Hepatitis viruses Flashcards

1. To recognise the sings and symptoms of viral hepatitis 2. To comprehend the dental implications of hepatitis viral infection 3. To explain the dental relevance of viral hepatitis and the need for precautionary measures during management in the dental surgery

1
Q

Outline liver functions

A
  • Metabolism: amino acids, proteins, lipids, carbohydrate
  • Controls the level of blood glucose through glycogen
  • Synthesis: albumin, a/B-globulins, clotting factors II, V, IX, X (II, VII, IX, X = vitamin K dependant), triglycerides, cholesterol and bile acid
  • Metabolism and detoxification of drugs, hormones, vitamins
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2
Q

What is the dental relevance of liver health

A
  • Metabolism and detoxification of drugs
  • Wound healing and haemostasis post extraction
  • Viral liver infections may put patients and dental team at risk of cross infection
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3
Q

What is jaundice

A

It is caused when a pathological process interferes with metabolism and excretion of bilirubin, and the problem can be pre-hepatic, hepatic or post-hepatic

It causes yellowing pigmentation of the skin, conjunctiva and mucous membranes

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4
Q

What is pre-hepatic jaundice

A

Due to haemolytic anaemia (sickle cell anaemia, thalassemia), Gilbert’s syndrome (genetic disorder of bilirubin metabolism) and malaria

This occurs prior to the liver

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5
Q

What is hepatic jaundice

A

Occurring within the liver due to acute/chronic viral hepatitis, leptospirosis (parasite), hepatotoxicity, cirrhosis, drug induced hepatitis or alcoholic liver disease

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6
Q

What is post-hepatic jaundice

A

Occurring after the conjugation of bilirubin in the liver due to gallstones, pancreatic cancer, liver flukes, stricture of bile duct, obstruction of biliary tree

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7
Q

Outline the structure of hepatitis B virus

A
  • Enveloped DNA virus of hepadnaviridae
  • Antigens = HBsAg protein, glycoproteins, cellular lipid
  • Core/nucleocapside contains hep B core antigen HBcAg
  • HBeAg is truncated from core polypeptide and is released from the infected liver
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8
Q

Modes of transmission for hepatitis B virus

A
  1. Virtical/ perinatal (mother to child)
  2. Sexual
  3. Transfusion of contaminated blood/ blood products
  4. IV drug users
  5. Needlestick injuries
  6. Horizontally between children in Africa
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9
Q

What are the clinical features of HBV infection

A
  1. Acute hepatitis
    - Symptomatic (jaundice, dark urine, fatigue, nausea, vomitting, right hypochondrial pain) 5-10% lead to cirrhosis)
    - Fulminant hepatic failure (rare)
  2. Chronic
    - Cirrhosis
    - Hepatocellular carcinoma
    - End stage liver disease
    - Extrahepatic manifestations (arthropathy)
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10
Q

What is the hepatitis B vaccine and how is it given

A

= HBsAg absorbed onto aluminium hydroxide adjuvant
It is prepared from yeast cells using recombinant DNA
- 3 doses are given at 0, 1 + 2 or 0, 1 + 6 months or 0, 7, 21 days
- Testing is done 1-2 months after third dose

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11
Q

What is the antibody titre of someone who is a non responder to the hepatitis B vaccine

A

<10

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12
Q

What is the antibody titre of someone who is a poor responder to the hepatitis B vaccine

A

10 - 100 = partially immune

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13
Q

What is the antibody titre of someone who is a good responder to the hepatitis B vaccine

A

> 100 = immune

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14
Q

Interpret the following data

  1. HBsAg = negative
  2. Anti-HBc = negative
  3. Anti-HBs = negative
A

This patient is susceptible to hepatitis B virus

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15
Q

Interpret the following data

  1. HBsAg = negative
  2. Anti-HBc = positive
  3. Anti-HBs = positive
A

This patient is immune due to natural infection from HBV

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16
Q

Interpret the following data

  1. HBsAg = negative
  2. Anti-HBc = negative
  3. Anti-HBs = positive
A

This patient is immune due to HBV vaccination and so they do not contain the core antigen so are only positive for the surface antigen

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17
Q

Interpret the following data

  1. HBsAg = positive
  2. Anti-HBc = positive
  3. Anti-HBs = negative
  4. IgM anti-HBc = positive
A

This patient is acutely infected (if there is high HbeAg then the person is highly infective and can pass the infection on to others)

18
Q

Interpret the following data

  1. HBsAg = positive
  2. Anti-HBc = positive
  3. Anti-HBs = negative
  4. IgM anti-HBc = negative
A

The patient is chronically infected

19
Q

Interpret the following data

  1. HBsAg = negative
  2. Anti-HBc = positive
  3. Anti-HBs = negative
A

This laboratory test is unclear and could be due to

  1. Resolved infection
  2. False positive in the laboratory result
  3. Low level chronic infection
  4. Resolving acute infection
20
Q

