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Viral Hepatitis Flashcards

1
Q

Define hepatitis?

A

6 viruses known to infect humans- A, ,C,D,E nd G other viruses that inect liver= CMV, EBV, yellow fever, herpes

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2
Q

what are the six different viruses known to infect

A
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3
Q

what is the typical presentation for hepatitis?

A

fever, jaundice, raised ALT, AST

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4
Q

what is the typical presentation for hep A?

A

Travel, faecal-oral (contaminated water is a major source/ poor hygiene), acute, usually asymptomatic, supportive management , 2 weeks incubation - Asia and Africa

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5
Q

what is the typical presentation for hep B?

A

acute, MSM, unprotected sex, blood transfusion/ IVDU, causes high ALP as well, most clear the infection, 4-12wks, health care workers, likely in children, Africa

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6
Q

what is the typical presentation for Hep C?

A

chronic, rf for hepatocellular carcinoma, TRANSFUSIONS, blood to blood transmission/IVDU, 2wks-6mnths, Eastern Mediterranean

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7
Q

what is the typical presentation for Hep D?

A

only with Hep B

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8
Q

what is the typical presentation for Hep E?

A

Enteric, faecal oral (water), Pregnancy, immunocompromised, supportive management, acute

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9
Q

Define hepatitis A and E?

A

hepatitis caused by infection with RNA viruses, hepatitis A or hepatitis E that follow an acute course with progression to chronic carriage

go to A and E with Hep A and E

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10
Q

what type of viruses are Hep A and E?

A

small non-enveloped single stranded linear RNA viruses of roughly 7500 nucleotides-> with transmission via faeco-oral route

HAV- picornavirus

HEV - calcivirus

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11
Q

describe the aetiology of hepatitis A and E?

A 
HAV = picornavirus
HEV = calicivirus

Transmission = faecal-oral route

Both viruses replicate within hepatocytes and are secreted into bile

Liver inflammation and hepatocyte necrosis is caused by the immune response

Infected cells are targeted by CD8+ T cells and NK cells

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12
Q

What is the transmission of hepatitis A and E?

A

faecal -oral route

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13
Q

describe the histological features of hepatitis A and E

A

Inflammatory cell infiltration of portal tracts (neutrophils, macrophages, eosinophils, lymphocytes)

Zone 3 necrosis

Bile duct proliferation

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14
Q

what are the risk factors for hepatits A and E?

A

endemic region with poor sanitation

homosexual men

close contact with infected person

think went on hols and had some shellfish

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15
Q

summarise the epidemiology of viral hepatitis?

A

Hep A – more common than Hep E

HAV is endemic in the developing world

Infection often occurs sub-clinically (no clinical findings)

Better sanitation in the developed world means that it is less common, age of exposure is higher and, hence, patients are more likely to be symptomatic

Annual UK incidence: 5000

HEV is endemic in Asia, Africa and Central America

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16
Q

what is the incubation period of HAV and HEV?

A

3-6 weeks

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17
Q

what are the prodromal period symptoms ( early symptoms) of Hepatitis A and Hep E?

A

malaise

anorexia- distaste in cigarettes in smokers

fever

nausea and vomiting

RUQ pain

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18
Q

what are the symptoms of hepatitis?

A

dark urine

pale stools

jaundice lasting around 3 weeks

ocassionally, itching and jaundice may last several weeks in HAV infection

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19
Q

what are the signs of hep A and Hep E?

A

pyrexia

jaundice

tender hepatomegaly

spleen may be palpable

ABSENCE of stigmata of chronic liver disease (although some spider naevi may appear transiently)

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20
Q

what are the appropriate investigations for Hep A and Hep E and interpret the results?

