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GI II Test 2 > Infectous Disorders of Liver > Flashcards

Infectous Disorders of Liver Flashcards

1
Q

What kind of disease does Hep A Virus (HAV) cause?

A

benign self-limited disease

DOESN’T CAUSE CHRONIC HEPATITIS OR CARRIER STATE

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2
Q

How is HAV transmitted?

A

fecal-oral via contaminated water, or consumption of raw/undercooked shellfish

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3
Q

HAV characteristics?

A

SSRNA

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4
Q

How does HAV appear clinically?

A

the disease is mild or asymptomatic and rare after childhood; confers immunity with IgG

anti-HAV immunoglobulin IgM seen in serum w/onset of symptoms (IgM = acute)

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5
Q

What kind of disease does Hep A Virus (HAV) cause?

A

can cause a wide spectrum of disease manifestations, with most of the
cases leading to asymptomatic chronic disease or clearance

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6
Q

What are the 5 different forms of HBV induced illness?

A
  • acute hepatitis w/recovery and clearance of virus
  • Non-progressive chronic hepatitis*
  • Progressive chronic disease ending in cirrhosis
  • Acute hepatic failure with massive liver necrosis
  • Asymptomatic, ‘healthy’ carrier state

*clinically important precursor for HCC

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7
Q

How is HBV transmitted?

A
  • in high-prevalence areas (africa, asia) = childbirth
  • in intermediate-prevalence areas = horizontal (breaks in skin/mucus membranes)
  • in low prevalence areas = unprotected sex, IV drug abuse
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8
Q

HBV characteristics?

A

Partially dsDNA virus

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9
Q

What are the serum markers for HBV?

A
  • HbsAg: appears before sxs, peaks during overt dz, lasts ~12 wks (donated blood screened for this)
  • Anti- HBs Ab: doesn’t rise until dz over, about same time HbsAg disappears. IgG form provides immunity
  • HbeAg, HBV-DNA, DNA polymerase: all appear after HbsAg, indicate active viral replication
    • persistent HBeAg = indicator of continued viral replication, infectivity, probably progression to chronic hepatitis
  • Anti-HBc ab- appears before onset of sxs, shows up w/ increased ALT/AST levels
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10
Q

Clinically relevant info about HBV?

A
  • age of infection is best indicator of chronicity (younger = increased probability of chronicity)
  • host immune response is main determinant of outcome of infection
  • hard to completely cure because of viral insertion into host DNA
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11
Q

How does HBV cause hepatocyte injury?

A
  • indiretly; CD8+ cytotoxic T cells attack infected hepatocytes
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12
Q

What is the morphological appearance of liver in HBV infection?

A

in chronic HBV, liver biopsy shows finely granular ‘ground glass’ hepatocytes packed with HBsAg

  • cells w/ER swollen by HbsAg
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13
Q

Hep C virus characteristics?

A
  • SSRNA virus

- b/c of genomic instability + antigenic variability, there’s no vaccine

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14
Q

HCV infection and clearance?

A
  • milder clinically than HBV, but

- 80-90% of pts develop chronic infection, and 20% get cirrhosis

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15
Q

What are clinical characteristics of HCV infection?

A
  • characteristic repeated bouts of hepatic damage
  • chronic HCV infection = persistent elevation in serum aminotransferases (wax and wane, but never normal)
  • cryoglobulinemia found in ~35% of individuals w/ CHC
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16
Q

How do you diagnose HCV?

A

Detect HCV-RNA, which is in the blood 13 weeks during active infection w/ increase in ALT/AST

17
Q

What is HCV associated with?

A
  • metabolic syndrome (genotype 3)

- can give rise to insulin resistance and NAFLD

18
Q

Liver morphology in HCV?

A
  • HCV leads to portal lymphoid follicle, bile duct reactive changes and lobular regions of macovesicular steatosis
  • chronic HCV shows lymphoid aggregates or fully formed lymphoid follicles; fatty change of scattered hepatocytes
  • also can maybe mimic primary biliary cirrhosis (histologically)
19
Q

Characteristics of HDV?

A
  • external coat antigen of HBsAg surrounds an internal “delta antigen”
20
Q

How does infection with HDV arise?

A
  • co-infection: following exposure to serum containing HDV and HBV (HBV must be established first for HDV to make virions)
  • Superinfection: when HBV carrier is exposed to new inoculum of HDV
21
Q

What are the phases of HDV superinfection?

