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PBL SEM 4 > viral hepatitis 1 > Flashcards

viral hepatitis 1 Flashcards

1
Q

what is hepatitis?

A

inflammation of the liver

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2
Q

what are the infectious causes of hepatitis?

A

viral, bacterial, fungal , parasitic

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3
Q

what are the non-infectious causes of hepatitis?

A
  • alcohol — alcoholic liver disease
  • drugs eg. paracetamol
  • autoimmune eg. primary biliary cirrhosis, autoimmune hepatitis
  • metabolic — fatty liver disease caused by metabolic syndrone, diabetes
  • ischaemic
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4
Q

what hepatitis viruses are transmitted via the faecal-oral route?

A

A and E

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5
Q

what hepatitis viruses are transmitted via blood and body fluids?

A

E (transmitted both ways), B, Delta, C

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6
Q

all hepatitis viruses can lead to CHRONIC infection except what?

A

hepatitis A

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7
Q

what is chronic infection defined as?

A

> 6 months

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8
Q

why does hepatitis A not cause chronic liver disease?

A

because it never causes chronic infection

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9
Q

chronic viral hepatitis causes ___________, and subsequent healing with _____, which over time can progress to _______

A
  • chronic liver inflammation
  • fibrosis
  • cirrhosis
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10
Q

describe viral hepatitis pathogenesis

A
  • non-cytopathic — hepatitis viruses don’t cause damage themselves to hepatocytes, it is the immune response to the virus that gives rise to the damage
  • hepatocyte damage is IMMUNE-MEDIATED
  • eg. hep B enters hepatocyte, then the hepatocyte will express on its surface certain antigens recognised by cytotoxic T ells, which will then destroy the hepatocyte
  • antigen recognition by cytotoxic T cells : apoptosis
  • chemokine driven recruitment of Ag-nonspecific cells
  • damage depends on strength of immune response
  • mild inflammation to massive necrosis of liver (‘fulminant’ hepatitis, acute liver failure)
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11
Q

what does injury to hepatocytes lead to?

A

necrosis

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12
Q

what enzymes are released into the bloodstream from the breakdown of hepatocytes, and are indicative of liver inflammation and injury?

A

ALT and AST — both usually contained within hepatocytes

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13
Q

alkaline phosphatase (ALP) is indicative of what?

A

damage to bile canaliculi

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14
Q

ALP and bilirubin are elevated in what?

A

cholestasis

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15
Q

The liver cells synthesise clotting factors (measured by __, ___) and other proteins such as _____, and hence these tests are the best indicator of how the liver is functioning

A
  • prothrombin time, INR
  • albumin
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16
Q

how do you assess synthetic liver function?

A

INR, albumin

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17
Q

what does the presentation of acute viral hepatitis depend on?

A

age and immune status

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18
Q

what are the ranging presentations of acute viral hepatitis?

A

asymptomatic (childhood) vs mild, non-specific vs fulminant (adulthood)

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19
Q

what are the commonest symptoms of acute viral hepatitis?

A

prodrome of nausea, fatigue, malaise, fever

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20
Q

other symptoms of acute viral hepatitis?

A

jaundice (when fever settles), dark urine (due to conjugated bilirubin in urine), pale stools, RUQ tenderness, hepatomegaly

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21
Q

what are dark urine and pale stools due to?

A

cholestasis

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22
Q

what is pain felt in hepatomegaly?

A

pain felt because there are only pain receptors in the capsule of the liver. there are none in the actual substance. therefore if liver is enlarged, the patient may experience pain

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23
Q

what investigations are doing in acute viral hepatitis?

A
  • elevated ALT/AST
  • bilirubin, ALP less marked
  • FBC, INR
  • liver ultrasound to rule out obstruction of biliary tract
  • viral screen — Hep A antibody (IgM), Hep B surface Ag, Hep C antibody, consider Hep E IgM
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24
Q

what is produced first out of IgG and IgM?

A

IgM

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25
Q

describe chronic viral hepatitis

A

ongoing inflammation in cycles with an immune response to the virus infection of the liver cells. liver tries to heal itself with fibrosis = connective tissue. as inflammation progresses with secondary fibrosis, get less and less of liver cells present as they are replaced with fibrotic tissue which cannot carry out the function of the liver.

  • progression of fibrosis to cirrhosis (20-30 years)
  • accerelated by co-factors eg. alcohol, HIV, diabetes, steatohepatitis
  • asymptomatic, until liver decompensation (so little functioning liver left so patient develops complications such as ascites or jaundice)
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26
Q

what is the gold standard for diagnosing cirrhosis and fibrosis?

