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GI 2 Pathology--Chapt. 18 and 19 > Chapter 18 part 2: infectious disorders > Flashcards

Chapter 18 part 2: infectious disorders Flashcards

1
Q

Types of infectious disorders of the liver

A
  • Viral Hepatitis: A, B, C, D, E

- Bacterial, Parasitic and Helminthic infections

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2
Q

Systemic viral infections that can involve the liver

A
  • Epstein-Barr virus
  • CMV
  • Yellow fever virus
  • Less commonly: rubella, adenovirus, enterovirus, herpesvirus
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3
Q

Unless specified, hepatitis refers only to what kind of infections??

A
  • infections of the liver by the hepatotropic viruses: A, B, C, D, or E!!!
  • All produce similar clinical and morphological patterns of acute hepatitis but vary in their routes of transmission and potential to induce carrier states or chronic disease
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4
Q

Hepatitis A virus

A
  • ssRNA that causes a benign, self limited disease
  • fulminant HAV is rare (0.1-0.3% fatality)
  • not directly cytopathic
  • hepatocyte damage is due to CD8+ T cell responses
  • Accounts for 25% of acute hepatitis in world
  • Acute infxn marked by anti HAV IgM in serum; IgG appears as IgM declines (in few months) and persists for years conferring long-term immunity
  • vaccine available
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5
Q

Hep B virus can cause:

A
  • Acute, self-limited hepatitis
  • Nonprogressive chronic hepatitis
  • Progressive chronic disease culminating in cirrhosis and increased risk of HCC
  • Fulminant hepatitis with massive liver necrosis
  • Asymptomatic carrier state
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6
Q

Potential outcomes of Hep B infection in adults and frequencies

A
  • Acute infection–>subclinical dz (65), acute hepatitis (25), chronic hepatitis (5-10)
  • Subclinical dz–>recovery (100)
  • Acute hepatitis–>Recovery (99) or Fulminant Hep (<1)–>death or transplant
  • Chronic hep–>HCC (2-3), cirrhosis (20-30), recovery
  • cirrohhosis and HCC–>death or transplant

*acute hepatic failure and fulminant hep are same thing

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7
Q

Major determinant of the outcome of Hep B infection is?

A
  • Host immune response to virus
  • Younger age at infection has higher probability of chronicity
  • Innate immunity is protective during initial phases of infection and strong responses by virus-specific CD4+ and CD8+ interferon (IFN-y) producing cells are associated with resolution
  • Abs prevent subsequent reinfection and form basis of effective vaccines
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8
Q

How is hepatocyte killing mediated in HBV infection?

A
  • HBV is not cytopathic
  • hepatocyte killings is mediated by cytotoxic CD8+ T lymphocytes against virus-infected cells
  • Viral DNA sequences can also integrate into host genomes, constituting a pathway for cancer development
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9
Q

Structure of HBV

A
  • ciruclar, partially DsDNA
  • mature virus exists as a spherical “Dane particle” with outer surface protein and lipid envelop encasing an electron dense core
  • 8 viral genotypes with distinct global distributions
  • HBV genome has 4 open reading frames
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10
Q

4 open reading frames of HBV

A
  • Nucleocaspid core Ag (HBcAg) plus a longer polypeptide transcript (HBeAg) that is secreted into bloodstream
  • Hep B surface Ag (HbsAg) envelope glycoproteins (large, middle and small); infected hepatocytes can synthesize and secrete massive quantities of noninfective HbsAg (mostly small HBsAg)
  • Polymerase with both DNA polymerase and reverse transcriptase activity; viral replication occurs through an intermediate RNA template: DNA–>RNA–>DNA
  • Hbx protein, a transcriptional transactivator of host and viral genes, necessary for viral replication
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11
Q

HbsAg, HBe Ag and HBV DNA

A
  • HbsAg appears before symptoms (anorexia, fever, jaundice)
  • peaks during overt disease and declines over months
  • HBeAg and HBV DNA appear soon after HBsAg and before disease onset
  • HbeAg is detectable in serum during viral replication but some mutant strains do not produce it
  • HbeAg usually declines within weeks
  • persistence suggests progression to chronic disease
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12
Q

Abs that appear in Hep infection

A
  • IgM and anti-HBcAg are first to appear, followed by:

- anti-HbeAg and IgG anti-HBcAg

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13
Q

Anti-HBSAg signifies

A
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14
Q

Chronic carrier defined by

A

-presence of HBsAg in serum for 6 months

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15
Q

Chronic Hep B infection Tx

A

-difficult to cure due to development of resistant mutant strains

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16
Q

Hep B transmission–differences based on geography

A
  • in high prevalence areas (Africa, Asia), transmission during childbirth=90%
  • in intermediate prevalence regions (Southern and eastern europe), horizontal transmission in childhood by minor cutes or breaks in mucus membranes is most common
  • in low prevalence areas (US and western Europe), IV drug abuse and unprotected intercourse are major modes of transmission
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17
Q

