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DERS (GIT) > L17- GI Infections VII (viral hepatitis) > Flashcards

L17- GI Infections VII (viral hepatitis) Flashcards

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1
Q

Viral Hepatitis:

  • (1) are the main viruses that cause primary inflammation of the liver
  • (2) are the other viruses causing liver inflammation
  • (3) name the types of viral hepatitis (define them)
A

1- HepA/B/C/D/E

2- HSV, CMV, EBV, YFV (yellow fever)

3- Acute <6mos, Chronic >6mos

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2
Q

for each Hepatitis virus, list its envelope status, genome type, and viral family

A

HepA: non-enveloped, (+)ssRNA, picornavirus

HepB: enveloped, partial dsDNA, hepadnavirus

HepC: enveloped, (+)ssRNA, flavivirus

HepD: enveloped, (-)ssRNA, deltavirus

HepE: non-enveloped, (+)ssRNA, hepevirus

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3
Q

list the Viral Hepatitis symptoms (including phases)

A

1) Prodrome / pre-icteric: fever, n/v, loss of appetite, chronic fatigue, abdominal pain/swelling, leg swelling, easily bruised, itchy skin
2) Icteric / jaundice: jaundice, bilirubinemia, dark urine color, pale stool color (or bloody or tarry)

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4
Q

In LFTs:

  • (1) are liver injury indicators
  • (2) are liver function indicators
A

1- AST, ALT, LDH, ALP

2- bilirubin (total, direct, indirect), albumin, PT

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5
Q

describe the distribution of Hepatitis viruses based on infectious type

A

HepA, HepE = ‘infectious’; enteric transmission (fecal-oral)

HepB, HepD, HepC: ‘serum’, parenteric transmission (transmission thru blood, sex)

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6
Q

HAV:

  • (1) genome, structure [family]
  • stable in the following conditions, (2)
  • inactivated in the following conditions, (3)
A

1- non-enveloped, icosahedral // (+)ssRNA // picornavirus

2- pH = 1.0, solvents (ether, chloroform), detergents, saltwater, groundwater, drying, temperature (survives wks at 4C, 1/2hr at 56C)

3- formalin, UV radiation, chlorine Tx of drinking water, temperature (partial form at 61C for 20 mins)

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7
Q

HAV replication (initial steps):

  • enters the body via (1)
  • attached to (2) cells
  • genome is delivered to (cytoplasm/nucleus)
A

1- ingestion (fecal-oral) of contaminated food/water/ect

2- Kupffer cells (liver macrophages)

3- cytoplasm

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8
Q

HAV replication (later steps):

  • genome is translated into (1) and then processed via (2)
  • (3) is one of the results from (2) and is responsible for (4)
  • (5) is the final step
A

1- (cytoplasm) single long polypeptide
2- cleaved via proteases into protein (peptides)
3- RNA dependent RNA polymerase
4- copies RNA –> (+)/(-)ssRNA
5- viral assembly and release via exocytosis

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9
Q

Most cases of viral hepatitis result from Hep(1). The most deaths from viral hepatitis results from Hep(2).

A

1- HepA (40%)

2- HepB (~47% of total deaths), HepC (~48%)

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10
Q

describe the transmission of HepA

A

-fecal-oral: virus can shed before or in the absence symptoms (90% children, 25-50% adults) and is shed at high concentrations
(rarely has person-to-person transmission, via blood)

  • extremely stable virus
  • most outbreaks occur at schools, camps, daycare, restaurants
  • worldwide, all year long
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11
Q

HepA:

  • Sxs are milder in (adults/children)
  • (2) incubation period
  • (3) main Sxs
  • (4) main signs (excretions / labs)
A

1- children

2- 3-4wks (~30 days, range 15-50 days)

3- (abrupt onset, intensified before icteric phase) fever, fatigue, nausea, loss of appetite, abdominal pain [inc chance of jaundice with inc age]

4- (same as other hepatitis) dark urine, pale feces, elevated ALT > AST

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12
Q

describe the detection (/diagnosis) of a HAV infection

A

-clinically: Sxs time course, common sources

Serology (in chronological order):

1) virus in feces (2-6wks)
2) IgM (starts 4wks, peaks 6wks) –> acute infection
3) IgG (starts 5wks, peaks 8wks and beyond) –> previous infection

