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Gastrointestinal 2 > Viral Hepatitis > Flashcards

Viral Hepatitis Flashcards

1
Q

What is the commonest cause of hepatocellular carcinoma?

A

HepB

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2
Q

What forms of hepatitis are transmitted through the faecal-oral route?

A

Hepatitis A
Hepatitis E

Think FAECAL

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3
Q

Which forms of forms of hepatitis have a bloodborne vertical transmission?

A

BCD

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4
Q

Which of the hepatitis viruses lead to chronic infection?

A

BCD

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5
Q

What is the incubation time of the BCD hepatitis viruses?

A

60-120

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6
Q

What are the viral classifications of the hepatitis viruses?

A

A

B

C

D

E

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7
Q

What are the clinical outcomes for the chronic forms of hepatitis?

A

Hepatitis B and C - hepatocellular carcinoma and cirrhosis.

Hepatitis D - co-infection

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8
Q

Co-infection

A

Coinfection is the simultaneous infection of a host by multiple pathogen species. In virology, coinfection includes simultaneous infection of a single cell by two or more virus particles.

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9
Q

Table of Hepatitis viruses

A
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10
Q

All of the hepatitis viruses are RNA except…

A

Hepatitis B which is DNA

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11
Q

Hepatits A summary

A
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12
Q

How is spread of HAV prevented?

A

Good hygeine

Vaccines

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13
Q

Who are at risk groups of HAV?

A

Travellers, MSM, patients with haemophilia, drug users, chronic liver disease, occupational risk.

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14
Q

HEV affects who and where?

A
  • Endemic in Asia, Africa, Central America and Middle East.
  • Transmission: Faecal-oral route, travellers, needle-sharers.
  • High mortality in pregnancy (25%).
  • Most as a result of zoonotic infection (Primary hosts are pigs).
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15
Q

How do patients with HEV present?

A

Most patients are asymptomatic and present with mild and persistent LFT abnormalities.

However Immunosuppressed patients can progress to chronic hepatitis.

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16
Q

Who are classed as immunosuppressed groups?

A

Immunosuppressed groups:

  • Solid organ transplant recipients. 50–66% of HEV-infected organ transplant recipients develop chronic hepatitis.
  • Patients with haematological disorders.
  • Individuals living with HIV.
  • Patients with rheumatic disorders receiving heavy immunosuppression.
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17
Q

What are the symptoms of hepatitis A?

A

Fever, malaise, nausea, arthralgia, then jaundice, hepatosplenomegaly, adenopathy.

Increased ALT and AST.

IgM increases from day 25 indicating infection.

Note: HepE has a very similar presentation.

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18
Q

What type of virus is HBV and where does it replicate?

A

DNA virus replicates in liver cells.

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19
Q

How does HBV spread?

A

Blood products, IV drug users, sexual contact, carers and healthworkers also at risk, heamophiliacs, homosexuals.

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20
Q

What are the clinical signs and symptoms of HBV?

A

Acute Hepatitis.

Flu like symptoms.

Can cause RUQ discomfort.

Jaundice.

Arthralgia and utricaria.

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21
Q

What do lab results show in HBV?

A

Raised AST and ALT

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22
Q

What does raised ALT indicate?

A

Raised ALT levels are an early sign of fatty liver disease. Viral hepatitis, side effects from prescription drugs and genetic or autoimmune conditions that affect the liver can also cause ALT levels to rise.

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23
Q

What do raised AST levels indicate?

A

High levels of AST in the blood may indicate hepatitis, cirrhosis, mononucleosis, or other liver diseases. High AST levels can also indicate heart problems or pancreatitis. If your results are not in the normal range, it doesn’t necessarily mean that you have a medical condition needing treatment.

AST levels increase when there’s damage to the tissues and cells where the enzyme is found.

24
Q

Hepatitis Antigens:

A
  • HBsAg – Surface antigen indicating infection.
  • Anti-HBs – Indicates vaccination and thus immunity.
  • Anti-HBc- Previous infection.
  • HBeAg – Present 1-3months after acute infection and indicates high infectivity.
  • HBeAb – Low infectivity.
25
Q

What do the presence of Anti-HBs antibodies indicate?

