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My Pathoma Unit 6 > Chapter 11 Exocrine pancreas, gall bladder, and liver > Flashcards

Chapter 11 Exocrine pancreas, gall bladder, and liver Flashcards

1
Q

What is an annular pancreas and what does it carry increased risk for?

A

Developmental malformation in which the pancreas forms a ring around the duodenum; risk of duodenal obstruction

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2
Q

What is Acute pancreatitis and what is it due to? How is this set off?

A

Inflammation and hemorrhage of the pancreas. Due to autodigestion of pancreatic parenchyma by pancreatic enzymes. Premature activation of trypsin leads to activation of other pancreatic enzymes

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3
Q

What does acute pancreatitis result in?

A

liquefactive hemorrhagic necrosis of the pancreas and fat necrosis of the peripancreatic fat.

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4
Q

What is acute pancreatitis most commonly due to? (2) what are some other causes(7)

A

Most common: Alcohol and gallstones

Others: trauma, hypercalcemia, hyperlipidemia, drugs,, scorpion stings, mumps, and rupture of a posterior duodenal ulcer

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5
Q

What are 5 clinical features of acute pancreatitis?

A

1 Epigastric abdominal pain that radiates to the back
2 Nausea and vomiting
3 Periumbilical and flank hemorrhage (necrosis spreads into the periumbilical soft tissue and retroperitoneum)
4 Elevated serum lipase and amylase; lipase is more specific for pancreatic damage.
5 Hypocalcemia (calcium is consumed during saponification in fat necrosis)

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6
Q

What is a poor prognostic indicator in acute pancreatitis?

A

hypocalcemia

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7
Q

What are 4 complications of acute pancreatitis (further questions on each)?

A

1 Shock
2 Pancreatic pseudocyst
3 pancreatic abscess
4 DIC and ARDS

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8
Q

What causes shock in acute pancreatitis?

A

due to peripancreatic hemorrhage and fluid sequestration

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9
Q

What forms pancreatic pseudocysts? how do they present? What is a complication?

A

formed by fibrous tissue surrounding liquefactive necrosis and pancreatic enzymes. Presents as an abdominal mass with persistently elevated serum amylase. rupture is associated with release of enzymes into the abdominal cavity and hemorrhage.

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10
Q

What are pancreatic abscesses commonly due to in acute pancreatitis? how do they present?

A

often due to E. Coli; presents with abdominal pain, high fever, and persistently elevated amylase.

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11
Q

What causes DIC and ARDS in Acute Pancreatitis?

A

DIC- enzymes activate coag cascade.

ARDS- enzymes chew up alveolar/capillary interface

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12
Q

What is chronic pancreatitis and what is it most commonly due to?

A

Fibrosis of pancreatic parenchyma, most often secondary to recurrent acute pancreatitis. Most commonly due to alcohol (adults) and cystic fibrosis (children); however many cases are idiopathic.

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13
Q

What are 5 clinical features of chronic pancreatitis?

A

1 Epigastric pain that radiates to the back
2 pancreatic insufficiency
3 Dystrophic calcification of pancreatic parenchyma on imaging.
4 secondary diabetes mellitus - complication due to destruction of islets
5 Risk for pancreatic carcinoma

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14
Q

What does pancreatic insufficiency in chronic pancreatitis result in? Are amylase and lipase useful markers?

A

results in malabsorption with steatorrhea and fat-soluble vitamin deficiencies. Amylase and lipase are not useful serologic markers of chronic pancreatitis because vast majority of the pancreas has been destroyed and you are not making them.

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15
Q

What does dystrophic calcification in chronic pancreatitis show on imaging?

A

Contrast studies reveal a “chain of lakes” pattern due to dilation of pancreatic ducts.

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16
Q

What is pancreatic carcinoma, where does it arise and who is it most commonly seen in?

A

Adenocarcinoma arising from the pancreatic ducts. Most commonly seen in elderly (average age is 70 years)

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17
Q

What are the 2 major risk factors for pancreatic carcinoma?

