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Liver Symposium Flashcards

1
Q

What are the main liver diseases?

A
  • ALCOHOL RELATED LIVER DISEASE
  • Viral Hepatitis
  • Non-alcoholic fatty liver disease
  • Autoimmune liver diseases
  • LIVER TRANSPLANTATION
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2
Q

What are the 5 main types of hepatitis?

A

ABCD and E

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3
Q

Which strains of hepatitis are enteric viruses and self limiting, acquired through food and water?

A

Enteric viruses hep A and E

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4
Q

How are Hep B,C and D caused?

A

Acquired through blood - cause chronic disease

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5
Q

Who often gets Hep A?

A

5-14 years old is the commonest group

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6
Q

Is Hep A symptomatic?

A

Asymptomatic cases are very common

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7
Q

How is acute Hepatitis A diagnosed?

A

By IgM antibodies

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8
Q

Who gets Hep A immunisation?

A
  • Travellers
  • Patients with chronic liver disease
  • IDU (especially with HCV or HBV)
  • Haemophiliacs
  • Occupational exposure
  • lab workers
  • Men who have sex with men (MSM)
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9
Q

What are the three antigens associated with HepB?

A

Surface antigen

E antigen - secreted out, it interferes with host immune system and prevents destruction by the host

Core antigen

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10
Q

What do the following substances in the blood indicate?

  • Hepatitis surface antigen (HBsAg)
  • Hepatitis e antigen (HBeAg)
  • Hepatitis core antigen (HBcAg)
  • HBV DNA Active replication
A

Surface antigen - presence of virus

E antigen - active replication

Hepatitis core antigen - Active replication (although this is not detected in blood)

HBV DNA - Active replication

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11
Q

What does the presence of the following antibodies indicate?•Anti-HBs

  • IgM anti- HBc
  • IgG anti HBC

Anti-HBe

A
  • Anti-HBs - Protection
  • IgM anti-HBc - Acute infection
  • IgG anti HBc - Chronic infection/exposure

Anti-HBe - Inactive virus

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12
Q

What is the approach when a patient maight have detectable levels of Hepatitis surface antigen?

A

If positive - find out if it is an active infection or chronic

Acitve infection if clinical evidence or known cause exists with corresponding raise in IgM anti HBVc

Chronic infection requires ongoing monitoring and treatment

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13
Q

What is the natural history of chronic hepatitis B?

A

After cirrhosis it can cause end stage liver disease or Hepatocellular carcinoma

A liver which is fibrotic but not is cirrosed still has a high risk of HCC

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14
Q

What are treatment options for HBV?

A
  • Pegylated interferon
  • Oral antiviral drugs
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15
Q

What percentage of HCV patients report jaundice?

A

10%

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16
Q

When does HCV often become symptomatic?

A

When the liver becomes cirrhotic

May have normal LFT’s

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17
Q

How is HCV different to the other hepatitis viruses?

A

Hep C is RNA virus which is different to hepatitis which is a DNA virus

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18
Q

What is the natural progression of Hepatitis C?

A
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19
Q

When does hepatits D arise?

A

Only in conjunction with hepatitis B - The small RNA virus is enveloped in the Hepatits B surface antigen

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20
Q

What is the disease progression of Hepatits E?

A

Self - limiting - no long term sequelae

No specific treatment, no efective vaccine currently available

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21
Q

What is the effect of herpes on the liver?

A

Rare but can cause acute hepatitis

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22
Q

What does NAFLD encompass? Non alcoholic fatty liver disease

A

Simple steatosis

Non alcoholic steatohepatits

Fibrosis and cirrhosis

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23
Q

What components of metabolic syndrome are associated with NAFLD?

A

Diabetes mellitus

Obesity

Hyperglyceridemia

Hypertension

24
Q

What are other risk factors of NAFLD?

