L8: Viral Hepatitis Flashcards

(108 cards)

1
Q

Examples of Hepatotropic viruse

A

HAV, HBV, HCV, HDV, HEV

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2
Q

Examples of Non Hepatotropic viruse

A

Mumps, measles, rubella, CMV, HSV, VZV, Dengue virus.

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3
Q

What are Other causes of hepatitis?

A
  • Salmonella typhi, Plasmodium.
  • Drugs: ATT, Antiepileptics, Halothane.
  • Autoimmune Hepatitis.
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4
Q

Causes of Acute viral hepatitis

A

Commonly HAV, HEV.

Rarely HCV, HBV.

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5
Q

Causes of Chronic viral hepatitis

A

HBV, HCV, HDV.

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6
Q

CP of Hepatotropic viruses

A

Hepatotropic viruses 3 possible courses:

  1. Acute viral hepatitis.
  2. Chronic viral hepatitis.
  3. Acute liver failure.
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7
Q

Signs of Prodromal phase of Acute Viral Hepatitis

A
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8
Q

Symptoms of Prodromal phase of Acute Viral Hepatitis

A
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9
Q

Labs in of Prodromal phase of Acute Viral Hepatitis

A
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10
Q

Signs of Icteric phase of Acute Viral Hepatitis

A
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11
Q

Symptoms of Icteric phase of Acute Viral Hepatitis

A
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12
Q

Labs in Icteric phase of Acute Viral Hepatitis

A
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13
Q

Signs of Convalesent phase of Acute Viral Hepatitis

A
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14
Q

Symptoms of Convalesent phase of Acute Viral Hepatitis

A
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15
Q

Labs in Convalesent phase of Acute Viral Hepatitis

A
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16
Q

DDx of Viral Hepatitis

A

 Malaria
 Dengue hepatitis
 Enteric hepatitis
 Chronic liver disease
 Liver abscess
 Cholangitis

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17
Q

Genome & Family of HAV

A

Picornavirus single-stranded RNA genome

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18
Q

Antibodies of HAV

A

Anti-HAV-IgM and Anti-HAV-IgG

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19
Q

Site of Replication of HAV

A

cytoplasm of liver cells

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20
Q

Epidemeology of HAV

A

Most common Viral Hepatitis

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21
Q

Source of infection by HAV

A

patients

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22
Q

Route of spread of HAV

A

Feco-oral

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23
Q

Infectivity period of HAV

A

Patient remains infectious 2 weeks prior to & for up to 1 week after onset of illness

