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

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Flashcards in L19- GI Infections VIII (viral hepatitis, liver parasites) Deck (44):
1

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

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

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

3- Dane particles

4- small

2

HBV structure:
-(1) list important surface Ags
-(2) list important core proteins

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]

3

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

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)

4

HBV:
-HBcAg = (1)
-HBsAg = (2)

1- core protein / Ag

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

5

describe HBV replication

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

6

name the function for each HBV protein
-(1) ORF P
-(2) ORF S
-(3) ORF C
-(4) ORF X

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

7

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

1- hepatocytes, Kupffer cells

2- nucleus

3- HCC

4- 7 days

8

list the routes of HBV transmission

(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

9

HBV:
-acute infection mostly in (1) patients
-chronic infection mostly in (2) patients

1- adults

2- children (immuno-compromised)

10

list the Sxs HBV infections

1st: fever, rash, arthritis (type III hypersensitivity reaction)

2nd: malaise, nausea, anorexia, jaundice, dark urine, RUQ pain

Last: itching

11

(T/F) HBV directly kills liver cells

F- not directly cytopathic

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

12

HBV infections will result in Igs against ______ Ag

-HBcAg (core protein)
-HBsAg (surface glycoproteins)
-polymerase

13

list the techniques used for HBV diagnosis

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

14

how is chronic HBV infection defined clinically

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

15

HBV Tx

-IFN

with or without

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

16

HBV prevention

Vaccines: subunit or immune globulin

-screening blood supply
-elimination of 'risky' behavior (sex, IV drug use, etc)

17

HBV Serology (indicate disease status):
-HBsAg (-)
-anti-HBc Ig (-)
-anti-HBs Ig (-)

susceptible

18

HBV Serology (indicate disease status):
-HBsAg (-)
-anti-HBc Ig (+)
-anti-HBs Ig (+)

immune via natural infection

19

HBV Serology (indicate disease status):
-HBsAg (-)
-anti-HBc Ig (-)
-anti-HBs Ig (+)

immune via vaccine

20

HBV Serology (indicate disease status):
-HBsAg (+)
-anti-HBc Ig (+)
-IgM anti-HBc (+)
-anti-HBs Ig (-)

acute infection

21

HBV Serology (indicate disease status):
-HBsAg (+)
-anti-HBc Ig (+)
-IgM anti-HBc (-)
-anti-HBs Ig (-)

chronic infection

22

HBV Serology (indicate disease status):
-HBsAg (-)
-anti-HBc Ig (+)
-anti-HBs Ig (-)

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

23

HDV:
-(1) alternate name
-(2) genome, shape, family
-(3) important Ags

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

list the HDV clinical manifestations

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

HDV diagnosis requirements

detection of the following:
-anti-HDAg
-HDV RNA
-HDAg (acute phase of disease)

26

HDV Tx and prevention

Tx: IFN-α, no real 100% effective Tx

Prevention: HBV vaccination

27

list the main parasites for liver and biliary tree infections

(trematodes)
-fascioliasis
-clonorchiasis
-opistorchiasis

28

Clonorchiasis clinical manifestations...

-cholangitis
-biliary hyperplasia / obstruction
-cholangiocarcinoma

29

Fascioliasis clinical manifestations

-hepatic fibrosis / necrosis
-cholangitis
-biliary obstruction
-biliary cirrhosis

30

Opisthorchiasis clinical manifestations

-cholangitis
-biliary hyperplasia and obstruction
-cholangiocarinoma

31

describe the key trematode features

-unsegmented
-incomplete digestive tract
-two striated suckers

-most are hermaphrodites
-most of the body is reproductive organs

32

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

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

33

Fasicola spp.
-(1) is the method of human infection via (2) as intermediate hosts
-(3) form in hosts, leaves host via (4)

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

34

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)

1- immature eggs
2- miracidia
3- (fresh water) snail
4- *cercariae (rediae, sporocysts)
5- aquatic vegetation (watercress)
6- **metacercariae encyst

35

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

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

Fasicoliasis:
-often (a-/symptomatic)
-(2) incubation period
-(3) list the phases

1- asymptomatic (Sxs 15% of time)

2- days - months

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

37

Fasioliasis acute phase: form, duration, Sxs

-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

Fasioliasis acute phase: form, Sxs

-adult flukes

-biliary colic, RUQ pain, epigastric pain
-nausea, intolerance to fatty food, obstructive jaundice
-pruritus
-biliary lithiasis

39

Fasioliasis:
-(1) Dx
-(2) geographic prevalence
-(3) Tx
-(4) prevention

1- Ova, stool sample microscopy

2- worldwide

3- antiparasitics

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

40

Clonorchis sinesis = (1):
-associated with (2) consumption
-(3) 1st host, 2nd host, reservoirs

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

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

41

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)

1- embryonated eggs (shed in feces)
2- (fresh water) snail
3- miracidia
4- *cercariae (rediae, sporocysts)
5- fish
6- **metacercariae encyst

42

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

1- **metacercariae (encyst)
2- fish
3- metacercariae excyst
4- liver parenchyma into biliary ducts (via intestinal wall / peritoneal cavity)
5- adult flukes

43

list the range of clinical manifestations of C. sinesis infections

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

C. sinesis:
-(1) geographic incidences
-(2) main risk factor
-(3) Dx
-(4) Tx

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

2- eating infected fish (raw)

3- Ova in stool sample microscopy

4- antiparasites