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GI Pathology > 9. Liver Symposium: Viral liver disease/alcohol & transplantation issues > Flashcards

9. Liver Symposium: Viral liver disease/alcohol & transplantation issues Flashcards

1
Q

Which viruses cause hepatitis?

A

Five main: Hepatitis A,B,C,D and E

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2
Q

Hepatitis viruses:

  1. Which ones are enteric viruses?
  2. Which ones are parenteral viruses?
  3. Which ones cause self limiting acute infections?
  4. Which ones cause chronic disease?
A
  1. Hepatitis A and E
  2. Hepatitis B, C and D
  3. Hepatitis A and E
  4. Hepatitis B, C and D
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3
Q

Describe clinical course of Hepatitis A virus?

A

Initial rise in IgM and ALT.
ALT peaks at 4 weeks after infection and returns to normal around 8 weeks.
IgM peak around 4 weeks after infection and then continues to fall.
IgG rises linearly after initial infection.

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4
Q

Hepatitis A:

  1. T/F: only occurs in epidemic form.
  2. How is it transmitted?
  3. Which age group is the infection more common in?
  4. T/F: Asymptomatic cases very common.
  5. How is it diagnosed?
A
  1. False. Occurs sporadically or in epidemic form.
  2. Through faecal-oral route, sexually, or through blood
  3. 5-14 year olds.
  4. True
  5. Acute disease diagnosed by IgM antibodies.
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5
Q

Which group of people are immunised against Hepatitis A virus?

A
  • Travellers
  • Patients with chronic liver disease: IDU (IV drug users) (especially with HCV or HBV)
  • Haemophiliacs
  • Occupational exposure: lab workers
  • Men who have sex with men (MSM)
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6
Q

Name different types of Hepatitis B virus antigens and comment on what they indicate in respect to viral replication.

A
  1. Hepatitis surface antigen (HBsAg): Presence of virus
  2. Hepatitis e antigen (HBeAg): Active replication. HBeAg is a protein formed via specific self-cleavage of the pre-core/core gene product, which is secreted separately by the cell.
  3. Hepatitis core antigen (HBcAg): Active replication (not detected in blood). HBcAg contains incomplete double-stranded circular DNA and DNA polymerase/reverse transcriptase.
  4. HBV DNA: Active replication
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7
Q

HBV antibody:

  1. Which antibody indicates immunity from HBV?
  2. Which antibody indicates acute infection?
  3. Which antibody indicates chronic infection/ exposure?
  4. Which antibody indicates inactive virus?
A
  1. Anti-HBs indicate protection could be due to previous exposure or immunisation.
  2. IgM anti-HBc
  3. IgG anti-HBc
  4. Anti-HBe
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8
Q

Approach to HBV infection:

  1. Which antigen would you test for?
  2. What does negative result for the above antigen indicate?
  3. What does positive result for the above antigen indicate?
  4. What would you do if positive for above antigen?
A
  1. HBsAg
  2. No active infection so can initiate or complete vaccination series.
  3. Chronic or active infection.
  4. Look for clinical evidence of active or epidemiologic link to identified case. If there is evidence then check for IgM anti-HBc, if positive then the patient has acute infection. If there is no evidence of IgM anti-HBc is negative then the patient might have chronic infection so evaluate for ongoing monitoring and treatment.
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9
Q

Outline natural history of chronic hepatitis B.

A

Normal liver > chronic hepatitis B > either no further progression or it progresses to cirrhosis which can the lead to ESLD (end-stage liver disease) or HCC (hepatocellular carcinoma) and then ESLD.

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10
Q

What are the treatment options for Hep B infection? Comment on advantages and disadvantages.

