Liver Diseases Explained Clearly (Acute vs Chronic Hepatic Diseases)

Liver Diseases Explained Clearly (Acute vs Chronic Hepatic Diseases)

okay so welcome to another MedCram
lecture we’re talking about liver function tests it’s the third lecture
where we talk about actual diseases and I wanted to break them up into acute
liver diseases chronic and finally cholestatic so let’s get started okay so
here I’ve made a table of some of the characteristics of hepatitis in the
acute form let’s talk about hepatitis A remember that hepatitis A is is an oral
transmission so you don’t get it by blood you get it by the soil not washing
their hands and then getting into the food and then there’s sort of a fecal
oral transmission you get it but because this is the liver you’re going to see an
increased amount of alt over ast both go up but you’re going to see more of an
alt type of bound up over the ast and so how are you going to diagnose this
remember it’s the eye G m and T hepatitis A virus okay so that’s how you
make the diagnosis now with hepatitis B on the other hand it’s not oral but it’s
intravenous intravenous or body fluid okay and in this situation it’s very
similar to hepatitis A and that the alt is going to be higher than the ast
because this is the liver that’s being attacked and not muscle or something
else with hepatitis B remember there’s different antigens there’s surface
antigens and there’s cor antigens and that’s important because if you get an
immunization you’re going to have antibodies against the surface antigen
so if I could draw a little example here if this is the virus particle the blue
is the surface and the core is the green the core is the actual
viral particle so when they give a vaccine they’re just using the blue
portion of the virus the non-infectious so you’re going to have antibodies that
are going to be made against the surface antigen so you so if you have an
immunization you should be surface antibody positive but you should be core
antibody negative because they never gave you the core and so what this means
is that you should the IgM antibody to the hepatitis B core antigen should be
positive if you actually have the infection let me restate that here so
the i GM core antibody is positive again the IgM antibody to the hepatitis B core
antigen is positive that’s called the IGM anti-hbc c stands for the core and
you should also have it positive to the surface antigen so both of those should
be positive okay because in an actual infection you’re getting the surface and
you’re also getting the core so you should have IgM you should have both of those so again
the IgM antibodies of the hepatitis B core antigen and to the hepatitis B
surface antigen both should be positive okay what about hepatitis C again
hepatitis C is actually a little bit more chronic and so you’re not going to
see as much of an increase here but again the key point here is the ast is
going to be less and increased than the alt again this is intravenous drug use
or IV DEA abuse okay there’s other things that are associated
with this like tattoos also sharing razors multiple sex partners these sorts
of things can increase the risk of spreading hepatitis C now how do you
check for that it’s very simple it’s simply the anti HCV antibody into IgM
you could also check for the hepatitis C virus RNA within the first three months
of the exposure you should have an antibody reaction though okay alright
let’s talk about alcohol now whereas before the alt was higher than the ASD
because this is the liver be aware that in alcohol they’re about the same or you
might even see that the ast is going to be higher than the alt is that
interesting and obviously here instead of intravenous drug use we’re going to
get alcohol use so that’s that’s obviously very important difference
there obviously you want to make sure that there’s not other things going on
here so the diagnosis is basically based based on history
what about ischemic now remember an ischemic you’re getting no blood flow to
the liver so the liver is going to be really upset with that and it’s going to
tell you that and so what you’re going to see is humongous raises
the ast and the alt and we’re talking several thousand here okay so they
really go up in ischemic disease and obviously you’re going to have blood
pressures here in the 50s / 30s or something really bad like that or a code
situation and again you’re going to be ruling out other things here but if you
see this go up and shoot up pretty quickly I want you to think of ischemia
and you just again is going to be based on the history okay let’s talk about the
chronic diseases now obviously you can get chronic hepatitis B and C and you
don’t get chronic hepatitis A or it’s very rare so I left those off of here
basically they look identical as to the acute situation except the liver enzymes
are not as elevated let’s talk about mash probably one of the most common it
stands for non-alcoholic steatohepatitis basically these patients are fat obese
so you’re talking about patients with for instance the metabolic syndrome
insulin resistance hypertriglyceridemia and in the history you’re going to
basically get for the diagnosis is that of exclusion you certainly don’t want to
just look at someone say they’re fat and that’s why you’ve got nash but these
type of patients what do they look like these patients are liver patients so
