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

B5.026 Liver Disorders II Flashcards

1
Q

diseases affecting hepatocytes

A

hepatitic diseases- viral, autoimmune
fatty liver disease- NASH and alcohol
DILI
hepatocellular carcinoma

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2
Q

causes of viral hepatitis

A 
EBV
CMV
yellow fever
herpes
Hep A, B, C, D, E
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3
Q

features of herpes hepatitis

A

immunocompromised pts
patchy coagulative necrosis, no particular zonal distribution
eosinophilic intranuclear inclusions
3 Ms: multinucleation, molding, margination

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4
Q

features of CMV hepatitis

A

mostly after renal and liver transplant
immunocompetent people- infectious mono with mild hepatitis
focal hepatocyte necrosis, microabscesses, and occasional sinusoidal lymphocytic infiltration
owl’s eye intranuclear inclusions

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5
Q

features of EBV hepatitis

A

immunocompetent and immunocompromised people

diffuse sinusoidal lymphocytic infiltrate (string of pearls) with varying degrees of portal inflammation

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6
Q

overview of hep A

A

endemic in countries with substandard sanitation
fecal-oral contamination- food industry, school, nurseries, raw shellfish
vaccine developed in 1992
no carrier or chronic state

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7
Q

hep A symptoms

A

sporadic febrile illness with jaundice, fatigue, loss of appetite

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8
Q

what is problematic about how hep A spreads?

A

it can be shed in feces before an individual shows symptoms, they don’t know they’re transmitting it

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9
Q

epidemiology of hep B

A

1/3 of world pop have been infected
5% have chronic infection (400 million)
75% of carriers in asia and west pacific

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10
Q

modes of transmission of hep B

A

high prevalence areas- perinatal transmission during childbirth accounts for 90% of cases
low prevalence areas (US)- sexual contact and IV drugs
vaccination induces protective anti-HBs antibody response in 95%

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11
Q

outcomes of hep B by frequency

A

65% subclinical disease
25% acute hep B
5-10% chronic hep B

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12
Q

outcome of acute hep B

A

99% recovery

1% fulminant hep

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13
Q

outcome of chronic hep B

A

20-30% cirrhosis
2-3% HCC
recovery in the rest

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14
Q

protective antibody against hep B

A

anti-HBs (antibody against surface antigen)

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15
Q

what determines outcome of hep B infection?

A

host immune response to virus
strong CD4 and CD8 interferon producing T cells associated with resolution of acute infection
HBV does not cause direct hepatic injury, injury is caused by CD8 cytotoxic T cells attacking infected cells

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16
Q

histo of hep B

A

ground glass hepatocytes

cells with ER swollen with HSsAg

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17
Q

epidemiology of hep C

A

3.9 mil have Ab to hep C
75% have chronic infection (viral DNA in serum)
most common blood bourne infection in US
accounts for almost 1/2 of pts in US with chronic liver disease

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18
Q

transmission of hep C

A 
IV drugs - 60%
transfusion - 10% prior to 1991
hemodialysis and health care- 5%
sexual - 15%
vertical transmission - 6%
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19
Q

description of hep D

A

unique RNA virus that is replication defective
only causes infection when it is encapsulated by HBsAg
dependent on hep B for multiplication

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20
Q

2 types of hep D infection

A 
acute coinfection (simultaneous exposure with hep B)
superinfection (exposure of chronic hep B carrier)
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21
Q

hep E overview

A

enterically transmitted, water bourne
mostly self limiting
high mortality in pregnant women (20%)

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22
Q

4 primary courses of hepatitis

A
  1. acute asymptomatic infection with recovery- serologic evidence only
  2. acute symptomatic hepatitis with recovery
  3. chronic hepatitis- with or without progression to cirrhosis
  4. fulminant hepatitis- massive to submassive hepatic necrosis
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23
Q

acute hepatitis on histo

A 
dominant features are in lobular/acinus
disordered, "dirty" appearance
acidophilic (apoptotic) cells
liver plate disarray
confluent bridging or submassive necrosis
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24
Q

appearance of sinusoidal lymphocytes

A

blue dots in typically empty sinusoidal white spaces

25
Q

clinical definition of chronic hepatitis

A

persistent inflammatory reaction of the liver with more than 6 months of clinical signs and symptoms

26
Q

chronic hepatitis on histo

A 
marked and patchy expansion of the portal tracts by predominantly lymphocytes
interface hepatitis
varying degrees of bile duct damage
steatosis
lobular inflammation
27
Q

who gets progressive chronic hep C?

A 
>40 at infection
immunodeficient
viral heterogeneity
genotype 1
males
long duration of infection
ethanol
28
Q

grading hep C

A

activity

  • portal inflammation
  • interface hepatitis
  • confluent necrosis
  • apoptosis
29
Q

staging hep C

A

fibrosis

30
Q

what is harvoni?