A
  1. Pegylated Interferon
  2. Oral Antiviral Drugs:
    - Lamivudine: good clinical data especially in ESLD and pregnant patients. But high rate of resistance.
    - Adefovir: studied in ESLD patients and Lamivudine failures. But lower potency. Resistance = moderate.
    - Entecavir: High potency and genetic barrier to resistance but not in Lamivudine-resistant HBV patients
    - Telbivudine: Moderate potency, cat B in pregnancy. Not active in Lamivudine-resistant HBV patients.
    - Tenofovir: Moderate potency, cat B in pregnancy, low resistance, studied in HIV-coinfected. But renal toxicity.
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11
Q

Hepatitis C virus:

  1. T/F: always causes acute liver failure
  2. T/F: Causes chronic HCV infection
  3. T/F: most symptomatic before developing cirrhosis
  4. T/F: May have normal LFTs.
  5. T/F: It is a single-stranded RNA virus.
A
  1. False. Rarely causes acute liver failure
  2. True
  3. False. Most asymptomatic until cirrhotic
  4. True
  5. True
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12
Q

Outline natural history of Hepatitis C virus.

A

Exposure (acute phase) > resolved or chronic (majority). Chronic > majority are stable, in 20% cases = cirrhosis.
Cirrhosis > slowly progressive (majority) or leads to HCC.
HIV and alcohol increases chances of progression to HCC/death.

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13
Q

Hepatitis C virus:

  1. How is it diagnosed?
  2. How is it treated?
A
  1. Check for HCV antibody in the serum using ELISA.
  2. Many drugs available. Treatment changed from interferon-based regimes to all-oral combination regimes using directly acting antiviral agents.
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14
Q

Hepatitis D virus/Delta:

  1. T/F: HDV is a small RNA virus enveloped by HBsAg.
  2. T/F HDV codes for it’s own protein coat.
  3. T/F: May present with co-infection or super-infection with HBV.
  4. T/F: Very resistant to treatment.
  5. How is it transmitted?
A
  1. True.
  2. False. Does not code for its own protein coat.
  3. True.
  4. True.
  5. Transmission similar to HBV. Vertical transmission from mother to child. Horizontal transmission occurs via minor abrasions or close contact with other children. Also transmitted via blood or sexually.
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15
Q

Hepatitis E virus:

  1. T/F: Commonest cause of acute hepatitis in Grampian.
  2. T/F: Self-limiting, no long-term sequelae
  3. Are there any effective treatments or vaccines?
  4. T/F: causes fulminant hepatic failure in pregnant women.
A
  1. True
  2. True
  3. No effective vaccine. No specific treatment available.
  4. True. Fulminant hepatic failure = development of severe liver injury with impaired synthetic capacity and encephalopathy in patients with previous normal liver.
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16
Q

Name other viruses that can cause viral hepatitis.

A
  1. Hepatitis F: variant of HBV?
  2. Hepatitis G: related to HCV
  3. Hepatitis GB: cause liver disease?
  4. EBV and CMV: generally cause mildly deranged LFTs only in immunocompromised hosts.
  5. Herpes simplex: Rare severe acute hepatitis
17
Q

What 3 entities does Non-alcoholic fatty liver disease encompass?

A

Simple steatosis (abnormal retention of fat)
Non-alcoholic steatohepatitis (fat + inflammation)
Fibrosis and cirrhosis

18
Q

What is Non-alcoholic fatty liver disease associated with? Name other risk factors as well.

A
  • Diabetes mellitus
  • Obesity
  • Hypertriglyceridemia
  • Hypertension
  • Other risk factors: Age, Ethnicity (e.g. Hispanics), Genetic factors (e.g. PNPLA3 gene)
19
Q

Outline natural history of Non-alcoholic fatty liver disease.

A

Normal liver > steatosis > non-alcoholic steatohepatitis +/- fibrosis > cirrhosis.
Throughout there is increased CV risk.

20
Q

How is Non-alcoholic fatty liver disease diagnosed?

A
  • Biochemical tests: AST/ALT ratio
  • Enhanced liver fibrosis panel (ELF) (hyaluronic acid, TIMP-1, and PIIINP)
  • Cytokeratin-18
  • Ultrasound
  • Fibroscan
  • MR/CT
  • MR Spectroscopy: Actually quantify fat
  • Liver biopsy
21
Q

What is NAFLD score?

A

A scoring system for the patients who are believed to have NAFLD. Patients are classed as high risk for 3 or more following categories:

  • Age >45
  • Diabetic or impaired fasting glucose (IFG) >/or equal to 7mmol/L
  • BMI >30
  • AST: ALT ratio >1 (AST>ALT)
  • Platelet count low (<150)
  • Albumin low (<34)
22
Q

What is the treatment for Non-alcoholic fatty liver disease?

