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Year 3 > Hepatitis (GI) > Flashcards

Hepatitis (GI) Flashcards

1
Q

What are two types of hepatitis (non-viral)?

A
  • autoimmune hepatitis - these flashcards focus on AIH
  • ischaemic hepatitis
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2
Q

Define autoimmune hepatitis.

A

Chronic inflammatory disease of the liver of unknown aetiology

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3
Q

Who does autoimmune hepatitis tend to affect more?

A

Young females (4:1)

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4
Q

What are the three types of autoimmune hepatitis?

A
  • type 1 AIH (classic, 80% of cases) - children and adults
  • type 2 AIH - children only
  • type 3 AIH
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5
Q

What are the most common antibodies present in type 1 autoimmune hepatitis? (2 + 2)

A
  • antinuclear antibodies (ANA)
  • anti-smooth muscle antibodies (ASMA)
  • (anti-actin antibodies - AAA)
  • (anti-soluble liver antigen - anti-SLA)
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6
Q

What antibodies are present in type 2 autoimmune hepatitis? (1 + 1)

A
  • anti-liver kidney microsomal-1 (anti-LKM-1)
  • (anti-liver cytosol - ALC-1)
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7
Q

What antigen is targeted in type 3 autoimmune hepatitis?

A

Anti-soluble liver antigen (anti-SLA)

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8
Q

What is the aetiology of autoimmune hepatitis?

A

Idiopathic

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9
Q

What are some examples of autoimmune diseases that autoimmune hepatitis is commonly associated with? (4)

A
  • Hashimoto’s thyroiditis
  • Graves disease
  • ulcerative colitis
  • Coeliac disease
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10
Q

What gene plays a role in autoimmune hepatitis?

A

HLA gene (HLA-DR3/4)

Genetically predisposed individual –> environment e.g. viruses/drugs may lead to hepatocyte expression of HLA-DR3/4 –> T-cell mediated autoimmune attack against hepatocytes

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11
Q

What is autoimmune hepatitis characterised by?

A

Presence of circulating autoantibodies with a high serum globulin concentration (hyperglobulinaemia), inflammatory changes on liver histology (chronic inflammation) and a favourable response to immunosuppressive treatment

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12
Q

When can ischaemic hepatitis occur?

A

Following acute hepatic hypoperfusion e.g. after sepsis or cardiac arrest

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13
Q

What is ischaemic hepatitis characterised by? (2)

A
  • marked elevation of AST and ALT 1-3 days after insult
  • significant rise in LDH (very sensitive for ischaemic hepatitis)
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14
Q

What are the clinical features of hepatitis? (13)

A
  • fatigue
  • malaise
  • anorexia
  • abdominal discomfort
  • hepatomegaly
  • splenomegaly
  • jaundice
  • encephalopathy
  • pruritus
  • arthralgia
  • nausea
  • amenorrhoea
  • spider naevi
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15
Q

What might you see on examination of hepatitis?

A
  • ascites
  • hepatomegaly
  • splenomegaly
  • jaundice
  • spider naevi
  • GI bleeding
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16
Q

What are some risk factors for hepatitis? (4)

A
  • female
  • genetics
  • viral triggers
  • drug triggers
17
Q

What are the first-line investigations in hepatitis? (2)

A
  • LFTs - AST, ALT, BR, GGT
  • prothrombin time
18
Q

What do we see in bloods/LFTs in hepatitis?

A
  • high AST and ALT
  • BR, GGT and ALP - mild to moderately increased
  • low serum albumin (when synthetic function affected)
  • high globulins (hypergammaglobulinaemia)
19
Q

What do we suspect instead of hepatitis if ALP was raised a lot (rather than mild-moderate)?

A

Bile duct pathology

20
Q

What serum autoantibodies can be found in type 1 and type 2 autoimmune hepatitis?

A
  • type 1 AIH: ANA & ASMA
  • type 2 AIH: anti-LKM-1
21
Q

What is characteristic of type 1 autoimmune hepatitis?

A

Decreased albumin, increased prothrombin time

22
Q

What is prothrombin time like in hepatitis?

A

Prolonged PT

23
Q

What would serum protein electrophoresis show in hepatitis?

A

Hypergammaglobulinaemia (increased IgG)

24
Q

Why would a liver biopsy be done in hepatitis and what would it show?

A

Confirms diagnosis - inflammation and bridging necrosis seen

25
Q

What LFTs are markedly raised in hepatitis? (2)

A
  • aspartate transaminase (AST)
  • alanine transaminase (ALT)
26
Q

What investigations can we do in hepatitis to rule out other causes? (6)

A
  • viral serology (hepatitis B/C)
  • urinary copper/caeruloplasmin (Wilson’s disease)
  • ferritin and transferrin saturation (haemochromatosis)
  • alpha-1-antitrypsin (deficiency)
  • anti-mitochondrial antibodies (PBC)
  • ERCP (PSC)
27
Q

What are some differential diagnoses for hepatitis? (13)

A
  • primary biliary cirrhosis (PBC)
  • primary sclerosing cholangitis (PSC)
  • chronic hepatitis
  • drug-induced hepatitis
  • granulomatous hepatitis
  • genetic haemochromatosis
  • alpha-1-antitrypsin deficiency
  • Wilson’s disease
  • cholangiopathy related to AIDS
  • non-alcoholic steatohepatitis (NASH) - presence of 1+ components of metabolic syndrome
  • alcoholic liver disease
  • SLE
  • Graft vs Host disease
28
Q

What are the indications for management of hepatitis? (3 + 3)

A
  • aminotransferases >10x upper limit of normal
  • symptomatic
  • histology:
    • significant interface hepatitis
    • bridging necrosis
    • multiacinar necrosis
29
Q

How do we manage hepatitis?

A
  • corticosteroid - prednisolone followed by maintenance treatment with gradual reduction in dose
  • immunosuppressant - azathioprine
  • maintenance phase: steroid-sparing agents, frequent LFT and FBC monitoring
  • often long term treatment
  • definitive Rx: liver transplant
30
Q

What do we test for before starting azathioprine in hepatitis?

A

Test for TPMT1

31
Q

What is the definitive treatment for hepatitis?

A

Liver transplant (if refractory/intolerant/end-stage)

32
Q

How do we monitor disease progression in hepatitis? (3)

A
  • ultrasound and alpha-feroprotein level every 6-12 months if cirrhosis present - to detect hepatocellular carcinoma
  • repeat liver biopsies to check disease progression
  • frequent FBC+LFTs
33
Q

What vaccinations could we give in hepatitis?

A

Hepatitis A and B vaccinations

34
Q

What are some complications of hepatitis? (7)

A
  • fulminant hepatic failure (severe impairment in absence of pre-existing liver disease)
  • cirrhosis
  • portal hypertension (ascites, varices)
  • hepatocellular carcinoma
  • corticosteroid side effects
  • azathioprine side effects (malignancy, BM suppression, cholestatic hepatitis, pancreatitis, teratogenic)
  • infections due to immunosuppression
35
Q

Describe the prognosis of hepatitis.

A
  • majority of patients with moderate/severe AIH respond to treatment within 2 weeks
  • achieve remission with serum aminotransferases falling into normal range after 12+ months of treatment

Year 3 (95 decks)

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