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22 Cards in this Set

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finely branching telangectasias (spider nevi), Fetor hepaticus (dead body breath), gynecomastia, testicular atrophy, asterixis, ankle edema, scleral icterus, juandice, and coma... all can be caused by what?
Liver cell failure.
Micronodular liver regeneration (<3mm), uniform... usually due to what types of damage?

Macronodcular (>3mm), varied size?

which increases risk of hepatocellular carcinoma?
metabolic (alcohol, hemochromatosis, Wilson's)

usually due to significant liver injury leading to hepatic necrosis (e.g. posinfectious or drug induced hepatitis).

Macronodular.
Explain how melana and hematemesis can be signs of portal HTN.
portal HTN can cause esophageal varices because of the backup circulation trying to relieve HTN. they can then bleed --> sx mentioned.

also, portal HTN can cause PUD, which can go thru the stomach wall and cause the same sx.
Which is elevated in MI, AST or ALT?

Alcoholic hepatitis?

viral hepatitis?
AST

AST>ALT

ALT>AST
What is GGT?
- increased with what?
gamma-glutamyl transpeptidase)
- various liver diz, also with heavy EtOH consumption.
Elevated alk phos can be a result of which type of dz?
obstructive liver dz (hepatocellular carcinoma), bone dz, or bile duct dz.
Amylase is elevated in which two types of dz?
- how to tell the difference?
Acute pancreatitis, mumps
- if lipase is up too, it's probably acute pancreatitis.
Lipase is elevated in what?
acute pancreatitis.
What does a decrease in ceruloplasmin signal?
Wilson's dz.
Hypoglycemia in a child that just had a viral infection (VZV or influenza B especially) that Dr. Mom tx'ed with ASA. Dz?
- histological changes?
- mechanism?
Reye's syndrome.
- mitochondrial abnormalities, fatty liver, coma.
- ASA metabolites \\B-oxidation (of fatty acids) by reversible inhibition of mitochondrial enzyme.
What is the severity order (and reversibility) of hepatic steatosis, alcoholic cirrhosis, and alcoholic hepatitis?
steatosis (least severe, reversible)
hepatitis (still might be reversible)
cirrhosis (irreversible)
AST/ALT is usually > ___ in alcoholic hepatitis?

What is seen on histology?
1.5

swollen and necrotic hepatocytes with PMN infiltration. Intracytoplasmic eosinophilic inclusions (Mallory bodies) are present.
Macrovesicular fatty change in liver due to alcohol is called what?
hepatic steatosis.
Micronodular, irregularly shrunken liver w/ "hobnail" appearance is what stage of alcoholic liver dz?
- what would you expect to see on histology and where?
- associated sx?
alcoholic cirrhosis
- sclerosis around central vein (Zone III)
- associated with manifestation of chronic liver dz (jaundice, hypoalbuminemia)
Pt from Asia presents with jaundice, tender hepatomegaly, ascities, polycythemia, and hypoglycemia.

a-FP lvls are elevated.

Dz?
- how does it commonly spread in the pt?
- why is it common in asia?
Hepatocellular carcinoma/hepatoma.
- hematologous spread (unlike most carcinomas)
- they have more HBV, HCV.
Besides HCV and HBV, which other things are risk factors for hepatocellular carcinoma?
Alcoholics, a1-antitrypsin deficiency, Wilson's dz, hemochromatosis, carcinogens.
Hepatocellular carcinoma can lead to what syndrome? Why?
Budd-Chiari syndrome: clinical picture caused by occlusion of the hepatic veins and/or IVC. It presents with the classical triad of abdominal pain, ascites and hepatomegaly.

the cancer can obstruct the hepatic vein!
What is Nutmeg liver? causes?
- if the condition persists and you progress... getting centrilobular congestion and necrosis... what is this called?
liver looks like a mottled nutmed, due to backup of blood. Caused by Right heart failure or Budd-Chiari syndrome.
- cardiac cirrhosis.
Absence of JVD, visable back veins, and varices.. .all can be signs of what?
- 3 things associated with it?
- eventually leads to?
Budd-Chiari syndrome.
- hepatocellular carcinoma, pregnancy, polycythemia vera
- congestive liver disease (hepatomegaly, ascities, abdominal pain).... --> eventual liver failure.
Why does a1-antytrypisn deficiency cause hepatocellular carcinoma? What other sx would you expect?
- what would be seen i/ liver on histo?
- type of inheritance?
misfolded gene product accumulates in hepatocellular ER.
- would see panacinar emphysema.
- PAS (+) globules in liver
- Codominant trait.
At birth, which liver enzyme is immature can lead to jaundice/kernicterus?
- what type of jaundice is this?
- tx?
immature UDP-glucuronyl transferase --> unconjugated hyperbilirubinemia --> jaundice/kernicerus
- phototx converts unconjucated bilirubin to water-soluble form --> gets peed out.
Give me the type of hyperbilirubinemia, Urine biliruin, and urine urobilinogen lvls seen i/:
- hepatocellular jaundice
- obstructive jaundice
- hemolytic
- conjugated/unconjugated, increased, wnl or decreased (because the liver isn't conjugating much anymore)
- conjugated, increased urine bilirubin, decrease urine urobilinogen
- unconjugated, absent (acholuria.. the liver is working fine, it's just doing alot... hence -->) increased urine urobilogen (the normal breakdown product).