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Clinical Pathology > Theme 11 L7: Medical liver diseases > Flashcards

Theme 11 L7: Medical liver diseases Flashcards

1
Q

What are the functions of the liver?

A
  1. Produce bile
  2. Protein production e.g clotting factors
  3. Cholesterol production
  4. Store excess glucose as glycogen
  5. Convert ammonia to urea for renal excretion
  6. Vitamin metabolism/ storage
  7. Metabolise drugs/ toxins
  8. Regulate clotting
  9. Create immune factors & filter bacteria from blood
  10. Clearance of billirubin
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2
Q

Explain bilirubin metabolism

A
  • bilirubin is produced by red blood cell breakdown in the spleen (“unconjugated”)
  • then “conjugated” in liver with glucuronic acid to make it soluble and excreted
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3
Q

What is enterohepatic circulation?

A

some bilirubin is re-absorbed from gut; bile acids secreted with it are reabsorbed

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4
Q

What is the intermediate compound before heme breaks down into bilirubin?

A

biliverdin

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5
Q

When is jaundice visible?

A

when bilirubin > 40 umol/l

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6
Q

What is the cause of pre-hepatic jaundice?

A

too much bilirubin produced

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7
Q

Which conditions is pre-hepatic jaundice associated with?

A
  • haemolytic anaemia

- Gilbert’s syndrome - harmless deficient conjugation of billirubin

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8
Q

What is the cause of hepatic jaundice?

A

too few functioning liver cells –> fails to break down bilirubin

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9
Q

Which conditions is hepatic jaundice associated with?

A
  • acute diffuse liver cell injury
  • end stage chronic liver disease
  • inborn errors of metabolism
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10
Q

What is the cause of post-hepatic jaundice?

A

bile duct obstruction by a stone, stricture, tumour

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11
Q

How is bilirubin transported to the liver?

A

it is insoluble so it is transported in the plasma bound to albumin

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12
Q

Which type of bilirubin accumulates in pre-hepatic jaundice?

A

unconjugated bilirubin - bound to albumin, insoluble, not excreted

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13
Q

What is the symptoms of pre-hepatic jaundice?

A

yellow eyes and skin

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14
Q

Which type of bilirubin accumulates in hepatic jaundice?

A

Mostly conjugated, water soluble

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15
Q

What is the symptoms of hepatic jaundice?

A

yellow skin/ eyes and dark urine

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16
Q

Which type of bilirubin accumulates in post-hepatic jaundice?

A

conjugated - soluble, excreted but cant get into gut

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17
Q

What is the symptoms of post- hepatic jaundice?

A

yellow eyes, dark urine, pale stool

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18
Q

What is included in LFTs?

A
  • bilirubin (conjugated and unconjugated)

- liver enzymes: ALT, AST aminotransferases

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19
Q

What is raised in obstructive jaundice and chronic biliary disease?

A

raised alk phos

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20
Q

What are most non-obstructive cases of jaundice caused by?

A

acute hepatitis

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21
Q

What is the first histopathological sign in liver with obstructive jaundice?

A

bile in the liver parenchyma

22
Q

Very high levels of liver enzymes suggests what?

A

acute liver disease / hepatitis

23
Q

What are the symptoms of acute hepatitis?

A 
asymptomatic
malaise
jaundice
coagulopathy (failure of clotting)
encephalopathy
deayh
24
Q

What is confluent panacinar necrosis of the liver?

A

all hepatocytes have died

25
Q

What are some causes of chronic hepatitis?

A
  1. immunological injury - viral, autoimmune, drugs
  2. toxic/metabolic injury - fatty liver disease, alcoholic or non-alcoholic fatty liver, drugs
  3. genetic inborn errors - iron, copper, alpha 1 antitrypsin accumulate in liver and damage it
  4. biliary disease - autoimmune, duct obstruction, drugs
  5. vascular disease - clotting disorders, drugs
26
Q

Explain the pathology of cirrhosis?

