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pathoma unit 6 > exocrine, gallbladder, liver > Flashcards

exocrine, gallbladder, liver Flashcards

1
Q

annular pancreas

A

developmental malformation in which the pancreas forms a ring around the duodenum. may cause obstruction of the duodenum.

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2
Q

acute pancreatitis

A

inflammation of the pancreas, usually with hemorrhage. due to autodigestion of the pancreatic parenchyma by pancreatic enzymes.

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3
Q

what happens if trypsin is prematurely activated

A

then all the enzymes will activated. results in liquefactive hemorrhagic necrosis of the pancreas. also fat necrosis of the peripancreatic fat.

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4
Q

what are the most common causes of pancreatitis

A

alcohol and gall stones

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5
Q

what are other causes of pancreatitis

A

trauma, hypercalcemia, hyperlidemia, drugs, scorpion stings, mumps, rupture of posterior duodenal ulcer.

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6
Q

clinical features of pancreatitis

A

epigastric abdominal pain that radiates to the back. nausea and vomiting. periumbilical and flank hemorrhage. elevated serum lipase and amylase, lipase is more specific for pancreatic damage. hypocalcemia

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7
Q

why is there hypocalcemia in pancreatitis

A

calcium is consumed during saponification of fat necrosis

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8
Q

what are the complications of pancreatitis

A

shock due to pancreatic hemorrhage and fluid sequestration. pancreatic pseudocyst formed by fibrosis tissue surrounding liquefactive necrosis and pancreatic enzymes. pancreatic abscess often due to E coli. DIC and ARDS

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9
Q

what is the presentation of pancreatic abscess

A

abdominal pain, high fever, persistently elevated amylase.

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10
Q

chronic pancreatitis

A

often due to acute. fibrosis of parenchyma.

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11
Q

what are the most common causes of chronic pancreatitis.

A

alcohol and cystic fibrosis. many causes are idiopathic

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12
Q

clinical features of chronic pancreatitis

A

epigastric pain radiates to back, pancreatic insufficiency that leads to malabsorption with steatorrhea and fat soluble vitamin deficiency. dystrophic calcification on imaging. there is a chain of lakes pattern on the imaging due to dilation of pancreatic ducts. secondary DM, increased risk of pancreatic carcinoma

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13
Q

are amylase and lipase reliable markers for chronic?

A

no.

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14
Q

pancreatic carcinoma

A

adenocarcinoma arising from the pancreatic ducts.

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15
Q

when is pancreatic carcinoma most commonly seen

A

average age is 70

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16
Q

what are the major risks for pancreatic carcinoma

A

smoking and chronic pancreatitis

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17
Q

clinical features of pancreatic carcinoma

A

epigastric abdominal pain and weight loss, obstructive jaundice with pale stool and palpable gallbladder. pancreatitis, migratory thrombophlebitis

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18
Q

what is associated with tumors that arise in the heads of the pancreatitis

A

obstructive jaundice with pale stool and palpable gallbladder

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19
Q

what is the serum marker for pancreatic carcinoma

A

CA 19-9

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20
Q

how does migratory thrombophlebitis present

A

swelling, erythema and tenderness in the extremities.

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21
Q

what is associated with secondary DM in pancreatic carcinoma

A

tumors of the body and tail.

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22
Q

what is whipple procedure and what is it used for.

A

pancreatic carcinoma. involves surgical resection involving removal of the head and neck of the pancreas, duodenum and gallbladder.

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23
Q

what is the prognosis of pancreatic cancer

A

very poor. 1 year survival is 10%

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24
Q

billiary atresia

A

failure to form or early destruction of the extra hepatic biliary tree. leads to biliary obstruction within the first two years of life. presents as jaundice and progresses to cirrhosis

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25
Q

cholelithiasis

A

solid round stones in the gallbladder. due to precipitation of cholesterol or bilirubin in bile. arises with supersaturation of cholesterol or bilirubin decreased phospholipid or bile acids or stasis. gallstones are usually asymptomatic.

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26
Q

what are the most common gallbladder stones

A

cholesterol 90%. they are yellow stones. they are usually radiolucent, but can be opaque due to calcium.