A

smoking and chronic pancreatitis

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18
Q

What are 5 clinical features of pancreatic carcinoma and when do they occur?

A

Occur late
1 Epigastric abdominal pain with weight loss
2 Obstructive jaundice with pale stools and palpable gallbladder; associated with tumors that arise in the head of the pancreas (most common location)
3 Secondary diabetes mellitus; associated with tumors that arise in the body or tail
4 pancreatitis (tumor blocks ducts)
5 migratory thrombophlebitis (trousseau sign)

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19
Q

What is the serum tumor marker for pancreatic carcinoma?

A

CA-19-9

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20
Q

How does migratory thrombophlebitis present in pancreatic carcinoma?

A

Presents as swelling, erythema, and tenderness in the extremities. seen in 10% of patients

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21
Q

What does treatment of pancreatic carcinoma involve?

A

Surgical resection en bloc removal of the head and neck of the pancres, proximal duodenum, and gall bladder (whipple procedure)

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22
Q

What is the prognosis of pancreatic carcinoma?

A

very poor prognosis; 1 year survival is <10%

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23
Q

What is biliary atresia, how does it arise and when, how does it present?

A

failure to form or early destruction of extrahepatic biliary tree. leads to biliary obstruction within the first 2 months of life. Presents with jaundice and progresses to cirrhosis

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24
Q

What is cholelithiasis?

A

solid, round stones in the gallbladder

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25
Q

What are gallstones due to and what are 3 situations that cause them?

A

due to precipitation of cholesterol or bilirubin in bile. Arises with (1) supersaturation of cholesterol or bilirubin. (2) decreased phospholipids (e.g. lecithin) or bile acids (normally increase solubility). (3) stasis (bacteria deconjugate bilirubin)

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26
Q

What color are cholesterol stones? what percentage of stones? how do they appear on Xray?

A

Cholesterol stones are yellopw and the most common type of stone (90%), especially in the west. They are usually radiolucent (10% are radiopaque due to associated calcium)

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27
Q

What are 6 risk factors for cholesterol stones?

A

1 Age (40s)
2 Estrogen (female gender, obesity, multigravida, OC)
3 Clofibrate (increases HMG-CoA red, and decreases conversion of cholesterol into bile acids.)
4 Native american ethnicity
5 Crohn Disease (damage to terminal ileum decreases reuptake of bile acids)
6 Cirrhosis (decreased production of bile acids)

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28
Q

What color are bilirubin stones and how do they appear on xray?

A

pigmented stones that usually appear radiopaque.

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29
Q

What are risk factors for bilirubin stones?

A

extravascular hemolysis (increases bilirubin in bile) and biliary tract infection (e.g., E coli, Ascaris lumbricoides, and Clonorchis Sinensis –> all deconjugate bilirubin)

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30
Q

What is Ascaris Lubricoides?

A

common roundworm that infects 25% of the world’s population, especially in areas with poor sanitation (fecal oral transmission); infects the biliary tract, increasing the risk for gallstones

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31
Q

What is Clonorchis Sinensis?

A

endemic in China, Korea, and Vietnam (chinese liver fluke); infects the biliary tract, increasing the risk for gallstones, cholangitis, and cholangiocarcinoma

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32
Q

Describe the symptoms of gallstones and 6 complications?

A 
Gallstones are usually asymptomatic
complications:
1 Biliary colic
2, acute cholecystitis
3 Chronic cholecystitis
4 ascending cholangitis
5 gallstone ileus
6 gallbladder cancer
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33
Q

What is Biliary Colic? what is it due to? how are symptoms relieved? What are some complications?

A

Waxing and waning RUQ pain. Due to gallbladder contracting against a stone lodged in the cystic duct. Symptoms are relieved if the stone passes. Common bile duct obstruction may result in acute pancreatitis or obstructive jaundice.

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34
Q

What is acute Cholecystitis? What causes it?

A

Acute inflammation of the gallbladder wall. Impacted stone in the cystic duct results in dilation with pressure ischemia, bacterial overgrowth (E. coli), and inflammation

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35
Q

How does acute cholecystitis present and what is a risk if left untreated?

