Hepatitis

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Hepatitis

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Both hepatitis viruses affect the kidneys and are associated with membranous and membranoproliferative glomerulonephritis. 

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A patient is admitted to the hospital because of a chronic untreated hepatitis C infection. He reports a history of heavy alcohol consumption. The physical findings are notable for jaundice and icterus (see the image below). Reduction of which hematopoietic factors would be most concerning from a clinical standpoint given this patient's history?

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Content Reviewers:

Rishi Desai, MD, MPH

Contributors:

Tanner Marshall, MS

Hepatitis, meaning like this inflammation, of the liver, most commonly comes about because of a virus.

These viruses tend to target the cells in the liver, and when they get in and infect these cells, they tend to cause them to present these weird and abnormal proteins via their MHC class 1 molecules, and at the same time, you’ve also got these immune cells infiltrating the liver and trying to figure out what’s going on, and so the CD8 positive T cells recognize these abnormal proteins as a sign that the cells are pretty much toast, and the hepatocytes go through cytotoxic killing by the T cells and apoptosis.

Hepatocytes undergoing apoptosis are sometimes referred to as Councilman bodies, shown on histology here, and this typically takes place in the portal tracts and lobules of the liver.

This cytotoxic killing of hepatocytes is the main mechanism behind inflammation of the liver, and eventual liver damage in viral hepatitis!

As someone’s hepatitis progresses, we’ll see a couple classic symptoms related to your immune system mounting an attack, like fever, malaise, and nausea.

Additionally though, patients might have hepatomegaly, where their liver is abnormally large from inflammation, which might cause some pain.

Also, as more and more damage is done to the liver, the amount of transaminases in their blood will increase.

Your liver has these transaminase enzymes so it can do its job of breaking down various amino acids.

Typically the serum amino transaminase, or the amount in your blood, is pretty low, but when your hepatocytes start getting damaged they start leaking these into the blood, so a common sign is a greater amount of both alanine aminotransferase, or ALT, and aspartate aminotransferase, or AST, typically even though both are elevated, ALT will be greater than AST in viral hepatitis and will also be the last of the two liver enzymes to return to normal.

Also, elevated levels of atypical lymphocytes are common to see with viral hepatitis, known as atypical lymphocytosis.

The lymphocytes are usually like huge, very large, due to stimulation from antigens, in our case the hepatitis virus antigens.

Patients often also end up developing jaundice, with a mix of both conjugated bilirubin and unconjugated bilirubin.

The conjugated bilirubin leaks out when bile ductules are damaged or destroyed when the hepatocytes die, which make up some of its lining!

Also, since these hepatocytes are dying, you start to lose the ability to conjugate bilirubin and make it water soluble, and so you also end up with unconjugated bilirubin as well.

So since there’s both conjugated and unconjugated bilirubin in the blood, some of the water soluble conjugated bilirubin gets filtered into the urine, giving it a darker color.

If symptoms continue or the virus sticks around for more than 6 months, viral hepatitis goes from being called acute to being called chronic hepatitis.

At this point, inflammation mostly happens in the portal tract, and if inflammation and fibrosis keep persisting, we consider that a bad sign, since it might be progressing to postnecrotic cirrhosis.

When things progress to cirrhosis, there may also be increased urobilinogen in the urine.

Normally, urobilinogen is made by intestinal microbes that convert the bilirubin in bile to urobilinogen.

And usually, most of the urobilinogen is reabsorbed from the intestine and goes back to the liver, where it’s converted back to bilirubin.

However, with cirrhosis, liver cells aren’t working properly anymore, so there’s a lot of liver fibrosis, so hepatocytes can’t process the urobilinogen, which is redirected to the kidneys and excreted, so you end up with more urobilinogen in your urine.

Now there are five known flavors or types of hepatitis virus, that have slightly different and unique properties.

Hepatitis A is transmitted through ingestion of contaminated food or water, in other words the fecal-oral route, and is known to be acquired by travelers.

Hepatitis A virus, or HAV, is almost always acute only, and there is essentially no chronic HAV.

If we’re talking serological markers, an HAV-IgM antibody indicates an active infection, whereas HAV-IgG antibody is a protective antibody and tells us that there’s been recovery from HAV or vaccination in the past.

Hepatitis E virus’s actually pretty similar to HAV, with the same route of transmission, oral-fecal, and is most commonly acquired through undercooked seafood or contaminated water.

It also doesn’t have much of a chronic state, and HEV-IgM antibodies tell us there’s an active infection and HEV-IgG antibody is protective and signals recovery.

Two big differences to note though between these two guys, is that (1) only HAV has the option for immunization and (2) HEV infection for pregnant women can be very serious, and can lead to acute liver failure, also sometimes called fulminant hepatitis.

Alright next on the docket is Hepatis C virus, this guy is transmitted via the blood, so could be from childbirth, intravenous drug abuse, and there’s also a small chance of getting it through unprotected sex, if there are open lesions, like cuts or sores, in the genital area.