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27
Q

what are the risk factors for gall stone

A

age (40), female due to estrogen, obesity, multiple pregnancies, and oral contraceptives. clofibrate, native americans, crohn’s and cirrhosis

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28
Q

.bilirubin stones

A

usually radioopaque. extravascular hemolysis, biliary tract infections

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29
Q

complications of gallstones

A

biliary colic, acute and chronic cholecystitis. ascending cholangitis, gallstone ileus, and gallbladder cancer

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30
Q

biliary colic

A

waxing and waning right upper quadrant pain. due to gallbladder contracting against stone lodged in the cystic duct. symptoms relieved if stone passed.

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31
Q

what happens f the common bile duct is obstructed

A

acute pancreatitis or obstructive jaundice.

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32
Q

acute cholecystitis

A

acute inflammation of the gallbladder wall. impacted stone results in dilation and ischemia, e coli growth and inflammation. presents in right upper pain often radiates to the right scapula. there is fever with increased WBC and nausea and vomiting. there is sometimes increased serum phosphatase from duct damage.

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33
Q

what are the risks of acute cholecystitis

A

rupture if left untreated.

34
Q

chronic cholecystitis

A

chronic inflammation of the gallbladder. chemical irritation from longstanding cholelithiasis with or without superimposed bouts of acute cholecystitis. characterized by herniation of gallbladder mucosa into the muscular wall rokitansky-achoff sinus. presents with vague upper right quadrant pain especially after eating. there is an increased risk of carcinoma.

35
Q

porcelain gallbladder

A

late complication of chronic cystitis, shrunken hard gallbladder due to longstanding inflammation. fibrosis and calcification. need to remove

36
Q

ascending cholangitis

A

bacterial infection of the bile ducts. usually due to an ascending infection of gram negative enterics. presents as sepsis, jaundice and abdominal pain. increased incidence of stone in the biliary duct.

37
Q

gallstone illeus

A

gall stone enters and obstructs the small bowel. due to cholecystitis and fistula formation between the gallbladder and small bowel.

38
Q

gall bladder carcinoma

A

adenocarcinoma that arises from the glandular epithelium that lines the gallbladder. gall stones are a major risk factor especially when complicated by porcelain. classically presents as cholecystitis in elderly women.

39
Q

what is the prognosis of gall bladder carcinoma

A

poor

40
Q

jaundice

A

yellow discoloration of the skin. earliest sign is scleral icterus. due to increased serum bilirubin arises with disturbances in bilirubin metabolism.

41
Q

viral hepatitis

A

inflammation of the liver parenchyma due to either hepatitis, EBV, CMV. acute hepatitis can lead to chronic hepatitis.

42
Q

how does acute hepatitis present?

A

jaundice and dark urine. fever malaise, nausea, and elevated liver enzymes.

43
Q

what does the inflammation of hepatitis look like

A

involves the lobules of the liver and portal tracts and is characterized by apoptosis. some cases are asymptomatic with elevated enzymes. the symptoms last less than 6 months.

44
Q

what characterizes chronic hepatitis

A

symptoms lasting longer than 6 months. inflammation involves mainly the tracts. there is a risk to cirrhosis.

45
Q

cirrhosis

A

end-stage liver damage characterized by disruption of normal parenchyma by bands of fibrosis and regenerative nodules of hepatocytes.

46
Q

how is the fibrosis mediated in cirrhosis

A

TGF-beta from stellate cells that lie underneath the endothelial cells that line the sinusoids

47
Q

what are the clinical features of cirrhosis

A

portal hypertension leads to ascites, congestive splenomegaly portosystemic shunts (esophageal varices, hemorrhoids, and caput medusae). hepatorenal syndrome (renal failure caused by renal failure. there is decreased detoxification and decreased protein synthesis

48
Q

what characterizes the decreased detoxification in liver failure

A

mental status changes, asterixis and eventually coma. all due to increased ammonia. this is metabolic and thus reversible hyperesterinism leads to gynecomastia, spider angiomata and palmer erythema. jaundice.

49
Q

what happens to the blood when there is liver failure.