A

Bloods

- LFTs - high AST, ALT, ALP and bilirubin

  • High ESR
  • Low albumin + high platelets (if severe)

Vital Serology

  • Hep B and C serology must be done to rule them out
  • Hepatitis A:
  • Anti-HAV IgM (during acute illness, disappears after 3-5 months)
  • Anti- HAV IgG (recovery phase and lifelong persistence)
  • Hepatitis E:
  • Anti-HEV IgM (raised 1-4 weeks after onset)
  • Anti-HEV IgG

Urinalysis

  • Positive for bilirubin
  • Raised urobilinogen
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21
Q

outline the management plan for viral hepatitis?

A

There is no specific management other than bed rest and symptomatic treatment (e.g. antipyretics, antiemetics or cholestyramine (for severe pruritus))

Prevention and Control

  • Public Health - safe water, sanitation and food hygiene
  • These are notifiable diseases
  • When travelling, personal hygiene and dietary precautions
  • Immunisation is available for HAV only

Passive immunisation with IM human immunoglobulin (effective for a short time)

Active immunisation with attenuated HAV vaccine offers safe and effective immunity for those travelling to endemic areas and high-risk individuals

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22
Q

what are the possible complications of Hep A and Hep E?

A

Fulminant hepatic failure (in a very small proportion of patients but is more common in pregnant women)

Cholestatic hepatitis with prolonged jaundice and pruritus can develop after HAV infection

Post-hepatitis syndrome: continued malaise for weeks to months

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23
Q

summarise the prognosis of viral hepatitis?

A

Recovery is usually within 3-6 weeks

Occasionally patients may relapse during recovery

There are no chronic sequelae

Fulminant hepatic failure has a mortality of 80%

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24
Q

Define Hep B?

A

Hepatitis caused by infection with hepatitis B virus (HBV), which may follow an acute or chronic course

Chronic is defined as viraemia and hepatic inflammation continuing for > 6 months

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25
Q

what

A
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26
Q

Define Hep D?

A

a defective virus, that may only co-infect with HBV or superinfect people who are already carriers of HBV – D is Dependent

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27
Q

describe the transmission of hep B and hep D?

A

sexual contact, blood and vertical transmission (from mother to baby)

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28
Q

what are the risk factors for Hep B and Hep D?:

A

IV drug use

Unscreened blood and blood products inc haemodialysis

Infants of HBeAg/HBsAg-positive mothers

Sexual contact with HBV carriers

Younger individuals (particularly babies) are more likely to become chronic carriers

Genetic factors are associated with varying rates of viral clearance

29
Q

what type of virus is HBV?

A

enveloped, partially double stranded DNA virus

30
Q

What type of virus if HDV

A

HDV is a single-stranded RNA virus coated with HBsAg

31
Q

What are the various viral proteins produced by Hep B?

A

Core antigen (HBcAg)

Surface antigen (HBsAg)

e antigen (HBeAg)

32
Q

describe the histology of Hep B?

A

mild to severe inflammation and changes to cirrhosis

33
Q

outline the aetiology of Hep B and Hep D?

A

HBV is an enveloped, partially double-stranded DNA virus

Transmission: sexual contact, blood and vertical transmission (from mother to baby)

Various viral proteins are produced such as:

Core antigen (HBcAg)

Surface antigen (HBsAg)

e antigen (HBeAg)

This is a marker of high infectivity

HDV is a single-stranded RNA virus coated with HBsAg

Antibody and cell-mediated immune response to viral replication leads to liver inflammation and hepatocyte necrosis

34
Q

what are the risk factors for Hep B and Hep D?

A

IV drug use

Unscreened blood and blood products inc haemodialysis

Infants of HBeAg/HBsAg-positive mothers

Sexual contact with HBV carriers

Younger individuals (particularly babies) are more likely to become chronic carriers

Genetic factors are associated with varying rates of viral clearance

35
Q

summarise the epidemiology of viral hepatitis?

A

Common

1-2 million deaths annually

Common in Southeast Asia, Africa and Mediterranean countries

HDV is also found worldwide

36
Q

what is the incubation period of viral hepatitis?

A

3-6 months

6 months in chronic carriers

37
Q

what are the presenting symptoms of Hep B and Hep D?

