Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

CMV hepatitis features

A

mostly after renal and liver transplant

immunocompetent people - mono with mild hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

histo of CMV hepatitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q
A

CMV hepatitis

intranuclear inclusions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
A

microabscesses in CMV hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

feature of EBV hepatitis

A

immunocompetent and compromised

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
A

sinusoidal lymphoctytosis in EBV hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

hepatitis A features

A

endemic in countries with substandard sanitation

sporadic

fecal oral

1992

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

hepatitis B features

A

1/3 world pop infected

chronic or acute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

transmission of HBV

A

perinatal

sexual contacts

IV drugs

transfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

natural history of HBV

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

injury from HBV

A

injury caused by CD8+ cytotoxic T cells attacking infected cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

HBV histo

A

ground glass hepatocytes

cells with endoplasmic retuculum swollen with HSsAg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
A

HBV ground glass hepatocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

most common blood bourne infection in US

A

HCV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

HCV transmission

A

inoculations and blood transfusions

IV drug use - 60%

transfusions

hemodialysis and healtcare workers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

natural history of HCV

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

HDV features

A

unique RNA virus that is replication defective

only causes infection when encapsulated by HBsAg

Dependent on HBV for multiplication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

HEV features

A

enterically transmitted, water bourne

mostly self limiting, except in high mortality in pregnant women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q
A

sinusodal lymphocytes and kupffer cells top

apoptotic hepatocyte bottom

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q
A

acute hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q
A

normal liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

grade and stage for chronic hepatitis C

A

grade - activity

stage - fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what are sofosbuvir and ledipasvir

A

sofosbuvir - nucleotide polymerase inhibitor

ledipasvir - NS5A inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q
A

portal inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q
A

interface hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q
A

confluent necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q
A

apoptosis and lobular inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q
A

apoptotic hepatocyte

34
Q
35
Q
36
Q
A

a finding in cirrhosis

seen when fibrosis crosses from one structure to another

37
Q
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
54
Q
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

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

74
Q
A

Endothelial cells wrapped around expanded hepatic plates

75
Q
A

expanded trabeculae 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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions