Term
| what is the incidence of cholelithiasis? |
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Definition
| 10-20% of the population - most of which are clinically silent |
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Term
| what do gallstones in most western countries contain? |
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Definition
| crystalline cholesterol monohydrate as well as bilirubin, Ca salts (pigment stones) |
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Term
| what are the risk factors for cholelithiasis? |
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Definition
| female over 40 (increases w/age), obsese, fertile, OCP |
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Term
| what plays a major role in cholelithiasis? other factors? |
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Definition
| hypersecretion of biliary cholesterol (not directly related to serum cholesterol). increased expression of hepatic lipoprotein receptors and increased hepatic HMG-CoA activity. all of these factors lead to a net increase in cholesterol uptake and biosynthesis. (cholesterol taken up better & precipitates & causes layers on layers leading to stones) |
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Term
| can incidence of cholelithiasis be inherited? |
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Definition
| yes, often pts w/gallstones have a family hx of the same. |
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Term
| what is the pathogenesis of inherited cholelithasis? |
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Definition
| inborn errors can lead to impaired bile salt synthesis, secretion, production of serum and biliary levels of cholesterol, and defects in lipoprotein receptors |
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Term
| what characterizes cholesterol stone formation? what % of these end up being radiopaque? |
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Definition
| bile in the gallbladder *saturated with cholesterol (sludgy, thick) and *decreased motility of the gall bladder lead to acceleration of cholesterol nucleation/precipitation, then mucus trapping the crystals leads to stone. 10-20% of these will end up radiopaque (depends on calcium carbonate composition). |
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Term
| why is the wall of a gallbladder with stones more thick usually? |
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Definition
| b/c of some associated cholecystitis |
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Term
| what is the path of formation for cholesterol gallstones? |
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Definition
| bile & lipids -> hypersaturation -> lamellar vesicles -> gall bladder hypomotility -> mucus hypersecretion -> calcium abnormalities -> stones |
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Term
| what are pigment gallstones? is there anything which can increase the chance of these forming? |
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Definition
| gallstones composed of insoluble calcium salts and unconjugated bilirubin. black stones: in sterile GB, often present in great #. brown stones: infected bile ducts, composed of Ca++ soaps and radiolucent. infections of e. coli/ascaris lumbricoides increases the chance of pigment stone formation. 50-70% of these are radiopaque. |
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Term
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Definition
| RUQ pain, fever, jaundice: associated with complications of gallstones |
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Term
| what are complications of cholelithiasis? |
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Definition
| perforation, fistulae, cholangitis, pancreatitis |
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Term
| what kind of gall stones are more likely to cause duct obstruction? cause ileus/bowel obstruction? |
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Definition
| small stones are more likely to cause duct obstruction, which is associated with pain. large stone may erode into the small bowel and produce "gallstone ileus" and bowel obstruction |
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Term
| do gallstones increase the risk of GB CA? |
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Definition
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Term
| what is the morphology of acute cholecystitis? |
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Definition
| inflammation of the gall bladder; large, tense, red, blotchy - may be purulent exudate, the lumen may have pus/stones/turbid bile, or there may be empyema (lumen filled w/pus) |
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Term
| what is the general pathophysiology of acute cholecystitis? |
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Definition
| acute cholecystitis is usually caused by obstruction of the neck or cystic duct by stones. there can also be *acalculous cholecystitis due to biliary sx, trauma, burns, hyperalimentation, and postpartum state. |
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Term
| what is the specific pathophysiology associated with acute calculous cholecystitis? |
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Definition
| chemical irritation/inflammation. luminal lecithins are converted to lysolecithins. bile salts injure the mucosal epithelium. prostaglandins contribute to inflammation. intraluminal pressure increases and impairs blood flow. |
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Term
| what is the specific pathophysiology associated with acute acalculous cholecystitis? |
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Definition
| this is more insidious, symptoms are less defined and there is increased incidence of gangrene/perforation associated with *salmonella typhi/staph. *clostridium may also be involved and form gas pockets. |
