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GIR Test 2 > B5.026 - Liver Disorders 2 > Flashcards

B5.026 - Liver Disorders 2 Flashcards

1
Q

causes of viral hepatitis

A

EBV

CMV

Yellow fever

herpes

viral hepititis

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2
Q

herpes hepatitis features

A

immunocompromised pts

patchy coagulative necrosis, no particular zonal distribution

eosinophilic intranuclear inclusions

3 M’s of Herpes

Multinucleation

Molding

Margination

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3
Q

CMV hepatitis features

A

mostly after renal and liver transplant

immunocompetent people - mono with mild hepatitis

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4
Q

histo of CMV hepatitis

A

focal hepatocyte necrosis, microabscesses, occasional sinusodal lymphocytic infiltration, owls eye

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5
Q
A

CMV hepatitis

intranuclear inclusions

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6
Q
A

microabscesses in CMV hepatitis

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7
Q

feature of EBV hepatitis

A

immunocompetent and compromised

diffuse sinusoidal lymphocytic infiltrate with varying degrees of portal inflammation “string of pearls”

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8
Q
A

sinusoidal lymphoctytosis in EBV hepatitis

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9
Q

hepatitis A features

A

endemic in countries with substandard sanitation

sporadic

fecal oral

1992

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10
Q

hepatitis B features

A

1/3 world pop infected

chronic or acute

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11
Q

transmission of HBV

A

perinatal

sexual contacts

IV drugs

transfusion

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12
Q

natural history of HBV

A
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13
Q

injury from HBV

A

injury caused by CD8+ cytotoxic T cells attacking infected cells

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14
Q

HBV histo

A

ground glass hepatocytes

cells with endoplasmic retuculum swollen with HSsAg

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15
Q
A

HBV ground glass hepatocytes

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16
Q

most common blood bourne infection in US

A

HCV

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17
Q

HCV transmission

A

inoculations and blood transfusions

IV drug use - 60%

transfusions

hemodialysis and healtcare workers

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18
Q

natural history of HCV

A
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19
Q

HDV features

A

unique RNA virus that is replication defective

only causes infection when encapsulated by HBsAg

Dependent on HBV for multiplication

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20
Q

HEV features

A

enterically transmitted, water bourne

mostly self limiting, except in high mortality in pregnant women

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21
Q
A

sinusodal lymphocytes and kupffer cells top

apoptotic hepatocyte bottom

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22
Q
A

acute hepatitis

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23
Q
A

normal liver

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24
Q

clinically chronic hepatitis

A

presistent inflammatory reaction of the liver with more than 6 months of linical signs and symptoms

maked patchy expansion of the portal tracts by predominantly lymphocytes, interface hepatitis, varying degrees of bile duct damage, steatosis, lobular inflammation

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25
Q

grade and stage for chronic hepatitis C

A

grade - activity

stage - fibrosis

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26
Q

what is harvoni

A

treatment of genotype 1 of hepatitis C

one pill, once a day

in clinical studies 96-99% of patients who had no prior treatment were cured in 12 weeks of therapy

combo of sofosbuvir, ledipasvir

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27
Q

what are sofosbuvir and ledipasvir

A

sofosbuvir - nucleotide polymerase inhibitor

ledipasvir - NS5A inhibitor

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28
Q

what are factors that are taken into account in activity (grade) of chronic hepatitis C

A

portal inflammation

interface hepatitis

confluent necrosis

apoptosis

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29
Q
A

portal inflammation

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30
Q
A

interface hepatitis

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31
Q
A

confluent necrosis

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32
Q
A

apoptosis and lobular inflammation

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33
Q
A

apoptotic hepatocyte

34
Q
A

fibrosis

35
Q
A

fibrosis

36
Q
A

a finding in cirrhosis

seen when fibrosis crosses from one structure to another

37
Q
A

fibrosis

38
Q

describe autoimmune hepatitis

A

young and middle aged women

ANA or anti SMA usually present

chronic disease, progressive and fatal without treatment

39
Q

treatment of autoimmune hepatitis

A

steroid therapy leads to symptomatic improvment but doesnt prevent progression

40
Q

diagnostic criteria for autoimmune hepatitis

A

female

polyclonal hypergammagolbulinemia

circulating autoAb (ANA, ASMA)