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13
Q

HAV:
-(1) is the main prevention method; (2) are other good practices

-(3) is about the only treatment

A

1- vaccine (killed / inactivated)

2- good sanitation, proper personal hygiene, preventing food/water contamination

3- prophylaxis with Immune Serum Globulin (passive immunity) –> prevents illness if given before or <2wks after exposure

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14
Q

HEV genome, structure [family]

A

non-enveloped, icosahedral
(+)ssRNA
hepevirus family

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15
Q

HEV:

  • (1) main geographic areas
  • can result in (acute/chronic/both) viral hepatitis
  • worst / life-threatening in (3) patients
A

1- Asia + India, Africa, Mexico

2- acute (presents like HAV- no chronic infections)

3- pregnant patients

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16
Q

HEV:

  • (1) Dx, Tx
  • (2) prevention
A

1- no standard tests (PCR is best but not always available), no standard Tx

2- (NO vaccine) avoid beverages with ice of unknown purity, uncooked shellfish, uncooked fruits/veggies

17
Q

describe HEV Serology (chronologically- include presence in blood/stool, jaundice timeframe, ALT, IgM, IgG)

A

1) (1-2 wks before Sxs) HEV in blood
2) (~1wk before Sxs, up to 3wks after) HEV in stool
3) (3-4wks once Sxs start) jaundice

ALT: 2-4wks after Sxs start, peaks at 2wks

IgM: 10wks after Sxs start, peaks at 2wks

IgG: (forever) surpasses IgM at 4wks

18
Q

HCV:

  • (1) genome, structure [family]
  • replication in (cytoplasm/nucleus)
  • (3) are the main structural proteins (membrane) in mature virons
A

1- enveloped, icosahedral // (+)ssRNA // flavivirus

2- cytoplasm

3- capsid + E1, E2 (virus-encoded membrane proteins)

19
Q

HCV replication:

  • after inoculation, particles will attach to (1) and enter cells via (2)
  • (3) briefly describe genomic replication
A

1- multiple LDL-R and or VLDL-R

2- receptor mediated endocytosis + acidification

3- translation into single polypeptide –> RNA dep. RNA poly. replicates RNA –> (+)/(-) ssRNA

20
Q

HCV:

  • (1) are the main reservoirs
  • (2) predominate transmission
  • mostly is seen as a (acute/chronic) infection
A

1- humans
2- blood (IV drug use, sex, transfusions)
3- chronic (+ asymptomatic) infections [5-30 yr development]

21
Q

HCV:

  • replicates in (1) cells, which will be destroyed via (2)
  • (3) is important in the resolution of HCV infections (indicate importance)
  • chronic infections lead to a higher risk for (4)
A

1- hepatocytes (although not cytopathic)
2- immunopathogenesis
3- humoral and cellular immunity- therefore worse in the immuno-compromised (co-morbidities)
4- HCC

22
Q

HCV Dx:

  • (1) and (2) are used to detect Igs
  • seroconversion occurs (3) post-infection
  • it is difficult to detect Igs in (4) patients
  • (5) is used to detect viral genome
A 
1- ELISA
2- RIBA (recombinant immunoblot assay)
3- 7-31 wks
4- viremic, immunocompromised, hemodialysis
5- RT-PCR (in blood or liver)
23
Q

what are the requirements for diagnosing a chronic HCV infection

A
  • elevated liver enzymes
  • positive anti-HCV Ab test
  • positive HCV RNA test
  • > 6 mos
24
Q

in HCV serology, (1) peaks first and (2) peaks second

A

1- ALT

2- IgG

25
Q

HCV:

  • (1) prevention
  • (2) Tx
A

1- (no vaccine) screening of blood for transfusions, eliminate ‘risky’ behavior

2- (prophylactic Igs ineffective) IFN, antiviral polymerase inhibitors (nucleo-side/-tide analogs), antiviral protease inhibitors

26
Q

GB-C virus = (1)

  • (2) describe genome
  • (3) reservoirs
  • (4) transmission
  • (5) is a unique feature
A

1- HepG virus
2- enveloped, (+)ssRNA, flavivirus
3- humans (GBV-C), monkeys (GBV-A, GBV-B)
4- sex, blood
5- interferes with HIV pathogenesis / replication

-causes decade long chronic infection

DERS (GIT) (21 decks)

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