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Y3R5: Medicine I 🩺 > L8: Viral Hepatitis > Flashcards

L8: Viral Hepatitis Flashcards

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
Q

IP of HAV

A

15 - 45 days

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26
Q

CP of HAV

A

 Asymptomatic (90%): Clinically silent OR Nonspecific Anorexia, Nausea Vomiting

 Symptomatic (10%): Jaundice, Dark urine & Pale stools

study clinical course of HAV

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27
Q

Dx (Labs) of HAV

A
  • 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
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28
Q

Atypical features of Acute Hepatitis A

A
  • Cholestatic hepatitis
  • Relapsing hepatitis
  • Extrahepatic manifestations
  • Autoimmune hepatitis
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29
Q

Characters of Cholestatic hepatitis

A

Recovering from acute HAV.

Deep icterus & intense pruritus during convalescent phase.
- Few weeks to months.
- Counseling & antipruritic measures.

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30
Q

Def of Relapsing hepatitis

A
  • Reinfection due to prolonged enterohepatic circulation of HAV
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31
Q

Characters of Relapsing hepatitis

A

Second attack of hepatitis 4-8 weeks following initial recovery

  • Subclinical elevation of transaminases.
  • Either mildly symptomatic disease or full blown
    hepatitis attack.
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32
Q

Extrahepatic manifestations of HAV

A
  • Renal
  • Nervous System
  • Pancreatobiliary system
  • Hematological
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33
Q

Extrahepatic manifestations of HAV

  • Renal
A

proteinuria, AGN, nephrotic syndrome, ARF

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34
Q

Extrahepatic manifestations of HAV

  • Nervous System
A

aseptic meningitis, encephalitis, seizures.

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35
Q

Extrahepatic manifestations of HAV

  • Pancreatobiliary
A

acalculous cholecystitis, acute pancreatitis.

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36
Q

Extrahepatic manifestations of HAV

  • Hematological
A

autoimmune hemolytic anemia, aplastic anemia

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37
Q

TTT of HAV

A

 DIET: Fresh food & Plenty of water & Sugary food

 REST

 Ursodeoxycholic acid

 Avoid: Alcohol, Fried and fatty foods

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38
Q

Prevention of HAV

A

Vaccine → Formalin inactivated
- 2 doses 0, (6-12) months
- IM deltoid or gluteal

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39
Q

Genome of HBV

A
  • DNA virus (hepadnavirus)
  • Genome is composed of incomplete double-stranded DNA.
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40
Q

Complete HBV Particle is Named …..

A

Dane-particle

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41
Q

MOT of HBV

A

Body fluids contain viral particles

  • Semen & vaginal secretions
  • Blood & Saliva
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42
Q

Risky Groups for HBV

A

 Multiple sex partners

 IV drug abusers

 Hemodialysis patients

 Patients requiring repeated blood transfusions: Hemophilia & Thalassemia

 Health care workers

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43
Q

Serological Markers for HBV

A
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44
Q

HBsAg

A

Marker of infectivity

45
Q

Anti-HBs

A

Marker of immunity

46
Q

HBcAg

47
Q

Anti-HBc

A
  • IgM anti-HBc: Recent infection.
  • IgG anti-HBc: Older infection.
48
Q

HBeAg

A

Marker of high degree of infectivity.

49
Q

Anti-HBe

A

May be present in infected or immune person.

50
Q

Chart of Acute HBV Infection with Recovery

51
Q

Factors associated with the severity of hepatitis B

A
  • Infecting dose
  • Age
  • Immunological Status
52
Q

Factors associated with the severity of hepatitis B

  • Infecting Dose
A

Higher the dose of HBV → shorter is incubation period → more severe hepatitis.

53
Q

Factors associated with the severity of hepatitis B

  • Age
A

Young age: mild initial hepatitis & more chance of chronicity.

54
Q

Factors associated with the severity of hepatitis B

  • Immunological Status
A

lmmunological impaired hosts: Milder initial disease.

55
Q

Phases of Acute HBV

A
  • Pre-Icteric
  • Icteric
56
Q

Pre-Icteric Phase of Acute HBV

A

Symptoms are nonspecific:
 Moderate fever & Headache
 Malaise and weakness
 Right upper quadrant pain.

57
Q

Icteric Phase of Acute HBV

58
Q

Characters of Acute anicteric hepatitis

A
  • No jaundice otherwise similar to acute icteric hepatitis
  • The symptoms are less severe than that in acute
59
Q

Dx of Acute HBV

A
  • HBsAg
  • Anti HBc IgM
  • HBV DNA by PCR is most sensitive test
60
Q

Complications of Acute HBV

A
  1. Fulminant Hepatitis: liver failure within weeks
  2. Chronic Hepatitis (around 15% in adults & 85% in young children)
  3. Rare complications:
61
Q

Rare Complications of Acute HBV

A

 Pancreatitis
 Myocarditis
 Atypical pneumonia
 Aplastic anemia
 Transverse Myelitis

62
Q

Def of Chronic HBV

A

Inflammatory disease of the liver > 6 months.