A

Age

Ethnicity

Genetic factors

25
What is the natural pathway for NAFLD?
Steatosis: Infiltration of liver cells with fat, associated with disturbance of the metabolism NASH: Nonalcoholic steatohepatitis
26
How do we diagnose NAFLD?
**Biochemical tests: AST /ALT ratio** (Aspartate transaminase vs alinine transaminase) AST to ALT ratio of 2:1 or greater is suggestive of alcoholic liver disease, particularly in the setting of an elevated gamma-glutamyl transferase The AST to ALT ratio can also occasionally be elevated in a liver disease pattern in patients with nonalcoholic steatohepatitis **Enhanced liver fibrosis pane**l (ELF) - Liver markers **Cytokeratin - 18** (Good non-invasive marker to determine presence of NASH) **Ultrasound** **Fibroscan** **MR/CT** **MR spectroscopy** **Liver biopsy**
27
Which diagnosing investigation is effective at determining the actual quantity of fat
MR spectroscopy
28
What are the levels of platelets and albumin in a high risk NAFLD patient?
Platelets are low and albumin is low
29
What is the criteria to assess the NAFLD score?
30
What is the treatment for NAFLD?
* 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 * Weight reduction surgeries
31
What is the two hit process involved in the development of NASH?
1.Normal liver becomes fatty as a result of the diet - increased fat import to the hepatocytes and reduced export. ## Footnote Hyperinsulinemia causes fatty liver. (insulin pushes glucose into the liver) Fatty liver causes insulin resistance. Insulin resistance leads to compensatory hyperinsulinemia. 2. Inflammation and fibrosis
32
What use is an ultrasound scan for NAFLD?
Ultrasound cannot differentiate between fatty liver with no fibrosis and NASH - in both cases the liver will appear bright.
33
What is notable difference in the clinical features of alcoholic liver disease and NAFLD?
Jaundice only occurs after cirrhosis in NAFLD
34
When is NAFLD the most likely diagnosis?
Elevated serum transaminases No history of alcohol abuse Negative chronic liver disease screen
35
What are the autoimmune liver diseases?
* Autoimmune hepatitis * Primary biliary cholangitis (PBC) used to be called primary billiary cirrhosis * Primary sclerosing cholangitis (PSC)
36
Which gender is more susceotible to autoimmune hepatitis?
Female
37
What would you find in the serum of autoimmune hepatitis?
High levels of serum immunoglobulins (hypogammaglobulinaemia) and autoantibodies ## Footnote * Type 1: ANA, SMA * Type 2: LKM1 * Type 3: SLA
38
What is the presentation of autoimmune hepatitis?
Fatigue Anorexia Jaundice Non - resolving viral hepatitis Fever Arthralgia Vitiligo Epistaxis Signs of chronic liver disease such as spider naevi and hepatosplenomegaly Cushingoid face
39
What autoimmune diseases might also be present for someone with autoimmune hepatitis?
Hashimoto's thyroiditis Renal tubular acidosis Rheumatoid arthritis
40
What is the diagnosis for autoimmune hepatitis?
Liver biopsy
41
What is cholestasis?
Cholestasis is defined as a decrease in bile flow due to impaired secretion by hepatocytes or to obstruction of bile flow through intra-or extrahepatic bile ducts. Therefore, the clinical definition of cholestasis is any condition in which substances normally excreted into bile are retained.
42
What causes the loss of small and middle sized bile ducts in primary biliary cholangitis?
Granulomatous inflammation of the portal tracts
43
What is the effect of the loss of the bile ducts?
Fibrosis and cirrhosis of the liver
44
What is the presentation of primary biliary cholangitis?
Itching Tiredness
45
What is the diagnostic for primary biliary cholangitis?
IgM elevated Antimitochondrial antibody positive
46
What is the treatment of choice for primary biliary cholangitis?
UDCA -Ursodeoxycholic acid
47
Define biliary cirrhosis
Primary biliary cirrhosis (PBC) is a progressive disease of the liver caused by a buildup of bile within the liver (cholestasis) that results in damage to the small bile ducts that drain bile from the liver. Over time, this pressure build-up destroys the bile ducts leading to liver cell damage.
48
What is the difference between primary biliary cholangitis and primary sclerosing cholangitis in terms of which bile ducts are involved?
Primary biliary cholangitis: Intrahepatic ducts are involved Primary sclerosing cholangitis: •Intra and extrahepatic bile ducts involved
49
What is the progression of primary sclerosing cholangitis?
Biliary cirrhosis Portal hypertension Hepatic failure
50
Who does primary primary sclerosing cholangitis affect?
Males : Female is 2:1 Most patients present at 25-40 Important cause of liver disease in children
51
What are the clinical features of patients with Primary sclerosing cholangitis?
2/3rds of patients also have ulcerative cholitis Persistently raised serum alkaline phosphatase in a patient with ulcerative cholitis Common symptoms: Fatigue, intermittent weight loss, right upper quadrant abdominal pain and pruritis Hepatomegaly Splenomegaly
52
What is diagnosis of Primary sclerosing cholangitis?
Perinuclear antineutrophil cystoplasmic antibodies (ANCA) have been detected in 60-80% of patients with primary sclerosing cholangitis MRCP is the test of choice
53
What is treatment for Primary sclerosing cholangitis?
Liver transplant Biliary stents
54
Who receives liver transplants?
* 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
55
What are contraindications for transplant?
Active extrahepatic malignancy Hepatic malignancy with macrovascular or diffuse tumor 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
56
What is the difference between orthotopic and heterotopic transplantation?
Orthotopic transplantation is the replacement of a whole diseased liver with a healthy donor liver. Heterotopic transplantation is the addition of a donor liver at another site, while the diseased liver is left intact.
57
What is post operative treatment for Transplantation?
* Post operative ICU care * Multidisciplinary care * Prophylactic antibiotics and anti-fungal drugs * Anti-rejection drugs * Steroids * Azathioprine (immunosuppressant) * Tacrolimus/Cyclosporine (immunosuppressant)

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