week 6- upper and lower GI Flashcards
What is liver fibrosis? Causes? Ssx? Dx?
o excess CT scar dt chronic, repeated liver cell injury
o Causes: dos w hepatic effects, affecting hepatic blood flow, drugs, chemicals
o Ssx: asx, unless develop 2nd do
o Dx: bx
• What is liver cirrhosis? Ssx? PE?
o late stage of hepatic fibrosis → widespread distortion of normal hepatic architecture
o ssx: often non-specific (anorexia, fatigue, weight loss); Late: portal HTN
o PE: Skin: Pallor, jaundice, petechiae, purpura; Abdomen: Ascites, SM; Extremities: nail clubbing
• What is work-up for cirrhosis? Px?
o LFTs often normal, Albumin and bilirubin, more helpful
o PT (coag), CBC, Viral tests (to look for cause)
o Liver bx
o Px: irreversible
• What is primary biliary cirrhosis? Ssx? PE? Work-up?
o AI liver do, progressive destruction of bile ducts →cholestasis, cirrhosis, liver failure
o Ssx: (insidious). Suspect in mid-age F w classic sxs: unexplained pruritis, fatigue, RUQ pn, jaundice, dry mouth
o PE: HM firm NNTP, mb SM
o Work-up: ↑GGT, ALP. abN AST and ALT. ↑ a-mito Abs. confirm w bx
• How is blood supplied to liver?
o dual blood supply
o Portal v (2/3): rich nutrients, oxygen
o Hepatic a (1/3): O2 rich
o Hepatic veins: drain liver to IVC
• How can the liver be injured?
o Ischemia: ischemic hepatitis, ischemic cholangiopathy
o Insufficient venous drainage: focal, diffuse, or → portal HTN
o Specific vascular lesions
• What is ischemic hepatitis? Casues? Ssx? Work-up?
o diffuse liver damage dt inadequate blood, O2
o Causes: usu systemic, perfusion prob (HF, acute hypotension), Hypoxemia (resp failure, ↑CO2), ↑metabolic demand (sepsis)
o Ssx: N/V, tender HM
o Work-up: ↑aminotransferases (1000-3000IU/L), ↑bilirubin, ↑LDH (hrs). US, MRI, arteriography to identify obstructed vessel
• What is ischemic cholangiopathy? Casues? Ssx? Work-up?
o focal damage to biliary tree dt disrupted flow from hepatic a via peribiliary arterial plexus
o Causes: procedure vascular injury: liver transplant, laparoscopic cholecystectomy, chemoembolization, radiation therapy→bile duct injury → cholestasis, cholangitis, biliary strictures
o SSX: Pruritis, pale stool
o Work-up: labs reveal cholestasis; UA (dark urine). US, MRCP, ERCP to r/o cholelithiasis, cholangiocarcinoma
• What is congestive hepatopathy? Ssx? PE? Labs?
o RCHF →diffuse venous congestion in liver
o Ssx: usu asx, RUQ discomfort (liver capsule stretches), massive jaundice (severe)
o PE: ascites, HM, hepatojugular reflex (unlike in hepatic congestion dt Budd-Chiari syndrome)
o Lab: ↑ LFTs
• What are the 2 hepatic artery dos? Causes, sxs, work-up?
o Hepatic a occlusion: dt thrombosis, emboli, iatrogenic, vasculitis, structural abn, eclampsia, cocaine, sickle cell crisis. Infarction mb asx, RUQ pain, fever, N/V, jaundice. US, angiography
o Aneurysm: uncommon. Usu saccular and multiple. Dt arteriosclerosis, trauma, vasculitis, infx. US, CT to confirm. Un-tx may → death
• What are the 2 hepatic vein dos?
o Budd-chiari syndrome
o Veno-occlusice dz (Sinusoidal Obstruction Syndrome)
• What is Budd-chiari syndrome?