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Term
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Definition
| cholesterol hypersecretion from the liver within the lamina propria of the gallbladder. this can give rise to strawberry gallbladder: yellow deposits on the mucosal surface |
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Term
| what are causes/associations w/chronic cholecystitis? |
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Definition
| chronic cholecystitis usually occurs after repeated bouts of acute cholecystitis, but may not every time. supersaturation of the bile can also lead to chronic inflammation over time. |
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Term
| what is the morphology of chronic cholecystitis |
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Definition
| grossly: the gallbladder wall may be thickened, gray-white and less flexible. histologically: variable influx of chronic inflammatory cells and *rokitansky-ashcoff sinuses (outpouchings of mucosal epithelium) |
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Term
| what is porcelain gall bladder? |
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Definition
| dystrophic calcification due to chronic cholecystitis associated with an increased risk of CA |
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Term
| what is xanthogranulomatous cholecystitis? |
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Definition
| this describes a shrunken, nodular, chronically inflamed gallbladder with foci of necrosis/hemorrhage, lipid-filled macrophages and fibrosis. |
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Term
| what is hydrops of the gall bladder? |
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Definition
| this describes an atrophic, obstructed gall bladder containing clear secretions |
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Term
| what are the clinical features of chronic cholecystitis? |
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Definition
| more insidious, n/v, fatty food intolerance, variable degree of pain, and same possible complications as acute form |
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Term
| what is choledocholithiasis? |
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Definition
| stones in the bile duct which may be asymptomatic or cause obstruction in the biliary tree. choledocholithiasis may be associated with pancreatitis, abscesses, and *secondary biliary cirrhosis. |
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Term
| what is ascending cholangitis? |
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Definition
| marked inflammation and (bacterial) infection of the biliary tract |
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Term
| what are common causes of ascending cholangitis? |
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Definition
| choledocholithiasis, tumors, catherization, pancreatitis, infections (e. coli, klebsiella, and clostridium) |
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Term
| what are symptoms of ascending cholangitis? |
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Definition
| fever, chills, abdominal pain, jaundice. suppurative cholangitis may be present (puss fills the biliary tree) and *sepsis (rather than cholestasis) is the dominant clinical presentation. reynold's pentad: RUQ pain, fever, jaundice, *septic shock, and *CNS depression (last 2 differentiate from cholecystitis or cholelithiasis). |
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Term
| what are the 2 forms of biliary atresia? |
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Definition
| *fetal form: ineffective establishment of latency of thoracic and abdominal organ development. *perinatal form: normally developed biliary tree is destroyed after birth, possibly due to virus. |
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Term
| what is the pathophysiology of biliary atresia? can cirrhosis occur? |
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Definition
| there is inflammation and fibrotic stricture of the hepatic or common bile duct, destruction of the intrahepatic biliary tree and there may be extrahepatic biliary obstruction. this leads to biliary duct proliferation, portal tract edema and fibrosis and if not recognized or controlled, *cirrhosis may occur in 3-6 mos |
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Term
| what are the clinical features of biliary atresia? |
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Definition
| infants present with neonatal cholestasis, which can be treated with sx, but liver transplant is the best tx. w/o sx intervention, death occurs within ~2 years of birth |
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Term
| what characterizes CA of the extrahepatic bile ducts? risk factors? |
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Definition
| CA of the extrahepatic bile ducts is uncommon but aggressive and can lead rapidly to jaundice. most are adenomcarcinomas which appear as firm gray nodules (not surgically resectable) and mean survival is 6-18 mos. there is an increased risk for CA of the extrahepatic bile ducts among pts with primary sclerosing cholangitis, *ulcerative colitis (UC), cystic liver disease, fluke infections |
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Term
| what characterizes CA gallbladder? |
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Definition
| most gallbladder CA are adenocarcinoma, stones are present in 60-90% of cases, and most cases are seen in the pt's 7th decade. chronic inflammation plays a role and most have invaded the liver by dx. they have exophytic and infiltrating patterns and the peritoneum, GIT, and lymph nodes are sites of common spread. these have a poor survival rate. |
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