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Pathoma > Exocrine Pancreas, Gallbladder and Liver > Flashcards

Exocrine Pancreas, Gallbladder and Liver Flashcards

1
Q

What is an annular pancreas? Risk?

A

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

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2
Q

Acute pancreatitis is due to what? (specifically, premature activation of what?)

A

Due to auto digestion of pancreatic parenchyma by pancreatic enzymes. Caused by premature activation of trypsin which leads to activation of other pancreatic enzymes.

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3
Q

What type of necrosis occurs with acute pancreatitis?

A

Liquefactive hemorrhagic necrosis of the pancreas and fat necrosis of peripancreatic fat

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4
Q

Most common causes of acute pancreatitis? Other causes?

A

Alcohol and gallstones
Other: trauma (automobile accident in children), hypercalcemia (activates enzymes), hyperlipidemia, drugs, scorpion stings, mumps, and rupture of a posterior duodenal ulcer

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5
Q

How do alcohol and gallstones cause acute pancreatitis?

A

OH: causes contraction of spincter of Oddi (pancreatic enzymes drain - pancreatic duct to ampulla to duodenum)
Gallstones: block in the same area
Contraction -> decreased drainage -> increased risk of premature activation

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6
Q

Clinical features of acute pancreatitis?

A

Epigastric abdominal pain that radiates to the back
N & V
Periumbilical and flank hemorrhage (necrosis spreads into the periumbilical soft tissue and retroperitoneum)
Elevated serum amylase and lipase (lipase is more specific)
Hypocalcemia (Ca+2 is consumed during saponification in fat necrosis)

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7
Q

Are calcium levels high or low in acute pancreatitis?

A

Low (Ca+2 is consumed during saponification in fat necrosis)

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8
Q

4 Complication of acute pancreatitis

A

1) shock (due to peripancreatic hemorrhage and fluid sequestration)
2) pancreatic pseudocyst
3) pancreatic abscess
4) DIC and ARDS (pancreatic enzymes can get into the bloodstream and act on coagulation factors leading to DIC, they can also chew on the alveolar-capillary interface leading to ARDS)

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9
Q

What is the usual cause of a pancreatic abscess? Symptoms?

A

A complication of acute pancreatitis usually due to E. coli

Presents with abdominal pain, high fever and persistently elevated amylase

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10
Q

What is a pancreatic pseudocyst?

A

A complication of acute pancreatitis, formed by fibrous tissue surrounding the liquefactive necrosis and pancreatic enzymes (walled off fibrous tissue, no true lining). Presents as an abdominal mass with persistently elevated amylase. Rupture is associated with release of enzymes into the abdominal cavity and hemorrhage

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11
Q

What are the most common causes of chronic hepatitis in children and adults?

A

Children - CF

Adults - alcohol

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12
Q

Chronic pancreatitis has a increased risk of what?

A

Pancreatic carcinoma

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13
Q

Clinical features of chronic pancreatitis (4)

A

1) epigastric abdominal pain that radiates to the back
2) pancreatic insufficiency - malabsorption with steatorrhea and fat-soluble vitamin deficiencies (ADKE)
3) dystrophic calcification of pancreatic parenchyma on imaging; contrast studies reveal a ‘chain of lakes’ pattern due to dilation of pancreatic ducts
4) secondary DM - late complication due to destruction of islets

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14
Q

Are amylase and lipase good markers for acute or chronic pancreatitis? Which is more specific for pancreatic damage?

A

Acute (most are destroyed in chronic)

Lipase is more specific

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15
Q

Where does pancreatic carcinoma arise? Who is it most commonly seen in? What are the major risk factors?

A

Adenocarcinoma - from the pancreatic ducts
Most commonly seen in the elderly (70s)
Risk factors include smoking and chronic pancreatitis

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16
Q

Serum marker for pancreatic carcinoma

A

CA 19-9

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17
Q

Treatment for pancreatic carcinoma

A

Whipple procedure: Surgical resection involving en bloc removal of the head and neck of the pancreas, proximal duodenum and gallbladder

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18
Q

Clincal features of pancreatic carcinoma (5)

A

1) epigastric abdominal pain and WL
2) obstructive jaundice with pale stools and palpable gallbladder (tumors in the head - block flow)
3) DM (tumors in the body or tail)
4) Pancreatitis
5) Migratory thrombophlebitis (Trousseau sign) swelling, erythema and tenderness in the extremities

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19
Q

Most common location of pancreatic carcinoma

A

Head of the pancreas

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20
Q

What is biliary atresia? What results?