o obstructed intra/extra-hepatic vessels → congested sinusoids, HM, portal HTN, ↓ portal blood flow, ascites, SM. Dt hypercoagulable state, clot of veins, IVC. Acute: fatigue, RUQ pn, n/v, mild jaundice, tender HM, ascites; ↑ aminotransferases. Chronic: wks-mos. Asx →fatigue, abdominal pain, HM lower extremity edema. Untx: die liver failure in 3 yrs
• what is veno-occlusive dz?
o endothelial injury→non-thrombotic occlusion of terminal hepatic venules and sinusoids. dt irradiation, graft vs host disease, hepatotoxins. Suspect if unexplained liver dz AND matching hx (bone marrow transplant, irradiation, etc.). Sudden jaundice, Ascites, tender, smooth HM. ↑LFTs. US, liver bx
• what are portal vein dos? Example?
o obstruct portal vein → portal HTN. Mb extra or intrahepatic
O Portal vein thrombosis: dt surgery, hypercoagulable states, CA, cirrhosis, trauma →GI bleeding from varices (usu esophagus, stomach). Usu asx unless assoc w another painful do (pancreatitis). ↑LFTs. US
• What is peliosis hepatitis?
O Mult blood-filled cystic spaces randomly in liver, mm to 3 cm
O Usu dt damage to sinusoidal lining cells from hormones (OCPs, anabolic steroids), tamoxifen, vit A
O Usu asx. cysts rupture →hemorrhage, death. jaundice, HM, liver failure
O Often found incidentally on US, CT
• What causes portal HTN? Ssx? PE?
O Cirrhosis (developed countries), Schistosomiasis (in endemic areas), hepatic vascular abn. →Esophageal varices, Portal-systemic encephalopathy O often asx, usu dt complications, acute variceal bleeding →sudden, painless upper GI bleeding O PE: ↓systolic BP, SM, ascites, peripheral edema, dilated abdominal wall veins, caput medusae (umbilicus), jaundice, spider angioma
• What is work-up for portal HTN? Px?
O transjugular catheter (rare, invasive, to measure portal pressure). US, CT: dilated intra-abdominal collateral arteries
O Mortality >50% if acute variceal hemorrhage, depends w degree bleed and degree of hepatic reserve
• What is portal-systemic encephalopathy? Causes? Pathophysiology?
O Aka hepatic encephalopathy: neuropsychiatric syndrome
O Causes: usu cirrhosis, portal HTN; fulminant hepatitis dt virus, drug, toxin
O Precipitators w liver dz: Metabolic stress (infx, electrolyte imbalance, dehydration, diuretics), dos that inc gut protein (GI bleeding, high protein diet), non-specific cerebral depressants (alcohol, sedatives, analgesics)
O Path: liver doesn’t detox →circulation →brain, mb toxic
• What are ssx of portal-systemic encelpahlopathy? Work-up?
O Constructional apraxia. Uncommon: agitation and mania. Liver flap (asterixis) when arms outstretched, wrists dorsiflexed
O Wu: Psychometric eval. CMP: electrolytes, albumin, LFT. EEG: diffuse slow-wave activity
• What is post-operative liver dysfunction?
O St after major surgery, even w/o of preexisting liver dos; usu dt hepatic ischemia, anesthesia
O Pts w well-compensated liver dz (eg, cirrhosis w normal LFTs) usu do well w surgery but may ↑severity of preexisting liver dos
• What are the 3 types of post-op liver dysfunction?
O Jaundice: ↑bilirubin formation, ↓hepatic clearance, usu w multiple transfusions, worse few days post, clears gradually
O Hepatitis: dt insufficient liver profusion (not inflammation) → transient peri-op hypotension or hypoxia, ↑aminotransferases (>1000 units/L), mild ↑bili. only few days after, clears
O Cholestasis: extrahepatic biliary obstruction dt intra-abdominal complications, post-op drugs
• What are the types of liver masses, CA, granulomas?