they’re going to have a slightly increased alt over that of the AST but
the alt will be higher than the ASD but it’ll be it’ll be elevated now as we
said with alcohol it’s very it’s just backwards the alt is high but the ast is
what’s elevated and again the history is going to be that of EtOH and a guess
it’s also going to be of exclusion you want to just make sure that you’re not
just subscribing somebody to the old alcohol reason for their liver disease
make sure that even though they’re drinking make sure you rule out the
other things autoimmune hepatitis that’s that’s the reason why we need to rule
this out if you have a middle-aged woman who drinks a lot you certainly don’t
want to say that it’s due to just for drinking because it could be due to
autoimmune disease these are the type of patients that get autoimmune disease
these young women so because it’s an autoimmune hepatitis
itis again it’s in the liver they’re going to have a higher alt than AST so
the history in this is that they’re young women that’s the type of people
who get these autoimmune diseases and the thing here that you got to know is
this this is for boards and it’s the anti smooth muscle antibody if that’s
positive it’s going to be very difficult to say that this is all related to
alcohol disease so look for positive Auto antibodies and to nuclear
antibodies but specifically the answer they’re looking for is anti smooth
muscle antibodies ok humic row mitosis this is uncommon in women it’s usually
because why they have periods and they lose iron so they it’s very hard to
store up with iron but the history here is that it’s typically in men and what
are we going to see here well if you take the ferritin level and the iron
saturation that’s the where you take the iron the serum iron and divided by the T
IBC you’re going to get something greater than 55 percent and usually
you’re ferritin level is greater than a thousand so you’re off the charts with
this and of course the history is that of something called bronze diabetes and
this shows up on test a lot and the reason does is because it’s got a very
specific presentation basically iron infiltrates a lot of the endocrine
organs of the body the iron infiltrates the pituitary okay so they can get
pituitary problems it infiltrates the pancreas so what do they get they get
diabetes it infiltrates the heart so they get what and CHF or some sort of
constrictive cardiomyopathy okay so look for this patient with diabetes who has a
bronze look to themselves now there’s an iron metabolism
deficiency that you should know it is on chromosome six and how do you remember
that I remember that comes in a 2 plus form and also in a 3
plus form the Pharos and the ferric form and I know that 2 times 3 is equal to 6
so that’s how I remember it’s on chromosome 6 I don’t think they will
ever ask you that but you can certainly impress your friends with that bit of
knowledge ok what about Wilson’s disease I think Wilson’s disease showed up on a
famous television show once and those of us who studied knew what the diagnosis
was before the end of the show you’re going to have increased alt and ast the
history here with Wilson’s disease is that they’re young they get this kind of
korea form movement disorder and psychiatric disease but the key here is
this thing’s called the kaiser ka y ser Fleischer f.l.e.i.j.a h ER rings so
Google that or look that up on the internet and see what Kaiser Fleischer
rings are in the eyes and you will see that and the key here is not a high but
a low zero plasmon and why is that because it’s trying to suck up all the
copper this is a abnormal copper deposition so you get hemolysis and
actually you get a low alch foss and a low serum and plasma ratio okay and now
the one that’s most near and dear to my heart is alpha 1-antitrypsin you
specifically we see this with patients with lung disease
remember antitrypsin alpha 1-antitrypsin is an enzyme that is in your lungs it’s
made in your liver as well and what it does is it protects these elastase –is
from breaking your elastin fibers and so if you don’t make alpha 1-antitrypsin
you have something called alpha 1-antitrypsin deficiency and you tend to
get emphysema more quickly well that’s not the only thing that can happen
you can get a buildup of this abnormal protein in the law in the liver and
you’ll see these past positive pass positive granules in the liver and you
will get liver disease it’s a very kind of a low-level liver disease so you’re
not going to see it going very high but on the history you’re going to have COPD
asthma certainly if they smoke very early in life if they don’t smoke
they’ll have COPD later in life and they’ll scratch your head say well how
did I get the COPD I’ve never smoked well get an alpha 1-antitrypsin level
the thing that you should know there is the worst form of it is the p i– z z
allele okay and the normal is the mm but the z z is the worst
and that’s homozygote recessive okay so this is autosomal recessive autosomal
recessive inheritance and so you check how do you make the diagnosis you don’t
obviously do a liver biopsy first off but you simply get an alpha
1-antitrypsin level and then have them see a liver doc okay so let’s talk about
next the characteristics of cholestatic liver disease and for that join me for
the next lecture number four you you