A

Failure to form or early destruction to the extrahepatic biliary tree (bile ducts outside the liver)
Leads to biliary obstruction within the first two months of life
Presents with jaundice (CB) and progresses to cirrhosis (back pressure)

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21
Q

What are the two types of gallstones (cholelithiasis)? Which one is more common? How do they precipitate?

A

Cholesterol (most common - 90%) or bilirubin
Arise with supersaturation, decreased phospholipids (lecithin) or biles acids or stasis (increase bacterial growth - deconjugate bilirubin)

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22
Q

Cholesterol stones: radiolucent or opaque? Risk factors?

A

Usually radiolucent (don’t show up on x-ray), 10% are radiopaque due to associated calcium

Risk factors: age (40s), estrogen (female gender, obesity, multiple pregnancies and oral contraceptives), clofibrate (lipid lowering drug - decreased conversion of cholesterol to bile acids), Native American ethnicity, Crohn disease (decreased uptake of bile salts and acids) and cirrhosis (decreased production of biles salts)

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23
Q

Bliirubin stones: radiolucent or opaque? Risk factors?

A 
Usually radiopaque (show up on x-ray)
Risk factors: extravascular hemolysis (increased bilirubin in bile from heme and protoporphyrin breakdown) and biliary tract infections (E. Coli, Ascaris lumbricoides and Clonorchis sinensis)
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24
Q

5 key complications of cholelithiasis

A 
Biliary colic
Acute  and chronic cholecystitis 
Ascending cholangitis
Gallstone ileus 
Gallbladder cancer
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25
Q

What is Clonorchis sinensis?

A

Chinese liver fluke, endemic in China, Korean and Vietnam. Infects the biliary tract, increasing the risk for gallstones, cholangitis, and cholangiocarcinoma

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26
Q

What is Ascaris lumbricoides?

A

A common roundworm that infects 25% of the world’s population. Infects the biliary tract, increasing the risk for gallstones

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27
Q

Biliary colic - what is it and how does it present?

A

Due to gallbladder contracting against a stone lodged in a cystic duct
Presents as waxing and waning RUQ pain that is relieved if the stone passes
Common bile duct obstruction may result in acute pancreatitis or obstructive jaundice

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28
Q

Acute cholecystitis - what is it, how does it present and what is the risk if left untreated?

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
Presets with RUQ pain often radiating to the R scapula, fever with increased WBC count, N, V and increased serum alkaline phosphatase (from duct damage - contained within the epithelium)
Risk of rupture if left untreated

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29
Q

Where does pain radiate with acute cholecystitis?

A

RUQ pain radiating to the R scapula

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30
Q

Chronic cholecystitis - what is it, how does it present and what are the late complications?

A

Chronic inflammation of the gallbladder - due to chemical irritation from longstanding cholelithiasis w/ or w/o superimposed bouts of acute cholecystitis
Presents w/ vague RUQ pain, especially after eating
Late complications: porcelain gallbladder (shrunken, hard gallbladder due to chronic inflammation, fibrosis, and dystrophic calcification) and increased risk for carcinoma

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31
Q

What key finding characterizes chronic cholecystitis?

A

Herniation of gallbladder mucosa into the muscular wall (Rokitansky-Aschoff sinus)

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32
Q

What is a gallstone ileus?

A

Occurs when a gallstone enters and obstructs the small bowel, due to cholecystitis with fistula formation between the gallbladder and small bowel (fistula ruptures allowing gallstone to move into the small bowel)

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33
Q

What is ascending cholangitis? How does it present?

