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3 GI 2/5 Liver
Step Up to Medicine, Chap 3, Liver
| Question | Answer |
|---|---|
| Which classification is used to estimate hepatic reserve in liver failure: measures disease severity, and is predictor of morbidity and mortality? | Child's classification |
| Which Child's class indicates milder liver disease? Most severe liver disease? | Class A=mild (bili <2). Class C= most C-vere (severe) (bili >3). |
| 2 MCC of cirrhosis? | Alcoholic liver disease (MCC) and chronic viral infection (esp Hep C) |
| Gold std for diagnosing cirrhosis? | Liver biopsy |
| Name 2 drugs commonly assoc'd with cirrhosis. | Acetaminophen toxicity and methotrexate |
| Which complication of bone marrow transplant can lead to cirrhosis? | Hepatic veno-occlusive disease |
| Treatment for portal HTN? | Use transjugular intrahepatic portal-systemic shunt (TIPS) to lower pressure |
| Most dangerous complication of portal HTN? | Bleeding (hematemesis, melena, hematochezia) 2/2 esophogastric varices is MC |
| Tx for bleeding varices? | Give fluids for stabilization of hemodynamics, octreotide drip (fewer SE than vasopressin), beta blocker (prevents recurrence as long-term therapy). Can also do variceal ligation or banding. |
| Test of choice to diagnose pt with hematemesis? | Emergent upper GI endoscopy |
| If IV vasopressin is given to treat bleeding varices, what drug is also given to prevent complications and side effects? | Nitro (prevents coronary vasoconstriction/MI, decreased CO, HTN) |
| Indications for paracentesis of ascitic fluid? | New-onset ascites, worsening ascites, or suspected SBP. |
| What measurement of ascitic fluid helps determine the cause of the ascites? Which numbers point toward portal HTN as the likely cause? | Serum ascites albumin gradient. >1.1=portal HTN. <1.1= consider other causes |
| Tx for ascites? | Bed rest, low-sodium diet, and diuretics (furosemide and spironolactone). Theraptueic paracentesis if dyspnea or early satiety. Peritonovenous shunt or TIPS to reduce portal HTN. |
| What is the mechanism of lactulose in treating hepatic encephalopathy? | Metabolism of lactulose by bacteria in the colon favors formation of NH4+ which is poorly absorbed by the GI tract thus promoting excretion of ammonia |
| What is the mechanims of neomycin in treating hepatic encephalopathy? | Decreases ammonia production by bacteria in intestines |
| How often should labs be ordered on cirrhotic pts? Which labs should be ordered? | Every 3-4 mos. Order CBC, renal f'n tests, electroyltes, LFTs, and coag tests. Also do endoscopy to look for esophageal varices. |
| Name two things that often precipitate hepatorenal syndrome? | Infection or diuretics. |
| Azotemia, oliguria, hyponatremia, hypotension, low urine sodium (<10mEq/L) in a pt with cirrhosis. | Hepatorenal syndrome. Indicates end-stage liver disease. |
| Tx for hepatorenal syndrome? | Liver transplant. Very poor prognosis, and usually fatal w/out transplant. |
| Top 3 bacteria causing SBP? | E coli (MCC), Klebsiella, Strep pneumo |
| Diagnostic parameters in paracentesis fluid for SBP? | WBC >500, PMN >250 with positive culture. |
| How long must a pt abstain for alcohol before being considered for liver transplantation? | 6mos |
| AR disease of copper metabolism | Wilson's disease |
| Cause of Wilson's disease? | Deficiency of ceruloplasmin (copper-binding protein necessary for excretion) in liver--> hepatocyte death--> leakage of copper into various organs (corneas, kidneys, brain) |
| 3 findings used to diagnose Wilson's disease? | 1. Hepatic disease (elevated aminotransferases, impaired coag factors and albumin synthesis). 2. Serum ceruloplasmin levels (normal levels don't exclude dx though). 3. Liver biopsy (elevated [copper]) |
