B5-025 Liver Disorders I Flashcards

1
Q

the dual blood supply of the liver comes from

2

A
  • portal vein
  • hepatic vein
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2
Q

macrophages that live in the sinusoids of the liver

A

Kupffer cells

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3
Q

lined with simple cuboidal epithelium

“string of pearls”

A

bile duct

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4
Q
A
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5
Q

blood in zone one is […] in oxygen

A

rich

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6
Q

blood in zone 3 is […] in oxygen

A

low

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7
Q

there is a more dense distribution of cytochrome p450 enzymes in zone […]

A

3

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8
Q

large cells with centrally located nucleus and prominate nucleolus

A

hepatocytes

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9
Q

hepatocytes are connected to their neighbor hepatocytes through a

A

bile cannaliculus

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10
Q

space between hepatocytes and sinusoids

A

space of Disse

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11
Q

stellate cells live in the

A

space of Disse

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12
Q

what do stellate cells do in their quiescient state?

A

store fat-soluble vitamins

ADEK

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13
Q

in a normal adult state, the cell plates should be […] cells thick

how many cells

A

1
2 cells max (regenerative state)

3+ indicates neoplastic process

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14
Q

feathery degeneration indicates an accumulation of

A

bile

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15
Q

steatosis can be due to

3

A

obesity, alcohol, diabetes

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16
Q

accumulation of iron in a canalicular distribution

A

hemochromatosis

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17
Q

accumulation of copper

Cu not excreted in bile

A

Wilson’s disease

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18
Q

accumulation of misfolded protein in the RER

A

a1 antitrypsin deficiency

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19
Q

old age/”wear and tear” pigment seen in hepatocytes

A

lipofuscin

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20
Q
  • clumped cytokeratin filaments
  • ballooned degeration
A

Mallory hylanine

steatohepatitis, alcohol use

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21
Q
  • hyperpigmentation of the skin
  • jaundice
  • diabetes
A

genetic hemochromatosis

“bronze diabetes”

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22
Q

what lab values would you expect to be elevated in hemochromatosis?

4

A
  • AST/ALT
  • serum iron
  • transferrin
  • serum ferritin
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23
Q

treatment for hereditary hemochromatosis

A

weekly phlebotomy and deferoxamine

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24
Q

inheritance pattern of hereditary hemochromatosis

bonus points if you name the gene

A

autosomal recessive inheritance of HFE gene

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25
Q

HFE regulates

A

hepcidin

controls how much iron is absorbed in intestine

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26
Q
  • caused by inappropriately high intestinal iron absorption
  • results in excess body iron stores
A

hereditary hemochromatosis

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27
Q

why do most cases of hereditary hemochromatosis present after age 40?

A
  • takes a long time to accumulate
  • cirrhosis occurs when the body iron exceeds 30-40 g around age 40
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28
Q

risk factors for hereditary hemochromatosis

A
  • male gender
  • hepatitis C
  • alcohol
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29
Q

PAS-diatase resistant globules

A

a1 antitrypsin deficiency

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30
Q

Piz allele

A

alpha 1 antitrypsin deficiency

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31
Q

present with cirrhosis of the liver
and early onset empysema, chronic bronchitis, asthma, etc

A

alpha 1 antitrypsin deficiency

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32
Q

all patients with PiZZ genotype accumulate […] in hepatocytes

A

alpha 1 antitrypsin deficiency

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33
Q
  • resting tremor
  • brownish ring around cornea
A

wilson’s disease

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34
Q

what labs would you expect to be abnormal in Wilson’s disease?

A
  • decreased ceruloplasmin
  • elevated urine copper
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35
Q

mutation in ATPase leading to defective conjugation of copper in ceruloplasmin

A

Wilson’s disease

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36
Q

increased copper absorption in gut but decreased excretion in bile

A

wilson’s disease

37
Q

treatment for Wilson’s

A

penicillamine

copper chelation

38
Q

what kind of stain is used to visualize copper?

A

rhodadine

39
Q

apoptosis is commonly seen in

“dead reds”

A

viral hepatitis

40
Q

zonal toxic necrosis is due to

A

ischemia or toxins

41
Q

causes centrolobular necrosis

A

acetaminophen overdose

42
Q

midzonal necrosis is caused by

2

A

adenovirus
acute hepatitis

43
Q

submassive or massive necrosis is due to

A

toxins
viral hepatitis

44
Q

laboratory tests to evaluate biliary function

4

A
  • total bilirubin
  • direct bilirubin
  • alk phos
  • GGT
45
Q

laboratory tests to determine hepatocyte function

3

A
  • serum albumin
  • PTT
  • serum ammonia
46
Q

what labs would you expect to be elevated in an obstructive liver disease pattern?

