HistoPath - Liver CPC Flashcards

1
Q

What may cause high bilirubin

A

Pre-hepatic: Haemolysis, Gilbert’s
Hepatic: Hepatitis, cirrhosis, Liver failure
Post-hepatic: Obstruction, Cholecystitis, pancreatic Ca

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2
Q

What makes the endothelial cells of the liver unique

A

The endothelial cells are discontinuous - there are spaces between cells and between the endothelium and hepatocytes (Space of Disse)

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3
Q

What investigations should be done for an isolated raised bilirubin

A

Is it pre-hepatic, hepatic or post hepatic?
a. Pre-hepatic: haemolysis → FBC + blood film
b. Hepatic → repeat LFTs
c. Post-hepatic: Obstructed

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4
Q

What is the Van den Bergh reaction

A

Measures serum bilirubin via fractionating
Direct reaction: conjugated
Indirect reaction: Unconjugated

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5
Q

What are the considerations for jaundice in children

A

Need to know whether unconjugated or conjugated.
Jaundice is normal >24h, but bilirubin should be unconjugated (liver immaturity + fall in the Hb in early life)
If it does not settle, other rare causes should be looked for including hypothyroidism, other causes of haemolysis (including Coomb’s test or DAT) and the unconjugated bilirubin will be useful

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6
Q

What is Gilbert’s syndrome and what is its inheritance

A

A common condition that causes an isolated raised bilirubin in the absence of any deranged liver values
Causes jaundice that is worsened by fasting
Recessive inheritance (50% carry the gene)

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7
Q

What is the prevalence of Gilbert’s syndrome

A

1 in 20

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8
Q

What is the pathophysiology of Gilbert’s syndrome

A

UDP glucoronyl transferase activity is reduced to 30%
Unconjugated bilirubin tightly albumin bound → does NOT enter urine

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9
Q

Which measurements assess liver function

A

Prothrombin time (most representative)
Bilirubin
Albumin (production is slow)

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10
Q

How is hep A transmitted and what is the timeline for infection

A

Faeco-oral transmission

  1. Virus excreted in the 4 weeks before becoming ill (incubation)
  2. IgM response
  3. Jaundice develops
  4. IgG response → immunity
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11
Q

What is the timeline for hepatitis B infection

A
  1. Infection
  2. Hbe antigen production - acutely infectious, exposed to the LIVE virus
  3. Anti-Hbe production to neutralise Hbe Ag
  4. Anti-Hbc and anti-Hbc IgM production
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12
Q

What is seen on histology of the liver for alcoholic hepatitis

A

“clear spaces” - fatty change (due to reversible fatty change in the liver)
Mallory hyaline bodies - pink, dense material
Neutrophils and lymphocytes present
Damaged hepatocytes
Brown/green pigment (bile) due to accumulation

Collagen stains blue to show collagen surrounding hepatocytes (scarring)

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13
Q

What are the defining histological features of liver damage

A

Liver cell damage (Balloon cells with Mallory hyaline, mixed neutrophilic and lymphocytic)
Inflammation
Fibrosis
Fatty change
Mega/giant mitochondria seen

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14
Q

What is the management for alcoholic hepatitis

A

Vitamin B1
Thiamine
Stop drinking
Supportive
Nutrition

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15
Q

What does vitamin B1 deficiency cause

A

Beri-Beri

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16
Q

What are the clinical signs of chronic liver disease

A

Multiple spider naevi
Palmar erythema
Gynaecomastia (liver is unable to break down oestradiol)
Dupuytren’s contracture (fourth finger most commonly affected)

17
Q

What are the features of portal hypertension

A

Splenomegaly
Visible veins
Ascites

18
Q

What is a flap on examination indicative of

A

Liver failure

19
Q

What are the functional deficits in liver failure and what can it lead to

A

Synthetic function
Clotting factor and albumin -> bleeding tendencies
Clearance of bilirubin -> jaundice
Clearance of ammonia

Can lead to encephalopathy

20
Q

What is the histology of liver failure

A

Gross: pale liver, made up of fat, uniform nodules with a cuff of fibrous tissue around each, whole liver involved

Micro: nodule of regenerating hepatocytes with a fibrous cuff around the nodule

21
Q

Why may liver failure lead to encephalopathy and varices

A

Scarring between the portal tracts and portal veins which allows the blood to bypass the hepatocytes (intra-hepatic shunting of blood), while formation of varices/haemorrhoids are extra-hepatic shunts

22
Q

What are the causes of liver cirrhosis

A

Fatty liver disease (alcoholic and non-alcoholic) -> micronodular
Viral hepatitis (Hep B, C and D) -> macronodular
Haemochromatosis (iron)
Wilson’s disease (copper)
Primary biliary cholangitis
Primary sclerosing cholangitis

23
Q

Give examples of portal-systemic anastomoses

A

Oesophageal varices
Rectal varices
Umbilical vein recanalising
Spleno-renal shunt

24
Q

What do scratch marks suggest in liver disease

A

Obstruction of the bile ducts → bile salts/acids enter the skin

25
Q

What is Courvoisier’s law

A

Gall bladder is palpable in a jaundiced patient - likely to be pancreatic cancer (and NOT gallstones)

Gallstones = Gall bladder becomes thickened and fibrosed → cannot enlarge