A

Presents with RUQ pain, often radiating to right scapula, fever with increased WBC count, nausea, vomiting, and increased serum alkaline phosphatase (from duct damage). risk of rupture if untreated.

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36
Q

What is chronic cholecystitis and what is it due to??

A

Chronic inflammation of the gallbladder. Due to chemical irritation from longstanding cholelithiasis, with or without superimposed bouts of acute cholecystitis.

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37
Q

What is Chronic cholecystitis characterized by? and how does it present?

A

Characterized by herniation of gallbladder mucosa into the muscular wall (rokitansky-aschoff sinus). Presents with vague RUQ pain, especially after eating.

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38
Q

What is a late complication of chronic cholecystitis? What does it increase risk for?

A

Porcelain gallbladder. Shrunken, hard gallbladder due to chronic inflammation, fibrosis, and dystrophic calcification. Increased risk for carcinoma

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39
Q

What is treatment of chronic cholecystitis?

A

Cholecystectomy, especially if porcelain gallbladder is present.

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40
Q

What is ascending cholangitis and what is it usually due to?

A

Bacterial infection of the bile ducts. usually due to ascending infection with enteric gram negative bacteria from bowel.

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41
Q

How does ascending cholangitis present and what other disease shows increased incidence of ascending cholangitits?

A

Presents as sepsis (high fever and chills), jaundice, and abdominal pain. Increased incidence with choledocholithiasis (stone in the biliary ducts)

42
Q

What is gallstone ileus and what is it due to?

A

Gallstone enters and obstructs the small bowel. Due to cholecystitis with fistula formation between the gallbladder and small bowel.

43
Q

What is gallblader carcinoma? what does it arise from, what is the major risk factor?

A

Adenocarcinoma arising from the glandular epithelium that lines the gallbladder. Gallstones are a major risk factor, especially when complicated by porcelain gallbladder.

44
Q

How does gallbladder carcinoma present and what is the prognosis?

A

Classically presents as cholecystitis in an ELDERLY woman. Poor prognosis

45
Q

What is jaudnice and what is it due to and when does it arise?

A

Yellow discoloration of the skin; earliest sign is scleral icterus. Due to increased serum bilirubin, usually >2.5 mg/dL. Arises with disturbances in bilirubin metabolism

46
Q

What are the steps of bilirubin metabolism (7)?

A

1 RBCs are consumed by macrophages of the RES
2 protoporphyrin (from heme) is converted into unconjugated bilirubin (UCB).
3 albumin carries UCB to liver
4 Uridine glucuronyl transferase (UGT) in hepatocytes conjugates bilirubin
5 Conjugated bilirubin (CB) is transferred to bile canaliculi to form bile, which is stored in the gallbladder
6 Bile is released into the small bowel to aid in digestion
7 intestinal flora convert CB to urobilinogen, which is oxidized to stercobilin (makes stool brown) and urobilin (partially reabsorved into blood and filtered by kidney, making urine yellow)

47
Q

Wrt to jaundice, what is the etiology, laboratory findings and clinical features of extravascular hemolysis or ineffective erythropoiesis?

A

Etiology: High levels of UCB overwhelm the conjugating ability of the liver.
Laboratory Findings: increased UCB
Clinical Features: Dark urine due to increased urine urobilinogen (UCB is not water soluble, and this is absent from urine) Increased risk for pigmented bilirubin gallstones

48
Q

Wrt to jaundice, what is the etiology, laboratory findings and clinical features of Physiologic jaundice of the newborn?

A

Etiology: newborn liver has transiently low UGT activity.
Laboratory findings: Increased UCB
Clinical Features: UCB is fat soluble and can deposit in the basal ganglia (kernicterus) leading to neurological deficits and death. Treatment is phototherapy (makes UCB more water soluble)

49
Q

Wrt to jaundice, what is the etiology, laboratory findings and clinical features of Gilbert syndrome?

A

etiology: mildly low UGT activity; AR
Laboratory findings: Increased UCB
Clinical features: Jaundice during stress (e.g. severe infection); otherwise, not clinically significant.

