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Clinical > Hepatology > Flashcards

Hepatology Flashcards

1
Q

A build up of what causes hepatic encephalopathy? How many stages are there?

A

Build up of ammonia
Stages 1 - 4

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2
Q

How is hepatic encephalopathy managed?

A

Lactulose to reduce ammonia production, IV mannitol to reduce cerebral oedema.
Rifaximin (an antibiotic that reduces gut production of ammonia) can be used to prevent recurrence.

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3
Q

What are the stages of hepatic encephalopathy?

A

1) altered mood/behaviour, sleep disturbance, dyspraxia
2) speech becomes slurred and personality change
3) incoherent speech, restless, asterixis, somnolent but rousable
4) coma

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4
Q

How is jaundice catagorised?

A
  • Pre-haptic
  • Hepatic
  • Pots-hepatic
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5
Q

What causes a rise in ALT?

A

Liver damage (hepatic jaundice)

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6
Q

What causes a rise in AST?

A

Liver damage, muscle damage, MI

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7
Q

What causes a rise in AST:ALT?

A

hepatocellular damage - more specifically alcoholic liver disease

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8
Q

What causes a rise in ALP?

A

This is unfairly unspecific: cholestasis, increased bone breakdown, pregnancy, etc.
If raised independently it indicates bone disease.

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9
Q

What causes a rise in GGT?

A

This is fairly specific to cholestasis

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10
Q

Why might clotting be affected in the context of liver damage?

A

Production of factors 10, 9, 7, 2 is impacted as liver function declines = prolonged PT.

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11
Q

Why might someone have a raised unconjugated bilirubin?

A
  • Increased production of bile (haemolysis)
  • decreased liver uptake
  • decreased conjugation (gilbert’s)

Essentially pre-hepatic or hepatic jaundice.

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12
Q

Why might someone’s conjugated bilirubin be raised?

A

Hepatic (liver disease) or post-hepatic jaundice

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13
Q

What causes a rise/fall in urinary urobilinogen?

A

Elevated levels in haemolytic (pre-hepatic)y and hepatic jaundice.
Decreased in post-hepatic jaundice.

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14
Q

A serum-ascites albumin gradient above what indicates portal hypertension?

A

1.1

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15
Q

WCC over what suggests spontaneous bacterial peritonitis?

A

> 250 in ascetic fluid (this is predominantly neutrophils)

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16
Q

Does a negative gram stain rule out spontaneous bacterial peritonitis?

A

NO! It is often -ve.

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17
Q

What are the most common causes of spontaneous bacterial peritonitis?

A

E.Coli and Klebsiella

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18
Q

What is Primary Sclerosing Cholangitis?

A

Inflammation of medium/large intra and extrahepatic bile ducts leading to scarring, fibrosis and narrowing of the passages.
This causes bile to build up within the liver, causing more damage.

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19
Q

Someone presenting with raised ALP and bilirubin alongside fatigue, jaundice, and reduced appetite, who is ANA and P-ANCA positive has likely got what diagnosis?

A

PSC

20
Q

What type of malignancy should someone with PSC be screened for?

A

Cholangiocarcinoma: regular imaging

21
Q

How can we diagnose PBC? What type of jaundice does this cause?

A

MRCP, post hepatic.

22
Q

What is Primary Biliary Cholangitis?

A

Inflammation and scarring of mainly small intrahepatic ducts leading to cirrhosis of the liver.

23
Q

What are the signs of PBC? Which antibody is it associated with?

A

Pruritis, fatigue, dry skin, dry eyes, jaundice.
Antimitochondrial antibodies are present in 90% (may also have a raised serum IgM).

24
Q

How do we manage PBC?

A

Cholestyramine manages pruritus, ursodeoxycholic acid may help slow disease progression.

25
Q

Which antibodies are most commonly seen in autoimmune hepatitis type 1?

A

Anti-smooth muscle antibodies

26
Q

What is the difference between type 1 and 2 autoimmune hepatitis?

A

Type 2 is more common in children/young people.

27
Q

What is the 1st line management for ascites secondary to chronic liver cirrhosis?

A

Spironolactone 100-400mg daily.

28
Q

What causes ischaemic hepatitis? How is this seen on LFTs?

A

Acute hypoperfusion which is usually due to cardiac arrest of sepsis.
Massively raised ALT but normal bili and ALP.

29
Q

What is Reye’s Syndrome?

A

Liver failure and encephalitis after taking aspirin for viral infection.
It is due to microvascular hepatocyte stenosis.

30
Q

What are the components of the Child-Pugh score?

A
  • Bili >51 mg/dL
  • Albumin <28 g/dL
  • PT >6 seconds
  • Marked encephalopathy
  • Marled ascites
31
Q

What is the triad associated with acute liver disease?

A
  • Encephalopathy
  • jaundice
  • coagulopathy (INR>1.5)
32
Q

What indicates the need for liver transplant post paracetamol OD?

A
  • pH <7.3 after 24 hours
  • prothrombin time >100s/INR >6.5, creatinine >300, grade 3/4 hepatic encephalopathy
33
Q

HBsAg (surface antigen) is +ve in who?

A

Acute or chronic HepB infection

34
Q

HBeAg is +ve in who?

A

The most infectious Hep B pts

35
Q

Anti-HBe is +ve in who?

A

low viral load pts

36
Q

IgG anti-HBc (core antibody) is +ve in who?

A

chronic infection of HepB

37
Q

IgM anti-HBc (core antibody) is present in who?

A

acute Hep B infection

38
Q

anti-HBs (surface antigen) antibody is +ve in who?

A

vaccinated or infection (if this is the only +ve then it is due to vac)

39
Q

What is Budd-Chiari syndrome?

A

Blocked hepatic vein causing congestion + ischaemia.
Can be thrombosis or external compression (e.g., pregnancy)

40
Q

What are the indications for a TIPS procedure in chronic liver disease? What is the potential complication?

A
  • Blood in vomit or black tarry stools (oesophageal bleeds)
  • Refractory (resistant to treatment) ascites
  • Budd-Chiari syndrome (jaundice, abdo pain, hepatomegaly)
    Cx: hepatic encephalopathy.
41
Q

How often should someone with hepatitis B or cirrhosis be checked for hepatocellular carcinoma? How is this screened?

A

6 monthly AFP and USS

42
Q

What do you see on USS of NAFLD?

A

Increased echogenicity (fatty infiltrates).

43
Q

Which is usually higher in NAFLD:
ALT or AST?

A

ALT

44
Q

How does alcoholic liver progress?

A

Fatty liver, hepatitis, fibrosis/cirrhosis, hepatocellular carcinoma.

45
Q

How is hepatocellular carcinoma seen on USS?

A

Hypodense heterogenous lesions.

46
Q

How do you manage hepatic encephalopathy?

A
  • Lactulose
  • Rifaximin (kills off gut bacteria to reduce ammonia produced)
  • Chlordiazepoxide (reduce agitation)
47
Q
A

Clinical (27 decks)

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