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DERS (GIT) > L19- GI Infections VIII (viral hepatitis, liver parasites) > Flashcards

L19- GI Infections VIII (viral hepatitis, liver parasites) Flashcards

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1
Q

HBV:

  • (1) genome, structure, family
  • (2) conditions where it is uniquely stable/resistant
  • particles are termed (3)
  • requires (small/large) inoculation dose
A

1- partial dsDNA (circular, relaxed), enveloped // hepadnaviridae

2- low pH, resistant to freezing, detergents, moderate heat

3- Dane particles

4- small

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2
Q

HBV structure:

  • (1) list important surface Ags
  • (2) list important core proteins
A

1- envelope has 3 glycoproteins: L, M, S (large, medium, small) = HBsAg

2- core protein = HBcAg and reverse transcriptase [note- viral DNA genome is in core also]

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3
Q

HBV is unique because in addition to replicating, it also produces…..(explain)

A

Subviral Lipoprotein Particles

  • 20nm spheres / filaments
  • ***contains envelope glycoproteins
  • *outnumbers infectious virions 1000-10000:1

-aka decoy particles w/o DNA, non-infectious (although it will produce an immune reponse)

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4
Q

HBV:

  • HBcAg = (1)
  • HBsAg = (2)
A

1- core protein / Ag

2- surface glycoprotein (on envelope): either L/M/S (large, medium, small)

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5
Q

describe HBV replication

A

1) partial dsDNA –> cccDNA in the nucleus (covalently closed circular DNA)
2) transcription of cccDNA –> 4 mRNA molecules (host machinery)

3a) mRNA –> viral proteins (host machinery)
3b) RNA dep. DNA poly. (reverse transcriptase) converts mRNA –> dsDNA

Note- creation of Dane particles and partial HBV particles

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6
Q

name the function for each HBV protein

  • (1) ORF P
  • (2) ORF S
  • (3) ORF C
  • (4) ORF X
A

1- P, viral polymerase (reverse transcriptase)

2- S, surface protein (L, M, S) –> attachment to liver cells (hepatocytes, Kupffer cells)

3- C, core protein for capsid

4- X, HBx protein –> transactivator to establish infection + HCC development

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7
Q

HBV:

  • infects (1) cells
  • replication in (nucleus/cytoplasm)
  • risk to develop (3)
  • can survive outside of body in blood for (4)
A

1- hepatocytes, Kupffer cells

2- nucleus

3- HCC

4- 7 days

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8
Q

list the routes of HBV transmission

A

(highest at acute stage of infection, most amount of virions)

  • unprotected sex
  • contact with infected blood, blood transfusions, open wound
  • IV drug use, tattoos, piercings
  • vertical: mother to child
  • sharing razors, toothbrushes
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9
Q

HBV:

  • acute infection mostly in (1) patients
  • chronic infection mostly in (2) patients
A

1- adults

2- children (immuno-compromised)

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10
Q

list the Sxs HBV infections

A

1st: fever, rash, arthritis (type III hypersensitivity reaction)
2nd: malaise, nausea, anorexia, jaundice, dark urine, RUQ pain

Last: itching

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11
Q

(T/F) HBV directly kills liver cells

A

F- not directly cytopathic

-MHC-I / CD8 Tc cells directed against HBV Ags –> kills infected hepatocytes
AND
-non-specific inflammatory response

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12
Q

HBV infections will result in Igs against ______ Ag

A
  • HBcAg (core protein)
  • HBsAg (surface glycoproteins)
  • polymerase
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13
Q

list the techniques used for HBV diagnosis

A

ELISA, immunochromatographic assay, qualitative immunoassay, and agglutination assay: detects viral Ags (HBsAg, HBeAg, HBcAg) and Igs against viral Ags

qRT-PCR –> HBV titers

Biochemical assays: monitors liver enzymes (ALT, AST) for acute or chronic infections

Liver biopsy: assess liver damage when ALT is high

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14
Q

how is chronic HBV infection defined clinically

A

> 6mos
persistence of HBsAg in blood
(no window period)