50
Q

Wrt to jaundice, what is the etiology, laboratory findings and clinical features of Crigler-najjar syndrome

A

etiology: absence of UGT
laboratory findings: increased UCB
Clinical Features: Kernicterus; usually fatal

51
Q

Wrt to jaundice, what is the etiology, laboratory findings and clinical features of Dubin-Johnson syndrome?

A

Etiology: deficiency of bilirubin canalicular transport protein; AR
Laboratory findings: increased CB
Clinical features: Liver is dark; otherwise, not clinically significant.

52
Q

What is Rotor syndrome?

A

Similar to Dubin-Johnson syndrome, but lacks liver discoloration

53
Q

Wrt to jaundice, what is the etiology, laboratory findings and clinical features of biliary tract obstruction (obstructive jaundice)?

A

Etiology: associated with gallstones, pancreatic carcinoma. cholangiocarcinoma, parasites, and liver fluke (clonorchis sinensis).
Laboratory Findings: Increased CB (water soluble), decreased urine urobilinogen, and increased alkaline phosphatase
Clinical Features: Dark urine (due to bilirubinuria) and pale stool. pruritus due to increased plasma bile acid deposits in skin. Hypercholesterolemia with xanthomas. steatorrhea with malabsorption of fat soluble vitamins.

54
Q

Wrt to jaundice, what is the etiology, laboratory findings and clinical features of Viral hepatitis?

A

Etiology : Inflammation disrupts hepatocytes and small bile ductules.
Laboratory Findings: Increase in both CB and UCB
Clinical Features: Dark urine due to increased urine bilirubin; urine urobilinogen is normal or decreased.

55
Q

REVIEW TABLE 11.2 on page 119

A

REVIEW TABLE 11.2 on page 119

56
Q

REVIEW TABLE 11.3 on page 120

A

REVIEW TABLE 11.3 on page 120

57
Q

What is viral hepatitis and what two types of hepatitis may result? What causes it?

A

Inflammation of liver parenchyma, usually due to hepatitis virus; other causes include EBV and CMV. Hepatitis virus causes acute hepatitis, which may progress to chronic hepatitis.

58
Q

How does the hepatitis virus cause damage?

A

Viral antigen is presented on hepatocytes by MHC class 1 and then recognized by CD8 T cells.

59
Q

How does acute hepatitis present?

A

Jaundice (mixed UCB and CB) with dark urine (due to CB), fever, malaise, nausea, and elevated liver enzymes (ALT>AST)

60
Q

Describe the inflammation in acute hepatitis? and describe how long symptoms last?

A

Inflammation involves lobules of the liver and portal tracts and is characterized by apoptosis of hepatocytes. Some cases may be asymptomatic with elevated liver enzymes. Symptoms last less than 6 months.

61
Q

What is chronic hepatitis characterized by and what does the inflammation involve and what is it at risk of progressing to?

A

Characterized by symptoms that last longer than 6 months. Inflammation predominantly involves portal tract and has the risk of progression to cirrhosis

62
Q

What is Cirrhosis?

A

End stage liver damage characterized by disruption of the normal hepatic parenchyma by bands of fibrosis and regenerative nodules of hepatocytes.

63
Q

What is fibrosis mediated by in cirrhosis?

A

mediated by TGF-Beta from stellate cells which lie beneath the endothelial cells that line sinusoids.

64
Q

What are 3 clinical features of Cirrhosis?

A

Portal hypertension
Decreased detoxification
Decreased protein synthesis

65
Q

What doe portal hypertension lead to in cirrhosis? (4)

A

1 Ascites (fluid in the peritoneal cavity)
2 Congestive splenomegaly/hypersplenism
3 portosystemic shunts (esophagela varices, hemorrhoids, and caput medusae)
4 Hepatorenal syndrome (rapidly developing renal failure secondary to cirrhosis)

66
Q

What does decreased detoxification in cirrhosis result in? (3)

A

1 Mental status changes, asterixis, adn eventual coma (due to increased serum ammonia); metabolic, hence reversible
2 gynecomastia, spider angiomata, and palmar erythema due to high estrogen levels
3 Jaundice

67
Q

What does decreased protein synthesis in cirrhosis lead to? (2)

A

1 hypoalbuminemia with edema

2 coagulopathy due to decreased synthesis of clotting factors; degree of deficiency is followed by PT

68
Q

What is Alcohol related liver disease? what does it result in?