A

Bacterial infection of the bile ducts usually due to ascending infection with enteric gram negative bacteria
Presents as sepsis (high fever and chills), jaundice, and abdominal pain
Increased incidence with choledocholithiasis (stone in biliary ducts)

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34
Q

Gallbladder carcinoma - what is it, what is the major risk factor, how does it present

A

Adenocarcinoma arising from the glandular epithelium that lines the gallbladder wall
Gallstones are a major risk factor, especially when complicated by porcelain gallbladder
Classically presents as cholecystitis (usually occurs in 40/50s) in an elderly woman
Poor prognosis

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35
Q

Jaundice occurs with bilirubin levels above…

A

2.5mg/dL

36
Q

Describe normal bilirubin metabolism

A

RBCs are consumed by macrophages of the reticuloendothelial system (spleen). Protoporphyrin (from heme) is converted to UCB. Albumin carries UCB to the liver where it is conjugated by uridine glucuronyl transferase (UGT) in hepatocytes. CB is transferred to bile canaliculi to form bile and stored in the gallbladder. Bile is released into the small bowel to aid in digestion. Intestinal flora convert CB to urobilinogen which is oxidized to form stercobilin (makes stool brown) and urobilin (reabsorbed in blood and filtered into urine making it yellow)

37
Q

Causes of Jaundice:

Extravascular hemolysis or ineffective erythropoiesis

A

High levels of UCB (from excessive destruction of RBCs) overwhelm the conjugating liver. Dark urine due to increased urine (urobilinogen), increased risk for pigmented bilirubin gallstones (excessive CB in bile)

38
Q

Does increased UCB cause dark urine?

A

No - UCB is not water soluble and is thus absent from the urine

39
Q

Physiologic jaundice of the newborn

A

Newborn liver has transiently low UGT activity. Increased UCB. UCB is fat soluble and can deposit in the basal ganglia (kernicterus) leading to neurological deficits and death. Treatment is phototherapy (makes UCB water soluble)

40
Q

Gilbert syndrome

A

Mildly low UGT activity, autosomal recessive. Increased UCB. Jaundice during stress (severe infection), otherwise not clinically significant

41
Q

Crigler-Najjar syndrome

A

Absence of UGT, increased UCB. Kernicterus, usually fatal.

42
Q

Dubin-Johnson syndrome

A

Deficiency of bilirubin canalicular transport protein, AR. Increased CONJUGATED BILIRUBIN (builds up in liver cells, leaks into blood). Liver is dark, otherwise not clinically significant. Rotor syndrome is similar but lacks liver discoloration.

43
Q

Biliary tract obstruction (obstructive jaundice)

A

Associated with gallstones, pancreatic carcinoma, cholangiocarcinoma, parasites and liver fluke (Clonorchis sinensis). Increased CB, decreased urine urobilinogen, and increased alkaline phosphatase. Dark urine (due to bilirubinuria - CB is water-soluble) and pale stool. Pruritus due to increased plasma bile acids. Hypercholesterolemia with xanthomas. Steatorrhea with malabsorption of fat-soluble vitamins.

44
Q

Viral hepatitis (cause of jaundice)

A

Inflammation disrupts hepatocytes and small bile ductules. Increase in both CB and UCB. Dark urine due to increase urine bilirubin; urine urobilinogen is normal or decreased.

45
Q

Hepatitis A

A

Fecal-oral transmission, commonly acquired by travelers
Acute hepatitis, no chronic state
Anti-virus IgM marks active infection, anti-virus IgG is protective and its presence indicates prior infection or immunization

46
Q

Hepatitis E

A

Fecal-oral transmission, commonly acquired from contaminated water or undercooked seafood
Acute hepatitis, no chronic state
Anti-virus IgM marks active infection, anti-virus IgG is protective and its presence indicates prior infection (no vaccine)
HEV infection in pregnant woman is associated with fulminant hepatitis (liver failure with massive liver necrosis)

47
Q

Hepatitis B

A 
Parenteral transmission (childbirth, unprotected intercourse, IV drug use, needle stick)
Results in acute hepatitis, chronic disease occurs in 20% of cases
48
Q

Hepatitis C

A 
Parenteral transmission (childbirth, unprotected intercourse, IV drug use, needle stick). Risk from transfusion is almost nonexistent due to screening of the blood supply
Results in acute hepatitis, chronic disease occurs in most cases
HCV-RNA test confirms infection; decreased RNA levels indicate recovery; persistence indicates chronic disease
49
Q

Hepatitis D

A

Dependent on HBV for infection; superinfection upon existing HBV is more severe than coinfection

50
Q

Which hepatitis viruses lead to chronic states?