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15
Q

HBV Tx

A

-IFN

with or without

-anti-virals: polymerase inhibitors as nucleoside / nucleotide analogs

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16
Q

HBV prevention

A

Vaccines: subunit or immune globulin

  • screening blood supply
  • elimination of ‘risky’ behavior (sex, IV drug use, etc)
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17
Q

HBV Serology (indicate disease status):

  • HBsAg (-)
  • anti-HBc Ig (-)
  • anti-HBs Ig (-)
A

susceptible

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18
Q

HBV Serology (indicate disease status):

  • HBsAg (-)
  • anti-HBc Ig (+)
  • anti-HBs Ig (+)
A

immune via natural infection

19
Q

HBV Serology (indicate disease status):

  • HBsAg (-)
  • anti-HBc Ig (-)
  • anti-HBs Ig (+)
A

immune via vaccine

20
Q

HBV Serology (indicate disease status):

  • HBsAg (+)
  • anti-HBc Ig (+)
  • IgM anti-HBc (+)
  • anti-HBs Ig (-)
A

acute infection

21
Q

HBV Serology (indicate disease status):

  • HBsAg (+)
  • anti-HBc Ig (+)
  • IgM anti-HBc (-)
  • anti-HBs Ig (-)
A

chronic infection

22
Q

HBV Serology (indicate disease status):

  • HBsAg (-)
  • anti-HBc Ig (+)
  • anti-HBs Ig (-)
A

unclear could be:

i) resolved infection, most common
ii) false positive (therefore susceptible)
iii) low level chronic infection
iv) resolving acute infection

23
Q

HDV:

  • (1) alternate name
  • (2) genome, shape, family
  • (3) important Ags
A

1- defective virus (HBV = helper virus)

2- enveloped, (-)ssRNA, rod-shaped (extensive base pairing) // deltavirus

3- HBsAg, S-HDAg (small capsid protein), L-HDAg (large capsid protein)

24
Q

list the HDV clinical manifestations

A

Co-infection (<5%):

  • co-administration of HBV/HDV with HBV infection followed by HDV infection
  • low risk of chronic liver disease

Superinfection (70-80%):

  • established HBV infection
  • HDV administration with immediate infection
  • high risk of chronic liver disease

Fulminant hepatitis / acute liver disease (w/ encephalopathy)

25
Q

HDV diagnosis requirements

A

detection of the following:

  • anti-HDAg
  • HDV RNA
  • HDAg (acute phase of disease)
26
Q

HDV Tx and prevention

A

Tx: IFN-α, no real 100% effective Tx

Prevention: HBV vaccination

27
Q

list the main parasites for liver and biliary tree infections

A

(trematodes)

  • fascioliasis
  • clonorchiasis
  • opistorchiasis
28
Q

Clonorchiasis clinical manifestations…

A
  • cholangitis
  • biliary hyperplasia / obstruction
  • cholangiocarcinoma
29
Q

Fascioliasis clinical manifestations

A
  • hepatic fibrosis / necrosis
  • cholangitis
  • biliary obstruction
  • biliary cirrhosis
30
Q

Opisthorchiasis clinical manifestations

A
  • cholangitis
  • biliary hyperplasia and obstruction
  • cholangiocarinoma
31
Q

describe the key trematode features

A
  • unsegmented
  • incomplete digestive tract
  • two striated suckers
  • most are hermaphrodites
  • most of the body is reproductive organs
32
Q

Fasicola hepatica = (1)
Fasicola = (2)
-infects (3) organ
-(4) reservoirs (definitive host), with (5) as intermediate host

A 
1- liver fluke, sheep liver fluke
2- giant fluke
3- liver + biliary passages
4- sheep, goat, cattle, other herbivorous
5- fresh water snails
33
Q

Fasicola spp.