A

liver biopsy

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27
Q

what non invasive methods can be sued to diagnosis fibrosis/cirrhosis?

A

elastography, Fibrotest

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28
Q

what’s APRI score?

A

combination of blood tests - uses platelet count and the AST in a formulation

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29
Q

describe a fibroscan

A
  • ultrasound elastography is performed by the fibroscan machine
  • probe sounds out US waves which are reflected through the liver. they are reflected more quickly as the liver stiffness increases
  • machine will tell you in real time a numerical score
  • there are settings on the score on which above you would call someone cirrhotic
  • can repeat and say there and then if they’re cirrhotic, unlike biopsy

WAVES REFLECTED MORE QUIUCKYL AS LIVER ‘STIFFNESS’ INCREASES IE. AS LIVER BECOMES MORE FIBROTIC

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30
Q

what are complications of cirrhosis?

A

progression to decompensation liver disease and hepatocellular carcinoma

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31
Q

the fibrous tissue laid down through the liver alters the blood flow and leads to _________

A

portal hypertension

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32
Q

what are complications of portal hypertension?

A
  • ascites
  • variceal bleeding
  • encephalopathy
  • subacute bacterial peritonitis = infection of ascites
  • acute on chronic liver failure
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33
Q

what is the % 5 year survival for decompensated liver disease?

A

50%

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34
Q

what type of virus is hepatitis A?

A

RNA virus from picornavirus family

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35
Q

what is the incubation period for hep A?

A

30 days (4-6 weeks) = relatively short

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36
Q

how is hepatitis A transmitted?

A

faecal-oral transmission, associated with poor sanitation

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37
Q

hep A in developing vs developed world

A
  • endemic in developing world — infection in childhood, mild or subclinical (>90% if <5 years)
  • in developed world, hep A is a disease of adults, contaminated food/water, travel to endemic countries, IVDU, occupational
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38
Q

what does hepatitis A not lead to?

A

chronic infection

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39
Q

what are 2 complications of hepatitis A?

A

prolonged cholestasis, liver failure - RARE but more likely in adults and in pre-existing liver disease

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40
Q

how is Hep A diagnosed?

A

acute infection — HAV IgM
recovery or vaccinated — HAV IgG

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41
Q

how is Hep A prevented?

A
  • vaccine (given at 0, 6-12 months)
  • immunoglobulin given in outbreak as vaccine takes several weeks to work
  • improvement in sanitation

DECLINING UK INCIDENCE since 2005

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42
Q

what type of virus is hepatitis E?

A

RNA virus from herpevirus family

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43
Q

what is average IP for hep E?

A

40 days (slightly longer than hep A)

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44
Q

how is Hep E transmitted?

A

faecal-oral transmission, HEV contaminant of blood supply in many countries

45
Q

global HEV?

A

big problem globally — 3.4 million acute cases (Pakistan, India, Mexico)

46
Q

what are the different HEV genotypes?

A

Genotype 1,2 — large ‘water borne’ outbreaks
Genotype 3,4 — zoonotic, sporadic cases — associated with undercooked pork, wild boar, deer

47
Q

in who is there a higher mortality of hep E?

A

cirrhotics (underlying liver disease) and pregnant women (30% mortality in 3rd trimester)

48
Q

what is hep E linked to?

A

a range of acute neurological syndromes eg. transverse myelitis

49
Q

what hep E genotypes can become chronic in immunosuppressed? example?

A

3, 4

eg. solid organ and stem cell transplant patients, neonates, age <1, HIV with CD4 <250

50
Q

how is HEV diagnosed?

A

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

51
Q

what do you check for in chronic HEV?

A

Hep E RNA in blood

52
Q

hep E prevention?

A

improvements in sanitation

vaccine currently only in china

53
Q

what is the most common cause of acute viral hepatitis in UK?

A

HEV

54
Q

HEV neurological syndromes — dont often seen much in the way of raised _____. if someone comes in with _______ with transverse myelitis or ____________ — check for Hep E

A

dont often seen much in the way of raised ALT. if someone comes in with Guillain Barre with transverse myelitis or meningoencephaltiis — check for Hep E

55
Q

what type of virus in HBV?

A

DNA virus from hepadnaviridae family - has multiple genotypes (subtypes)

56
Q

what is the HBV IP?