A

Acute phase: active HDV replication and suppresion of HBV with high ALT/AST levels

Chronic phase: HDV repl. decreases, HBV repl. increases, transferase levels fluctuate, dz progresses to cirrhosis and sometimes HCC

22
Q

Clinical signs of HDV infection? (lab-wise)

A
  • HDV RNA is detectable in the blood and liver just before and in the early days of acute symptomatic disease
  • IgM anti-HDV is the most reliable indicator of recent HDV exposure
23
Q

HEV characteristics?

A

ssRNA

  • self-limiting
  • not associated w/chronic liver dz or persistent viremia in immunocompromised pts
24
Q

How is HEV transmitted?

A
  • enterically transmitted, water-borne infection

- zoonotic, has animal reservoirs (cats, monkeys, dogs, PIGS)

25
Q

What is the most important characteristic feature of HEV?

A

causes higher mortality among pregnant women (almost 20%)

26
Q

What is the morphology of acute hepatitis?

A
  • Lymphoplasmacytic (mononuclear) infiltrate
  • ‘Spotty necrosis’ or lobular hepatitis scattered throughout a lobule
  • Necrosis: empty cytoplasm, cell membrane ruptures leads to hepatocyte dropout
  • Collapsed sinusoidal collagen reticulin framework
  • Apoptosis: hepatocytes shrink, become eosinophilic, pyknotic, fragmented
  • Lack of portal inflammation
27
Q

What is the morphology of severe acute hepatitis?

A
  • confluent necrosis of hepatocytes around central veins
  • Cellular debris, collapsed reticulin fibers, congestion +/- hemorrhage
  • Variable inflammation
  • Central-portal bridging necrosis leads to parenchymal collapse
28
Q

What is the morphology of chronic hepatitis?

A
  • mononuclear portal inflammation
  • Mild: inflammatory infiltrates are limited to portal tracts
  • Progressive disease: extension of chronic inflammation from portal tracts with interface hepatitis
  • Linking of portal & portal-central regions = bridging necrosis
29
Q

What people are at risk of autoimmune hepatitis?

A
  • caucasians w/ DRB1 allele

- females

30
Q

What are the types of autoimmune hepatitis?

A

Type 1 - middle aged older ppl
- ANA, **ASMA* (anti-smooth muscle), ANTI-SLA/LP, AMA antibodies

Type 2 - children, teens

  • **Anti-LMK1 (anti-liver kidney microsome-1) abs against CYP2D6
  • ACL1 antibodies
31
Q

What are the phases of autoimmune hepatitis?

A

early phase: severe parenchymal destruction followed rapidly by scarring (takes years to develop)
-shows hepatocyte ‘rosettes’ in areas of activity

progressive or indolent phase: leads to liver failure

  • initial sign is severe hepatocyte injury w/necrosis but little scarring
  • chronic: burned out cirrhosis w/little necroinflamm. activity
32
Q

Clinical progression/signs of autoimmune hepatitis

A

• Acute onset with fulminant disease in 8 weeks
• Hepatic encephalopathy
• Untreated: 40% mortality in 6 months (both type 1 & type 2 lead to liver failure)
• 40% of survivors have cirrhosis
• plasma cells are a prominent and characteristic component of the inflammatory infiltrate in biopsy specimens showing
autoimmune hepatitis

33
Q

What is the prognosis of autoimmune hepatitis?

A

Prognosis: better in adults than in children (delay in diagnosis in pediatric populations)
• 80% of patients respond to immunosuppression for long term survival
• End stage: liver transplant with 75% survival at 10 years, recurrence in 20% of patients

34
Q

Describe acetominophen toxicity’s effect on the liver

A
  • it’s the most common cause of acute liver failure requiring transplant in the US
  • it’s caused by a toxic metabolite produced in CYP450 breakdown in acinus zone 3 hepatocytes (closest to central vein and furthest from portal vein)
  • zone 2 tries to compensate and gets injured
35
Q

What are other drugs that can cause toxic effects on the liver (2 specific)

A

chlorpromazine: causes cholestasis in ppl who are slow to metabolize it to harmless byproduct
halothane: can cause fatal immune-mediated hepatitis in some ppl exposed on multiple occasions

GI II Test 2 (7 decks)

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