  • (1) is the method of human infection via (2) as intermediate hosts
  • (3) form in hosts, leaves host via (4)
A

1- (incidental hosts) contaminated water OR aquatic plants (watercress)
2- fresh water snails
3- adult worm (intestinal)
4- feces

34
Q

Fasicola spp. life cycle (pre-host / human):

  • (1) form in feces
  • forms (2) in water, and (2) invades (3)
  • (2) develops into (4) within (3)
  • (4) form is release from (3) and infects (5) and becomes (6)
A 
1- immature eggs
2- miracidia
3- (fresh water) snail
4- *cercariae (rediae, sporocysts)
5- aquatic vegetation (watercress)
6- **metacercariae encyst
35
Q

Fasicola spp. lifecycle (starting with infectious form):

  • mammals ingest (1) form from (2)
  • (3) conversion occurs in the duodenum
  • migration to (4) occurs, and (5) maturation occurs
A 
1- **metacercariae (encyst)
2- aquatic vegetation (watercress)
3- metacercariae excyst
4- liver parenchyma into biliary ducts (via intestinal wall / peritoneal cavity)
5- adult flukes
36
Q

Fasicoliasis:

  • often (a-/symptomatic)
  • (2) incubation period
  • (3) list the phases
A

1- asymptomatic (Sxs 15% of time)

2- days - months

3-
acute (larvae, 2-4mos)
–> latent (mos-yrs, asymptomatic, parasite maturation)
–> chronic (adults)

37
Q

Fasioliasis acute phase: form, duration, Sxs

A
  • migration of larvae (metacercariae)
  • 2-4 mos

Sxs:

  • general allergic / toxic rxns
  • fever, urticaria
  • generalized / RUQ abdominal pain, hepatomegaly
  • loss of appetite, flatulence, n/d
  • cough, SOB, chest pain
38
Q

Fasioliasis acute phase: form, Sxs

A

-adult flukes

  • biliary colic, RUQ pain, epigastric pain
  • nausea, intolerance to fatty food, obstructive jaundice
  • pruritus
  • biliary lithiasis
39
Q

Fasioliasis:

  • (1) Dx
  • (2) geographic prevalence
  • (3) Tx
  • (4) prevention
A

1- Ova, stool sample microscopy

2- worldwide

3- antiparasitics

4- use non-contaminated veggies (water/feces) by washing and cooking + control intermediate hosts

40
Q

Clonorchis sinesis = (1):

  • associated with (2) consumption
  • (3) 1st host, 2nd host, reservoirs
A

1- Opisthorchis sinensis // Chines or Oreintal liver fluke
2- raw, pickles, smoked fish

3- fresh water snail –> freshwater fish –> fish + cats, dog, carnivores

41
Q

C. sinensis life cycle (pre-host / human):

  • (1) form in feces
  • invades (2) and develops into (3)
  • (3) develops into (4)
  • (4) form is released and infects (5) and becomes (6)
A 
1- embryonated eggs (shed in feces)
2- (fresh water) snail
3- miracidia
4- *cercariae (rediae, sporocysts)
5- fish
6- **metacercariae encyst
42
Q

C. sinesis lifecycle (starting with infectious form):

  • mammals / humans ingest (1) form from (2)
  • (3) conversion occurs in the duodenum
  • migration to (4) occurs, and (5) maturation occurs
A 
1- **metacercariae (encyst)
2- fish
3- metacercariae excyst
4- liver parenchyma into biliary ducts (via intestinal wall / peritoneal cavity)
5- adult flukes
43
Q

list the range of clinical manifestations of C. sinesis infections

A

1) mild / asymptomatic
2) severe infection: fever, diarrhea, epigastric pain, hepatomegaly, anorexia, jaundice (occasionally)
3) biliary obstruction
4) chronic infection: adenocarcinoma of bile duct
5) Gallbladder invasion: cholescystitis, cholelithiasis, impaired liver function, liver abscess

44
Q

C. sinesis:

  • (1) geographic incidences
  • (2) main risk factor
  • (3) Dx
  • (4) Tx
A

1- Asia (Korea, China, Taiwan, Vietnam, Japan, Russia)

2- eating infected fish (raw)

3- Ova in stool sample microscopy

4- antiparasites

DERS (GIT) (21 decks)

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