Hep C Virus characteristics

A
  • ssRNA, enveloped virus
  • low fidelity of HCV RNA polymerase causes substantial genomic variability and constitutes a major obstacle to vaccine development–any person can harbor a population of related but divergent quasi species and the presence of high titers of anti-HCV IgG does not confer effective immunity
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18
Q

Viral replication of Hep C virus

A
  • begins with translation of a single polypeptide that is processed into nucleocapsid protein, envelope proteins and seven nonstructural proteins
  • E2 envelope protein is a target of several anti-HCV Abs but is also the most variable region of genome allowing escape from otherwise neutralizing titers
  • Anti-HCV Abs do not confer protection
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19
Q

characteristic feature of HCV infection

A

-repeated bouts of damage

20
Q

difference bw HCV infection and HBV infection

A
  • In contrast to HBV, progression to chronic disease occurs in most (80-90%) of HCV infected patients and cirrhosis occurs in 20%
  • Like HBV hepatocellular damage is immune mediated, although the cellular immune responses are largely unable to completely eradicate HCV infections
21
Q

Incidence of HCV infection

A
  • half of U.S burden of chronic liver dz

- incidence has significantly declined as a result of blood supply screening

22
Q

What ppl are at risk for HCV infection?

A

-Primary=IV drug abusers and multiple sexual partners

23
Q

Dx of HCV infection

A
  • HCV RNA detectable in blood for 1-3 weeks during active infection, coincident with transaminase elevations
  • Anti-HCV Abs occur in only 50-70% of patients in acute setting although 90% will eventually develop such Abs
24
Q

Treatment for chronic HCV infection

A
  • potentially curable
  • older Tx=IFN-a and ribovarin
  • newer drugs that target viral protease and polymerase can achieve undetectable levels of virus in majority of pts
25
Q

Hep D virus

A
  • defective RNA virus that can replicate and cause infection ONLY when encapsulated by HBsAg
  • so ONLY develops when there is confection by HBV infection
  • Acute confection by HDV and HBV leads to hepatitis that ranges from mild to fulminant but chronicity rarely develops
  • BUT HDV SUPERINFECTION of an unrecognized HBV carrier or in a pt with chronic HBV leads to eruption of acute hepatitis with frequent conversion to chronic disease and cirrhosis
26
Q

High prevalence areas for HDV coinfection

A
  • Africa
  • Middle East
  • Italy
  • Amazon basin
  • *UNCOMMON in US, Southeast Asia and China
27
Q

structural features of HDV

A
  • has an HBV envelope
  • the only protein produced by virus is an internal polypeptide assembly called the delta Ag (HDAg) associated with small circular ssRNA
  • Viral replication requires host RNA polymerase activity
28
Q

HDV Dx

A
  • HDV RNA appears in blood and liver before and ruing early acute symptomatic infection
  • IgM anti-HDV indicates recent HDV exposure
  • IgM anti-HbcAg suggests acute HBV confection whereas serum HBsAg implies superinfection
  • Vaccination against HBV can prevent HDV infection
29
Q

Hep E virus

A
  • nonenveloped ssRNA virus
  • enterically transmitted, water-borne infection with several animal reservoirs (monkeys, cats, pigs, and dogs)
  • HEV epidemics have occurred in Asia, Mexico, and Africa and also endemic in India where 30-60% of acute hepatitis cases
  • typically self-limited with no chronicity but high rate of fatal fulminant hepatitis (20%) in pregnant women
30
Q

Hep E–Dx

A
  • HEV Ag found in hepatocytes during active infection and visions and RNA can be detected in stool and serum before symptom onset
  • Subsequent development IgG anti-HEV confers long-lived protection against reinfection
31
Q

Clfinicopathologic syndromes of viral hepatitis

A
  • any hep virus can be asymptomatic or symptomatic
  • fulminant course uncommon
  • serologic and molecular studies essential for viral hep Dx and to distinguish type
  • Acute asymptomatic infection with recovery, Acute symptomatic infection with recovery, Acute liver failure
32
Q

Acute asymptomatic infection with recovery

A
  • Pts identified only incidentally based on elevated transaminases or by antiviral Ab titers
  • HAV and HBV are frequently subclinial
33
Q

Acute symptomatic infection with recovery

A
  • Acute symptomatic infections are all similar with variable incubation pds, asymptomatic preicteric phase, symptomatic icteric phase, and convalescence
  • Peak infectivity occurs during last asymptomatic days of incubation pd and early days of acute symptoms
34
Q

