Ouch my liver :(
LFTs
Billybilly
Oope it's hepatitis
Test Your Knowledge
100

Obstruction or damage to liver canaliculi can result in this condition

Intrahepatic cholestasis 

100

This crucial serum protein is decreased in cases of liver failure, inflammation, or protein malnutrition,

Albumin

100

This hyperbilirubinemia results from >80% total bilirubin being indirect

Unconjugated Hyperbilirubinemia

100

This phase of hepatitis infection is associated with very aminotransferase levels, sometimes greater than 1000 U/L

Acute hepatitis

100

You're a heavy drinker and notice you've been bruising more easily. Your buddies say man up...but you're not about toxic masculinity and also a hypochondriac. After paying 30% co-insurance your labs come back:

total bilirubin: Elevated

indirect bilirubin: normal

Vitamin K: normal

Albumin: normal

INR: elevated


Liver synthetic dysfunction

200

This clotting measurement is an early and sensitive marker for liver dysfunction

INR

200

These amino transferases transfer aminogroups to ketoglutaric acid

Aspartate aminotransferase (AST)

Alanine aminotransferase (ALT)

200

This hyperbilirubinemia results from either impaired hepatic secretion or decreased hepatic uptake/function (advanced liver injury)

Conjugated Hyperbilirubinemia

200

This compound can reverse acetaminophen induced DILI

N-acetylcysteine

200

In liver failure, the prolonged INR improves with vitamin K administration (T/F)

False.

Vitamin K administration will improve INR when the liver has a normal synthetic function but vitamin K is not being adequately absorbed from the gut, as occurs in cholestasis

300

Name three potential causes of extrahepatic cholestasis

Tumors, stones, cysts

300

Elevation in alkaline phosphatase indicates either of these two conditions

Cholestasis (intrahepatic or extrahepatic obstruction to bile flow)

Infiltration of liver parenchyma

300

This modality is used to differentiate intrahepatic vs extrahepatic cholestasis

Endoscopic retrograde cholangiopancreatography (ERCP)

Ultrasound/MRI

300

This strain of hepatitis is responsible for a majority of fulminant hepatic failure cases

Hep B

300

A 43-year-old woman with a long history of non-insulin dependent diabetes mellitus was noted to have an alanine aminotransferase (ALT) that was twice the upper limit of normal on routine screening. She said that she did not drink alcohol and never had done. She was obese (BMI 28). Which is the most likely cause for her elevated ALT?

Hepatic Steatosis

400

During your last CE shift your spidey senses twitch. Youre the only one to notice the patients characteristic yellowing and empathically sense pain originating from their RUQ


You dont need labs. You taste their blood directly and find:

Elevated direct bilirubin, elevated indirect, elevated AP

AST and ALT of 900

Normal albumin and INR

Hepatitis.

AST/ALT higher than AP --> hepatocellular

Even when the liver is really sick, bilirubin conjugation is conserved

400

Your patient has markedly elevated AST and ALT (>1000) and is negative for all hepatitis titers and negative for DILI. What would you tests would you order next and what is the treatment plan

Most likely autoimmune

Test for ANA or ASMA

Lower inflammation with corticosteroids

400

A predominantly direct hyperbilirubinemia is present in all of the following causes of jaundice, except:

a. Hemolysis

b. Bile duct obstruction

c. Drug-induced liver injury

d. Primary biliary cirrhosis

Hemolysis

400

Youre holding a human liver in your hand. You mull over its intricacies, hearing Dr. Zhang appreciate each individual feature. You know this liver's owner was suffering from jaundice, but this jawn (liver) looks fine. Inspired, you lurk on EPIC and find the biopsy results confirming your suspicion of priary biliary cholangitis. 

The halmark antibody and pathology of PBC is

Anti-mitochondrial antibody (95% of cases)

Microscopic destruction of canalicular cells

400

Stranded, hungry, cold. Youve survived in the artic wilderness for weeks. Despite your Bear Grylls style survival skills, your primary biliary cholangitis starts to act up. 

What animal can you feast upon to stabilize your hepatocytes and which compound is responsible for the protective effects

  • Ursodeoxycholic acid
  • First, it increases the rate of bile flow from the hepatocytes, thereby combating cholestasis and diluting toxic bile acids in bile.
  • Second, it inhibits the body's production of toxic bile acids, thereby preventing further injury to the hepatocytes.
  • Third, it inhibits apoptosis (genetically programmed cell death), thereby preventing hepatocytes from dying.
  • Fourth, it mildly inhibits the immune response in the liver, thereby possibly reducing immunological injury to the bile ducts and liver.
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