A

there is decreased protein synthesis and thus hypoalbuminemia with edema, coagulopathy due to decreased synthesis of clotting factors

50
Q

alcohol related liver disease

A

most common cause of liver disease. results from chemical injury to hepatocytes generally seen with binge drinking

51
Q

fatty liver

A

accumulation of fat in hepatocytes, results in heavy greasy liver resolves with abstinence

52
Q

what mediates the injury in alcoholic liver

A

acetaldehyde

53
Q

what does alcoholic liver damage look like

A

swelling of hepatocytes with formation of mallory bodies. necrosis and acute inflammation. presents as painful hepatomegaly with elevated liver enzymes.

54
Q

how often does cirrhosis occur

A

10-20%

55
Q

nonalcoholic fatty liver disease

A

fatty change, hepatitis, cirrhosis associated with obesity. there is elevated liver enzymes.

56
Q

hemochromatosis

A

excess body iron leads to deposition in tissues and organ damage.

57
Q

how is the tissue damage mediated in hemochromatosis

A

free radicals.

58
Q

what causes hemochromatosis

A

AR defect in iron absorption or chronic transfusion.

59
Q

what causes primary hemochromatosis

A

defect in HFE. usually a C282Y usually presents in childhood

60
Q

what is the classic triad of hemochromatosis

A

cirrhosis, secondary DM, and bronze skin. dilated cardiomyopathy, cardiac arrhythmia, and gonadal dysfunction

61
Q

what are the labs for hemochromatosis

A

increased ferritin, decreased TIBC, increased serum iron and increased % saturation.

62
Q

what does a biopsy of hemochromatosis look like

A

there is brown pigment in hepatocytes

63
Q

what are the risks associated with hemochromatosis

A

hepatocellular carcinoma. treatment is a phlebotomy.

64
Q

wilsons disease

A

AR defect ATP7B gene. hepatocyte copper transport. there is a lack of copper incorporation into ceruloplasm.

65
Q

what happens to copper in wilsons

A

builds up in hepatocytes, leaks into the serum and deposits into tissues. copper mediated tissue damage.

66
Q

how does wilsons present

A

childhood cirrhosis neurologic manifestations, kayser-flecher rings in the cornea.

67
Q

what are the neurological manifestations of wilsons

A

dementia, corea, parkinsonian due copper in the basal ganglia

68
Q

what are the labs for wilsons

A

increased urinary copper, decreased ceruloplasm, increased copper on liver biopsy.

69
Q

what are the risks for wilson

A

hepatocellular carcinoma

70
Q

what is the treatment for wilson

A

D-penicillamine

71
Q

primary billiary cirrhosis

A

autoimmune granulomatous destruction of intrahepatic bile ducts classically arises in women average age of 40. associated with other autoimmune.

72
Q

what is the etiology of primary billiary cirrhosis

A

unknown. there is antimitochondrial antibody.

73
Q

how does primary billiary cirrhosis present

A

features of obstructive jaundice, cirrhosis is a late complication

74
Q

primary sclerosing cholangitis

A

inflammation and fibrosis of the intrahepatic and extra hepatic bile ducts.

75
Q

what does primary sclerosing cholangitis look like

A

periductal fibrosis with an onion-skinning appearance. the uninvolved regions are dilated and look like beads.

76
Q

what is the etiology of primary sclerosing cholangitis

A

unknown, but there is a positive p-ANCA. presents as an obstructive jaundice with cirrhosis as a late complication. there is an increased risk for cholangiocarcinoma.

77
Q

reye syndrome

A

fulminant liver failure and encephalopathy in children with viral illness who take aspirin. likely due to mito damage. presents as hypoglycemia, elevated enzymes, nausea, vomiting, coma, death.

78
Q

hepatic adenoma

A

benign tumor of hepatocytes, associated with oral contraceptive use. there is a risk of intraperitoneal bleeding especially during pregnancy. the tumors are sub capsular and respond to estrogen.

79
Q

hepatocellular carcinoma risk factors

A

chronic hepatitis, cirrhosis, aflatoxin from aspergillus. there is an increased risk for budd-chiari syndrome.

80
Q

what is budd-chiari syndrome

A

liver infarction secondary to hepatic vein obstruction. presents with painful hepatomegaly and ascites.

81
Q

mets to liver

A

more common than primary. arises from colon, pancreas, lung and breast. there are multiple nodules. may be detected as hepatomegaly with a nodular free edge of the liver.

pathoma unit 6 (3 decks)

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