A

Anti-HBs – Indicates vaccination and thus immunity.

26
Q

What does the present of HBsAg indicate?

A

HBsAg - is the surface antigen indicating current infection.

27
Q

What does the presence of HBeAg indicate?

A

HBeAg is present 1-3 months after acute illness and indicates high infectivity.

28
Q

What does Anti-HBc in blood indicate?

A

Antibodies showing a previous HBV infection.

29
Q

What does the presence of HBeAb indicate?

A

Low infectivity.

30
Q

What are the goals and endpoint of HBV treatment?

A
  • Improve survival and quality of life by preventing disease progression and HCC.
  • Prevent mother-to-child transmission, hepatitis B reactivation, and prevent and treat HBV-associated extrahepatic manifestation.
  • Main Endpoint: Induction of long-term suppression of HBV DNA.
  • Valuable endpoint: Induction of HBeAg loss (± anti-HBe seroconversion) in HBeAg-positive patients with chronic hepatitis B.
  • Additional Endpoint: ALT normalization (biochemical response)
  • Optimal endpoint: HBsAg loss (± anti-HBs seroconversion)
31
Q

How is hepatitis B treated?

A

If you have only had the infection for a few weeks or months (acute hepatitis B), you may only need treatment to relieve your symptoms while your body fights off the infection.

32
Q

Summary of Hepatitis A, C and E

A
33
Q

What does the presence of IgM vs IgG antibodies indicate in hepatitis infections?

A

IgM indicates current infection.

IgG indicates patient is recovering from infection / may be vaccinated.

34
Q

HCV is transmitted how?

A

Childbirth and sex.

35
Q

Breakdown HBsAg

A

HBsAg

Hepatitis B surface Antigen

36
Q

How is chronic viral hepatitis defined?

A

Presence of HBsAg after 6 months.

37
Q

What is the treatment for Hepatitis B?

A

Treatment for chronic hepatitis B may include: Antiviral medications.

Several antiviral medications:

Entecavir (Baraclude), tenofovir (Viread), lamivudine (Epivir), adefovir (Hepsera) and telbivudine (Tyzeka)

These medications can help fight the virus and slow its ability to damage your liver.

38
Q

How is hepatitis B infection approached in pregnancy?

A
39
Q

Vaccinate high risk groups of people with hepatitis and sexual partners etc.

A

Vaccinate high risk groups of people with hepatitis and sexual partners etc.

40
Q

What is unique about HDV?

A

HDV can only infect people with HBV.

41
Q

How is HDV treated and transmitted?

A

Transmitted by same routes as HBV- esp in IVDUs. Treatment of HBV will treat HDV.

No vaccine available, but HBV vaccine will prevent HBV and thus HDV.

PEG IFN for 48 weeks mainstay of treatment.

42
Q

Should be suspected in patients with HBV with particularly severe persistent hepatitis, esp. with suppressed HBV DNA.

How is HDV confirmed?

A

Should be confirmed by HDV RNA.

43
Q

PEG IFN

A

They are used to treat both hepatitis B, hepatitis C and multiple sclerosis. Pegylated interferon is contraindicated in patients with hyperbilirubinaemia.

44
Q

HCV Summary:

A

RNA virus

Bloodborne transmission

Can be asymptomatic . Chronic infection leads to cirrhosis and cancer.

Detection of hepatitis C antibodies suggests infection at some time.

Chronic infection suggested by HCV RNA (viral load).

45
Q

Prognosis of HCV

A
  • 20% clear the virus.
  • 80% develop chronic hepatitis.
  • 10-20% have jaundice or flu like illness.
  • 20% develop cirrhosis over 20 years.
46
Q

Hepatitis with a vowel comes from the bowel!

A

HAV HEV

47
Q

HIV co-infection

A

Co-infection with hepatitis C:

When people have both HIV and hepatitis C, this is often described as co-infection. The liver has an essential role in processing medicines used to treat HIV and other conditions.