A

75 days (6 weeks to 6 months)

57
Q

what is the outcome of infection with HBV linked to?

A

maturity of immune system and effectiveness of response (linked to age)

58
Q

HBV globally?

A

approx 350 million infected (180 000 in UK)

> 0,6 million deaths/year from end stage liver disease and liver cancer

59
Q

HBV prevention?

A

vaccine - 3 doses at 0, 6 weeks, 6 months

60
Q

link with HBV infection outcome and age at infection

A
61
Q

what are the routes of transmission for HBV?

A
  • contact with infected blood
  • sexual
  • mother to baby
62
Q

what is the epidemiology of chronic HBV infection?

A

45% of the global population lives in areas with a high prevalence of HBV infection

63
Q

UK HBV prevelance

A

0.3%

95% new cases of chronic infection are immigrants from high prevalence areas

64
Q

most new HBV infections in the uk occur in who?

A

adults by sexual or parenteral (drug) route

65
Q

Hep B serology : viral proteins

A
  • Hepatitis B surface antigen HBsAg
  • Hepatitis B e antigen HBeAg
66
Q

Hep B serology : host antibodies

A
  • hepatitis B e Antibody - Anti-Hbe — made in response to exposure to E antigen
  • hepatitis B core antibody - Anti-HBc (IgM, IgG) — made in response to hepatitis B core antigen
  • hepatitis B surface antibody - Anti-HBs
67
Q

presence of what over 6 months defines chronic HBV infection?

A

surface Ag

68
Q

what is seen in someone with a prior Hep B vaccination only?

A

Hep B surface antibody

69
Q

if patient clears Hep B (which as an adult you have over a 95% chance of doing), left in blood after infection = what?

A

IgG antibodies to Hep B core antigen, and antibodies to surface antigen

70
Q

what is the first then second thing to appear in blood after HBV exposure?

A

HBsAG, then HBeAg

71
Q

what do you test for if screening someone for chronic HBV infection?

A

1) Hep B surface antigen
2) Hep B core antibody

72
Q

what is seen in blood in someone with - HBV

  1. no exposure
  2. previous exposure
  3. chronic infection
A
  1. HBV sAg -ve, core Ab -ve
  2. HBV sAg -ve, Core Ab +ve
  3. HBV sAG +ve, Core Ab +ve
73
Q

if infected with HBV at birth, what are the different phases you go through throughout life?

A
  • immune tolerant
  • immune clearance (HBeAg-positive chronic hepatitis)
  • inactive carrier phase - at older age, can have acquired significant fibrosis or even cirrhosis by this stage
  • reactivation (HBeAg-negative chronic hepatitis)
74
Q

how can high dose steroids cause reactivation in hep B?

A

high dose steroids given in inactive carrier phase — these suppress immune system so virus becomes more active again - reactivation

75
Q

what are the Hep B phases characterised by?

A

fluctuating levels of ALT and hep B virus DNA

76
Q

how can some people with HBV lose the virus?

A

some people can lose virus — lose surface antigen and make surface antibody. however could have developed quite severe fibrosis by this time

77
Q

what is seen in immature vs mature immune system in Hep B?

A
  1. immature immune system = high levels of Hep B DNA - virus replicating unchecked but immune system is not destroying virally infected hepatocytes so ALT levels are normal
  2. mature immune system (20+) - fluctuating ALT and virus level. see raised ALT when immune system is active and destroying the hepatocytes
78
Q

what % per year does fibrosi progress to cirrhosis?

A

2-10%

79
Q

describe tenofovir and entecavir treatment for chronic HBV

A

= nucleoside analogues
- block hepatitis B DNA polymerase - switch off replication in cell, but do not eradicate CCC DNA stored in hepatocyte nucleus. therefore if medication stopped the whole process starts up again
- LIFELONG MEDICAITON

80
Q

describe interferon treatment for chronic HBV

A

injection given 1x week. stimulates our immune response to recognise that the hepatocytes are infected with a virus. immune system therefore destroys these cells.

81
Q

HBV life cycle — part of it is in the _____. part involves _______ being inserted into host genome (our DNA) — sits like a viral reservoir and is hard to get rid of unless ______ is destroyed

A
  • cytoplasm
  • CCC DNA = covalently closed circular DNA
  • hepatocyte
82
Q

current HBV treatment clinical trial research involves what?