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24
Q

Risk Factors for HAV

A

Overcrowding & Poor Sanitation

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25
IP of **HAV**
15 - 45 days
26
CP of **HAV**
 Asymptomatic (90%): Clinically silent OR Nonspecific Anorexia, Nausea Vomiting  Symptomatic (10%): Jaundice, Dark urine & Pale stools ## Footnote study clinical course of HAV
27
Dx (Labs) of **HAV**
- Anti HAV IgM: +ve in acute infection & disappears within 3 months of recovery - Anti HAV IgG: is of no diagnostic value as it persists years after infection
28
Atypical features of Acute Hepatitis A
- Cholestatic hepatitis - Relapsing hepatitis - Extrahepatic manifestations - Autoimmune hepatitis
29
Characters of **Cholestatic hepatitis**
**Recovering from acute HAV.** **Deep icterus & intense pruritus during convalescent phase.** - Few weeks to months. - Counseling & antipruritic measures.
30
Def of Relapsing hepatitis
- Reinfection due to prolonged enterohepatic circulation of HAV
31
Characters of **Relapsing hepatitis**
**Second attack of hepatitis 4-8 weeks following initial recovery** - Subclinical elevation of transaminases. - Either mildly symptomatic disease or full blown hepatitis attack.
32
Extrahepatic manifestations of HAV
- Renal - Nervous System - Pancreatobiliary system - Hematological
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Extrahepatic manifestations of HAV - Renal
proteinuria, AGN, nephrotic syndrome, ARF
34
Extrahepatic manifestations of HAV - Nervous System
aseptic meningitis, encephalitis, seizures.
35
Extrahepatic manifestations of HAV - Pancreatobiliary
acalculous cholecystitis, acute pancreatitis.
36
Extrahepatic manifestations of HAV - Hematological
autoimmune hemolytic anemia, aplastic anemia
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TTT of **HAV**
 DIET: Fresh food & Plenty of water & Sugary food  REST  Ursodeoxycholic acid  Avoid: Alcohol, Fried and fatty foods
38
Prevention of **HAV**
Vaccine → Formalin inactivated - 2 doses 0, (6-12) months - IM deltoid or gluteal
39
Genome of **HBV**
- DNA virus (hepadnavirus) - Genome is composed of incomplete double-stranded DNA.
40
Complete HBV Particle is Named .....
Dane-particle
41
MOT of **HBV**
**Body fluids contain viral particles** - Semen & vaginal secretions - Blood & Saliva
42
Risky Groups for **HBV**
 Multiple sex partners  IV drug abusers  Hemodialysis patients  Patients requiring repeated blood transfusions: Hemophilia & Thalassemia  Health care workers
43
Serological Markers for **HBV**
44
HBsAg
Marker of infectivity
45
Anti-HBs
Marker of immunity
46
HBcAg
....
47
Anti-HBc
- IgM anti-HBc: Recent infection. - IgG anti-HBc: Older infection.
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HBeAg
Marker of high degree of infectivity.
49
Anti-HBe
May be present in infected or immune person.
50
Chart of Acute HBV Infection with Recovery
51
Factors associated with the severity of hepatitis B
- Infecting dose - Age - Immunological Status
52
Factors associated with the severity of hepatitis B - Infecting Dose
Higher the dose of HBV → shorter is incubation period → more severe hepatitis.
53
Factors associated with the severity of hepatitis B - Age
Young age: mild initial hepatitis & more chance of chronicity.
54
Factors associated with the severity of hepatitis B - Immunological Status
lmmunological impaired hosts: Milder initial disease.
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Phases of Acute HBV
- Pre-Icteric - Icteric
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Pre-Icteric Phase of Acute HBV
**Symptoms are nonspecific:**  Moderate fever & Headache  Malaise and weakness  Right upper quadrant pain.
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Icteric Phase of **Acute HBV**
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Characters of **Acute anicteric hepatitis**
- No jaundice otherwise similar to acute icteric hepatitis - The symptoms are less severe than that in acute
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Dx of **Acute HBV**
- HBsAg - Anti HBc IgM - **HBV DNA by PCR is most sensitive test**
60
Complications of **Acute HBV**
1. Fulminant Hepatitis: liver failure within weeks 2. Chronic Hepatitis (around 15% in adults & 85% in young children) 3. Rare complications:
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Rare Complications of **Acute HBV**
 Pancreatitis  Myocarditis  Atypical pneumonia  Aplastic anemia  Transverse Myelitis
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Def of **Chronic HBV**
Inflammatory disease of the liver > 6 months.
63
CP of **Chronic HBV**
**Non-Specific** - Fatigue, anorexia, abdominal distension. - Hepatomegaly, splenomegaly, hepatic facies, palmar erythema - Spider angioma & liver cell failure (ascites- encephalopathy).
64
Dx (Serology) of **Chronic HBV**
 HBsAg positive > 6 months  Anti-HBc IgG in blood  Serum HBV DNA  HBeAg or Anti HBeAg may be present
65
TTT of **Chronic HBV**
66
Hepatocellular carcinoma is a complication of hepatitis B even before cirrhosis occurs so ........
screening of HCC in HB patients is a must.
67
Drugs of HBV despite not eradicating the virus they decrease the risk of transmission and disease progression to cirrhosis or HCC
....
68
Prevention of **Chronic HBV**
- HBV Vaccine - PEP - Perinatal Prophylaxis of Inhants
69
Prevention of **Chronic HBV** - HBV Vx
**DNA Recombinant vaccine** - IM (deltoid but not gluteal) - 3 doses 0, 1,6 - Duration of protection: 5 to 10 yrs. (Very effective) - Booster doses may be needed
70
Prevention of **Chronic HBV** - PEP
Combination of HBIG & HB vaccine (within 24 hours of exposure)
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Prevention of **Chronic HBV** - Perinatal Prophylaxis of infants