A

20% Hep B

Almost all Hep C

51
Q

HBsAG

A

First serologic marker to rise, key marker of infection. + in acute and chronic states

52
Q

First serologic marker to rise with Hep B?

A

HBsAG

53
Q

HBcAB

A

Acute battle - IgM (acute and window - only thing positive during the window period)
Sign of victory - IgG (resolved and chronic)

54
Q

HBsAB

A

IgG (protective) - resolved and immunized

55
Q

HBeAG and HBV DNA

A

+ in acute and +/- in chronic

56
Q

Causes of viral hepatitis

A

Hepatitis virus
EBV
CMV

57
Q

Acute hepatitis presents as…Inflammation involves?

A

Jaundice (CB and UCB) with dark urine (CB), fever, malaise, nausea and elevated liver enzymes (ALT> AST)
Inflammation involves lobules of the liver and portal tracts and is characterized by apoptosis of hepatocytes

58
Q

How long must symptoms last for to be considered chronic hepatitis? Where does inflammation usually occur? Risk?

A

6 months
Inflammation predominantly involves portal tract
Risk of progression to cirrhosis

59
Q

What is cirrhosis?

A

End-stage liver damage characterized by disruption of the normal hepatic parenchyma by bands of fibrosis in between regenerative nodules of hepatocytes

60
Q

How is the fibrosis in cirrhosis mediated?

A

Mediated by TGF-B from stellate cells which lie beneath the endothelial cells that line the sinusoids

61
Q

Clinical features of cirrhosis

A

Portal HTN: ascites, congestive splenomegaly/hypersplenism, portosystemic shunts (esophageal varices, hemorrhoids and caput medusa), hepatorenal syndrome (rapidly developing renal failure secondary to cirrhosis)

Decreased detoxification: mental status changes, asterixis, end eventual coma (increased ammonia); metabolic, hence reversible. Gynecomastia, spider angiomata, palmar erythema due to hyperestrinism (liver removes excess estrogen from the blood). Jaundice (liver hepatocytes conjugate bilirubin)

Decreased protein synthesis: Hypoalbuminemia with edema, coagulopathy (decreased synthesis of clotting factors, degree of deficiency followed by PT)

62
Q

What mediates the damage in alcohol-related liver disease?

A

Acetaldehyde (metabolite of alcohol)

63
Q

Alcohol hepatitis is characterized by?

A

Swelling of hepatocytes with formation of Mallory bodies (damaged cytokeratin filaments), necrosis, and acute inflammation

64
Q

What are Mallory bodies?

A

Damaged cytokeratin filaments (IF) seen with alcohol hepatitis

65
Q

Is fatty liver reversible?

A

Yes with abstinence of OH

66
Q

What is higher in alcohol hepatitis ALT or AST? What else occurs?

A

AST > ALT, AST is located in mitochondria, OH is a mitochondrial poison
Painful hepatomegaly is also seen

67
Q

Non-alcoholic fatty liver disease: associated with what? how is it diagnosed?

A

Fatty change, hepatitis and or cirrhosis that develop without exposure to OH
Associated with obesity
Diagnosis of exclusion (ALT > AST)

68
Q

How is tissue damage mediated in hemochromatosis? Cause?

A

Organ damage by excess body iron via the generation of free radicals (fenton reaction)
Cause: AR defect in iron absorption (primary) or chronic transfusions (secondary)

69
Q

What mutation causes primary hemochromatosis?