How is HBV infection prevented

A
  • Education for mode of transmission
  • Standard infection control procedures
  • Screening of blood products
  • Post exposure vaccination (post needle stick and sex)
  • Exposure prone procedure regulations
21
Q

With regards to HBsAg, what should health care workers be

A

Negative (if it is positive then they should be HBeAg negative and the viral load should be 10^3 genome/ml)

22
Q

How is HBV treated

A
  1. Lamivudine

2. Interferon

23
Q

What is hepatitis D virus

A

It is a defective virus whose replication requires co-infection or superinfection with HBV and it has no specific treatment

24
Q

What is co-infection

A

Simultaneous infection with HBV and HDV resulting in severe or fulminant hepatitis

25
Q

What is superinfection

A

HBsAg carriers who subsequently acquire HDV resulting in exacerbation of hepatitis

26
Q

Outline the structure of hepatitis C virus

A
  • Enveloped spherical, positive single stranded RNA virus
  • Flavivirus
  • High viral turnover and absence of proofreading results in accumulation of mutation in genome (at least 7 genotypes)
  • There are multiple closely related but distinct HCV variants so n vaccine is effective
27
Q

Describe routes of transmission for HCV

A
  1. Transfusion of contaminated blood or blood products
  2. IVDUs
  3. Nosocomial transmission (needles tick, harm-dialysis, colonoscopy)
  4. Rarely sexual transmission/mother-to-child
28
Q

Outline the clinical features of HCV infection

A
  • Acute; similar to HBV with lower transaminases
  • Fulminant; Japan
  • Chronic; fatigue, malaise, reduced QoL, cirrhosis, decompensated liver disease, hepatocellular carcinoma
  • Extrahepatic manifestations; membranous glomerulonephritis, lymphocytic sialodenitis, cryoglobulinaemia
29
Q

How is infection with HCV treated

A

Pegylated interferon and rebavirin, length of treatment depends on the HCV genotype and there is no vaccine available

30
Q

How is HCV prevented

A
  • Education on modes of transmission
  • Screening of blood and blood products
  • Standard infection control
  • Needle exchange programme
  • Post needles tick injury screening
  • No vaccination
31
Q

With regards to HCAb, what should health care workers be

A

HCAb negative (if positive, HCV RNA should be negative)

32
Q

Outline the structure of hepatitis A virus

A
  • Non-enveloped, spherical, single stranded
  • Positive sense, linear RNA virus
  • Picornavirus with genotypes I - VII
33
Q

Amongst which groups of people is the incidence of HAV infection greatest

A
  1. Children and staff in childcare facilities
  2. Patients and staff in mental health institutions
  3. Men who sex men
  4. IVDU
  5. Travellers in endemic areas (developing world)
34
Q

Describe mode of transmission of HAV

A

Food and waterborne transmission (faeco-oral route)

35
Q

Outline the clinical features of HAV infection

A
  1. Common in children
  2. Acute hepatitis
    - common with increasing age with 2-6 week incubation
    - prodromal period = headache, fever, malaise, anorexia, vomitting weightloss
    - cholestasis = dark urine, pale stools
    - jaundice, hepatomegaly, splenomegaly, spider naevi
36
Q

What are the complications of HAV infection

A
  • Prolonged cholestasis
  • Relapsing disease within 1-3 months
  • Fulminant hepatitis
  • Extrahepatic disease
  • Triggering of autoimmune chronic active hepatitis
37
Q

Outline investigation and treatments for HAV

A

Investigations = antibody; HAV IgM indicates acute phase of infection , HAV IgG indicated past infection

Treatment is supportive, no chronic infection

38
Q

How can HAV infection be prevented

A
  • passive immunisation with pooled Ig for post exposure prophylaxis
  • active immunisation for travellers to endemic areas, MSM, IVDUs, regular recipients of blood products, high risk employees, military personnel with 2 doses of vaccine
39
Q

Outline the structure of HEV

A

Spherical, non-enveloped, single strand positive sense RNA virus = calicivirus, herpevirus

40
Q

Outline the routes of transmission for HEV infection

A
  1. Waterborne
  2. Foodborne
  3. Zoonotic transmission
  4. Blood transfusion

= Endemic to southeast and sentral Asia

41
Q

Outline the clinical features of HEV infection

A

Asymptomatic, mild hepatitis, fulminant hepatitis

25% mortality rate in pregnant ladies
No chronic liver disease

42
Q

How can HEV infection be prevented

A

Improved sanitation, cooking pork properly (preventing zoonotic transmission), unsuccessful passive immunisation