63
Q

CP of Chronic HBV

A

Non-Specific

  • Fatigue, anorexia, abdominal distension.
  • Hepatomegaly, splenomegaly, hepatic facies, palmar erythema
  • Spider angioma & liver cell failure (ascites- encephalopathy).
64
Q

Dx (Serology) of Chronic HBV

A

 HBsAg positive > 6 months
 Anti-HBc IgG in blood
 Serum HBV DNA
 HBeAg or Anti HBeAg may be present

65
Q

TTT of Chronic HBV

66
Q

Hepatocellular carcinoma is a complication of hepatitis B even before cirrhosis occurs so ……..

A

screening of HCC in HB patients is a must.

67
Q

Drugs of HBV despite not eradicating the virus they decrease the risk of transmission and disease progression to cirrhosis or HCC

68
Q

Prevention of Chronic HBV

A
  • HBV Vaccine
  • PEP
  • Perinatal Prophylaxis of Inhants
69
Q

Prevention of Chronic HBV

  • HBV Vx
A

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
Q

Prevention of Chronic HBV

  • PEP
A

Combination of HBIG & HB vaccine (within 24 hours of exposure)

71
Q

Prevention of Chronic HBV

  • Perinatal Prophylaxis of infants
A
  • HBIG 0.5ml IM in thigh immediately after birth
  • Full course of HB vaccine started within 12 hours of birth
72
Q

Genome of HDV

A

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
Q

MOT of HDV

A

similar to those for hepatitis B.

74
Q

Prevention of HDV

A
  • 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
Q

TTT of HDV

A

PEGylated interferon alpha is effective in reducing the viral load and the effect of the disease progression.

76
Q

Detection of HCV by PCR

A

Hepatitis C (PCR) is detectable in the blood within 3 weeks after infection.

77
Q

Detection of HCV Antibodies

A
  • 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
Q

Genome of HCV

A
  • Single stranded, enveloped RNA virus.
79
Q

Genotypes of HCV

A
  • 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
80
Q

Most Common HCV Genotype in Egypt

81
Q

CP of HCV

A
  • 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
Q

Pathology (Findings) of HCV

83
Q

MOT of HCV

84
Q

CP of Chronic HCV

A
  • Hepatic
  • Extra-Hepatic
85
Q

CP of Chronic HCV

  • Hepatic Manifestations
A

 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.

86
Q

CP of Chronic HCV

  • Extrahepatic manifestations
87
Q

CP of Chronic HCV

  • pathogenesis of Extrahepatic manifestations
A

a) Mediators of autoimmunity

b) Immune complex formation

c) Virus invasion and replication

88
Q

CP of Chronic HCV

  • Strongly associated Extra-Hepatic Manifesatations
A

1) Mixed cryoglobulinemia

2) Membranoproliferative glomerulonephritis

3) Porphyria cutenea tarda

4) Sjogren syndrome

5) Lymphoproliferative disorders

6) Leukocytoclastic vasculitis

7) Neuropathy

89
Q

CP of Chronic HCV

  • Rarely associated Extra-Hepatic Manifesatations
A

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)

90
Q

Prevention of Chronic HCV

91
Q

TTT of Chronic HCV

92
Q

TTT of Chronic HCV

  • All patients with +ve HCV RNA …….
A

should be considered potential candidate for therapy

93
Q

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.

VIP

94
Q

TTT of Chronic HBV

  • Ledipasvir + Sofosbuvir
A

which was released in 2014 and is approved to treat those with → genotypes 1, 4, 5 and 6 of hep C.

95
Q

TTT of Chronic HBV

  • Velpatasvir + Sofosbuvir
A

released in 2016.

  • Epclusa is approved for those with all genotypes of hep C, with or without cirrhosis.
96
Q

Source of HEV

A
  • 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
Q

IP of HEV

98
Q

CP of HEV

A

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
Q

Incidence of HEV

A

HEV is reported mainly among young adults (aged 14 - 45 yrs.)

100
Q

Fulminant HEV

A
  • HEV has a propensity to induce a fulminating form of acute disease particularly in pregnant women (causing fulminating HEV infection)
101
Q

Complications of HEV in Pregnant women

A
  • 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
Q

Dx of HEV

103
Q

Dx of HEV

  • EIA & ELISA & Western Blot
A
  • 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
Q

Dx of HEV

  • PCR
A

PCR tests for the detection of HEV RNA in serum and stool

105
Q

Dx of HEV

  • Immunofluorescent antibody blocking assays
A

Immunofluorescent antibody blocking assays to detect antibody to HEV antigen in serum and liver

106
Q

Dx of HEV

  • Immune electron microscopy
A

Immune electron microscopy to visualize viral particles in feces

107
Q

Treatment of acute HEV infection

108
Q

Treatment of acute HEV infection

  • Ribavirin
A
  • 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

Y3R5: Medicine I 🩺 (47 decks)

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