| Treatment for Wilson's disease? | Chelating agents (D-penicillamine), Zinc (prevents dietary uptake; give alone if no sx or with chelators if symptomatic), liver transplant (unresponsive to therapy or fulminant liver failure). |
| AR disease of iron absorption | Hemochromatosis |
| Cause of hemochromatosis | Excess absorption of iron in intestines--> increased accumulation of iron as ferritin and hemosiderin in organs--> organ fibrosis |
| Primary organ affected in hemochromatosis? | Liver (also affects pancreas, heart, skin,joints, thyroid, gonads, and hyopthalamus) |
| Name 2 endocrine disorders caused by hemochromatosis. | Bronze diabetes: iron deposition in pancreas and hyperpigmentation of skin. Also hypothyroidism. |
| Iron studies in hemochromatosis show? | Elevated seru iron and serum ferritin. Elevated iron saturation (transferrin near 100%). |
| Diagnostic test required for hemochromatosis? | Liver biopsy (determines hepatic iron concentration) |
| Tx for hemochromatosis? | Repeated phlebotomies. Liver transplant in advanced cases. |
| Benign liver tumor MC seen in young women (15-40yo). | Hepatocellular adenoma |
| Risk factors for hepatocellular adenoma? | OCP use, female sex, and anabolic steroid use. |
| Tx for hepatocellular adenoma? | D'C OCPs, surgical resection for tumors >5cm that don't regress after D'C'ing OCPs. Otherwise there's a risk of rupture. |
| MC type of benign liver tumor | Cavernous hemangioma |
| Diagnostic test of choice in cavernous hemangioma? Which diagnostic test is contraindicated? Why? | Diagnose with imaging tests (CT w/IV contrast, US). Do NOT use biopsy b/c of risk of rupture and hemorrhage. |
| Which conditions can increase the size of cavernous hemangiomas? | Pregnancy and OCP use. |
| Tx for cavernous hemangioma? | Most cases req' no tx. Consider resection if pt is symptomatic or if high risk of rupture (large tumors). |
| Benign liver tumor in women of reproductive age with NO assoc'n with OCP use? | Focal nodular hyperplasia |
| Tx for focal nodular hyperplasia? | None |
| 2 MC malignant liver tumors? | HCC and cholangocarcinomas |
| Which subtype of HCC is assoc'd with Hep B/C and cirrhosis? | Non-fibrolamellar (MC type of HCC). Usually unresectable with short survival time (months). |
| Which subtype of HCC is NOT assoc'd with Hep B/C or cirrhosis, and is more commonly seen in young people? | Fibrolamellar (more often resectable; longer survival time) |
| Name 3 chemical carcinogens assoc'd with HCC. | Aflatoxin, vinyl chloride, and thorotrast. |
| What is prognosis of HCC if unresectable? If resectable? | <1 yr if unresectable. 25% survival at 5 years if resectable. |
| Tumor marker used as screening tool in HCC? | AFP (also helpful in monitoring response to therapy) |
| Liver disease assoc'd with obesity, hyperlipidemia, and DM | NASH |
| AD condition with decreased activity of hepatic uridine diphosphate glucoronyl transferase causing isolated elevation of unconjugated bilirubin | Gilbert's syndrome |
| Pt on crash diet coming in with jaundice and elevation of unconjugated bilirubin | Gilbert's disease (also illness, fever, alcohol, infection) |
| Blood draining into duodenum via CBD | Hemobilia |
| MCC hemobilia | Trauma |
| Dx test for hemobilia? | Arteriogram |
| Which infections are associated with hyatid liver cysts? | Infection from tapeworm Echinococcus granulosus, or less commonly Echinococcus multilocularis |
| MC location for hyatid liver cysts? | right lobe of liver |
| Tx for hyatid liver cysts? | Surgical resection with mebendazole post-op. |
| MCC pyogenic liver abscess? | Biliary tract obstruction (obstruction of bile outflow allows bacterial proliferation). ALso GI infection (diverticulitis, appendicitis), penetrating liver trauma (GSW, trauma) |
