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

Front 19

tx of hepatic encephalopathy

Back 19

lactulose, rifaximin, and laxatives

Front 20

most common malignancy of liver

Back 20

metastasis from colon, breast, or lung

note: HCC usually accompanied by elevation of AFP -> one lesion with poorly defined margins instead of several masses of varying sizes.

Front 21

isoniazid can cause what?

Back 21

idiosyncratic liver injury with histological features similar to those seenin pts with viral hepatitis: panlobular monnuclear infilltration and hepatic cell necrosis

approx 10-20% of pts will develop mild aminotransferase elevation within first few weeks of tx (typically less than 100). This hepatic injury is typically self-limited and will resolve without intervention.

Front 22

hyperestrogenism in cirrhosis leads to?

Back 22

gynecomastia, testicular atrophy, decreased body hair, spider angiomas, and palmar erythema

Front 23

familial conjugated hyperbili

Back 23

dubin-johnson and rotor syndrome

only dubin johnson presents with a dark granular pigment present in hepatocytes

Front 24

poor surgical candidate for cholecystitis patient. next step?

Back 24

ursodeoxycholic acid to dissolve small radiolucent gallstones in pts with nl, functional gallbladdders who are poor surgical candidates.

however, med is very costly and a/w high risk of relapse when therapy is halted

Front 25

emphesematous cholecystitis

Back 25

common form of acute cholecystitis in elderly diabetic males. Arises due to infection of the galbladder wall with gas=forming bacteria

Front 26

hydatid cyst vs amebic liver abscess

Back 26

hydatid cyst: usually caused by infection with echinococcus granulosus, which is acquired by intimate contacts with dogs

amebic liver abscess: entamoeba histolytica is a protozoan -> remember mexico trip
- also look for dysentery and RUQ pain. primary infxn is in the colon leading to bloody diarrhea. however the ameba may be transported to the liver by portal circulationthus leading to an amebic liver abscess

Front 27

sphincter of oddi dysfunction. tx?

Back 27

ERCP with sphincterotomy

Front 28

liver failure -> p/w severe epistaxis, bleeding from IV sites, and bloody diarrhea

next step?

Back 28

give FFP -> coagulopathic!

Front 29

complications of acute pancreatitis

Back 29

pleural effusion, ARDS, ileus, and renal failure

Front 30

ischemic hepatic injury

Back 30

in setting of hypotension manifests as acute, massive increases in the AST and ALT with milder associated icnreases in the total bili and alkphos. (example showed AST and ALT in 2,000+, alk phos mildly elevatedp

In pts who survive the inciting condition, liver enzymes typically return to nl within a few weeks

Front 31

postoperative cholestasis

Back 31

can develop after a prolonged surgery characterized by hypotension, extensive blood loss into tissues, and massive blood replacement

thought to be due to 1) increased pigment load (caused by transfusion), 2) decreased liver functionality (due to hypotension), and decreased renal bili excretion (caused by tubular necrosis)

Front 32

acute liver failure

Back 32

elevated PT time and neurologic s/s suggestive of hepatic encephalopathy

Front 33

postcholecystecomy syndrome

Back 33

persistent abdominal pain or dyspepsia that occurs either postoperatively or mo to years after a cholecystectomy.

Can be biliary (retained common bile duct or cystic duct stone, biliary dyskinesia) or extra-biliary (pancreatitis, PUD, CAD), causes

patients usually notice the same pain they had prior to surgery, new pain just after surgery, or same pain that never went away.

with elevated alkphos and mildly abnl aminoserotransferases and dilated common bile duct on US, thinkof common bile duct stone or biliary sphincter of Oddi dysfunction.

next step involves endoscopic US, ERCP, or MRCP!!!

Front 34

SAAG

Back 34

distinguishes transudative from exudative process

subtract ascites albumin concentration from serum albumin concentration. A difference of 1.1 or greater is 95% accurate in diagnosing a transudative process consistent with portal hypertension.

(think of it as a wide open door which would be an exudative process as having a smaller difference)

Front 35

courvoisier's sign and virchow's node

Back 35

classic findings of pancreatic adenocarcinoma

courvoiser's sign: nontender but palpable gallbladder at the right costal margin in a jaundiced patient

Virchow's node: supraclavicular adenopathy in a pt with metastatic dz

lab eval: usually increased serum bili and alkphos in conjunction with mild anemia

use abdominal US first on pts with jaundice, and if nondiagnostic, use abdominal CT

Front 36

reversibility of liver conditions

Back 36

fatty liver (steatosis), alkhep, and early fibrosis of the liver can be REVERSIBLE with cessation of alcohol intake

true cirrhosis (with regenerative nodules) is IRREVERSIBLE, regardless of alcohol abstinence

Front 37

nl liver span

Back 37

6-12cm in the midclavicular line

Front 38

alkhep histologic findings

Back 38

mallory bodies, infiltration by neutrophils, liver cell necrosis and a perivenular distribution of inflammation

Front 39

cryoglobinemia

Back 39

immune complex disorder (IgM against anti-hepC virus IgG) most commonly due to chronic hep C.

pts may develop vasculitis involving hte skin, kidney, nerves, or joints.

Low complement levels, increased RF, increased liver transaminases, serum cryoglobulins, and kidney/skin bx can confirm the dx

2958

Front 40

unvaccinated Hep B individuals exposed to hep b. next step?

Back 40

administer hep B immune globulin and hepB vaccine now!