Usmle Step 2: Hepatology Qbank

Front 1

Define fulminant hepatic failure, populations at risk, and tx

Back 1

hepatic encephalopathy that develops within 8 weeks of the onset of acute liver failure.

Develops more commonly in pts who are heavier users of acetaminophen, alcohol, or methamphetamines and in those who are coinfected with hep B and D viruses

Tx: considered high-priority candidates for liver transplantation since mortality > 80%

Front 2

Primary sclerosing cholangitis features

Back 2

inflammation and fibrosis of the intrahepatic and extrahepatic biliary ducts diagnosed by cholangiography

Front 3

Tx for asymptomatic gallstones

Back 3

No treatment indicated (20% will eventually develop sx within 15 yrs)

Symptomatic = laparascopic cholecystectomy (70% of pts will experience sx recurrence within 2 yrs)

Front 4

pancreatic pseudocyst

Back 4

encapsulated area of enzyme-rich fluid, tissue, and debris that accumulates within the pancreas and causes an inflammatory response.

Complication of both acute and chronic pancreatitis, best diagnosed by U/S and tends to resolve spontaneously.

Front 5

How does hepatic encephalopathy occur?

Back 5

CNS complication of liver failure secondary to accumulation of ammonia in blood because of inability of liver to detoxify ammonia into urea

Front 6

Initial inciting event in acute cholecystitis minus any signs of liver damage

Sx?

Back 6

Impaction of gallstone into the cystic duct (if presenting with liver sx, into the common bile duct) with subsequent inflammation and infection

Sx include acute onset of F/N/V and RUQ abdominal pain, leukocytosis

Front 7

Findings in men with cirrhosis

Back 7

telangiectasias, palmar erythema, testicular atrophy, gynecomastia, and ED

Front 8

pt with newly diagnosed hep C infxn. next step in mgmt?

Back 8

should be evaluated for antiviral treatment with liver bx first!

offers the best clinical predictor of dz progression and helps assess likely response to tx. It also can determine the stage of the dz, r/o other concomitant liver dz (eg hemochromatosis), and guide tx decisions (duration, surveillance)

Front 9

presence of bili in urine

Back 9

conjugated hyperbilirubinemia

rotor syndrome = benign condition in which there is a defect of hepatic storage of conjugated bili, resulting in its leakage into the plasma. LFTs are nl, and tx unnecessary

unconjugated includes hemolytic anemia, thalassemia, gilbert's and PNH

Front 10

hepatic adenoma

Back 10

benign tumor most often seen in young and middle aged women who are taking OCPs. Severe intra-tumor hemorrhage and malignant transformation are the most dreaded complications

Front 11

nonalcoholic steatohepatitis risk factors + mechanism

Back 11

obesity, DM, HLD, TPN, and usage of certain meds

aka NASH

histologic features of hepatic tissue are indistinguishable from those of alkhep

mechanism: most likely mechanism is insulin resistance leading to increased peripheral lipolysis, trig synthesis, and hepatic uptake of fatty acids -> leads to intrahepatic fatty acid oxidation, which increases oxidative stress and proinflammatory cytokines with end result of liver inflammation, increased fat accumulation in thel ier, and fibrosis/cirrhosis

Front 12

pts with liver mass who traveled to an endemic area

Back 12

should be evaluated for amebic abscesses with serologic testing and receive empiric tx with oral metronidazole!!! Bc of associated risks, cyst aspiration is not typically recommended unless pt fails therapy

Front 13

immune clearance of hepB

Back 13

fluctuating level sof liver inflammation can produce variable liver transaminase levels and eventual clearance of HBeAg. During this phase, the presence of HBeAg indicates active replication of virus, even in pts with nl ALT. Such patients need serial measurements of both ALT and HBeAg every 3-6mo until they achieve viral clearance

Front 14

tx of acute cholangitis

Back 14

provision of supportive care and broad-spectrum antibiotics

pts who do not respond to this tx regimen should undergo biliary drainage with an endoscopic retrograde cholangiopancreatography

alternatives include transhepatic cholangiopancreatography or placement of large bore T tube (choledochotomy)

Front 15

lab tests in the evaluation of liver dz

Back 15

either assess liver functionality (PT time, bili, albumin, cholesterol) or structural integrity and cellular intactness (transaminases, GGTP, alkphos)

PT time considered the single most important test to assess liver function bc all clotting factors (except factor VIII) are synthesized in thel iver. When the liver is unable to create sufficient amts of clotting factors, PT is prolonged.

Elevated serum transaminases are indicative of hepatocyte damage bc these intracellular enzymes lea k from hepatocytes.

A marked increase in transaminases is indicative of active and ongoing tissue destruction. Progressive decrease in transaminase levels signals EITHER RECOVERY FROM LIVER INJURY or that VERY FEW HEPATOCYTES ARE FUNCTIONAL. thus the interpretation of transaminase levels should be made in light of other LFTs.

rise in PT with decrease in transaminase levels implies very little functional tisue remainsi n theliver, which can happen rapidly in cases of fulminant hepatic failu

Front 16

review gallstone characteristics

Back 16

review

Front 17

severe acute hepatic injury

Back 17

transaminase levels > 1000 most often due to: acute viral hep, ischemic hepatopathy (shock liver) or toxic livery injury (especially acetaminophen)

Front 18

infection with hepE in pregnant woman

Back 18

high rate of progression to fulminant hepatitis in pregnant women, especially in the third trimester