O Hepatic cysts O Benign liver tumors O Primary liver CA O Metastatic liver CA O Hematologic CAs O Hepatic granulomas
• What are hepatic cysts?
O =fluid-filled, usu asx, no clinical significance
O incidentally on US, CT
O Rare polycystic liver assoc w polycystic kidneys, but good hepatocellular fxn, portal HTN rare
• What are benign liver tumors?
o =solid, common, usu asx
o Types: Hepatocellualr adenoma, Focal nodular adenoma, Hemangiomas, lipomas, fibromas
o Ssx: HM, RUQ discomfort, IP hemorrhage
o LFTs usu normal to slightly abn; often incidental on US, CT; mb bx
• What is the major type of primary liver CA? ssx? Work-up? Px?
o Hepatocellular carcinoma: most common, esp East Asia and sub-Saharan Africa
o Usu w cirrhosis; common where HBV/HCV prevalent; also hemochromatosis, alcoholic cirrhosis
o Ssx: usu previously stable cirrhosis pt w RUQ pn/mass, weight loss, unexplained deterioration. St 1st sign is bloody ascites, shock, peritonitis, dt hemorrhage of tumor
o Work-up: a-Fetoprotein ↑ in40-65% (dedifferentiation of hepatocytes). CT, US, MRI. Liver bx if dx unclear
o Px: usu poor
• What are the other primary liver CAs?
o Fibrolamellar carcinoma, Cholangiocarcinoma, Hepatoblastoma, Angiosarcoma
o all uncommon
o Dx by liver bx, poor px
• What is metastatic liver CA? ssx? PE? Work-up?
o more common primary; from GI tract, breast, lung, pancreas
o asx early; non-specific: weight loss, anorexia, fever
o HM, hard, tender, palpable nodules (more severe=advanced), hepatic bruits rare, SM (esp if primary is pancreatic). Ascites from peritoneal seeding. mild jaundice
o Work-up: CT, MRI w contrast. Suspect in any pt w weight loss, HM, other primary tumor. LFTS non-specific. Dx liver bx
• What is the significance of the liver with hematologic cancers?
o Liver is commonly involved in advanced leukemia and blood related cancers
o Liver biopsy not needed
• What are hepatic granulomas? Causes? Ssx? Work-up?
o localized collections of chronic inflammatory, epithelioid, and giant multinucleated cells; not completely understood
o Causes: drugs, systemic do, infxs (TB and schistosomiasis worldwide)
o Ssx: usu asx, mb minor HM, mild jaundice; sxs reflect underlying cause (eg fever with infx)
o Work-up: LFTs; US, CT, MRI but not dx; dx by liver bx
• What are the inborn metabolic dos that cause hyperbilirubinemia?
o Unconj: gilbert syndrome, crigler-najjar syndrome, primary shunt hyperbilirubinemia
o Conj: dubin-johnson syndrome, rotor’s syndrome
• What is gilbert syndrome? Ssx? Labs?
o lifelong do, 5% of pop, dt defect in liver’s uptake of bilirubin, glucuronyl transferase activity is low, RBC destruction slightly accelerated
o usu asx
o Lab: mildly ↑ bilirubin, fluctuates 2-5mg/dL. normal LFTs, CBC. No urobilinogen
• What is crigler-najjar syndrome? 2 types?
o Rare inherited do, def glucuronyl transferase
o AR type I (complete) dz: Severe hyperbilirubinemia; usu die of kernicterus by 1 yr, may survive into adulthood; Tx: phototherapy, liver transplant
o AD type II (partial) dz: variable penetrance, less severe hyperbilirubinemia, live into adulthood, no neurologic damage
• What is primary shunt hyperbilirubinemia?
o Rare, familial, benign; overproduction of early-labeled bilirubin
• What are dubin-johnson and rotor syndromes?
