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26 Cards in this Set
- Front
- Back
What are the NANB viral heps technically?
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C, E, G, SEN, TTT, maybe others
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Common features of viral hepatitis?
Lab findings? |
RUQ abd pain, nausea, anorexia, fatigue, fever, jaundice, hepatomegaly
elevated liver enzymes, bilirubin in blood/urine, Alk Phos, LDH |
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HAV:
1. Family of viruses? 2. stable or unstable in environment? 3. acute, chronic infection? asymptomatic, symptomatic? 4. Transmission? Where? 5. single outbreak or community? 6. Vaccine? Who gets which kind? |
1. picornaviridae, +ssRNA, one serotype worldwide (enterovirus group)
2. stable in environment 3. acute, asymptomatic infections in kids, adults quick onset "infectious hepatitis" 4. fecal-oral, crowded, poor hygiene 5. community outbreaks 6. inactive vaccine for children. killed vaccine for the military, travelers to endemic regions, high risk groups. of infection. |
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Hep A pathogenesis? (incubation as well)
definitive dx of acute infection? definitive dx of past infection? Tx of HAV? |
intestine --> hepatocytes (replication) --> feces- incubation- 30 days
acute infection, >14 y/o anti-HAV IgM - acute infection anti-HAV IgG - past infection no antiviral tx, vaccinations, children @ 1 y/o, travelers |
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HBV:
1. Family? 2. Transmission? 3. How is the liver damaged? 4. When do clinical signs show up? 5. Who gets the active vaccine? 6. Who gets the passive vaccine? |
1. hepaDNA viridae, enveloped (partially) dsDNA
2. blood/semen, to liver 3. Damage to liver cells is immune mediated (due to release of toxic substances from infiltrating mononuclear cell and cytotoxic T-lymphocytes (CTLs) 4. When liver damage ensues clinical signs occur 5. children, infants, high-risk 6. health care workers |
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Hep B:
General serum marker of infection: why? Recovery/immunity to HBV by itself vs found with other Abs: Marker of acute infection: Marker of past/chronic infection: active replication: |
general: HBsAg- surface is what body sees first "s"
Recovery/immunity: anti-HBsAb (alone = vaccination) (with other Ab's = recovery) acute: anti-HBc IgM chronic: anti-HBc IgG active replication: HBeAg, HBV-DNA |
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Serum findings in active infections of Hep B?
Serum findings in recovery? Serum findings in chronic persistent? Chronic active? |
HBsAg, anti-HBcAg IgM
anti-HBsAg, anti-HBcAg IgG HBsAg, anti-HBcAg IgG, anti-HBeAg HBsAg+, HBeAg, HBcAg IgG, DNA Pol. |
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Which hepatitis often co-infects with Hep B?
What type of virus? risk group? Serologic dx? Which ones are more likely in chronic vs acute? |
Hep D
ssRNA, unclassified IVDA's and partners anti-HDV IgM (high in chronic) also found in acute, anti-HDV IgG (late in acute), HDV Ag |
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Hep C:
Family, type of virus? animal reservoir? Transmission? 90% of who will get this? commonly causes _________ infections. leading cause of ______________. |
Flavivirus, +ssRNA
humans, chimps injection, needle stick, sexual, 90%- drug users chronic liver transplantation |
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What are the "serum transmitted" Hep viruses?
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B and D
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HBV Ag or anti found from (acute infection)...
a. 4-24 weeks b. 6-32 weeks c. 32+ weeks d. 6+ weeks |
a. HBsAg
b. IgM anti-ABc c. Anti-Hbs d. Total anti- HBc |
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Factors that promote progression/severity of Hep C:
Ability to clear virus depends on ______ response. |
EtOH, age, HIV, male, HBV
T-cell (CD4, CD8) |
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Which hepatitis is not person-person transmitted?
Type of virus? Related to what virus? Best way to prevent Hep E infection? |
Hep E
NANB hep virus ,non-eveloped RNA genome similar to Calciviruses watch for contaminated H2O |
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Name the type of virus for the following...
a. AKA infectious hepatitis b. replicates via RNA intermediate c. High risk sexual drug abusers |
a. HAV- Hep A
b. HBV- Hep B b. HDV- Hep D |
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Types of HBV chronic infections?
Incubation period? More likely to develop chronic infection at what age? |
Chronic persistent- can still transmit but not symptomatic
Chronic active- symptomatic hepatitis - 100 days (about) - 0-5 yrs old |
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For Acute HBV infections at what times would you see...
a. HBeAg b. Anti- HBe |
a. 4-12 weeks
b. 12+ weeks |
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1. needs HBV as a helper to code its surface protein
2. Worrisome of mortalities in pregos |
1. Hep D
2. hep E |
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How does Hep D create Super-infection vs. coinfection...
Which is usually acute vs. chronic? |
Co-infection usually acute- D got while getting B
Super- usually chronic after already having B you get D |
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For superinfection of HDV how do you prevent?
How do you cure/prevent coinfection |
stop shitty behavior to prevent developing super infection
- Coinfection if you cure B you cure D |
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What serology studies find for Hep E?
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anti- HEV IgG, anti HEV IgM, viral detection
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What is the diagnostic process for HCV?
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1. anti- HCV first with ELISA
2. Confirm with RIBA test for RNA specific for Hep C 3. HCV PCR qualitative- (reverse transcriptase) to find out if presentand quantitative to find out how much present |
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1.1 Slutty Drugged Waitress Test show:
– HAV IgG: positive – HAV IgM: negative – HBsAg: positive – Anti-HBsAg: negative – Anti-HBcAg IgM: positive – HBeAg: positive – Anti-HBeAg: negative – Anti-HCV: negative |
Start with A's and then go C and then B
HAV IgG- not active then skip B See- Anti-HCV neg so no Hep C See "M" for HBV meaning she has acute infection, then others are used to confirm... but keep CHRONIC IN MIND IF PERSON IS DIRTY WHORE |
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1.2 Six month follow up of slutty waitress with normal liver enzymes
– HBsAg: positive – Anti-HBsAg: negative – Total Anti-HBcAg: positive – Anti-HBcAg IgM: negative – HBeAg: negative – Anti-HBeAg: postive |
more like chronic peristent not active, but can still transmit infections
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1.3 Two years later of dirty waitress:
– HAV: IgG positive --HAV IgM: negative – HBsAg: positive -Anti HBsAg: negative – Total Anti-HBcAg: positive – Anti-HBcAg IgM: negative – HBeAg: positive – HBV DNA: positive – Anti-HDV IgM: positive – Anti-HCV: negative |
now she has D most likely superinfection
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