another important thing is whenever we ask for growth time we throw tommy time we collect in the citrated samples the sodium cycle is the anticoagulant we use so that the blood is not clotted right now here normally the laboratories will just do it like this mix-up but that's not the liabilities the technicians should do it should be gradually just mix the blood right very gently rolling the test tubes and not the mix-up otherwise that improves hemolysis and that can alter the prothermic time it's very important if the patient has polycythemia a very high hemoglobin high rbc count then the plasma component of that sample would be less and the sodium citrated component will be more so that will also give a prolonged prothermic time because there is more anticoagulant added compared to the plasma so all these things we have to keep in mind when we interpret the face so finally i can say that the liver functions in liver biochemistry are not the same right when we ask for the liver biochemistry it's different than the liver functions the normally asked liver biochemists test are alt ast or scbt scot bilirubin alkaline phosphatase proteins and protonmentine and whenever it's extremely high more than 10-15 times think of acute hepatitis or drug induced or ischemic liver injury interpretation has to be done i repeat again in nagar over emphasizing in context of the patient's history examinations and the physical findings and patients can have advanced cirrhosis with mildly elevated abnormal results patient can have false abnormal laboratory tests patients additional tests are required more often if there is no clear-cut hepatitis or this suture may be having autoimmune hepatitis primary biliary cirrhosis or rare disease like wilson disease you need more tests to be ordered right or hemolytic jaundice we need to know the cause of hemolysis we need more taste let me ask for g6 pdsa and the hemoglobin electrophoresis always and currently we do not have tests which can non-invasive ask for the liver pathology but there are many tests which are in the pipeline or there will be elsewhere where the blood levels of certain of the metabolic proteins right the extracellular metabolic proteins which may be the future where we'll be able to just non-industry like our ltst and bilobian the we ask for the blood test and which will give the diagnosis of the liver cirrhosis or fibrosis somebody asked for the case the few tests are awaited right that they are in the clinical stage then lastly very importantly i always end my slides with saying that knowledge is power the medical science changing every day today there might have some new things which have come up so we have to keep updating ourselves i always say there are only two types of doctors or two type persons updated and outdated you have not updated for the topic you are outdated for the topic so i always believe that knowledge is power we keep on adding new informations new knowledge if you think that education is expensive try ignorance what we mean is if you don't know particular things you know how much blunder you can make for that person so thank you all for patient listening right and i'm glad that there are so many questions asked and even if there are any questions i am ready to answers right here thank you all monika stage is all yours yeah i can also look for any comments if there are any right so there is this uh there is one question related to uh is pregnancy liver problems is the causative factor for neonatal jaundice definitely definitely right new neutral jaundice um because of the mother but more often it is because if there is a premature delivery the liver of the child is not mature enough to handle the and you know that the hemoglobin is very high in the fetus right in the neonatals the hemoglobin level is 17 18 and because more hemoglobin more turnovers so more in the bilirubin comes to the liver and the liver is not mature so the neonatal journalist is more of physiological jaundice in most of the people more so if the child fetus is delivered prematurely so in all premature delivery or even in a normal delivery we expect the physiological jaundice in the first week if that is very high the indirect bilirubin which is high right indirect bilirubin is toxic indirect bloom is neurotoxic thankfully it is if it is a small quantity liver can handle it but it's a very large quantity it can produce chronic terrors chronic terrorist is something which is toxic and that is why the child is given to phototherapy it's kept in the neonatal icu and given the phototherapy most of the patients it recovers right but yes neonatal jaundice is more likely because more of this or there may be an in compatibility the mother's blood group and the fetal inclusion and it can be lethal also right it's a major incompatibility there are many issues but yes very very important questions and thank you for bringing that question sure yes we have taken a lot of questions sure yeah but we can go for if they are not tired right and we have enough time in this our own platform the time is not at all an issue right right right so there is this one question uh on which liver parameters elevated are elevated in sepsis in sepsis again it's just like an hepatic injury as a part of generalized plus there may be a vasodilatory sense and hypoperfusion the effective blood volume is reduced so basically what we expect is the increase in alt a est but there may be again cholesterol is influenced by rubin but main is acidity scp will be very high sepsis may also affect the platelet functions and we may get thrombocytopenia or bleeding tendencies because of the thrombocytopenia or metals because of the right the clotting factors which again as i said the long half-life so we don't expect in immediate future yeah then there is another in uh questions interesting questions indication of album infusion in clinical practice see albumin as i said uh is has itself as a very low half-life and very expensive so normally they give albumin when there is the hypoalbanemia established because of the chronic liver disease and patient is severe anxieties if the patient has severe anxieties right say patient raised in a accumulation of 10 liters of fluid just remaining one or two liters will not help right one or two liters will not reduce the respiratory embarrassment that the patient is having but if you remove more we can't remove more than one or two liters at a time right because it will produce hypovolemic stock right so in that situations we on one side we give albin on one side we give albumin and we can remove a large quantity so whenever we want to remove large quantity of the acidic fluid then we can give albin