| Which 4 organsisms are implicated in pyogenic liver abscesses? | E coli, Klebsiella, Proteus, Enterococcus |
| MC location for liver abscess (both pyogenic and amebic)? | Right lobe |
| Clinical features of pyogenic liver abscess? | Fever, malaise, anorexia, weight loss, nausea/vomiting, RUQ pain, and jaundice |
| Dx of pyogenic liver abscess? | US or CT with elevated LFTs |
| Treatment of pyogenic liver abscess. | IV antibiotics and percutaneous drainage of abscess (may need surgical drainage). Fatal if untreated. |
| Liver abscess most commonly seen in men, especially MSM | Amebic liver abscess |
| Causative organism in amebic liver abscess? | Entamoeba histolytica (fecal-oral transmission. amebae reach liver via hepatic portal vein) |
| Clinical features of amebic liver abscess? | Fever, RUQ pain, n/v, hepatomegaly, diarrhea |
| Dx of amebic liver abscess? | Serologic testing (IgG immunoassay) establishes diagnosis. Stool antigen test not sensitive. LFTs elevated. Difficult to distinguish from pyogenic abscess on imaging. |
| Tx for amebic liver abscess? | IV metronidazole. Therapeutic aspiration if risk of rupture due to large size or if no response to medical therapy. |
| Liver disease caused by occlusion of hepatic venous outflow-> hepatic congestion and microvascular ischemia | Budd Chiari syndrome |
| Which myeloproliferative disorder can cause Budd Chiari? | Polycythemia vera (also hypercoagulability, pregnancy, chronic inflammation, infection, cancer, trauma) |
| Tx for Budd Chiari? | Surgery (balloon angioplasty with stent placement in IVC, portocaval shunts) and liver transplantation w/cirrhosis |
| When does jaundice become clinically evident? | Bilirubin >2 |
| Dark urine is only seen with which type of bilirubin? Why? Toxicity? | Conjugated (direct) bilirubin b/c it's water soluble (loosely bound to albumin) so it can be excreted in urine. Non-toxic. |
| Name 3 major causes of jaundice. | 1. Hemolysis, 2. Liver disease, 3. Biliary obstruction |
| Why is unconjugated bilirubin toxic? | B/c the unbound form can cross BBB and cause neuro deficits |
| Dark urine and pale stools signify which type of hyperbilirubinemia? | Dark urine and pale stools |
| Where is the defect- prehepatic or posthepatic?: Unconjugated hyperbilirubinemia | Prehepatic |
| Where is the defect- prehepatic or posthepatic?: conjugated hyperbilirubinemia | Posthepatic |
| Jaundice, gray stools, dark urine, pruritus, elevated alk phos, increased serum cholesterol, skin xanthomas, malabsorption of fats and ADEKs | Cholestasis |
| Dubin-Johnson: unconj or conj hyperbilirubinemia? | Conj |
| Rotor's syndrome: unconj or conj hyperbilirubinemia? | Conj |
| Gilbert's syndrome: unconj or conj hyperbilirubinemia? | Unconj |
| Crigler Najar, types I and II: unconj or conj hyperbilirubinemia? | Unconj |
| Physiologic disease of newborn: unconj or conj hyperbilirubinemia? | Unconj |
| Urine positive for bilirubin: unconj or conj hyperbilirubinemia? | Conj |
| Urine negative for bilirubin: unconj or conj hyperbilirubinemia? | Unconj |
| Isolated unconjugated hyperbilirubinemia in an asymptomatic pt with no hemolysis? | Likely Gilbert's |
| Which aminotransferase is more sensitive for liver damage: AST or ALT? | ALT (L for Liver) |
| What is the expected AST:ALT ratio in alcoholic hepatitis? | >2:1 (AST never >500, ALT never >300) (the higher the ratio, the more likely alcohol is the cause) |
| Name 4 places alk phos is found. | Liver, bone, gut, placenta. |
| How is a GGT level useful in conjunction with an elevated alk phos? | If GGT is also elevated, suggests hepatic origin of obstruction. If GGT is normal, think pregnancy or bone disease as cause. |
| If LFTs show cholestasis, what test should be ordered? | Abd or RUQ ultrasound |
Created by:
sarah3148
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