A

alk phos
bilirubin
GGTP

all elevated

47
Q

what labs would you expect to be abnormal in an acute hepatitis pattern?

A

elevated AST/ALT
bilirubin +/-

48
Q

what labs would you expect to be abnormal in a cirrhosis pattern?

A

decreased albumin
decreased platelets
prolonged PTT

49
Q

multinucleation, margination, molding

A

herpesvirus hepatitis

50
Q
  • seen in immunocompromised after liver/renal transplant
  • microabscesses, “owl’s eyes”
A

CMV hepatitis

51
Q

sinusoidal lymphocytosis (“string of pearls”) with portal inflammation

A

EBV hepatitis

52
Q

one pill once a day for 12 weeks treatment for HCV

A

harvoni

really expensive

53
Q

this histology with plasma cells is characteristic of

A

autoimmune hepatitis

54
Q
  • ANA, ASMA +
  • AST, ALT > alk phos
  • hypergammaglobulinemia
  • absence of viral hepatitis
A

autoimmune hepatitis

55
Q

features of metabolic resistance

5

A
  • DM/insulin resistance
  • hypertension
  • dyslipidemia
  • central obesity
  • microalbuminemia
56
Q

just fat globules with very minimal risk to progression of cirrhosis

A

steatosis

57
Q
  • fat globules plus inflammation and ballooned hepatocytes
  • risk of progression to cirrhosis
A

steatohepatitis

58
Q

cytokines released from Kupffer cells to activate stellate cells

2

A

TNF-a
TGF-b

59
Q

what kind of cells deposit collagen in the liver?

A

stellate cells

60
Q

store fat soluble vitamins

A

stellate cells

61
Q

mallory hyaline =

A

alcoholic steatohepatitis

for testing purposes

62
Q
A

cirrhosis

63
Q

elevated AFP indicates

A

HCC

64
Q
A

HCC

65
Q
A

left: HCC
right: normal

66
Q

mutations associated with the development of HCC

3

A
  • b-catenin (activating)
  • TERT
  • TP53 (inactivating)
67
Q

round globular inclusions of misfolded proteins in hepatocytes that stain bright pink with PAS-diastase

A

a1-antitrypsin deficiency

68
Q

PAS stain removes […] with diastase

A

glycogen

69
Q

interface and lobular inflammatory activity

A

viral hepatitis

70
Q

broad fibrous bands and complete parenchymal nodules

A

cirrhosis

71
Q

cirrhosis causes

A

portal hypertension

72
Q

portosystemic venous shunts cause

3

A
  • esophageal varices
  • periumbilical caput medusa
  • hemorrhoids
73
Q

the livers inability to degrade estrogen in liver failure causes

4

A
  • skin spider angioma
  • palmar erythema
  • testicular atrophy
  • gyencomastia
74
Q

increased ammonia levels in liver failure cause

2

A

asterixis
encephalopathy

75
Q

decreased synthetic function in liver failure results in

A

low albumin

76
Q

what causes the prolongation of PT in liver failure?

A

factor IIV degradation

77
Q

how does alcohol cause hepatic steatosis?

A

excess NADH changes normal hepatic metabolism from catabolism of fat to anabolism of fats

results in decreased mitochondrial oxidation of fatty acids and increased triglyceride production

78
Q

lobular disarray with apoptotic hepatocytes and lobular inflammation

A

acute hepatitis

79
Q

AMA is associated with

A

primary biliary cholangitis

80
Q

extremely elevated transaminanses are associated with

A

acute hepatitis

81
Q

ANA is associated with

A

autoimmune hepatitis

82
Q

p-ANCA is associated with

A

primary sclerosing cholangitis

83
Q

interface activity and prominent lymphoplasmacytic infiltrate

A

autoimmune hepatitis

84
Q

more common in females
may be asymptomatic or present with fatigue, nausea, pruritis

A

autoimmune hepatitis

85
Q

associated with circulating anti-nuclear antibodies and high levels of serum immunoglobulins

A

autoimmune hepatitis

86
Q

autosomal recessive genetic disorder characterized by excessive iron absorption and toxic accumulation of iron

A

hereditary hemochromatosis

87
Q

diabetes, skin pigmentation, and cardiac failure

A

hereditary hemochromatosis

88
Q

prussian blue stain binds

A

iron

hereditary hemochromotosis

89
Q

heriditary hemochromatosis leads to

A

cirrhosis/HCC