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DTMH Block 4 > Viral Hepatitis > Flashcards

Viral Hepatitis Flashcards

1
Q

How many deaths occur worldwide due to viral hepatitis and what is the WHO goal?

A

1.5 million deaths annually
WHO goal = eliminate viral hepatitis by 2030

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2
Q

Which viral hepatitis is treatable, curable and preventable?

A

Treatable - HBV
Curable - HCV
Preventable - HAV, HBV

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3
Q

What are non-infectious causes of hepatitis?

A

Toxins
Medication
Alcohol
Autoimmune

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4
Q

Name non-viral infectious causes of hepatitis

A

Bacterial (TB, syphilis)
Protozoal (malaria, amoebiasis)
Cestodes (hydatid)
Trematodes (schistosomiasis)

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5
Q

Name hepatotrophic viral infectious causes of hepatitis

A

HAV
HBV
HCV
HDV
HEV

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6
Q

Name non-hepatotrophic viral infectious causes of hepatitis

A

Adenovirus
EBV
CMV
HSV
Yellow fever
Measles
Rubella

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7
Q

Which hepatotrophic virus is DNA?

A

HBV

HAV, HCV, HDV, HEV are RNA

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8
Q

Which hepatotrophic viruses are enteric?

A

HAV
HEV

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9
Q

Which hepatotrophic viruses are parenteral?

A

HBV
HCV
HDV

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10
Q

What are the clinical features of acute hepatitis?

A
  1. Asymptomatic
  2. Prodrome
  3. Illness
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11
Q

What are the clinical features of acute hepatitis prodrome?

A

Fever
Headache
Malaise
Fatigue
Anorexia
N+V
Abdominal pain

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12
Q

What are the clinical features of acute hepatitis illness?

A

Icterus (dark urine, pale stools, pruritis, jaundice)
Hepatomegaly
Extrahepatic (arthralgia, rash)

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13
Q

Can you identify causative organism of acute hepatitis based on laboratory markers?

A

No - virus specific assay is required for diagnosis

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14
Q

Which laboratory markers are altered in acute hepatitis?

A

ALT, AST, ALP
Bilirubin
PTT
Inflammatory markers

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15
Q

What is the epidemiology of HAV?

A

1.4 million cases annually
Sporadic vs epidemic
- poor sanitation
- day care
- travellers
- homeless

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16
Q

What is the transmission of HAV?

A

Feco-oral

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17
Q

What is the incubation period of HAV?

A

1 month (15-50d)

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18
Q

What do HAV symptoms depend on?

A

Age
Children <6y 70% asymptomatic
Adults 70% symptomatic

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19
Q

Discuss the outcomes of HAV infection

A

Usually mild and self-limiting (2-6m)
No chronicity
No re-infection
Complications increased with age

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20
Q

Name complications of HAV

A
  1. Fulminant hepatitis
  2. Cholestatic jaundice
  3. Relapsing hepatitis
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21
Q

Discuss the features of fulminant hepatitis in HAV

A

Encephalopathy
Coagulopathy
High fatality

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22
Q

Discuss the features of cholestatic jaundice in HAV

A

Persistent severe jaundice and pruritic for up to 3m that resolves spontaneously

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23
Q

Discuss the features of relapsing hepatitis in HAV

A

Biochemical and clinical relapse after initial recovery
Virus sheds in stool
Full recovery within 1y
Does not cause carrier state

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24
Q

Discuss serology concerning HAV

A

Anti-HAV IgM - active/recent infection
Anti-HAV IgG - persists for life (immunisation)

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25
Q

How long can anti-HAV IgM persist?

A

Up to 6 months

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26
Q

Which assay results confirm HAV infection?

A

Symptoms with positive anti-HAV IgM

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27
Q

Discuss prevention of HAV

A
  1. General
    - sanitation
    - proper food cooking
    - hand hygiene
    - infection control
    - food safety inspections
  2. Specific
    - HNIG
    - vaccine
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28
Q

What is HNIG?

A

Pooled human normal immunoglobulin

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29
Q

When can HNIG be used?

A
  1. PrEP
  2. PEP
  3. High risk (immunocompromised)
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30
Q

When can HAV vaccine be used?

A
  1. PrEP 2 weeks before travel and booster at 6 months
  2. PEP within 14 days of exposure
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31
Q

Which HAV PrEP is preferred?

A

Vaccine > HNIG

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32
Q

Discuss HAV vaccination

A

Targeted
- risk of exposure (travellers, occupational)
- risk of complications (immunocompromised, liver disease)
Universal
- childhood vaccination could eradicate HAV (humans are the only host)

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33
Q

Discuss treatment of HAV

A

Supportive
Avoid hepatotoxic drugs
Restrict activity until LFTs normalise
Liver transplant if fulminant hepatitis

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34
Q

Discuss the epidemiology of HBV

A

250 million carriers worldwide
Age inversely related to chronicity
SA prevalence is 7% with genotype A

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35
Q

What is important about the HBV genotype found in SA?

