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Flashcards in Viral Hepatitides Deck (56)
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1

How is Hep A spread

Faeco-oral route

2

Where are there high rates of Hep A

In communities with low standards of sanitation

3

Where are there outbreaks of Hep A

Daycare centres
association with sewage contaminated shellfish
Homosexual men
IV drug abusers

4

What is the incubation period for Hep A

15-50 days

5

What are the clinical features in symptomatic individuals

Acute febrile illness with jaundice
anorexia
nausea
abdominal discomfort
malaise
dark urine

6

What happens to the severity of Hep A as age increases

The severity increases

7

How is Hep A diagnosed

It relies on the detection of serum antibodies to HAV

8

What does high IgM indicate

Recent infection

9

What is the management of Hep A

Largely symptomatic
Vaccination is effective in preventing infection and disease

10

What is the vaccine for Hep A

Inactivated hepatitis A vaccines

11

Who is the Hep A vaccine recommended for

Those at high risk of infection
Those infected with Hep B and C
Travellers to countries with high rates of Hep A
Employees of early childhood services
Healthcare workers exposed to faeces
Men who have sex with men
Injecting drug users

12

How many people are estimated to be carriers of the Hep B virus

400 million worldwide

13

What are the risk factors for HBV infection

Transfusion
Needle sharing
sexual transmission
perinatal transmission
men who have sex with men
promiscuous heterosexuals
immunosuppressed patients
patients on haemodialysis
transplantation
health care transmission

14

How many genotypes are recognised for Hep B

8

15

What immune response is initiated in Hep B

Adaptive

16

What are the clinical manifestations of HBV in the acute phase

Most are asymptomatic or demonstrate mild fatigue

17

What are the clinical manifestations of HBV in the chronic phase

Some are asymptomatic,
Abnormal LFTs
Cirrhosis
HCC

18

What does the severity of the acute disease determine

The progression to chronicity

19

What are the 3 phases of Hep B

1. Replicative, during which aminotransferases are largely normal and there is little liver damage
2. Inflammatory - where the aminotransferases become elevated, liver biopsy shows chronic hepatitis and viral replication declines
3. Patients may enter the inactive phase where viral replication has stopped, the amino transferases normalise and there is no ongoing liver inflammation

20

How is a diagnosis of Hep B made

The hepatitis B surface antigen (HBsAg) must be positive for 6 months

21

What does the level of HBV-DNA correlate with

The amount of virus in the circulation and has prognostic implications

22

What is the management for Hep B

Prevention is the cornerstone!
Safe sex
Avoidance of sharing of IV drug use
Use of gloves
Careful cleaning of blood or body fluid spills
Disposal or adequate sterilisation of surgical instruments (tattoo and piercing)
Careful disposal of sharps
Use of goggle where there is a risk of infected material splashing into the eye
Immunisation

23

Who is the Hep B vaccination recommended for in the UK

Those exposed to blood or blood born products
Travellers who plan to spend long periods in high prevalence areas or with pre-existing medical conditions that place them at a higher risk of requiring medical procedures abroad
Haemophiliacs
Prisoners and prison officers

24

What is the treatment for Hep B

Oral nucleoside and nucleotide analogues (lamivudine)
IFN-alpha: used for a finite period with durable response in a subset of patients

25

What is Hep D

A subviral agent, dependent for its life cycle on HBV

26

What is it called when an individual receives both viruses

Co infection

27

What is superinfection

When a person chronically infected with HBV then contracts HDV

28

What is a requirement for the replication of HDV

The presence of HBV

29

What is the association with liver damage and HDV infection

Chronic HDV results in much more rapid progressing liver damage

30

What are the investigations for HDV

Should be considered in patients diagnosed with HBV.
HDAg-S is produced early and is required for viral replication
HDA-L is produced later and is an inhibitor of viral replication but is required for viral particle assembly