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MICRO Exam 7 > Hepatitis 89-90 > Flashcards

Hepatitis 89-90 Flashcards

1
Q

Differential Dx Hepatitis

A 
Hep A, B, C
EtOH injury
Drug induced
Gallstone
Amebic bacterial abscess
Viral Causes
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2
Q

Fecal Oral Hepatitis Viruses

A

HAV

HEV

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3
Q

Blood Borne Hepatits Viruses

A

HBV
HCV
HDV

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4
Q

OUtcomes of hepatitis

A
  1. anicteric
  2. icteric w/ resolution
  3. Fulminant
  4. Chronic
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5
Q

Hep A virus

A 
Picornaviridae
Small + sense
naked ss RNA
icosahedreal capsid
cap proteins bind hepatocytes
RESISTANT TO HARSH
Structural and non structural genes
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6
Q

HAV Epidemiology

A

Fecal Oral
Shed 2 weeks before
Continues 2 weeks after jaundice
Restaurant, daycare, shellfish, contaminated H2O

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7
Q

HAV clinical

A 
Acute Hepatitis
2-4 weeks incubation
Abrupt onset
Virus detectable prior to symptoms
IgM first
IgG next
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8
Q

Initial symptoms HAV

A

fever, loss appetite, abdominal pain

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9
Q

Later symptoms HAV

A

Dark Urine, Pale stool, Jaundice, pruitice 4-5 weeks long

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10
Q

HAV pathogenesis

A 
Fecal Oral
Internalized by hepatocytes
released in bile and GI
Humoral and CMI response
Non perm damage ADCC and CTL
jaundice, urine, stool bcuz of liver damage
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11
Q

HAV OUTCOME

A

Mild disease, complete recovery 99%
Fulminant hepatitis rare
NOT CHRONIC
LIFE LONG IMMUNITY

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12
Q

HAV Treatment

A

Post exposure prophylaxis, immune globulin

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13
Q

HAVE Prevention

A

Sanitation
Vaccine
HAVRIX Vaqta
Twinrix– HAV+HBV

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14
Q

HEV

A 
Hepeviridae
Small + naked ssRNA
icosahedral capsid
Cytoplasmic Replication
3 ORF
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15
Q

HEV Epidemiology

A

Fecal Oral
Mimics HAV
Higer fatality than HAV
Inadequate water supply and enviromental sanitation

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16
Q

HEV Clinical Features

A

Acute Hepatitis
2-8 week incubation
ABRUPT

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17
Q

HEV Pathogenesis

A

Fecal Oral
Both Humoral and CMI
Jaundice bcuz of damage

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18
Q

HEV Diagnosis

A

Mimics HAV

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19
Q

HEV Treatment and Prevention

A

Symptomatic

Prevention: Sanitation, recomb vaccine

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20
Q

HBV

A 
Hepadnaviridae
Small enveloped
partial dsDNA
Stable, icosahedral capsid
Glycoproteins in capsid
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21
Q

HBV Genome

A

Sgene
C gene
P gene
X gene

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22
Q

HBV S gene

A

HBsAg ( LMS proteins)

23
Q

HBV C gene

A

HBcAg

HBeAg—> not part of structure, is secreted

24
Q

HBV P gene

A

DNA polymerase

Reverse Transcriptase

25
HBV X gene
Transcriptional Transactivators, aid replication
26
HBV Replication
dsDNA by viral DNA polymerase -transcription into 4 mRNAs by HOST Pol full mRNA --> - DNA by reverse trancriptase Short mRNA--> synthesize viral proteins assembly- budding of virions=Dane particle Release of HBsAg + HBeAg
27
Purpose of - DNA template in HBV
partial + Synthesis
28
HBV Epidemiology
Blood Born Perinatal 20-49 age group 10 genotype A-D most common
29
HBV Clinical Features
``` incubation of 3 months INSIDIOUS if symptomatic 3 outcomes 1. acute hepatitis w/ resolution 2. acute hepatitis w/ progression to fulminant hep 3. Chronic Hepatitis 3. a. persistent 3.b. Active ```
30
Acute Hepatitis w/ resoltion HBV
``` hepatic inflammation fever RUQ pain dark urine pale stool resolves 3-6 months ```
31
Acute Hepatitis w/ fulminant hepatitis
rapid progrss liver necrosis acute severe rapidly fatal
32
Chronic Hepatitis
``` persistent infection initial mild infection cirrhosis liver failure or hepatocellular carcinoma ```
33
HBV pathogenesis
``` Enter blood infects hepatocytes No permanent liver damage DNA can insert in host... LATENT Effective CMI & Inflammation = resolution Ineffective CMI & inflammation= 1. immune complex 2. Cirrhosis 3. PHC/HCC ```
34
HBV Diagnosis
``` Acute Hep B -Elevated LIver -HBsAg and HBeAg appear first before symptoms -Chronic B -prolonged elevation of liver HBsAg HBeAg and HBV DNA persist ```
35
HBV Treatment
Acute Hepatitis: Symptomatic Fulminant Hepatitis- liver transplant Chronic Hepatiis-
36
HBV Prevention
``` Vaccination -Recombivax -Twinrix -C-Comvax HBIG - HepaGam HyperHep B Navi-HB ```
37
HDV
``` Small RNA virioid Circular - sense ssRNA surronded by delta Envelope contain HBsAg ** MUST HAVE HBV INFECTION** ```
38
HDV Epidemiology, Genotype
Genotype 1 most prevalent | 4% HBV infections in U.S. = HDV +
39
HDV Clinical Features
HBV but increased severity Coinfection- More acute symptoms Superinfection- increased severity of existing chronic hepatitis, increased fulminant hepatitis and cirrhosis
40
HDV Pathogenesis
Enters hepatocytes, Requires HBV infections | CAUSES CPE, also immune response culprable
41
HDV DIAGNOSIS Co INfection
Abs against HDV and HBcAg | HBsAg clears and appearance of anti-HBs
42
HDV DIAGNOSIS Superinfection
Persistence of HDV RNA and HBsAg for cronic Lack of ANTI HBs Total anti HDV mainly IgG, remain elevated.
43
HDV Treatment
Treat with HBV treatment
44
HDV Prevention
Vaccine for HBV protective against HDV
45
Hep C Virus
``` Flaviviridae + sense enveloped ssRNA Glycoprotein E1 E2 -enveloped Structural and non sturctural proteinsIFN resistance ```
46
HCV Replication
associates w/ LDL LDL + Cellular GAGs SRb1 and CD81
47
HCV Epidemiology
Six main genotypes Genotype 1 most prevalent in US Infected blood transmission *HIGH RISK: transplant, IVDU
48
HCV Clinical
Acute and Chronic Hepatitis INSIDIOUS ONSET-ACUTE Chronic- doulbe fatality compared to HBV
49
HCV Pathogenesis
Production of antiviral and proinflammartory cytokines | Activate other antiviral genes
50
HCV Persistence
Block type I and type II IFN Block production of antiviral cytokines Block production of ISG proteins IMMUNITY NOT LIFE LASTING
51
HCV Diagnosis
Detection of anti HCV antibodies ELISA and RIBA Recover= ALT levels; persistence of HCV RNA
52
Treatment HCV
Ribvirin | NS3/4a blockers
53
HCV Prevention
Education to prevent the spread of the virus

MICRO Exam 7 (14 decks)

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