A

Most children have an asymptomatic acute infection and 50% of adults have an asymptomatic acute infection (esp if they have HIV)

1-2 week prodrome consisting of:

  • Malaise
  • Headache
  • Anorexia
  • Nausea and vomiting
  • Diarrhoea
  • RUQ pain
  • Serum-sickness type illness may develop (e.g. fever, arthralgia, polyarthritis, urticaria, maculopapular rash)

Jaundice then develops with dark urine and pale stools

Recovery usually within 4-8 weeks

1% develop fulminant liver failure

Chronic carriage may be diagnosed after routine LFT testing or if cirrhosis or decompensation develops

38
Q

what are the signs of chronic Hep B infection?

A

Jaundice

Pyrexia

Tender hepatomegaly

Splenomegaly

Cervical lymphadneopathy (in 10-20% of patients)

Occasionally: urticaria and maculopapular rash

39
Q

what are the signs of chronic Hep B?

A

May be no findings

May have signs of chronic liver disease or decompensation

40
Q

describe the viral serology?

A
41
Q

describe the viral serology of acute HBV?

A

HBsAg positive

IgM anti-HBcAg

+/- HbEAg - if this is negative it reduces the likelyhood of transmission from mum to baby

42
Q

what is the viral serology for chronic Hep B?

A

HBsAg positive

IgG anti-HBcAg

+/- HBeAg (correlates with severity)

43
Q

describe serology for HBV cleared?

A

Anti-HBsAg antibody positive

IgG anti-HBcAg

44
Q

describe the serology of HBV that has been vaccinated against?

A

Anti-HBsAg antibody positive

45
Q

Describe the serology of HDV infection?

A

Detected by IgM or IgG against HDV

PCR is used for detection of HDV

46
Q

summarise serology for Hep B infection?

A
47
Q

what are the appropriate investigations for Hep B and what are the results?

A

viral serology

LFTs

  • High: AST, ALT, ALP, bilirubin
  • Also do a coag screen with baseline liver USS

FBC

  • Microcytic anaemia (indicative of portal HT)
  • Thrombocytopenia (indicative of portal HT)

Clotting

  • High PT (in severe disease)

TO CONSIDER: Liver Biopsy – percutaneous or transjugular if clotting is deranged or ascites peresent

48
Q

describe the prevention of Hep B?

A

blood screening, safe sex, instrument sterilisation

49
Q

what are the possible complications of Hep B?

A

1% get fulminant hepatic failure

Chronic HBV infection (10% of adults, much higher in neonates)

Cirrhosis

HCC

Extrahepatic immune complex disorders (e.g. glomerulonephritis, polyarteritis nodosa)

Superinfection with HDV may lead to acute liver failure or more rapidly progressive disease

50
Q

summarise the prognosis of Hep B?

A
51
Q

describe the management of acute hep B?

A

Symptomatic treatment (antipyretics, antiemetics and cholestyramine) and bed rest

Nucleoside/nucleotide analogues (entecavir OR tenofovir)

Notifiable disease - trace sexual and needle sharing contacts and offer a vaccination against HBV

52
Q

outline the management of chronic Hep B?

A

1st Line: Nucleoside/nucleotide analogues (entecavir OR tenofovir)

2nd Line OR + if coninfected by HepD: Interferon alpha (standard or pegylated – pegylated has inc half life)

  • Cytokine which augments natural antiviral mechanisms
  • Side-effects: flu-like symptoms such as fever, chills, myalgia, headaches, bone marrow suppression and depression – 5-10% discontinue
  • Signs of good response to interferon: high serum transminases, low HBV DNA, active histological changes, absence of complicating disease
  • Usually on these for life
53
Q

describe the passive immunisation of Hep B?

A

Hepatitis B immunoglobulin following acute exposure and to neonates born to HBeAg-positive mothers (in addition to active immunisation)

54
Q

Describe the active immunisation of Hep B?