absence of viral infection, drugs, EtOH

favorable response to immunosuppression

hepatic rather than cholestatic liver enzyme profile

41
Q

autoimmune hepatitis features during flare

A

marked interface hepatitis, lymphoplasmacytic infiltrate, hepatocyte rosettes, emperipolesis

lobular activity

42
Q

autoimmune hepatitis features during quiescent phase

A

no lobular activity/no to minimal interface activity

mild portal inflammation

43
Q
A

interfacing inflammation

44
Q
A

plasma cells

45
Q
A

Interface inflammation

46
Q
A

interface inflammation

47
Q
A

plasma cells

48
Q
A

hepatocyte rosettes

49
Q
A

emperipolesis

50
Q
A

resolved inflammation

51
Q

describe alcohol induced liver disease

A

steatoiss, production of excess reducing equivalents (NADH + H+) due to metabolism of alcohol

52
Q

describe hepatic steatosis

A

small and large fat droplets

initially centrilobular; progresses to entire lobule

fatty change is reversible with abstinence

53
Q
A

steatosis

54
Q
A

steatosis

55
Q

describe histo of alcoholic hepatitis

A

hepatocyte swelling and necrosis (ballooning)

mallory hyaline (ubiquinated cytokeratin intermediate filaments)

neutrophilic reaction

fibrosis

56
Q
A

ballooned hepatocyte

57
Q
A

mallory hyaline in ballooned hepatocyte

58
Q
A

chicken wire fibrosis

59
Q

causes of NAFLD

A

obesity

dyslipidemia, hyperinsulinemia, insulin resistance

60
Q

what is macrovesicular / large droplet fat defined as

A

fat droplets occupying greater than 1/2 of hepatocyte

61
Q

what is a small droplet defined as

A

a fat droplet occupying <1/2 of hepatocyte

not as bad as large droplet

62
Q

what is true microcesicular steatosis

A

very small uniform fat globules packed within hepatocytes visible at least as patches at 10x in fatty liver of pregnancy

63
Q
A

microvesicular steatosis

64
Q

causes of microvesicular steatosis

A

acute fatty liver of pregnancy

drugs

toxins

TPN

reye syndrome

infection

65
Q

what is reye syndrome

A

acute post viral illness in children who are given aspirin for fever

microvesicular steatosis

encephalopathy due to widespread mitochondrial injury

66
Q

what is fulminant hepatitis

A

hepatic insufficiency progresses from onset of sx to hepatic encephalopathy in 2-3 weeks

67
Q
A

centrilobular necrosis in acetaminophen OD

68
Q

describe acetaminophen OD effect on hepatocytes

A

centrilobular hepatocytes (zone 3) contain more microsomal biotransformation enzymes than the peripheral zone (1) hepatocytes

69
Q

where are most HCC found

A

asia

70
Q

etiology of HCC

A

viral infection

alcohol

food contaminants

hemochromatosis

71
Q

what are aflatoxins

A

found in regions where HBV is endemic

from aspergillus flavus

carcinogenic toxins in moldy grains and peanuts

toxins cause mutations in tumor suppressor genes (p53)

carcinogenesis only occurs in mitotically active liver

72
Q

describe characterisics of HCC

A

unifocal, multifocal, diffuse

green tinge

invade vascular channels, intrahepatic mets

well differentiated anaplastic

trabecular, acinar, solid, scirrhous

73
Q
A

HCC

74
Q
A

Endothelial cells wrapped around expanded hepatic plates

75
Q
A

expanded trabeculae HCC

76
Q
A

HCC

77
Q
A

HCC

78
Q

features of fibrolamellar HCC

A

young women 20-40

no risk factors

no cirrhosis

better prognosis potentially

79
Q
A

fibrolamellular HCC

Thick hyalinized fibrous bands

80
Q
A

HSV hepatitis

Note - purple ring on outside of cell is chromatin - margination

GIR Test 2 (17 decks)

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