A

HFE gene, usually C282Y, cysteine is replaced by tyrosine at amino acid 282

70
Q

Primary hemochromatosis:

Classic triad and other findings
Labs
Liver Biopsy
Increased risk
Treatment
A

Classic triad and other findings: cirrhosis, secondary diabetes, and bronze skin; other findings include dilated cardiopathy, cardiac arrhythmias, and gonadal dysfunction (due to testicular atrophy)
Labs: Increased ferritin, serum iron and % saturation with decreased TIBC
Liver Biopsy: accumulation of brown pigment in hepatocytes, distinguished from lipofuscin with prussian blue stain
Increased risk: hepatocellular carcinoma (free radicals)
Treatment: phlebotomy (remove RBC/iron)

71
Q

Wilson disease is a defect in what gene? What does it result in?

A

ATP7B in ATP-mediated hepatocyte copper transport
Results in lack of copper transport into bile and lack of copper incorporation into ceruloplasmin (carries copper in the blood)

72
Q

By what mechanism does Wilsons disease cause damage?

A

Copper build up in hepatocytes, leaks into serum and deposits in tissues. Copper-mediated production of hydroxyl free radicals leads to tissue damage

73
Q

How does Wilsons disease present?

A

Cirrhosis
Neurologic (behavioral changes, dementia, chorea and Parkinsonian syndrome due to copper deposit in the basal ganglia)
Kayser-Fleisher rings in the cornea

74
Q

Wilson disease treatment

A

D-penicillamine (chelates copper)

75
Q

Increased risk of what with Wilson disease?

A

Hepatocellular carcinoma

76
Q 
Primary biliary cirrhosis: 
What is it?
Associated with?
Etiology?
Presents?
Complication?
A

Autoimmune granulomatous destruction of intrahepatic bile ducts
Associated with autoimmune diseases (40 year-old female)
Etiology is unknown, anti-mitochondrial antibody is present
Presents with features of obstructive jaundice
Cirrhosis is a late complication

77
Q

What antibody is present in primary biliary cirrhosis?

A

Anti-mitochondiral antibody

78
Q

Reye syndrome: what is it, how does it present, mechanism?

A

Fulminant liver failure and encephalopathy in children with viral illness who take aspirin
Presents with hypoglycemia, elevated liver enzymes, N/V, may progress to coma and death
Likely related to mitochondrial damage of hepatocytes

79
Q

Reye syndrome mechanism?

A

Likely related to mitochondrial damage of hepatocytes

80
Q

Hepatic adenoma:

Related to use of what drug? Risk of? Describe the tumors

A

Benigin tumor of hepatocytes
Associated with oral contraceptive use, regresses upon cessation of the drug
Risk of rupture and intraperitoneal bleeding, especially during pregnancy
Tumors are subcapsular and grow with exposure to estrogen

81
Q 
Primary sclerosing cholangitis: 
What is it?
Appearance?
Etiology?
Presentation?
Increased risk for?
A

Inflammation and fibrosis of intrahepatic and extrahepatic bile ducts
Periductal fibrosis with ‘onion-skin’ appearance
Uninvolved regions are dilated resulting in beaded appearance on contrast imaging
Etiology is unknown, associated w/ *UC; p-ANCA is often positive
Presents with obstructive jaundice; cirrhosis is a late complication
Increased risk for cholangiocarcinoma

82
Q

Hepatocellular carcinoma risk factors

A 
Chronic hepatitis (HBV, HBC)
Cirrhosis (OH, nonOH fatty liver, Wilson disease, A1AT deficiency, hemochromatosis)
Aflatoxins* derived from Aspergillus (induce p53 mutations)
83
Q

What are Aflatoxins associated with? What is there mechanism of action?

A

Derived from Apergillus - in grains
Hepatocellular carcinoma
Induce p53 mutations

84
Q

Serum marker for hepatocellular carcinoma

A

Alpha-fetoprotein

85
Q

Hepatocellular carcinoma - increased risk for what?

A

Budd-Chiari syndrome
Liver infarction secondary to hepatic vein obstruction
Presents with painful hepatomegaly and ascites

86
Q

Common cancer that metastasize to the liver?

A 
Colon
Pancreas
Lung
Breast
*Results in multiple nodules in the liver (can be palpated on the free edge)

Pathoma (6 decks)

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