that is one second thing when we want to give albin when the patient is being prepared for the liver transplantations and patient residue aside is which is refracted into the treatment that's happened and the third when the patient has spontaneous spectral pareto noise which is one of the complications in cirrhosis where giving albumin and the antibiotics uh clear this spontaneous bacterial paration is earlier than patients who are not using albumin otherwise there are not much indications of the albumin in the setting any other questions you can also comment by the users that the session is really very wonderful valuable information thank you for that many users have enjoyed the session and so there is this one the last question probably which is the best marker for liver can cancer is it ca what what they were the for liver cancer seriously for liver cancers the alpha fetal protein is the marker right true yeah there was one questions are the hand raised by dr snack is a very senior surgeon and a big friend and one of the pioneer of the surgical on the plexus family so please allow dr nayak to join on the stage and give his questions or comments sure sir sure i will yeah being a surgeon you know we have learned motherboy that often function and structure are not two different things one affects the other and that is why even as a functional investigation sonography should be included because sometimes you might find something which is which is affecting the function so if you consider other things biopsy and ct scan and all as as a different form of investigations not deliver function test at least i think minimum sonography yeah definitely definitely i i have made a mention of this phonography also but basically what we were discussing were the blood markers right the blood liver biochemistry only that was the precise yeah yeah but as we function this if we say function all pieces of liver abnormal liver functions i would go for the sonography because it can pick up the undiagnosed chronically what is even in the acute setting there are so many patients who are compensated cirrhosis and we diagnose incidentally when we do for the sonography we can pick up splenomegaly small spin obligatory you know the spin will come up only when it is enlarged by two point five to three times but we can pick up the spleen size increase my left side is the liver which is sunken or maybe portal veil which is dilated so there are so many things we can definitely pick up and we can pick up the incidental chronic liver disease on sonography so yes i all patience of alternatives i would go first definitely it's a very positive thank you thank you now surely one of the doctor pitham dekka has asked for whether ca 19.9 marker indicated for liver cancers yeah there are many other markers definitely we can ask for there is no question about it but basically we wanted to relate to the liver functions that we asked for the liver biochemistry there are many other markers that definitely are indicated and one should go for but we usually do in relation to the onco physicians or the onco surgeons and that is why i have not included the markers but yes i agree that's even say 19.9 is a marker to ask for yeah please look at the other comments we don't want anybody to feel that their questions are not answered sure um so so there is somebody has asked about the fibroscan fibroscan is one of the tests in advancement of the sonography there is the fibroscan is one of the non-inverse test of knowing the fibrosis it knows basically it stays the elasticity of the liver which is way ahead of just simple sonography that we do here they are measuring the seer for velocity we don't need to go but it's a fibrous con is now one of the established states before going for the liver biopsy we can just do fibroscan and then see there are different values which are called kpa kilopascal units or something and there are different subsets if there is a beyond a particular limit kpa value is there then definitely it increases the chances of cirrhosis and doctrinal has asked about the hepatitis e raises delta rib in your common see basically dr angola delta bilirubin is something which is a a direct bilirubin called concha vivian so it is attached to the albumin so it is not clear if the patient has hepatitis e or any hepatitis for any reasons if there is cholestasis or it takes longer time to clear we see the total bilirubin directly lubin and delta and compare with the enzymes right if the patient is otherwise improving patient is improving and if you ask for the urine balsa and bile pigments they are absent that means ah that means it is not a direct conjugated bitumen that is increased it's a bilirubin which is delta bilobi so if the built-in rubin indicates that probably there is a cholestasis more and patient is bound to recover as long as the patient's appetite is report improved patient sense they will come down uh we assure the patient that he is going to come it's a matter of time because the delta bilirubin is an albumin uh bilirubin is attached to albumin so the half-life of the albumin is going to take care of but it's not something that is to be worried about so in fact that's a better marker if the patience is otherwise fine and the enzyme levels are less dr mustapha you can come and give your comments if you are not comfortable will turbine we already asked for yeah we'll be uploading our all slides right slowly right and thank you very much for kind words and if there are no more questions ah doctor monica you can just thank you very much for remaining yeah thank you so much sir thank you for wonderful uh and knowledgeable session yeah and there are other some comments that they would like to have more sessions right so i am thinking of another interpretation of maybe cbc or something which is also routinely asked for and there are so many things we can discuss on the analysis or the interpretation of complete blood count right and the peripherals me always another topic dear to my heart right so maybe some other time we can discuss that surely thank you so much good night you

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dr. Mahadev Desai

Dr. Mahadev Desai

Senior Consultant Physician | Ahmedabad

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dr. Monika Khurana

Dr. Monika Khurana

Researcher | Public Health Epidemiologist

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dr. Mahadev Desai

Dr. Mahadev Desai

Senior Consultant Physician | Ahmedabad

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dr. Monika Khurana

Dr. Monika Khurana

Researcher | Public Health Epidemiologist

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