Acute liver failure

A
  • Viral hepatitis causes 10% of cases of acute hepatic failure; globally hep A and E are the most common causes whereas HBV is more common in Asian and Mediterranean countries
  • Survival for more than a week may allow residual hepatocyte replication and activation of stem and progenitor cells yields prominent ductular reactions; recovery depends on restoration of missing parenchyma
  • Care is supportive and liver transplantation is only option when disease does not resolve
35
Q

Chronic hepatitis

A
  • symptomatic (fatigue, malaise, jaundice), biochemical or serologic evidence of ongoing hepatic disease for >6 months
  • Acute HCV infxn progresses to chronic hepatitis in 80%–1/3 develop cirrhosis
  • In addition to ongoing liver injury and risk of cirrhosis and/or HCC, immune complex disease (due to circulating Ab-Ag complexes) may develop w/vasculitis and glomerulonephritis
  • 35% of chronic hep C pts develop cryoglobulinemia
36
Q

Carrier state

A
  • A carrier harbors and can transmit hepatitis but has no manifest symptoms
  • includes patients with chronic disease but few or no symptoms and those with little or no adverse effects (healthy carriers); for HBV, healthy carriers lack HBe Ag but have anti-HBeAg, normal serum aminotransferase levels, low serum HBV DNA and a liver biopsy without significant necrosis or inflammation
  • In the US, adult HBV rarely produces a healthy carrier state but >90% of HBV infections acquired early in life in endemic areas result in healthy carrier state
37
Q

HIV and chronic viral hepatitis

A
  • similar transmission modes and risks result in frequent HIV and hepatitis virus confections
  • 10% of HIV patients are infected with HBV and 30% with HCV resulting in more aggressive liver disease
  • Chronic hepatitis is a major cause of morbidity and mortality in HIV infected patients and liver disease is the 2nd most common cause of death in AIDS
38
Q

Morphology of acute and chronic hepatitis–general

A
  • All hepatotropic viruses share most of the same morphologic changes
  • features are nonspecific and can be mimicked by drug reaction or autoimmune liver disease but some distinct features may be present (HBV, HCV)
39
Q

HBV morphology

A

-infected hepatocytes can show a finely granular “ground glass” cytoplasm packed with HBsAg

40
Q

HCV morphology

A

-portal lymphoid aggregates, bile duct reactive changes and lobular regions of macro vesicular steatosis

41
Q

Acute hepatitis morphology

A
  • Injured hepatocytes are eosinophilic and rounded with shrunken or fragmented nuclei (apoptosis) or swollen (ballooning degeneration)
  • In severe hepatitis, confluent damage causes bridging necrosis between portal and central regions of adjacent lobules; cholestasis can occur
  • Kupffer cell hyperplasia and macrophage aggregates mark the site of hepatocyte loss
  • Portal tracts exhibit mononuclear cell inflammation often with spillover into adjacent parenchyma associated with periportal apoptosis (interface hepatitis)
42
Q

Chronic hepatitis morphology

A
  • Histology ranges from mild to severe to cirrhosis
  • Mild: inflammatory infiltrates only in portal tracts
  • Progressive disease: extension of chronic inflammation from portal tracts with interface hepatitis; linking of portal-portal and portal-central regions constitutes bridging necrosis
  • continued loss of hepatocytes results in fibrous septum formation!! Associated hepatocyte regeneration results in cirrhosis
43
Q

Bacterial, Parasitic and Helminthic Infections–Extrahepatic infections

A

-especially sepsis can induce hepatic inflammation and varying degrees of cholestasis

44
Q

Bacterial, Parasitic and Helminthic Infections–Biliary obstruction and intrabiliary bacterial proliferation

A

-can cause severe acute inflammatory response (ascending cholangitis)

45
Q

Bacterial, Parasitic and Helminthic Infections–parasitic infections

A
  • e.g., amebic, echinococcal, malarial or helminthic organisms–are common causes of hepatic abscesses in developing countries
  • Liver flukes most common in southeast Asi case a high rate of CCA
46
Q

Bacterial, Parasitic and Helminthic Infections–Abscesses occurring in developed countries

A
  • rare; usually bacterial or candidal
  • sources are intra-abdominal (via portal vein), systemic (via arterial supply), biliary tree, direct extension, and penetrating injuries
  • Abscesses are associated with fever, right upper quadrant pain, tender hepatomegaly, and possibly jaundice
  • Mortality without daringe is 90%; survival is dramatically improved by early Tx
  • Rupture of echinococcal cysts can precipitate systemic spread of organism with severe immune mediated shock

GI 2 Pathology--Chapt. 18 and 19 (8 decks)

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