A

Damage to hepatic parenchyma due to consumption of alcohol. Most common cause of liver disease in the west. Fatty liver is the accumulation of fat in hepatocytes. results in a heavy, greasy liver; resolves with abstinence.

69
Q

What does Alcohol related liver disease result from? what is it characterized by. and how does it present?

A

Chemical injury to hepatocytes.
1 Acetaldehyde (metabolite of alcohol) mediates damage
2 Characterized by swelling of hepatocytes with formation of mallory bodies (damaged cytokeratin filaments), necrosis and acute inflammation
3 Presents with painful hepatomegaly and elevated liver enzymes (AST>ALT) because AST in mitochondria and EtOH is a mitochondrial poison. may result in death

70
Q

What is a complication of long-term. chronic alcohol induced liver damage?

A

Cirrhosis occurs in 10-20% of alcoholics

71
Q

What is nonalcoholic fatty liver disease? what is it associated with? and how is a diagnosis made?

A

Fatty change, hepatitis, and/or cirrhosis that develop without exposure to alcohol (or other known insult). Associated with obesity. Diagnosis of exclusion ALT>AST

72
Q

What is hemochromatosis and what mediates tissue damage in it?

A

Excess body iron leading to deposition in tissues (hemosiderosis) and organ damage (hemochromatosis). Tissue damage is mediated by generation of free radicals.

73
Q

What is hemochromatosis due to? Primary? Secondary?

A

AR defect in the iron absorption (primary) or chronic transfusions (secondary)

74
Q

What is primary hemochromatosis due to and what role do enterocytes play in iron regulation?

A

Primary hemochromatosis is due to mutations in the HFE gene, usually C282Y (cysteine is replaced by tyrosine at amino acid 282) Enterocytes take up almost all iron in our diet but only release it into blood if it is needed. Dysregulation in this process results in too much iron released into the blood.

75
Q

When does hemochromatosis present?

A

Late adulthood

76
Q

What is the classic triad of hemochromatosis and what are some other symptoms?

A

triad: cirrhosis, secondary diabetes mellitus, and bronze skin.
Other findings: dilated cardiomyopathy, cardiac arrythmias and gonadal dysfunction (due to testicular atrophy)

77
Q

What doe the following labs show in hemochromatosis?

ferritin, TIBC, serum iron, adn % saturation?

A

Ferritin is high
TIBC is low
Serum iron is high
% saturation is high

78
Q

What does liver biopsy show in hemochromatosis?

A

Reveals accumulation of brown pigment in hepatocytes. Prussian blue distinguishes between iron (blue) and liopfuscin.

79
Q

What is lipfuscin?

A

Brown pigment that is a by-product from the turnover (‘wear and tear’) of peroxidized lipids; it is commonly present in hepatocytes.

80
Q

What does hemochromatosis carry and increased risk for and what is the treatment?

A

increased risk for Hepatocellular carcinoma and treatment is phlebotomy.

81
Q

What is defective in Wilson disease, what is the inheritance pattern, what does this result in and how does this cause damage?

A

AR defect (ATP7B gene) in ATP mediated hepatocyte copper transport. Results in a lack of copper transport into bile and lack of copper incorporation into ceruloplasmin. Copper builds up in hepatocytes, leaks into the serum, and deposits in tissues. Copper mediated production of hydroxyl free radicals leads to tissue damage.

82
Q

how does wilson disease present and when?

A

Presents in childhood with:
1 Cirrhosis
2 Neurologic manifestations (behavioral changes, dementia, chorea, and parkinsonian symptoms due to deposition of copper in basal ganglia
3 Kayser Fleisher rings in the cornea

83
Q

What do the following lab values show in Wilson disease?

urinary copper, serum ceruloplasmin, and copper on liver biopsy?