A

Genotype A
- higher risk of chronicity
- higher risk of HCC

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36
Q

Discuss transmission of HBV

A

Horizontal
- blood exposure
- sexual exposure
- percutaneous
Vertical
- MTCT

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37
Q

Which factors increase risk for MTCT of HBV?

A

E antigen positive
High viral load

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38
Q

Which factors increase risk for percutaneous transmission of HBV?

A

E antigen positive

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39
Q

What is the incubation period of HBV?

A

3 months (1-6m)

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40
Q

Discuss the clinical features of acute HBV

A
  1. Asymptomatic
  2. Prodromal
  3. Pre-icteric
  4. Icteric
  5. Post-icteric

Symptoms resolve within 3 months but fatigue may persist

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41
Q

What is the definition of chronic HBV?

A

Persistence of HBsAg >6m
Often asymptomatic or non-specific symptoms

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42
Q

Discuss the risk of chronicity in HBV

A

Perinatal risk 90-95%
>20y risk <5%

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43
Q

Discuss the outcomes of chronic HBV

A
  1. Spontaneous surface antigen clearance (sAg negative and HBV DNA positive - occult infection)
  2. Inactive chronic carrier state (sAg positive)
  3. Disease progression (cirrhosis, decompensation, HCC)
44
Q

What makes HBV challenging to cure?

A

Covalently closed circular HBV DNA (cccDNA) is found within the nucleus
Persistent, stable “mini-chromosome” from which virus copies are made
Nucleoside analogues do not eliminate cccDNA

45
Q

What is the first serological marker in HBV?

46
Q

Which HBV serological marker indicates infection?

A

HBsAg
>6m = chronic infection

47
Q

Which HBV serological marker indicates active replication?

A

eAg (absent in some mutant viruses)

48
Q

What does anti-HBc IgG indicate?

A

Past infection

49
Q

What does anti-HBc IgM indicate?

A

Acute infection or reactivation

50
Q

What does anti-HBs indicate?

A

Immunity (past infection or vaccination)

51
Q

What is HBV DNA/VL useful for?

A

Identifying occult infection where HBsAg negative
Disease progression monitoring
Transmission risk
Treatment monitoring

52
Q

Discuss the treatment of acute HBV infection

A

Supportive
Prevent further transmission
Can consider nucleoside analogues in specific indications (severe disease)

53
Q

Which treatment is contraindicate in acute HBV infection?

A

Peg-interferon

54
Q

What is the pre-treatment assessment of HBV?

A

Age
Disease severity
Comorbidities
Serological profile
VL, genotype
HCC screening (U/S, AFP, fibrosis markers, biopsy, endoscopy)

55
Q

Discuss treatment options for HBV

A

Pegylated interferon
TAF
TDF
Entecavir
Lamivudine

56
Q

Discuss the advantages of interferon treatment of HBV

A

Finite duration (48w)
No drug resistance

57
Q

Discuss the disadvantages of interferon treatment of HBV

A

Injection
S/E
Contraindications (pregnancy, decompensated cirrhosis)

58
Q

Discuss the advantages of nucleoside analogue treatment of HBV

A

Oral
Potent
Well-tolerated
Multiple options

59
Q

Discuss the disadvantages of nucleoside analogue treatment of HBV

A

Long term treatment (>5y)
Drug resistance

60
Q

When can HBV treatment be stopped in certain patients?

A

Undetectable HBsAg and HBeAg
HBsAb and HBeAb
Undetectable HBV DNA
Normal LFTs

61
Q

Which nucleoside analogue is suitable for HBV treatment in children 2-11y?

62
Q

Discuss strategies for HBV prevention

A

Infection control
Blood product screening
Donor organ screening
Needle exchange programs
Counselling of infected persons
Vaccination (PrEP and PEP)

62
Q

Which factors indicate need for HBV treatment?

A

Cirrhosis (APRI >2)
HBV DNA > 20 000

63
Q

Which patients should be targeted for HBV PrEP vaccination?

A

HCWs
Household contacts of HBV patients
Dialysis, transplant, frequent transfusion recipients
Comorbidities (HIV, chronic liver disease)

64
Q

Which patients should be considered for HBV PEP vaccination?

A

Occupational exposure
Newborns of infected mothers
Sexual assault

65
Q

If patient is exposed to HBV but unvaccinated/non-immune, what should be added?

A

Hepatitis B immunoglobulin

66
Q

Discuss the epidemiology of HCV

A

70 million worldwide
1% low risk groups
>10% high risk groups

67
Q

Discuss HCV transmission

A
  1. Parenteral
  2. Sexual
  3. Vertical
68
Q

What is the incubation period of HCV?

A

2 months (2w-6m)

69
Q

Discuss the clinical features of HCV

A
  1. Usually asymptomatic
  2. Chronic - symptomatic when cirrhosis, HCC
70
Q

Discuss the natural history of HCV infection

A

15% resolve
85% chronic

20 year progression
20% of chronic become cirrhotic
6%/y develop ESLD
4%/y develop HCC
3-4%/y require transplant or die

71
Q

Name extra hepatic manifestations of HCV

A

Autoimmune (Sjogren’s)
Porphyria cutanea tarda
Lymphoproliferative disease
Insulin resistance

72
Q

What does HCV Ab negative HCV RNA negative indicate?