A
  • Diet and weight reduction
  • Exercise
  • Insulin sensitizers e.g. Metformin, Pioglitazone
  • Glucagon-like peptide-1 (GLP-1) analogues e.g. Liraglutide
  • Farnesoid X nuclear receptor ligand e.g. Obeticholic acid
  • Vitamin E (antioxidant that improves steatohepatitis)
  • Weight reduction surgeries
23
Q

List autoimmune liver diseases.

A 
Autoimmune hepatitis
Primary biliary cholangitis (PBC)
Primary sclerosing cholangitis (PSC)
Overlap syndromes
Autoimmune cholangiopathy
IgG 4 disease
24
Q

Autoimmune hepatitis:

  1. T/F: affects more females than males.
  2. Which immunoglobulin is elevated?
  3. Name 3 types of autoimmune hepatitis and the antibodies associated with?
  4. How is it diagnosed?
  5. How is it treated?
A
  1. True
  2. IgG is elevated.
  3. Type 1 with anti-nuclear (ANA) and anti-smooth muscle antibodies (SMA).
    Type 2 with anti-liver/kidney microsomal (anti-LKM1) antibodies.
    Type 3 with anti-soluble liver antigen (SLA) antibodies.
  4. Liver biopsy is diagnostic.
  5. Responds well to steroids. Long term azathioprine
25
Q

Primary biliary cholangitis (PBC):

  1. T/F: affects more females than males.
  2. Which immunoglobulin is elevated?
  3. T/F: Anti-mitochondrial antibody positive
  4. What are the symptoms of PBC?
  5. How is it treated?
  6. T/F: Intrahepatic bile duct involved.
A
  1. True
  2. IgM is elevated.
  3. True
  4. Pruritus and fatigue
  5. UDCA (Ursodeoxycholic acid) treatment of choice: increases rate of bile flow from the hepatocytes so thereby combats cholestasis and dilutes toxic bile acids in bile.
  6. True. Bile ducts are destroyed that leads to retention of toxic bile acids.
26
Q

Primary sclerosing cholangitis:

  1. T/F: affects more females than males.
  2. Which antibody is it positive for?
  3. Which ducts are involved?
  4. How is it diagnosed?
  5. T/F: associated with strictures and recurrent cholangitis and jaundice.
  6. How is it treated?
A
  1. False. It is male dominant.
  2. perinuclear anti-neutrophil cytoplasmic antibodies (pANCA) positive.
  3. Intra and extrahepatic bile ducts involved
  4. MRCP test of choice.
  5. True
  6. Liver transplant, biliary stents.
27
Q

Which patients normally get liver transplant?

A
  • Chronic liver disease with poor predicted survival
  • Chronic liver disease with associated poor quality of life
  • Hepatocellular carcinoma
  • Acute liver failure
  • Genetic diseases e.g. primary oxaluria, tyrosemia
28
Q

List contraindications for transplant.

A
  • Active extrahepatic malignancy
  • Hepatic malignancy with macrovascular or diffuse tumour invasion
  • Active and uncontrolled infection outside of the hepatobiliary system
  • Active substance or alcohol abuse
  • Severe cardiopulmonary or other comorbid conditions
  • Psychosocial factors that would likely preclude recovery after transplantation
  • Technical and/or anatomical barriers
  • Brain death
29
Q

How is transplantation prioritised in cirrhosis?

A

Based on:

  • Child’s Pugh scoring A, B and C
  • MELD score ( Bilirubin, Creatinine and INR)
  • UKELD( Bilirubin, Sodium, Creatinine and INR)
30
Q
  1. What kind of surgery is performed?

2. What is the post-operative treatment?

A
  1. orthotopic (previous liver is removed and the transplant is placed at that location in the body)
  2. Post operative ICU care
    - Multidisciplinary care
    - Prophylactic antibiotics and anti-fungal drugs
    - Anti-rejection drugs: Steroids, Azathioprine, Tacrolimus/Cyclosporine

GI Pathology (20 decks)

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