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Chem Path > Liver disease CPC > Flashcards

Liver disease CPC Flashcards

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1
Q

What does the portal triad consist of?

A

Hepatic vein, artery, bile duct

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2
Q

What is the Space of Disse?

A

The spaces between the hepatocytes and the endothelium (discontinuous organisation) of the sinusoids meaning that the blood comes into contact with the all the liver enzymes

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3
Q

What is Zone 1 damage and what substances cause it?

A

Periportal damage, caused by directly hepatotoxic substances

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4
Q

What is Zone 3 damage and what substances cause it?

A

Centrilobar damage, caused by metabolised hepatotoxic substances i.e. those that require bioactivation. Hypoxic damage as most oxygen lost by the time the blood reaches Zone 3

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5
Q

In which zone are the most metabolically active cells in the liver?

A

Zone 3

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6
Q

ALP rises more when which zone is damaged? Why?

A

Zone 1 due to proximity to bile ducts

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7
Q

What is Zone 2 damage?

A

Midzonal

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8
Q

Name 2 substances that cause Zone 1 damage

A

Iron salts, white phosphorus

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9
Q

Name 3 substances that cause Zone 2 damage

A

Furans, ngaione (myosporum spp.), beryllium

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10
Q

Name 4 substances that cause Zone 3 damage

A

Acetaminophen, aflatoxin, microcystin, ricin

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11
Q

How do you measure the split bilirubin? (conjugated and unconjugated)

A

van den Bergh reaction

Direct reaction to measure conjugated BR

Indirect reaction to measure unconjugated BR: add methanol which completes the reaction, allows measurement of total BR, so minus the conjugated value to get unconjugated value

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12
Q

Is the hyperbilirubinaemia conjugated or unconjugated in paediatric jaundice? Why?

A

Unconjugated in normal paediatric jaundice as caused by liver immaturity- cannot conjugate the BR fast enough.

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13
Q

What does phototherapy convert bilirubin to? Why is this helpful to treat paediatric jaundice?

A

Lumirubin and photo-bilirubin. These isomers do not need to be conjugated to be excreted.

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14
Q

What is the inheritance pattern of Gilbert’s syndrome?

A

Autosomal recessive

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15
Q

What do you see in LFTs in Gilbert’s?

A

Raised unconjugated bilirubin with otherwise normal LFTs

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16
Q

What makes the bilirubin levels worse in Gilbert’s?

A

Fasting

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17
Q

Pathophysiology of Gilbert’s

A

UDP glucuronyl transferase activity is reduced to 30%

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18
Q

What is the most representative marker of liver function?

A

Prothrombin time (if raised, shows liver isn’t making clotting factors so isn’t working properly)

(Albumin and BR also good)

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19
Q

Why are the enzyme LFTs (AST, ALT) not true markers of the liver’s synthetic function?

A

They tell you that there is damage rather than telling you how your liver is actually functioning

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20
Q

What do high AST and ALT indicate?

A

Hepatocyte damage e.g. hepatitis

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21
Q

In what type of hepatitis is AST > ALT?

A

Alcoholic hepatitis

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22
Q

In what type of hepatitis is ALT > AST?

A

All other heps other than alcoholic

23
Q

What does high ALP indicate?

A

Biliary obstruction

24
Q

3 key features of hepatitis

A

Fever, jaundice, raised ALT/AST

25
Q

Causes and findings in pre-hepatic jaundice

A

Causes: haemolysis, congestive heart failure

Findings: Raised unconjugated BR, raised LDH, reduced haemoglobin and haptoglobin

26
Q

Causes and findings in hepatic jaundice

A

Causes: acute or chronic liver failure, Gilbert’s, viral/alcoholic hep, PBC

Findings: raised unconjugated BR, raised ALT/AST, ~synthetic dysfunction

27
Q

Causes and findings in post-hepatic jaundice

A

Causes: anything causing biliary tree obstruction e.g. stones, inflammation (PBC/PSC), strictures, masses, extra-luminal masses e.g. pancreatic cancer/cholangiocarcinoma

Findings: raised conjugated BR, raised urinary BR, dark urine and pale stools

28
Q

Route of transmission of hep A

A

Faeco-oral

29
Q

Hep A presentation

A

ACUTE

Asymptomatic, or nausea, D+V, fever, jaundice, RUQ pain

30
Q

Hep A onset and symptom duration

A

2-6 wks, symptoms last ~8wks

31
Q

Explain natural history of hep A in terms of antibodies

A

After viral titres drop, get rise in IgM (–> unwell, jaundice)
After first few weeks, IgM drops and IgG rises –> immunity, cured

32
Q

Hep A treatment

A

Supportive

33
Q

Routes of transmission of hep B

A

Sexually, vertically, blood-to-blood

34
Q

Hep B presentation

A

Normally acute presentation (can be acute ± chronic)

Hepatitis symptoms – fever, jaundice, N+V, RUQ pain)
But a chronic infection follows in ~10% of people

35
Q

Hep B duration of onset

A

2-6 wks

36
Q

What percentage of hep B infections become chronic?

A

5-10%

37
Q

Antigens measured in hep B

A

HBsAg and HBeAg

Once these go down, produce antibodies against them (anti-HBs and anti-HBe)

38
Q

How could you distinguish between someone who has immunity to hep B through vaccinated and someone who has actually had hep B?

A

Vaccination contains HBsAg, so they will have anti-HBs antibodies but not anti-HBeAg

39
Q

Which antigen is never cleared in chronic hep B?

A

HBsAg (but levels decrease with time)

40
Q

Management of hep B

A

Acute: supportive

Chronic: antiviral therapy

41
Q

Which heps are associated with hepatocellular carcinoma?

A

B and C

42
Q

Route of transmission of hep C

A

Blood-to-blood

43
Q

Hep C duration of onset

A

6-8 wks

44
Q

Hep C presentation

A

Normally results in an asymptomatic presentation leading to a chronic infection (60-80%)

45
Q

Hep C management

A

Antiviral therapy (can be treated and eradicated)

46
Q

Which hep must hep D co-infect with?

A

Hep B

47
Q

Route of transmission of hep E

A

Faeco-oral

48
Q

Hep E presentation

A

Acute – asymptomatic, or – nausea, D+V, fever, jaundice, RUQ pain

49
Q

Hep E duration of onset

A

Onset = 2-6 weeks; symptoms last = ~8 weeks

50
Q

Which groups are at higher risk of hep E?

A 
Expectant mothers 
Immunocompromised patients (“E-mmunocompromised”)
51
Q

Key histological features of hepatitis (3)

A

Liver cell damage: Balloon cells (ballooning degeneration) containing mallory hyaline, Mallory-Denk bodies
Inflammation
Fibrosis

52
Q

What causes nutmeg liver?

A

Venous congestion (Budd-Chiari, congestive HF etc)

53
Q

What is Courvoisier’s Law?

A

If the gallbladder is palpable in a jaundiced patient, the cause is unlikely to be gallstones (i.e. it is more likely to be pancreatic cancer) – will also be a PAINLESS jaundice

Chem Path (6 decks)

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