A

No chronic infection (acute possible if very recent infection)

73
Q

What does HCV Ab negative HCV RNA positive indicate?

A

Acute infection

74
Q

What does HCV Ab positive HCV RNA positive indicate?

A

Acute OR chronic infection

75
Q

What does HCV Ab positive HCV RNA negative indicate?

A

Previous HCV infection
Confirm with repeat test in 12w

76
Q

Discuss HCV treatment

A

Antivirals to all chronic patients
If acute HCV, may defer and recheck HCV RNA due to spontaneous resolution possibility

77
Q

When do we say HCV is cured?

A

Undetectable HCV RNA >12w post treatment completion

78
Q

What should you monitor regularly with direct acting antivirals?

A

FBC
LFT
Creat
INR
HCV RNA VL

79
Q

Name the 3 targets of direct acting antivirals (DAAs) in HCV treatment

A
  1. NS3/4A protease
  2. NS5A
  3. NS5B polymerase
80
Q

Name examples of NS3/4A protease DAAs

A

Simeprevir
Grazoprevir
Voxilaprevir
Glecaprevir

81
Q

Name examples of NS5A DAAs

A

Daclastavir
Ledipasvir
Elbasvir
Velpatasir
Pibrentasvir

82
Q

Name examples of NS5B polymerase DAAs

A

Sofosbuvir
Dasabuvir

83
Q

Name HCV treatment options in patients >18y without cirrhosis

A

Sofos/velpa 12w
Sofos/dacla 12w
Gleca/pibre 8w

84
Q

Name HCV treatment options in patients <18y with compensated cirrhosis

A

Sofos/velpa 12w
Gleca/pibre 12w
Sofos/dacla 24w

85
Q

Name HCV treatment options in patients 12-17y

A

Genotypes
1, 4, 5, 6 - sofos/ledi 12w
2 - sofos/riba 12w
3 - sofos/riba 24w

86
Q

Which family does HAV belong to?

A

Hepatovirus

87
Q

Which family does HBV belong to?

A

Hepadnavirus

88
Q

Which family does HCV belong to?

A

Hepacivirus

89
Q

Which family does HDV belong to?

A

Deltavirus

90
Q

What are the features of acute hepatitis on pathology?

A
  1. Hepatocellular damage (minor cell swelling to apoptosis)
  2. Councilman bodies
  3. Varying degrees of necrosis
  4. Cholestasis
  5. Mild siderosis
  6. Mild steatosis
  7. Portal tracts infiltrated with mixed inflammatory cells
  8. Bile duct proliferation
91
Q

What are ‘councilman bodies’?

A

Apoptotic bodies

92
Q

What are the features of chronic hepatitis on pathology?

A

Inflammatory infiltrate
Interface hepatitis
Bridging necrosis -> fibrosis -> cirrhosis

93
Q

What is specific about the inflammatory infiltrate in HCV?

A

Lymphoid aggregates

94
Q

Discuss the features of hepatic steatosis

A

Moderate alcohol intake - microvesicular steatosis
Chronic alcohol intake - macrovesicular steatosis
Fatty change is initially centrilobular -> pan lobular in severe cases
Minimal fibrosis
Continued alcohol consumption -> fibrous tissue development around central veins

95
Q

Until what point is fatty change in hepatic steatosis reversible?

A

Until fibrosis appears

96
Q

Discuss the characteristics of alcoholic hepatitis

A

Hepatocyte swelling
Spotty necrosis
Neutrophil reaction (lobules)
Mallory bodies
Sinusoidal and perivenular fibrosis

97
Q

What are mallory bodies?

A

Eosinophilic inclusions in hepatocyte cytoplasm

98
Q

Can alcoholic cirrhosis develop without evidence of steatosis or alcoholic hepatitis?

99
Q

What can liver cysts mimic?

A

Malignant tumours

100
Q

What are 3 main types of liver cysts?

A
  1. Simple cysts
  2. Hydatid cysts (echinococcus granulosus)
  3. Choledochal cysts (congenital, intra vs extra hepatic)
101
Q

What is the most common visceral malignant tumour?

A

Hepatocellular carcinoma

102
Q

Discuss the epidemiology of hepatocellular carcinoma

A

M>F
20-40yo
Strongly linked to HBV
Vertical transmission 200x risk for HCC
<50% have cirrhosis

103
Q

What are other aetiologies of HCC?

A

Aflatoxins (aspergillus flavus)
Vinyl chloride
Thorotrast

104
Q

Discuss the pathology features of HCC

A

Usually solitary
Multifocal in cirrhosis
Hemorrhagic, necrotic masses
Bile stained
Rapidly growing
May infiltrate large veins eg vena cava
Seldom metastasises but can go to. lung
Death within 10m of diagnosis
Incr AFP in 75% of patients

DTMH Block 4 (14 decks)

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