o Conj hyperbilirubinemia wo cholestasis; only sx is jaundice
o DJ: rare, AR, impaired excretion of bilirubin glucuronides, dx liver bx, Liver is deeply pigmented dt melanin-like substance, histo normal
o R: rare, like DJ, but liver not pigmented
• What are the dos of the gall bladder?
o Cholelithiasis o Cholecystitis: acute/chronic o Acalculous biliary pain o Postcholecystectomy syndrome (PCS) o Choledocholithiasis o Cholangitis o Tumors of GB and bile ducts
• What is cholelithiasis? Prevalence? Risks?
o 1+ calculi (gallstones) in GB; most dos of biliary tract dt gallstones
o Prev: Developed countries: 10% adults, 20% ppl >65
o Risk: 5 F’s: female, fat, forty, fertile, FHx; American Indian ethnicity
• What is pathophysiology of cholelithiasis? 3 types?
o Biliary sludge, precursor to gallstones, develops during GB stasis
o Cholesterol stones: >85% in western world; bile supersaturated w cholesterol; dt excessive cholesterol secretion (obese, DM)
o Black pigment stones: small, hard; Ca2+ bilirubinate and inorganic salt
o Brown pigment stones: soft, greasy; Bilirubinate and fatty acids; dt infx, inflammation, parasites
• What are ssx of cholelithiasis? Work-up?
o 80% asx
o Biliary colic: RUQ pn may radiate to back, down R arm, sudden onset intense in 15-60 min, steady up to 12hr (usu <6), gradual disappear w dull ache
o n/v common w attacks
o Fever UNCOMMON unless cholecystitis has developed
o Work-up: labs unrevealing; dx abdominal US
• What is acute cholecystitis? Work-up?
o inflamed GB, develops over hrs, usu dt gallstone, obstructs cystic duct
o MC complication of cholelithiasis (≥95% w cholecystitis have cholelithiasis)
o Work-up: abdominal US; Cholescintigraphy if US equivocal or suspect acalculous cholecystitis; abdominal CT for complications like GB perforation (10%) → peritonitis, pancreatitis
• What are ssx of acute cholecystitis? PE?
o Ssx: pn like biliary colic but lasts longer (>6hr), subside 2-3 days, resolves 1 wk in 85%; Vomit common
o PE: R subcostal tenderness, (+) Murphy’s sign, Fever
• What is chronic cholecystitis? Ssx? PE? Work-up?
o > 1 wk, usu dt stones; range infiltrate of chronic inflam cells to fibrotic, shrunken GB; extensive calcification dt fibrosis = “porcelain gb”
o Ssx: Recurrent biliary colic; intensity not correlated to extent of damage
o PE: Upper abd tenderness, afebrile
o Work-up: abd US (Gallstones, st shrunken, fibrotic gb)
• What is acalculous biliary pain? Causes?
o biliary colic wo gallstones, dt structural or functional dos. Suspected when dx imaging can’t detect gallstones
o Causes: Microscopic stones, abn GB emptying, sensitive biliary tract, Sphincter of Oddi dysfunction, hypersensitive adjacent duodenum, mb gstones passed spontaneously
• What is work-up for acalculous biliary pan?
o Labs: abN biliary tract (↑ ALP, bilirubin, AST, ALT), or pancreatic abn (↑ lipase)
o abd US, mb endoscopic US (for small stones <1cm), ERCP w biliary manometry may reveal sphincter of Oddi dysfxn
• what is postcholecystectomy syndrome (PCS)? Sxs? Causes?
o abd sxs after cholecystectomy, 5-40%
o Ssx: Dyspepsia, Non-specific (not true colic), persistent pn
o altered bile flow dt loss of gb reservoir function
o Papillary stenosis (rare): fibrotic narrowing around sphincter dt trauma, inflammation dt pancreatitis, instrumentation (ERCP), prior stone passage
o retained stone
o Pancreatitis
o GERD
