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STEP 1 (1) > GI- Pathology II > Flashcards

GI- Pathology II Flashcards

1
Q

What pts most commonly get colorectal cancer?

A

50+ yo with ~25% having a family Hx

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2
Q

What are the risk factors for colorectal cancer?

A
  • adenomatous and serrated polyps
  • familial cancer syndrome

IBD

tobacco use

diet of process meat with low fiber

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3
Q

Where in the colon does cancer most commonly occur?

A

rectosigmoid > ascending > descending

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4
Q

How do ascending colorectal cancers present?

A

An exophytic mass, iron deficiency anemia, and weight loss

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5
Q

How do descending colorectal cancers present?

A

as an infiltrating mass, partial obstruction, colicky pain, and hematochezia

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6
Q

Colorectal cancer rarely presents with ________ bacteremia

A

Strept. Bovis

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7
Q

How is colorectal cancer diagnosed?

A

iron deficiency anemia in males (especially 50+) and postmenopausal females raises suspicion

screen pts 50+ with colonoscopy, flexible sigmoidoscopy, or stool occult blood test

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8
Q

How does colorectal cancer appear on a barium swallow test X-ray?

A

Apple core lesion

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9
Q

What is a good tumor marker for CRC?

A

CEA- good for MONITORING recurrence, but not for screening

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10
Q

What are the 2 molecular pathways that can lead to CRC?

A

1) Microsatellite instability pathway (~15%): DNA mismatch repair gene mutations (sporadic and Lynch syndrome)
2) APC/B-Catenin pathway (~85%) (sporadic cancer)

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11
Q

Describe the order of mutations in the APC/B-Catenin CRC pathway

A

Normal colon- loss of APC gene (decreases intercellular adhesions and increases proliferation)

Colon at risk- KRAS mutation (unregulated intracellular signal transduction)

Adenoma- loss of p53

Carcinoma

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12
Q

What is cirrhosis?

A

diffuse bridginf fibrosis and nodular regeneration via stellate cells disrupts normal liver architecture (increases the risk for hepatocellular carcinoma)

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13
Q

What are some common causes of liver cirrhosis?

A

alcohol (60-70%)

chronic viral hepatitis

biliary disease

genetic/metabolic disorders

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14
Q

What are the main effects of portal HTN?

A

-esophageal varices (leading to hematemesis)

peptic ulcers (leading to melena)

Splenomegaly

Caput medusae, ascites

anorectal varices

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15
Q

What are the main effects of liver cell failure?

A
  • hepatic encephalopathy
  • scleral icterus
  • fetor hepaticus (musty smelling breath)
  • Gynecomastia, spider nevi, and testicular atrophy (due to icnreased free estrogen)
  • jaundice
  • ankle edema
  • liver ‘flap’ (asterixis) (coarse hand tremor)
  • bleeding tendency
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16
Q

What are some conditions in which ALP would be elevated?

A

-cholestatic and obstructive hepatobiliary disease

HCC
infiltrative disorders

bone disease

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17
Q

What are some conditions in which AST and ALT would be elevated?

A

viral hepatitis (ALT > AST)

alcoholic hepatitis (AST > ALT)

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18
Q

What are some conditions in which amylase would be elevated?

A

acute pancreatitis, mumps

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19
Q

What are some conditions in which ceruloplasmin would be suppressed?

A

Wilson disease

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20
Q

What are some conditions in which y-glutamyl transpeptidase (GGT) would be elevated?

A

elevated in liver and biliary diseases but not in bone disease like ALP

associated with alcohol use

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21
Q

Elevated lipase is most specific for what?

A

acute pancreatitis

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22
Q

What is Reye Syndrome?

A

A rare, often fatal childhood heaptic encephalopathy caused by aspirin use in children (typically for home tx of viral infections such as VZV and influenza B

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23
Q

What are some findings with Reye Syndrome?

A

mitochondrial abnormalities

fatty liver and hepatomegaly

hypoglycemia

vomiting

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24
Q

How does aspirin cause Reye syndrome?

A

aspirin metabolites decrease B-oxidation by reversible inhibition of mitochondrial enzymes (avoid aspirin in children except in Kawasaki disease)

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25
Q

What are some alcoholic liver diseases?

A
  • hepatic steatosis
  • alcoholic hepatitis
  • alcoholic cirrhosis

this is a progression

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26
Q

Describe the histology of hepatic steatosis

A

Macrovesicular fatty change that may be reversible with alcohol cessation

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27
Q

Describe the histology of alcoholic hepatitis

A

this is marked by:

  • swollen and necotirc hepatocytes with neutrophilic infiltration
  • Mallory bodies (intracellular eosinophilic inclusions of damaged keratin filaments- below)
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28
Q

T or F. Alcoholic hepatitis requires sustained, long-term consumption

A

T.

