Liver disease Flashcards

1
Q

What are the two main physiological vascular changes that cause portal hypertension?

A
  • Initially increased intrahepatic vascular resistance

- Increased portal blood flow

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2
Q

Portal hypertension can be measure invasively with the hepatic venous pressure gradient. A finding of what represents clinically significant portal hypertension?

A

> 10mmHg

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3
Q

Noninvasive assessment of clinically significant portal hypertension involves which two investigations?

A

Liver stiffness on fibroscan
- ≥25kpa or 15-24 and plts <150
Measure of platelets

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4
Q

What is the mainstay of management of portal hypertension? What is the underlying mechanism of action?

A

Beta blockers
Decrease splanchnic vasodilation
Carvedilol also decreases intrahepatic vascular tone

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5
Q

What is the most common complication of portal hypertension?

A

Ascites

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6
Q

A total ascitic fluid protein count less than what is considered high risk for SBP?

A

<15g/L

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7
Q

What measurement is diagnostic for SBP?

A

PMN >250

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8
Q

What is empirical management for SBP?

A

Ceftriaxone IV, or Tazocin if already on prophylaxis

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9
Q

Apart from antibiotics, what forms a key part of treatment of SBP?

A

Concentrated albumin
Initial load followed by daily administration (>2 bottles/day) for at least 3 days
Aim 1-1.5g/kg/d over first 3 days

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10
Q

What are the three main parts of management of ascites?

A

Sodium restriction (<5g/day)
Diuretics - spironolactone +/- frusemide
Paracentesis

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11
Q

How do you define diuretic resistant ascites?

A

Ascites that cannot be mobilised or that recurs early post large volume paracentesis

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12
Q

How is diuretic refractory ascites managed?

A

Regular large volume paracentesis
Cease BB (causes decreases systolic function and renal perfusion)
Consider ceasing diuretics
Consider TIPS, transplant assessment

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13
Q
In those who develop oesophageal varices, what is the risk of haemorrhage?
A) <5%
B) 5-15%
C) 15-25%
D) 25-50%
A

B) 5-15%
RACP lectures said 12%
Some groups are of increased risk

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14
Q
Which of the following is not associated with increased risk of oesophageal varix haemorrhage?
A) Increased variceal size
B) Presence of red wale marks
C) Higher Childs-Pugh class 
D) Smoking
E) Continued alcohol abuse
A

D) Smoking

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15
Q

Primary prophylaxis for variceal ulcers consists of what?

A

B blockers or endoscopic banding

Similar efficacy

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16
Q
What constitutes secondary prophylaxis for patients with oesophageal varices that have bled?
A) Beta blocker
B) Endoscopic therapy
C) Beta blocker AND endoscopic therapy
D) Terlipressin
E) Norfloxacin
A

C) Beta blocker AND endoscopic banding > better than either therapy alone

17
Q
Which complication of cirrhosis carries the poorest prognosis?
A) Diuretic refractory ascites
B) Hepatic hydrothorax
C) Hepatic encephalopathy
D) Hepatopulmonary syndrome
E) Hepatorenal syndrome
A

E) hepatorenal syndrome

Median survival 1 months

18
Q

What is the histopathological hallmark of alcoholic hepatitis?

A

Neutrophil infiltration

19
Q
Which of the following does not form the part of management of alcoholic hepatitis? When are the others indicated?
A) Alcohol withdrawal management
B) PPI
C) Beta blocker
D) Glucocorticoids
E) NAC
A

C - beta blockers should be ceased due to increased risk of AKI

A - everyone
B - everyong, UGIB prophylaxis
D - in those with severe disease (MELD score >32)
E - consider in those with severe disease

20
Q

How is alcohol metabolised in the liver?

A

Primarily by alcohol dehydrogenase

Also by CYP450 and MEOS pathway

21
Q
Which of the following physiological changes is not seen in chronic alcoholism?
A) Hyperglycaemia
B) High NADH/NAD+ ratio
C) Lactic acidosis
D) Build up of acetaldehyde
A

A) usually see hypoglycaemia

22
Q

What is the most common autoantibody in autoimmune hepatitis?

A

ANA

23
Q

What is the most specific autoantibody in autoimmune hepatitis?

A

Anti-smooth muscle antibodies

24
Q

What is the most specific autoantibody in autoimmune hepatitis?

A

Anti-smooth muscle antibodies

25
Q

What is the main way HCC is diagnosed?

A

Quad phase CT

26
Q

What are the indications for immediate NAC commencement for a patient presenting post paracetamol overdose?

A
  • Ingestion > 8 hours prior or unknown time of ingestion
  • Modified release >10g
  • Multiple or staggered overdoses
27
Q

What is the mainstay of management for paracetamol overdose?

A

NAC infusion

28
Q

When should you check paracetamol levels post overdose?

A

Immediately if unknown time of ingestion

Otherwise 4-8 hours post ingestion

29
Q

Hereditary haemochromatosis is due to a mutation in (1), and inheritance follows a (2) pattern.

A
  1. HFE

2. Autosomal recessive

30
Q

HBsAg negative, HBcAb positive, HBsAb positive

A

Prior infection, inactive

31
Q

HBsAg -
HBsAb +
HBcAb -

A

Immunised

32
Q

HBsAg +
HBsAb -
HBcAb+

A

If IgM positive - acute infection

If IgM negative - chronic infection