A

Recombinant HBsAg vaccine for individuals at risk and neonates born to HBV +ve mothers

Immunisation against HBV protects against HDV

55
Q

define Hep C?

A

Hepatitis caused by infection with hepatitis C virus (HCV), often following a chronic course (in 80% of cases)

56
Q

describe the transmission of HCV?

A

PARENTERAL

Sexual transmission

Vertical transmission

57
Q

What type of virus of Hep C?

A

HCV is a small, enveloped, single-stranded RNA virus

RNA viruses have poor fidelity of replication and mutation rates are high - so, there are lots of HCV genotypes

58
Q

what are the risk factors for Hep C?

A

Recipients of blood and blood products

IV drug users

Non-sterile acupuncture

Tattooing

Haemodialysis

Health care workers

59
Q

describe the pathogenesis of Hep C?

A

The virus is not thought to be directly hepatotoxic

It is the humoral and cell-mediated responses to the viral infection that leads to hepatic inflammation and necrosis

60
Q

describe liver biospy of hep C?

A

Chronic hepatitis

Lymphoid follicles in portal tracts

Fatty change

Cirrhosis may be present

61
Q

Summarise the epidemiology of Hep C?

A

COMMON

Different genotypes of HCV have different geographical prevalence

62
Q

what are the presenting symptoms of Hep C?

A

90% of acute infections are ASYMPTOMATIC

10% become jaundiced with mild flu-like illness

May be diagnosed after incidental abnormal LFT or in older patients with complications of cirrhosis

63
Q

what are the signs of Hep C on physical examination?

A

May be NO SIGNS

There may be signs of chronic liver disease (if long-standing HCV infection) e.g. jaundice, ascites

May be signs of hepatic encephalopathy if advanced CLD

Extra-hepatic manifestations (rare) include:

  • Skin rash
  • Renal dysfunction (due to glomerulonephritis)
64
Q

what are the appropriate investigations for Hep C and describe the results?

A

HCV Serology

  • Anti-HCV antibodies - IgM (acute) or IgG (past exposure or chronic)

Reverse-transcriptase PCR

  • Allows detection and genotyping of HCV
  • Used to confirm antibody testing or if suspected in pt but serology negative

LFT

  • Acute infection: High ALT, AST and bilirubin
  • Chronic infection: 2-8 x elevation of AST + ALT (often fluctuates over time)
65
Q

what investigations would you consider for Hep C?

A

Liver Biopsy

  • Assess the degree of inflammation and liver damage (NOT for diagnosis)
  • NOTE: transaminase (AST and ALT) levels bear little correlation to histological changes
  • Useful for diagnosing cirrhosis – as these pts require monitoring for HCC
66
Q

describe the prevention management for Hep C?

A

Screen blood, blood products and organ donors

Needle exchange schemes for IV drug users

Instrument sterilisation

NO VACCINE AVAILABLE

67
Q

describe the medical management for Hep C?

A

Acute - mainly supportive (antipyretics, antiemetics, cholestyramine)

Chronic

  • Antivirals are now curative: NS5A inhibitors
  • Pegylated interferon-a
  • AND
  • Ribavarin

Monitor HCV viral load after 12 weeks to determine treatment efficacy

HCV RNA level measured by polymerase chain reaction on EDTA blood sample is used to monitor response to treatment. Undetectable HCV RNA at 48 weeks after completion of treatment defines cure (known as ‘sustained virological response’ or SVR)

Regular US of the liver may be needed if the patient has cirrhosis

There is no post exposure prophylaxis available for hepatitis C, unlike HIV.

68
Q

what are the possible complications of Hep C?

A

Fulminant hepatic failure

Chronic carriage of HCV

Hepatocellular carcinoma

Less common: porphyria cutanea tarda, cryoglobulinaemia, glomerulonephritis

69
Q

summarise the prognosis of Hep C?

A

80% of exposed will progress to chronic carriage

Of these, 20-30% will develop cirrhosis over 10-20 years

GI (51 decks)

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