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29
Q

What is the AST:ALT ratio in alcoholic hepatitis?

A

1.5+

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30
Q

Describe alcoholic cirrhosis

A

This is the final and irreversible form of alcoholic liver disease marked by jaundice and hypoalbuminemia

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31
Q

How does the liver grossly appear with alcoholic cirrhosis?

A

micronodular, and irregularly shrunken with ‘hobnail’ appearance

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32
Q

In alcoholic cirrhosis, sclerosis is most prominantly seen in which zone?

A

around the central vein (zone III)

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33
Q

Describe non-alcoholic fatty liver disease

A

This is a metabolic syndrome of insulin resistance marked by fatty infiltration of hepatocytes and cellular ‘ballooning’ and eventual necrosis independent of alcohol use

May cause cirrhosis and HCC

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34
Q

Which is more elevated in non-alcoholic fatty liver disease, ALT or AST?

A

ALT over AST

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35
Q

How does hepatic enchapelopathy arise?

A

cirrhosis causes portosystemic shunts, leading to decreased NH3 metabolism which directly causes the neuropsychiatric dysfunction

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36
Q

How does hepatic encephalopathy present?

A

can range from disorientation/asterixis (mild) to difficult arousal/coma (severe)

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37
Q

What are some triggers of hepatic enchepalopathy?

A
  • increased NH3 production and absorption (due to dietary protein, GI bleed, constipation, or infection)
  • decreased NH3 removal (due to renal failure, diuretics, bypassed hepatic blood flow post TIPS)
38
Q

What is the Tx of hepatic encephalopathy?

A

lactulose (increases NH4+ generation) and rifaximin

39
Q

What is the most common primary MALIGNANT tumor of the liver in adults?

A

Hepatocellular carcinoma/hepatoma

40
Q

What are some associations with hepatocellular carcinoma?

A
  • HBV (+/- cirrhosis)
  • all other causes of cirrhosis (including HCV, alcoholic and non-alcoholic fatty liver disease, hemochromatosis, a1-antitrypsin deificiency, and Wilson Disease)
  • carcinogens such as aflatoxin from Aspergillus
41
Q

Gross picture of hepatoceullar carcinoma

A

CT of hepatocellular carcinoma

42
Q

How might a HCC present?

A
  • jaundice
  • tender hepatomegaly
  • ascites
  • polycythemia
  • anorexia
43
Q

How do HCC spread?

A

via heme

44
Q

How are HCC diagnosed?

A

increased a-fetoprotein

ultrasound or contrast CT/MRI

biopsy

45
Q

Histology of HCC

A
46
Q

What are some other common liver tumors?

A
  • cavernous hemangionas
  • heptaic adenoma
  • angiosarcoma
  • METs
47
Q

Describe cavernous hemangiomas

A

common, BENIGN liver tumors typically occurring at ages 30-50

48
Q

T or F. Suspected cavernous hemangiomas should be biopsied

A

F. Due to risk of hemorrhage

49
Q

Describe hepatic adenomas

A

Rare, benign liver tumors often related to oral contraceptive or anabolic steroid use

These may regress spontaneously or rupture causing abdominal pain and shock

50
Q

Describe liver angiosarcomas

A

These are malignant tumors of endothelial origin associated with exposure to aresnic and vinyl chloride

51
Q

What is the most common cancer of the liver?

A

METs

52
Q

What places like to MET to the liver?

A

GI, breast, and lung

53
Q

What is Budd-Chiari Syndrome?

A

Thrombosis or compression of hepatic veins with centrilobular congestion and necrosis causing congestive liver disease (leading to hepatomegaly, varices, abdominal pain, and eventual liver failure)

May cause nutmeg liver

54
Q

T or F. Budd-Chiari Syndrome is marked by the absence of JVD

A

T.

55
Q

What are some associations of Budd-Chiari Syndrome?

A
  • hypercoagulable states
  • poylcythemia vera
  • postpartum state
  • HCC
56
Q

How does a1-antitrypsin deficiency affect the liver?

A

Misfolded gene products cause accumulation in the hepatocellular ER causing cirrhosis with PAS + globules (below) in the liver

NOTE: it causes panacinar emphysema in the lungs due to uninhibited elastase activity

57
Q

What causes jaundice?

A

billrubin deposition at high (2.5+ mg/dL) levels in blood secondary to increased production of defective metabolism

58
Q

What are some causes of unconjugated (indirect) hyperbilirubinemia?

A
  • hemolytic states
  • physiologic in newborns
  • Crigler-Najjar syndrome
  • Gilbert syndrome
59
Q

What are some causes of conjugated (direct) hyperbilirubinemia?

A
  • biliary tract obstruction (gallstones, cholangiocarcinoma, pancreatic or liver cancer, liver fluke)
  • biliary tract disease (primary sclerosing cholangitis or primary biliary cirrhosis)
  • excretion defects (Dubin-Johnson syndrome, Rotor syndrome)
60
Q

What are some causes of mixed hyperbilirubinemia?