A

urinary copper increased
serum ceruloplasmin decreased
copper on liver biopsy increased

84
Q

What does Wilson disease carry an increased risk for? what is the treatment?

A

Increased risk of hepatocellular carcinoma. Treatment is D-Penicillamine (chelates copper)

85
Q

What is primary biliary cirrhosis, who does it arise in and when, and what is it associated with?

A

Autoimmune granulomatous destruction of intrahepatic bile ducts. Classically arises in women (average age is 40 years). Associated with other autoimmune diseases.

86
Q

What is the etiology of primary biliary cirrhosis? what antibody is present?

A

Etiology is unknown; antimitochondrial antibody is present and helps mark the disease

87
Q

How does primary biliary cirrhosis present and what is a late complication?

A

Presents with features of obstructive jaundice. Cirrhosis is a late complication

88
Q

What is primary sclerosing cholangitis? What is seen on contrast imaging and on histologic examination?

A

Inflammation and fibrosis of intrahepatic and extrahepatic bile ducts. Periductal fibrosis with an ‘onion-skin’ appearance on histology. Univolved regions are dilated resulting in a ‘beaded’ appearance on contrast imaging

89
Q

What is the etiology of Primary sclerosing cholangitis and what is it associated with and what is a histologic marker?

A

Etiology is unknown, but associated with ulcerative colitis; p-ANCA is often positive.

90
Q

How does primary sclerosing cholangitis present, what is a late complication, and what does it pose and increased risk for?

A

Presents with obstructive jaundice; cirrhosis is a late complications. Increased risk for cholangiocarcinoma.

91
Q

What is Reye syndrome and what is it likely related to?

A

Fulminant liver failure and encephalopathy in children with viral illness who take aspirin. Likely related to mitochondrial damage of hepatocytes.

92
Q

How does Reye syndrome present?

A

Presents with hypoglycemia, elevated liver enzymes, and nausea with vomiting; may progress to coma and death.

93
Q

What is a hepatic adenoma and what is it associated with?

A

Benign tumor of hepatocytes. Associated with oral contraceptive use; regresses upon cessation of drug.

94
Q

What risks do hepatic adenomas carry and describe where they grow and what they respond to?

A

Risk of rupture and intraperitoneal bleeding, especially during pregnancy. Tumors are subcapsular and grow with exposure to estrogen.

95
Q

What is hepatocellular carcinoma and what are 3 risk factors?

A

Malignant tumor of hepatocytes. Risk factors:
1 Chronic hepatitis (e.g. HBV and HCV)
2 Cirrhosis (e.g. alcohol, nonalcoholic fatty liver disease, hemochromatosis, wilson disease, and A1AT deficiency)
3 Aflatoxins derived from aspergillus (induce p53 mutations)

96
Q

What complication does hepatocellular carcinoma carry a risk for? explain it.

A

Budd Chiari syndrome. liver infarction secondary to hepatic vein obstruction. Presents with painful hepatomegaly and acites.

97
Q

When are hepatocellular carcinomas detected and what is the prognosis?

A

Tumors are often detected late because symptoms are masked by cirrhosis; poor prognosis.

98
Q

What is the serum tumor marker for hepatocellular carcinoma?

A

AFP

99
Q

How common are metastases to the liver and what are 4 common sources?

A

More common than primary liver tumors; most common sources include colon, pancreas, lung, and breast carcinomas.

100
Q

What do metastases in the liver result in and how may they be detected clinically?

A

Results in multiple nodules in the liver. May be detected as hepatomegaly with a nodular free edge of the liver.

101
Q

How does hypercalcemia cause acute pancreatitis?

A

Calcium is an activator of enzymes

102
Q

How does alcohol cause acute pancreatitis?

A

Alcohol causes contraction of the sphincter of oddi which leads to impeded drainage of enzymes

My Pathoma Unit 6 (2 decks)

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