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Semester 4 > case 5 - viral hepatitis > Flashcards

case 5 - viral hepatitis Flashcards

1
Q

how are hep a and e transmitted

A

faecal or oral transmission

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2
Q

how are hep e b c and delta transmitted

A

via blood and bodily fluids

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3
Q

what hepatitis doesnt lead to chronic infection

A

hepatitis A

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4
Q

what is the pathogenesis

A

hepatitis viruses: non-cytopathic
Hepatocyte damage is immune-mediated
Antigen recognition by cytotoxic T cells: apoptosis
Chemokine driven recruitment of Ag-nonspecific cells

depending on strength of immune response
Mild inflammation to massive necrosis of the liver
‘Fulminant’ hepatitis which is a cause of acute liver failure

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5
Q

what does injury of hepatocytes lead to

A

necorosis

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6
Q

what can injury to bile canaliculi (cholestasis) lead to

A

Injury to bile canaliculi (cholestasis) leads to these results:
- ALP >150U/L
- Bilirubin >21umol/L

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7
Q

what are the investigations for hepatitis

A

elevated ALT, AST (can be >1000U/L)
Full blood count, INR
Liver ultrasound to rule out obstruction

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8
Q

describe features of viral hepatitis

A

sequelae of ongoing inflammation —> liver fibrosis
Progression of fibrosis to cirrhosis (20-30 years)
Accelerated by co factors - alcohol, HIV, diabetes, steatohepatitis
Asymptomatic, until liver decompensation

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9
Q

what are the non-invasive methods used to diagnose fibrosis

A

elastography and fibrotest

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10
Q

what is a fibroscan

A

waves are reflected more quickly as liver ‘stiffness’ increases, I.e the liver becomes more fibrotic

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11
Q

describe the complications of cirrhosis

A

progression to decompensated liver disease and hepatocellular carcinoma
Complications of portal hypertension
Ascites
Variceal bleeding
Encephalopathy
Subacute bacterial peritonitis
Acute on chronic liver failure

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12
Q

what is the survival rate for decompensated liver disease

A

50% 5 year survival

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13
Q

what type of virus is hep a

A

RNA virus - piconavirus

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14
Q

what are complications of hep a

A

prolonged cholestasis
Liver failure
Rare but more likely in older adults with pre-existing liver disease

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15
Q

diagnosis of acute hep a infection would show what

A

HAV and IgM

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16
Q

diagnosis of recovery or vaccinated hep a would show

A

HAV and IgG

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17
Q

what is the prevention for hep a

A

vaccine (given at 0, 6-12 months)
Immunoglobulin
Improvement in sanitation

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18
Q

what type of virus is hep e

A

RNA virus - herpesvirus

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19
Q

what are the different genotypes of hepatitis E

A

genotype 1,2 large ‘water borne’ outbreaks
Genotype 3,4 zoonotic, sporadic cases

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20
Q

what is the diagnosis for hep e

A

HEV, IgM (hepatitis E IgG, HEV RNA blood, stool)

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21
Q

what is the vaccination of hep e

A

Hecolin

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22
Q

what type of virus is hep b

A

DNA virus (hepadnaviridae) with multiple subtypes

23
Q

what is the outcome of infection closely linked to

A

Outcome of infection very closely linked to maturity of immune system and effectiveness of response

24
Q

what is the epidemiology of hep b in the UK

A

UK prevalence = 0.3%
Most new infections occur in adults, by sexual or parenteral route
Screwing programmes: identify non-immune, and chronic infection

antenatal clinical (Mother HBV sAG +ve)
Vaccination of baby +/- Ig
Prisons
GUM clinics, community drug services

25
Q

what are the hep b viral proteins

A

hepatitis B surface antigen - HBsAG
Hepatitis B e antigen - HBeAG

26
Q

what are the anti bodies for hep b

A

hepatitis B e antibody - anti-Hbe
Hepatitis B core antibody - Anti-HBc (IgM, IgG)
Hepatitis B surface antibody - anti-HBs

27
Q

what does surface antigen for more than six months define

A

chronic infection

28
Q

what does everyone have prior to vaccination

A

hepatitis B surface antigen only

29
Q

interpretation of no exposure to hep b serology

A

HBV sAG negative
Core Ab negative

30
Q

what would previous exposure show

A

HBV sAg negative
Core Ab positive

31
Q

what would chronic infection show

A

HBV sAg positive
Core Ab positive

32
Q

what are the phases for hep b infection

A

Immune tolerant
Immune clearance (HBeAg-positive chronic hepatitis)
Inactive carrier phase
Reactivation (HBeAg-negative chronic hepatitis)

33
Q

what are these phases characterised by

A

fluctuating levels of alt and hep b virus DNA

34
Q

What is mechanism of action of tenogovir and entcavir

A

they block a viral enzyme called hepatitis B DNA polymerase and switch off the replication in the cell. They do not eradicate the CCC DNA though.

35
Q

what does interferon do

A

Interferon - stimulates our immune response to recognise that these cells are infected with a virus of the hepatocytes

36
Q

why are CCC DNA hard to get rid of and how can we do so

A

Covalently closed circular DNA is inserted into the host genome and it sits like a viral reservoir
It is very difficult to get rid of this with out current treatments for hepatitis B
Only can get rid of this CCC DNA is by getting rid of the whole hepatocyte

37
Q

what is hepatitis delta virus

A

defective RNA virus that needs hep b machinery to replicate

38
Q

what does it use for envelope

A

uses surface antigen for hep b

39
Q

what are clinical features of hep d

A

severe hepatitis, 70% progress to cirrhosis
Lifetime risk of HCC doubled

40
Q

how is hep d diagnosed

A

hepatitis delta IgM, IgG, HDV RNA

41
Q

how is hep d treated

A
  • clearance of HBV sAG —> eradication of delta
    PEG IFN for >48 weeks
42
Q

what is the prevention for hep d

A

hep b vaccine

43
Q

what is hep c

A

RNA flavivirus

44
Q

what would no exposure to hep c show

A

HCV AB negative

45
Q

what would prior exposure to hep c show

A

HCV AB positive
Check HNC RNA if negative

46
Q

what would chronic infection of hep c show

A

HCV AB positive
HCV RNA positive

47
Q

what are direct acting antivirals

A

HCV poly protein

48
Q

what does IFN do

A

IFN stimulates immune system, direct inhibition of viral replication

49
Q

where does the life cycle take place

A

the cytoplasm

50
Q

what are the current therapies for chronic hep c

A

approval required from local MDT
Combinations of DAAs in single Tabley
Need to know genotype, if cirrhosis

51
Q

what are the suffixes of the drug name indicate

A

‘Previir’ = protease inhibitor
‘Asvir’ = NS5A inhibitor
‘Buvir’ = NS5B inhibitor

52
Q

what has a 98% cure

A

Velpatasvir/sofosbuvir (Epclusa) pan genotype

53
Q

what has a 90% cure

A

Elbasvir/grazoprevir (zepatier) genotype 1,4

Semester 4 (80 decks)

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