A

hepatitis and cirrhosis

61
Q

What causes physiologic neonatal jaundice?

A

At birth, immature UDP-glucuronosyltrasnferase leads to unconjugated hyperbilirubinemia causing jaundice and/or kernicterus

62
Q

What is kernicterus?

A

bilirubin deposition in the brain, especially the basal ganglia

63
Q

What is the tx for neonatal jaundice?

A

phototherapy (converts unconjugated bilirubin to water-soluble forms)

64
Q

What is Gilbert Syndrome?

A

Mildly decreased UDP-glucuronosyltransferase conjugation and impaired bilirubin uptake leading to an asymptomatic or mild jaundice state, and increased unconjugated bilirubin without overt hemolysis

Bilirubin increases with fasting and stress

65
Q

What is Type I Crigler-Najjar Syndrome?

A

Absent UDP-glucuronosyltransferase that presents as jaundice, kernicterus, and high levels of unconjugated bilirubin early in life (pts. die within a few yrs)

NOTE: Type II is less severe

66
Q

How is type I Crigler-Najjar Syndrome tx?

A

plasmapheresis and phototherapy

67
Q

How is Type II Crigler-Najjar Syndrome tx?

A

responds to phenobarbital, which increases liver enzyme synthesis

68
Q

Describe Dubin-Johnson Syndrome

A

Benign syndrome of conjugated hyperbilirubinemia due to defective liver excretion (MRP-2 is absent) causing a grossly black liver (note that Rotor syndrome is similar but milder and does not cause black liver)

69
Q

What enzyme converts unconjugated bilirubin to conjugated (water soluble) bilirubin?

A

UDP- glucuronosyltransferase (aka UGT 1A1)

70
Q

What are some sources of neonatal jaundice?

A

Infant UGT 1A1 is underdeveloped AND breast milk contains B-glucuronidase which can deconjugate bilirbuin

71
Q

Kernicterus is a clinical set of symptoms caused by deposition of bilirubin in the brain, particularly the _______

A

basal ganglia

72
Q

How is bilirubin made?

A

bilirubin is a breakdown product of hemoglobin and is made by:

  • heme oxygenase releasing the central Fe2+ to create bilverdin, and
  • bilverdin reductase using NADPH to create bilirubin
73
Q

What happens to bilirubin once its made?

A

it is bound to albumin an transferred via portal circulation to the liver for uptake

74
Q

What is Wilson disease?

A

A hepatic/neuro disease caused by inadequate excretion/circulation of copper in the copper

75
Q

What causes Wilson disease?

A

lack of ATP7B gene impairs the ability of copper to be loaded to ceruloplasmin

76
Q

What labs suggest Wilson disease?

A
  • elevated free copper
  • low levels of ceruloplasmin
  • high urine copper
77
Q

Why are ceruloplasmin levels low in Wilson Disease?

A

ceruloplasmin is relased from the liver without copper and thus is rapidly degraded

78
Q

What are the symptoms of Wilson Disease?

A
  • Cirrhosis
  • Hemolytic Anemia
  • Basal ganglia degeneration
  • Asterixis
  • Dyskinesia

Copper is Hella BAD

79
Q

What is the MOI of Wilson Disease? Chromosome?

A

AR; 13

80
Q

What is the tx of Wilson Disease?

A

All will require liver transplant and in the meantime give:

-penicillamine or trientine and zinc

81
Q

What is this?

A

Kayser-Fleischer ring in Wilson Disease

82
Q

What is hemochromatosis?

A

deposit of excess iron in the body (4 types)

83
Q

What is the most common (85-90%) cause of hemochromatosis?

A

C282Y mutation of hepcidin

84
Q

What are the symptoms of Hemochromatosis?

A
  • micronodular cirrhosis
  • DM
  • skin pigmentation
  • testicular atrophy
85
Q

Iron is best seen with a _______-____ stain

A

Prussian Blue

86
Q

What is the main tx of hemochromatosis?

A

phlebotomy

87
Q

How does biliary tract disease typically present?

A

-pruritis, jaundice, dark urine, light-colored stool, and HSM

88
Q

What are the main types of gallstones?

A
  • cholesterol stones
  • pigment stones
89
Q

What are the main risk factors for gallstones?

A

4F’s:

Female, Fat, Fertile, Forty

90
Q

What is this?

A

Porcelain gallbladder

91
Q

What is a Porcelain gallbladder?

A

a calcified gallbladder due to chronic cholecystitis usually found incidentally on imaging

92
Q

Pancreatic adenocarcinoma (terrible prognosis: 1 yr) is associated with what serum marker?

A

CA 19-9

STEP 1 (1) (28 decks)

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