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YEAR 5: Chemical Pathology JK > ChemPath: Liver Disease > Flashcards

ChemPath: Liver Disease Flashcards

1
Q

How may the causes of high bilirubin be categorized?

A

Pre-hepatic: Liver is OK but something beforehand is increasing the through put and that is haemolysis. Haemolytic anaemia is a good cause. Do a FBC and film. Film you can see if any RBCs are lysing and FBC may show anaemia.

Hepatic disease: Repeat the LFT, gamma GT, all the enzymes the liver makes will leak out into the circulation

Post-hepatic: Liver is fine but there’s something blocking the bile duct. Commonly either a gallstone and cancer of the head of the pancreas. Block the bile duct, end up with bilirubin in the circulation.

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2
Q

Where is bilirubin conjugated?

A

The liver

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3
Q

How do you measure conjugated and unconjugated bilirubin?

A

Van de Bergh Reaction

A direct reaction measures conjugated bilirubin

An indirect reaction measures unconjugated bilirubin

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4
Q

When may paediatric jaundice be normal and when may it be pathological?

A

Paediatric jaundice is usually normal, but the bilirubin should be unconjugated as the cause is usually liver immaturity coupled with a fall in the haemoglobin early in life. If it doesn’t settle, other rare causes should be looked for including hypothyroidism, other causes of haemolysis (including a Coombes test or DAT), and the unconjugated bilirubin will be useful.

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5
Q

What therapy may be used to help bilirubin conjugation?

A

Phototherapy - skin may also conjugate bilirubin. Converts bilirubin into two other compounds, lumirubin and photobilirubin which are isomers that do not need conjugation for excretion.

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6
Q

What type of inheritance pattern does Gilberts syndrome have?

A

Recessive

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7
Q

How prevalent is Gilbert’s syndrome?

A

About 6% of people will have it (1 in 20) 50% carry the gene.

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8
Q

What would you expect to see on LFTs for Gilberts?

A

Normal LFTs and high bilirubin. No need for liver biopsy.

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9
Q

What may exacerbate a high bilirubin level in Gilberts?

A

Fasting will increase bilirubin.

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10
Q

Describe the pathology of Gilberts.

A

UDP glucuronyl transferase activity reduced to 30%. This causes a slightly raised unconjugated bilirubin but this does not enter the urin and cause bilirubinurea.

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11
Q

What does it mean if you have urobilinogen in the urine?

A

That the enterohepatic circulation is intact. Urobilinogen is always present in the urine of normal people. It comes from the entero-hepatic circulation. If you have a normal GIT, the bilirubin that you make goes into the biliary tree, into the bowel, then bacteria in the bowel converts a small amount of bilirubin into stercobilinogen which is the same as urobilinogen and is reabsorbed and you poo it out.

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12
Q

What does a lack of urobilinogen in the urine suggest?

A

Blockage of the biliary tree. If you block the biliary tree then the bacteria cannot see the bilirubin, you get pale stools, don’t make any urobilinogen which means urine becomes negative. If urine is negative for urobilinogen but they are jaundice, suggests physical obstruction to biliary tree.

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13
Q

What is the best measure of Liver Function?

A
  • Prothrombin time (clotting factors PT, PTTK)
  • Albumin
  • Bilirubin
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14
Q

What do raised levels of all liver enzymes suggest?

A

Hepatitis

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15
Q

What does a high AST and ALT suggest?

A

Hepatocyte damage

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16
Q

What would an extremely high Alk phos suggest?

A
  • Obstructive Jaundice
  • Obstructive jaundice normally causes alk phos to rise a lot. Alk phos will increase by the greatest of the enzymes with obstructive jaundice.
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17
Q

What are prehepatic causes of hyperbilirubinaemia?

A
  • Gilberts
  • Haemolysis
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18
Q

What are hepatic causes of hyperbilirubinaemia?

A
  • Viral hepatitis
  • Alcoholic hepatitis
  • Cirrhosis
19
Q

What are post-hepatic causes of hyperbilirubinaemia?

A
  • Gallstones
  • Cancer of the head of the pancreas
20
Q

What are 3 main causes of hepatitis?

A
  • Viral - check viral titres
  • Autoimmune
  • Alcoholic
21
Q

Describe Hepatitis A serology.