A

During any chronic liver disease, scarring (fibrosis) gradually increases and starts to link vascular structures (bridging) eventually transforming the liver tissue into separate nodules – end stage

27
Q

What are the hepatotrophic viruses?

A
  • Hep A, B, C, D (only in patients with hepB), E

- other viruses: EBV, CMV, HSV (usually in immunocompromised host)

28
Q

Which hepatitis is most likely to progress to chronic hepatitis?

A

hepC

29
Q

How do we assess the severity of chronic hepatitis?

A 
grade = how inflamed
stage = how much fibrosis/ scarring
30
Q

Is liver fibrosis reversible?

A

yes - the liver can regenerate

31
Q

Explain the 3 stages that alcohol abuse has on the liver

A
  1. Fatty change (steatosis)
  2. Alcohol steatohepatitis
  3. Cirrhosis
32
Q

What is a common cause of non-alcoholic fatty liver disease (NAFLD)?

A

Obesity

33
Q

What is the pathogenesis of NAFLD?

A

Same as alcoholic liver disease:

  • steatosis
  • steatohepatitis
  • cirrhosis
  • HCC
34
Q

What is the commonest cause of acute liver injury?

A

Drug induced liver injury (DILI)

35
Q

When do you overdose on paracetamol?

A

when you run out of glutathione

36
Q

What is the antidote for paracetemol overdose?

A

n-acetylcysteine

37
Q

What happens in paracetmol overdose over the course of:
0-24 hours
24-72 hours
3-5 days

A

0-24 hrs mild symptoms - nausea, vomiting, sweating
24-72 hrs: increasing liver cell death
3-5 days: massive necrosis, liver failure and death

38
Q

What is haemochromatosis?

A

inherited inborn error of iron metabolism -

39
Q

Which locations does iron accumulate in in haemochromatosis and what are the effects of this?

A 
liver causing cirrhosis
pancreas causing diabetes
skin causing pigmentation
joints causing arthritis
heart causing cardiomyopathy
40
Q

How do you treat haemochromatosis?

A

venesection - to deplete iron stores to normal

41
Q

What is Wilson’s disease?

A

inherited inborn error of iron metabolism - usually presents at a younger age

42
Q

In wilson’s disease, copper accumulates where and what are the effects of this?

A
  • in liver causing cirrhosis
  • in eyes causing kayser-fleischer rings
  • in brain causing ataxia
43
Q

How do you diagnose Wilson’s disease?

A

serum copper & caeruloplasmin, urinary copper, slit lamp, liver biopsy

44
Q

How do we treat wilson’s disease?

A

drugs that chelate copper and enhance its excretion e.g penicillamine

45
Q

What is alpha 1 antitrypsin deficiency?

A
  • abnormal anti-protease which cannot be exported from hepatocyte
  • accumulates in liver cells and injures them - cirrhosis
  • insufficient in blood, failure to inactivate neutrophil enzymes - emphysema
46
Q

What is PBC?

A

Primary biliary cholangitis:

  • autoimmune
  • anti mitochondrial anti bodies
  • bile duct granulomas at early stage
  • then ductopenia (loss) and cirrhosis
47
Q

Which LFT will you expect to be elevated in PBC?

A

Alkaline phosphatase

48
Q

What is PSC?

A

Primary sclerosing cholangitis:

  • autoimmune
  • pruned tree on biliary imaging
  • peri ductal “onion skin” fibrosis
  • then ductopenia and cirrhosis
49
Q

What condition is PSC associated with?

A

ulcerative colitis, high alk phos

50
Q

What are the complications of cirrhosis?

A
  • increased blood flow - portal hypertension
  • pressure rises in portal vein
  • oesophageal varices/ haemorrhoids
  • blood by passes sinusoids so there is liver cell failure
51
Q

What are the signs of chronic liver failure?

A
  • ascites
  • muscle wasting
  • bruising
  • gynecomastia
  • spider naevi
  • viruses, caput medusae

Clinical Pathology (57 decks)

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