A

eradication CCC DNA

83
Q

HDV vs HBV virus type

A

HDV = RNA VIRUS, HBV = DNA VIRUS

84
Q

describe hepatitis delta virus

A

defective RNA virus — cannot replicate by itself — uses surface antigen of Hep B as its viral envelope

same routes of transmission as HBV

simultaneous vs superinfection

85
Q

HDV epidemiology

A
  • 5-20 million cases globally = 5% of HBV
  • pockets in mediterranean basin, turkey, russia, central asia, africa, s america
  • not as widespread as hep b
86
Q

clinical features of HDV

A
  • severe hepatitis, 70% progress to cirrhosis
  • lifetime risk of hepatocellular carcinoma is doubled

HDV accelerates the progression of liver disease in chronic HBV (cirrhosis can occur up to 10 years earlier) and also increases the risk of liver cancer.

87
Q

HDV diagnosis

A

hepatitis delta IgM, IgG, HDV RNA

88
Q

hep delta treatment

A

clearance of HBV sAg —> eradication of delta

pegylated interferon for > 48 weeks

89
Q

hep delta prevention

A

hepatitis B vaccine

90
Q

why can tenofovir not be used to treat HDV?

A

tenofovir inhibits hepatitis B DNA polymerase, and has no effect on HDV replication. pegylated interferon is currently the only licensed treatment for HDV

91
Q

Currently licenced treatments for chronic hepatitis B infection include _____ and ______ ( inhibitors of ________________ )and pegylated interferon. Interferon enhances the host immune response towards virally infected cells, and also inhibits various stages of viral replication.

A

Currently licenced treatments for chronic hepatitis B infection include Tenofovir and Entecavir ( inhibitors of Hepatitis B polymerase )and pegylated interferon. Interferon enhances the host immune response towards virally infected cells, and also inhibits various stages of viral replication.

92
Q

what type of virus is hepatitis C?

A

RNA flavivirus, six major subtypes

93
Q

HCV IP?

A

2 weeks to 6 months

94
Q

how does acute infection of hepatitis C often present?

A

asymptomatic

95
Q

hepatitis C — 75% develop chronic infection irrespective of what?

A

age and immune status

96
Q

HCV epidemiology

A
  • globally 180 million infected - UK 214 000
  • > 350 000 deaths/year
  • no vaccine available
97
Q

progression of hepatitis C: for every 100 people infected, how many will:

  1. develop chronic infection
  2. develop chronic liver disease
  3. develop cirrhosis
  4. die or cirrhosis or liver cancer
A
  1. 75-85
  2. 60-70
  3. 5-20
  4. 1-5
98
Q

how is hep C transmitted?

A
  • contact with infected blood = most important
  • sexual transmission
  • mother to baby (<5%) — less than 5% babies born to hepatitis C infected mothers will develop infection — dependent on viral load. risk increases if mothers viral load is >1000000 units/ml
99
Q

what country has the highest levels of HVC globally?

A

Egypt = 14-20%

100
Q

UK HCV epidemiology

A
101
Q

diagnosis of HCV — no vs prior vs chronic infection/exposure

A
102
Q

what do pegylated interferon and ribavirin do in HCV treatment?

A

IFN — stimulates immune system , direct inhibitor of viral replication

RBV — mechanism unclear, induces viral mutations

103
Q

what are poor prognostic indications in HCV?

A

cirrhosis, non caucasian, HIV co-infected, steatosis

104
Q

unable to treat people with HCV in those with contraindications to IFN/RBV — example?

A

decompensated liver disease

105
Q

in contrast to Hep B, the lifecycle of Hep C occurs entirely where?

A

in cytoplasm of hepatocyte

106
Q

what are the different types of direct acting anti virals (DAA)? drug suffixes?

A

DAA drugs block each of the enzymes involved in Hep E viral replication

  1. NS3/4 protease inhibitors - translation and only protein processing = ‘previr’
  2. NS5B polymerase inhibitor - RNA replication - ‘buvir’
  3. NS5A inhibitors - transport and release - ‘asvir’
107
Q

what is the current therapy for chronic HCV?

A
  • combinations of DAAs in single tablet
  • need to know genotype, if cirrhosis

‘ one pill a day (+ ribavirin if cirrhosis present)

  • average treatment length 8-12 weeks
108
Q

HCV pan genotyping 98% cure medications

A

Velpatasvir/Sofosbuvir (Epclusa)

109
Q

HCV genotype 1,4 90% cure medications

A

Elbasvir/Grazoprevir (Zepatier)

PBL SEM 4 (50 decks)

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