A

To get hep A you need to be exposed to the virus. Usually in developing country, drink contaminated water – virus replicates and you have an incubation period, Virus then excreted. Then you have immune response. IgM increases and jaundice – some people die at this point. IgG comes next. If you survive, you are cured and then immune. It is either kill or cure. Can’t get it twice.

22
Q

What are the two main antigens in Hepatitis B?

A
  • Antigen E
  • Antigen S
23
Q

Describe the serology of someone who has been infected with Hep B.

A
  • Anti-HBc +
  • Anti-HBs +
  • Anti-HBe +
24
Q

What antigen does the Hep B vaccine contain?

A

HBs

25
Q

Describe the serology of someone who has been vaccinated for Hep B.

A
  • Anti-HBs+
  • Anti-HBe -
  • Anti-HBc -
26
Q

What causes chronic hepatitis B?

A

When a patient has had Hep B and has the antibodies but never clears the virus. This person is a carrier and is infectious to others at all times.

27
Q

What are defining histology features of Alcoholic Hepatitis?

A
  • Liver cell damage:
    • ballooning degeneration
    • Mallory-Denk Bodies
  • Inflammation
  • Fibrosis
28
Q

What does NASH stand for?

A

Non-alcoholic steato-hepatitis

29
Q

What is the management of alcoholic hepatitis?

A
  • Supportive
  • Stop alcoholic
  • Nutrition
  • Vitamins (B1, thiamine)
  • Ocassionally steroids
30
Q

What diseases do deficiencies in these cause?

  • Vit D
  • Vit C
  • B12
  • B1
  • B3
  • Folic acid
A
  • Vit D = Rickets
  • Vit C = Scurvy
  • B12 / IF = Pernicious anaemia
  • B1 = Beri-beri
  • B3 = Pellagra
  • Folic acid = neural tube defects
31
Q

What are clinical features of chronic stable liver disease?

A
  • Multiple spider naevi
  • Dupuytren’s contracture
  • Plamar erythema
  • Gynaecomastia
32
Q

What else are you most likely to find on careful abdominal examination, given the visible vein on the anterior abdominal wall?

A

Splenomegaly. Increasing portal vein pressure goes up to the spleen. Splenomegaly is a sign of portal hypertension.

33
Q

What are 3 clinical features of portal hypertension caused by cirrhosis?

A
  • Visible veins
  • Splenomegaly
  • Ascites
34
Q

What causes a liver flap?

A

Liver flap is due to poison toxins to the brain due to inability of the liver to clear them.

35
Q

What are the consequences of liver failure?

A
  • Failed synthetic function
  • Failed clotting factor and albumin
  • Failed clearance of bilirubin
  • Failed clearance of ammonia (encephalopathy)
36
Q

What is the management of liver failure?

A
  • Minimize work done by the liver
  • Minimize GI bleeding
  • Wait and hope they recover OR give them a new liver
37
Q

What is intra-hepatic shunting of blood?

A

Blood comes into the portal tract via the portal vein and hepatic artery, trickles down the sinusoids and emerges through the hepatic vein. Here the patient develops scarring between the portal tract and the central vein so instead of trickling past the hepatocytes there is collagen tissue. Blood comes into the liver, it goes nowhere near the hepatocytes, it bypasses them completely, it comes in and then comes out. Nothing is done to the blood. This is called intra-hepatic shunting of the blood.

38
Q

What is a porto-systemic anastomoses?

A

Area where the portal blood meets the systemic blood.

39
Q

Where are the possible sites of porto-systemic anastamoses?

A
  • Oesophageal varices
  • Rectal varices
  • Umblical vein recanalising
  • Spleno-renal shunt
40
Q

What does scratching with jaundice suggest?

A

A post-hepatic cause

41
Q

What 2 things make up bile?

A

Bilirubin and bile salts

42
Q

What is the role of bile salts?

A

Bile salts emulsify fats. Bile salts deliberately excreted into the gut, emulsify fat then reabsorbed later downstream in the gut so there is enterhepatic circulation.

43
Q

What causes itching in post-hepatic jaundice?

A

Bile salts or bile acids. Both not in the blood stream usually but appear when you block the bile duct.

44
Q

What is Courvoisier’s Law?

A

In the presence of jaundice, if the gall bladder is palpable, the cause is unlikely to be gall stones. This is because a gall bladder with stones is usually small and fibrotic and incapable of being large.

YEAR 5: Chemical Pathology JK (26 decks)

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