48
Q

Hepatitis can lead to liver cirrhosis - how can this develop into hepatic encephalopathy?

A

Hepatic encephalopathy is largely believed to occur from accumulation of ammonia in the blood stream due to the livers decreased ability to detoxify ammonia that is produced and transported from the gastrointestinal tract.

49
Q

What are the features of hepatic encephalopathy?

A
  • confusion, altered GCS
  • asterix: ‘liver flap’, arrhythmic negative myoclonus with a frequency of 3-5 Hz
  • constructional apraxia: inability to draw a 5-pointed star
  • triphasic slow waves on EEG
  • raised ammonia level (not commonly measured anymore)
50
Q

What is the management of hepatic encephalopathy?

A

Management

  • treat any underlying precipitating cause
  • NICE recommend lactulose first-line, with the addition of rifaximin for the secondary prophylaxis of hepatic encephalopathy
  • lactulose is thought to work by promoting the excretion of ammonia and increasing the metabolism of ammonia by gut bacteria
  • antibiotics such as rifaximin are thought to modulate the gut flora resulting in decreased ammonia production
  • other options include embolisation of portosystemic shunts and liver transplantation in selected patients
51
Q

Causes of hepatitis:

A

Alcoholic hepatitis

Non alcoholic fatty liver disease

Viral hepatitis

Autoimmune hepatitis

Drug induced hepatitis (e.g. paracetamol overdose)

52
Q

What do LFT’s typically show in hepatitis?

A

Typical biochemical findings are that liver function tests become deranged with high transaminases (AST / ALT) with proportionally less of a rise in ALP. This is referred to as a “hepatitic picture”. Transaminases are liver enzymes that are released into the blood as a result of inflammation of the liver cells. Bilirubin can also rise as a result of inflammation of the liver cells. High bilirubin causes jaundice.

53
Q

Management of Viral Hepatitis:

A

Have a low threshold for screening patients that are at risk of hepatitis B.

Screen for other blood born viruses (hepatitis A and B and HIV) and other sexually transmitted diseases

Refer to gastroenterology, hepatology or infectious diseases for specialist management

Notify Public Health (it is a notifiable disease)

Stop smoking and alcohol

Education about reducing transmission and informing potential at risk contacts

Testing for complications: FibroScan for cirrhosis and ultrasound for hepatocellular carcinoma

Antiviral medication can be used to slow the progression of the disease and reduce infectivity

Liver transplantation for end-stage liver disease

54
Q

Summary of Autoimmune hepatitis

A

Autoimmune hepatitis is a rare cause of chronic hepatitis. We are not sure of the exact cause, however it could be associated with a genetic predisposition and triggered by environmental factors such as a viral infection that causes a T cell-mediated response against the liver cells. This is where the T cells of the immune system recognise the liver cells as being harmful and alert the rest of the immune system to attack these cells.

There are two types that have different ages of onset and autoantibodies:

Type 1: occurs in adults

Type 2: occurs in children

Type 1 typically affects women in their late forties or fifties. It presents around or after the menopause with fatigue and features of liver disease on examination. It takes a less acute course than type 2.

In type 2, patients in their teenage or early twenties present with acute hepatitis with high transaminases and jaundice.

Investigations will show raised transaminases (ALT and AST), IgG levels and it is associated with many autoantibodies.

55
Q

What antibodies are present in adults with Type 1 autoimmune hepatitis?

A

Anti-nuclear antibodies (ANA)

Anti-smooth muscle antibodies (anti-actin)

Anti-soluble liver antigen (anti-SLA/LP)

56
Q

How is autoimmune hepatitis treated?

A

Treatment is with high dose steroids (prednisolone) that are tapered over time as other immunosuppressants, particularly azathioprine, are introduced. Immunosuppressant treatment is usually successful in inducing remission however it is usually required life long. Liver transplant may be required in end stage liver disease, however the autoimmune hepatitis can recur in transplanted livers.

Gastrointestinal 2 (24 decks)

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