42 thoughts on “Liver Diseases Explained Clearly (Acute vs Chronic Hepatic Diseases)

  1. I am preparing for FRACGP and was browsing on the Internet to search for interesting medical lectures and fell in love with these lectures ..They are simple,appropriate very educative,easy to remember. A request to add some lectures on diabetes and management please. Thank you Sir for your lovely videos

  2. Hi
    This is amazing
    We in kuwait university want to interview you for our students magazine. Please reply back

  3. I am a Nurse in Singapore! Sincerely want to let u know that i am very glad that u have created and shared this video! They are very helpful to me!

    thank you very much!
    Looking forward to more of them! XD

  4. Correction: hep BsAg would be present during acute infection, while appearance of anti-Ag surface would represent clearance. Thanks for great lectures!


  6. Treating liver failure with transplanted hepatocytes is a promising new approach to reverse damage and stabilize liver metabolism. There are still many major challenges with this new cell therapy approach although not as many as with organ transplants.

  7. Awesome video! Was wondering if you would be interested in making a video about irritable bowel syndrome vs inflammatory bowel disease. Cheers

  8. Hep C is not just transmitted via IV drug use (sharing needles), sharing razors, tattoos, and multiple sexual partners. A large portion of the Hep C population today got it from blood transfusions before they screened for HepC, liver transplants, and children born to HSV positive mothers.

  9. There is a reason that serum ceruloplasmin is low in Wilson's disease.  First of all, serum copper normally is carried by a complex composed of copper + ceruloplasmin.  In wilson's disease, there is a defective enzyme, ATP7B.  A properly functioning ATP7B is necessary to bind copper to ceruloplsamin, with the resulting complex then being released into the blood as a stable complex.  When ATP7B is not working, Copper is not bound to ceruolplasmin.  The resulting unstable ceruloplasmin is quickly broken down in the blood stream.  So, the result is a paradoxically low serum copper even as the liver is toxic with elevated copper.  

    There is a second mechanism for the toxic accumulation of copper in the liver:  ATP7B has two roles (the first one is mentioned above), the second of which is in the excretion of excess copper into the bile.  When ATP7B malfunctions in wilson's disease, it fails to excreted excess liver copper into the bile.  

    This sum total result of the above leads to the observed phenomenon of paradoxically low serum copper coupled with copper toxicity in the liver. The culprit is the defective ATP7B enzyme that is coded recessively by chromosome 13.

  10. in hep B infection. antibodies to s is absent. antibodies to c is present. solo anti Hbs means vaccinated or immunized.

  11. don't the AST and ALT stay relatively normal with hep B and C, as they are chronic diseases? so like, don't they change, gradually becoming more pronounced?

  12. When the AST is higher than ALT, a muscle source of these enzymes should be considered. For example, muscle inflammation due to dermatomyositis may cause AST>ALT. This is a good reminder that AST and ALT are not good measures of liver function because they do not reliably reflect the synthetic ability of the liver and they may come from tissues other than liver (such as muscle).

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