A

treats genotype 1 of hep C
one pill, once a day
96-99% of patients who had no prior therapy cured with 12 weeks of therapy
$95,000 for full treatment

31
Q

appearance of fibrosis on histo

A

blue strands
blue is bad
can grow to bridge between different areas

32
Q

clinical signs of cirrhosis

A 
jaundice
hypoalbuninemia
hyperammonemia
hyperestrogenemia
coagulopathy
encephalopathy
hepatorenal syndrome
portal hypertension
33
Q

features of autoimmune hepatitis

A

young and middle aged women
ANA or anti-SMA usually present
chronic disease, fatal if left untreated
steroid therapy leads to symptomatic improvement
pts with LKM antibody positive diseases have poorer prognosis

34
Q

diagnosis of autoimmune hepatitis

A

very complex
multiple factors taken into account
scored based on features

35
Q

important diagnostic criteria of autoimmune hepatitis

A 
female
polyclonal hypergammaglobulinemia
circulating autoAb (ANA, ASMA)
absence of viral infection, drugs, EtOH
favorable response to immunosuppression
hepatic rather than a cholestatic liver enzyme profile
36
Q

autoimmune hepatitis on histo during flare

A

marked interface hepatitis
lymphoplasmacytic infiltrate
hepatocyte rosettes, emperipolesis
lobular activity

37
Q

autoimmune hepatitis on histo during quiescent phase

A

no lobular activity
no to minimal interface activity
mild portal inflammation

38
Q

what are hepatocyte rosettes

A

clusters of hepatocytes in a sea of lymphocytic infiltrates

39
Q

what is emperipolesis

A

hepatocytes engulf T cells

blue inclusions in hepatocytes

40
Q

causes of fatty liver disease

A

alcoholic steatohepatitis
NAFLD
NASH (non-alcoholic steatohepatitis)

41
Q

what causes steatosis in alcohol induced liver disease

A

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

42
Q

appearance of hepatic steatosis

A

small and large fat droplets
initially centrilobular; progressed to entire lobule
reversible with abstinence

43
Q

histo features of alcoholic hepatitis

A

hepatocyte swelling and necrosis (ballooning)
Mallory hyaline (ubiquinated cytokeratin intermediate filaments)
neutrophilic reaction
fibrosis

44
Q

unique feature of fibrosis in alcoholic hepatitis

A

chicken wire fibrosis

fibrosis around individual cells (usually in zone 3)

45
Q

2 types of steatosis

A

macrovesicular (large and small droplet)

microvesicular (VERY small droplets filling hepatocytes)

46
Q

etiologies of microvesicular steatosis

A

reye syndrome
fatty liver of pregnancy
valproic acid toxicity

47
Q

definition of large droplet

A

fat droplet occupying greater than one half of the hepatocyte

48
Q

definition of small droplet

A

fat droplet occupying less than one half of the hepatocyte

not as bad as large droplet

49
Q

reye syndrome

A

acute post viral illness in children who are given aspirin for fever
microvesicular steatosis
encephalopathy
due to widespread mitochondrial injury

50
Q

fulminant hepatitis

A

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

51
Q

causes of fulminant hepatitis

A

drug/chemical -52%
viral (HAV or HBV) - 12%
amanita phalloides (mushroom)
obstruction hepatic veins, Wilson disease, fatty liver of preg, Reye

52
Q

histo features of APAP overdose

A 
centrolobular necrosis
centrolobular hepatocytes (zone 3) contain more microsomal biotransformation enzymes than the peripheral (zone 1) hepatocytes
53
Q

HCC etiologies

A

viral infection
alcohol
food contaminants (aflatoxins)
hemochromatosis

54
Q

what are aflatoxins

A

from fungus aspergillus flavus
carcinogenic toxins in moldy grains and peanuts
cause mutations in tumor suppressor genes (p53)

55
Q

when does carcinogenesis occur in the liver

A

in mitotically active liver

chronic viral hepatitis with recurrent injury and regeneration

56
Q

features of HCC

A

can be unifocal, multifocal, diffusely infiltrative
green tinge
invade vascular channels
range from well differentiated to anaplastic
can be trabecular, acinar, solid, scirrhous
2/3 have AFP >1000
majority arise in background of cirrhosis

57
Q

what are expanded trabeculae

A

more than 1-2 cells thick between sinusoids

58
Q

features of fibrolamellar HCC

A

young woman (20-40 years)
no risk factors
no cirrhosis
better prognosis?

59
Q

histo fibrolamellar HCC

A

thick hyalinized fibrous bands

GIR Test 2 (20 decks)

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