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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
Q

HBV X gene

A

Transcriptional Transactivators, aid replication

26
Q

HBV Replication

A

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
Q

Purpose of - DNA template in HBV

A

partial + Synthesis

28
Q

HBV Epidemiology

A

Blood Born
Perinatal
20-49 age group
10 genotype A-D most common

29
Q

HBV Clinical Features

A 
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
Q

Acute Hepatitis w/ resoltion HBV

A 
hepatic inflammation
fever
RUQ pain
dark urine
pale stool
resolves 3-6 months
31
Q

Acute Hepatitis w/ fulminant hepatitis

A

rapid progrss liver necrosis
acute severe
rapidly fatal

32
Q

Chronic Hepatitis

A 
persistent infection
initial mild infection
cirrhosis
liver failure
or hepatocellular carcinoma
33
Q

HBV pathogenesis

A 
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
Q

HBV Diagnosis

A 
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
Q

HBV Treatment

A

Acute Hepatitis: Symptomatic
Fulminant Hepatitis- liver transplant
Chronic Hepatiis-

36
Q

HBV Prevention

A 
Vaccination
-Recombivax
-Twinrix
-C-Comvax
HBIG
- HepaGam
HyperHep B
Navi-HB
37
Q

HDV

A 
Small RNA virioid
Circular - sense ssRNA
surronded by delta
Envelope contain HBsAg
** MUST HAVE HBV INFECTION**
38
Q

HDV Epidemiology, Genotype

A

Genotype 1 most prevalent

4% HBV infections in U.S. = HDV +

39
Q

HDV Clinical Features

A

HBV but increased severity
Coinfection- More acute symptoms

Superinfection- increased severity of existing chronic hepatitis, increased fulminant hepatitis and cirrhosis

40
Q

HDV Pathogenesis

A

Enters hepatocytes, Requires HBV infections

CAUSES CPE, also immune response culprable

41
Q

HDV DIAGNOSIS Co INfection

A

Abs against HDV and HBcAg

HBsAg clears and appearance of anti-HBs

42
Q

HDV DIAGNOSIS Superinfection

A

Persistence of HDV RNA and HBsAg for cronic
Lack of ANTI HBs
Total anti HDV mainly IgG, remain elevated.

43
Q

HDV Treatment

A

Treat with HBV treatment

44
Q

HDV Prevention

A

Vaccine for HBV protective against HDV

45
Q

Hep C Virus

A 
Flaviviridae
\+ sense 
enveloped ssRNA
Glycoprotein E1 E2 -enveloped
Structural and non sturctural proteinsIFN resistance
46
Q

HCV Replication

A

associates w/ LDL
LDL + Cellular GAGs
SRb1 and CD81

47
Q

HCV Epidemiology

A

Six main genotypes
Genotype 1 most prevalent in US
Infected blood transmission
*HIGH RISK: transplant, IVDU

48
Q

HCV Clinical

A

Acute and Chronic Hepatitis
INSIDIOUS ONSET-ACUTE
Chronic- doulbe fatality compared to HBV

49
Q

HCV Pathogenesis

A

Production of antiviral and proinflammartory cytokines

Activate other antiviral genes

50
Q

HCV Persistence

A

Block type I and type II IFN
Block production of antiviral cytokines
Block production of ISG proteins
IMMUNITY NOT LIFE LASTING

51
Q

HCV Diagnosis

A

Detection of anti HCV antibodies
ELISA and RIBA
Recover= ALT levels; persistence of HCV RNA

52
Q

Treatment HCV

A

Ribvirin

NS3/4a blockers

53
Q

HCV Prevention

A

Education to prevent the spread of the virus

MICRO Exam 7 (14 decks)

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