- HBIG 0.5ml IM in thigh immediately after birth - Full course of HB vaccine started within 12 hours of birth
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Genome of **HDV**
**negative sense, single-stranded, closed circular RNA** - HDV recognizes its receptor via the N-terminal domain of the large hepatitis B surface antigen, HBsAg. - HDV envelope protein has three of the HBV surface proteins anchored to it.
73
MOT of **HDV**
similar to those for hepatitis B.
74
Prevention of **HDV**
- The vaccine for hepatitis B protects against hepatitis D virus because of the latter's dependence on the presence of hepatitis B virus for it to replicate.
75
TTT of **HDV**
PEGylated interferon alpha is effective in reducing the viral load and the effect of the disease progression.
76
Detection of **HCV** by PCR
Hepatitis C (PCR) is detectable in the blood within 3 weeks after infection.
77
Detection of **HCV** Antibodies
- HCV antibodies detection by ELISA is a screening test used to detect antibodies to the virus which appears within 12 weeks of infection (up to 1 y).
78
Genome of **HCV**
- Single stranded, enveloped RNA virus.
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Genotypes of **HCV**
- **There are 6 main genotypes:**  1, 2,3 in USA and Europe  4 in Egypt - **Genotypes 2&3 has the best prognosis and response to therapy** - **Genotypes 4 : is the most common in Egypt (>90%) mainly subtype 4a**
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Most Common **HCV** Genotype in Egypt
4a
81
CP of **HCV**
- HCV rarely causes acute hepatitis which may deteriorate into fulminant hepatitis and liver cell failure. - HCV most commonly causes chronic hepatitis ending in cirrhosis → liver cell failure and/or HCC
82
Pathology (Findings) of **HCV**
83
MOT of **HCV**
84
CP of Chronic **HCV**
- Hepatic - Extra-Hepatic
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CP of Chronic **HCV** - Hepatic Manifestations
 Usually asymptomatic, accidentally discovered  Fatigue, intermittent low grade fever, GIT symptoms  More advanced disease causes jaundice, itching, dark urine, edema LL, bleeding and abdominal enlargement.
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CP of Chronic **HCV** - Extrahepatic manifestations
87
CP of Chronic **HCV** - pathogenesis of Extrahepatic manifestations
a) Mediators of autoimmunity b) Immune complex formation c) Virus invasion and replication
88
CP of Chronic **HCV** - Strongly associated Extra-Hepatic Manifesatations
1) Mixed cryoglobulinemia 2) Membranoproliferative glomerulonephritis 3) Porphyria cutenea tarda 4) Sjogren syndrome 5) Lymphoproliferative disorders 6) Leukocytoclastic vasculitis 7) Neuropathy
89
CP of Chronic **HCV** - Rarely associated Extra-Hepatic Manifesatations
1) Lichen planus 2) Autoimmune thrombocytopenia 3) Thyroid disease 4) Type 2 diabetes 5) Corneal ulcers (Mooren ulcers) 6) Pulmonary fibrosis 7) Systemic vasculitis (polyarteritis nodosa)
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Prevention of **Chronic HCV**
91
TTT of Chronic **HCV**
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TTT of **Chronic HCV** - All patients with +ve HCV RNA .......
should be considered potential candidate for therapy
93
In the absence of contraindications as Hepatocellular carcinoma or Liver cell failure treatment is recommended because patients are source of infection and are at risk of developing complications. ## Footnote **VIP**
...
94
TTT of **Chronic HBV** - Ledipasvir + Sofosbuvir
which was released in 2014 and is approved to treat those with → genotypes 1, 4, 5 and 6 of hep C.
95
TTT of **Chronic HBV** - Velpatasvir + Sofosbuvir
released in 2016. - Epclusa is approved for those with all genotypes of hep C, with or without cirrhosis.
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Source of **HEV**
- Water or food supplies contaminated with feces in which the virus is n excreted have been implicated with a major outbreaks of HEV infection all over the world.
97
IP of **HEV**
2-9 Weeks
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CP of **HEV**
Following the incubation period a self-limiting acute viral hepatitis appears, lasting for several weeks - The acute infection is followed by recovery - No case of chronic disease has been reported - HEV is reported mainly among young adults (aged 14 - 45 yrs.)
99
Incidence of **HEV**
HEV is reported mainly among young adults (aged 14 - 45 yrs.)
100
Fulminant **HEV**
- HEV has a propensity to induce a fulminating form of acute disease particularly in pregnant women (causing fulminating HEV infection)
101
Complications of HEV in Pregnant women
- HEV has a propensity to induce a fulminating form of acute disease particularly in pregnant women (causing fulminating HEV infection) - HEV infection during pregnancy can cause intra uterine death, abortions & a high perinatal morbidity and mortality
102
Dx of **HEV**
103
Dx of **HEV** - EIA & ELISA & Western Blot
- To confirm the results of EIA or ELISA tests, Western blot assays to detect IgM and IgG anti-HEV in serum can be used
104
Dx of **HEV** - PCR
PCR tests for the detection of HEV RNA in serum and stool
105
Dx of **HEV** - Immunofluorescent antibody blocking assays
Immunofluorescent antibody blocking assays to detect antibody to HEV antigen in serum and liver
106
Dx of **HEV** - Immune electron microscopy
Immune electron microscopy to visualize viral particles in feces
107
Treatment of acute HEV infection
108
Treatment of acute HEV infection - Ribavirin
- Early therapy of acute HEV may shorten course of disease and reduce overall morbidity - Ribavirin treatment may be considered in cases of severe acute hepatitis E or if Hepatitis E occurred in patients already having chronic liver disease