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Clinical Pathology > CP11-5 Liver and Pancreatic Disease > Flashcards

CP11-5 Liver and Pancreatic Disease Flashcards

1
Q

What cells is the liver mainly made up of?

A

60% hepatocytes which each connect with a sinusoid, a biliary canaliculus and a neighbouring hepatocyte

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2
Q

What are the functions of the liver?

A

Stores glycogen, iron and vitamins A, D, E and B12
Synthesises glycogen, glucose (gluconeogenesis), proteins, clotting factors, urea, lipoproteins, cholesterol and bile acid
Catabolism of glucose (glycolysis) and proteins
Metabolism of amino acids, fatty acids and vitamins A, D, E and B12
Excretion of bile acid, bilirubin, drugs and steroid hormones
Detoxification/inactivation of drugs and steroids.

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3
Q

What are some systemic effects/signs and symptoms of liver disease?

A

Jaundice
excess oestrogen e.g. presenting as gynecomastia, spider naevi, liver palms, testicular atrophy
Bruising
Pigmentation
Clubbing
Dependent oedema
Ascites
Encephalopathy
Osteomalacia/osteoporosis

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4
Q

What is a common liver related symptom seen in babies?

A

Neonatal jaundice

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5
Q

What substances can be tested for to assess liver function?

A

Glucose
Albumin
Urea
Prothrombin - and prothrombin time
Cholesterol
Triglycerides
Bile acids
Bilirubin
Ferritin
Drugs
Steroid hormone

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6
Q

What do liver function tests test for?

A

Production of metabolites
Clearance of endogenous substances
Clearance of exogenous substances
Hepatocellular and biliary tract damage

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7
Q

What are some routine LFTs?

A

ALP (alkaline phosphatase)
ALT (alanine aminotransferase)
AST (aspartate aminotransferase)
Bilirubin
Albumin
Total protein
GGT (gamma glutamyl transferase)

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8
Q

What tests are done for viral hepatitis?

A

Serology for hepatitis viruses (A-E), CMV and HIV

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9
Q

What tests are used to investigate chronic active and autoimmune hepatitis?

A

Tests for anti-smooth muscle, anti-liver/kidney, anti microsomal and anti-nuclear antibodies

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10
Q

What tests are done into primary biliary cirrhosis?

A

Anti mitochondrial antibodies

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11
Q

What tests are done into hereditary hemochromatosis?

A

Ferritin, transferrin saturation, liver biopsy and genetic testing

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12
Q

What tests are done into Wilson’s disease?

A

Caeruloplasmin, urine copper, plasma copper and liver biopsy

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13
Q

What tests are done into alpha 1 antitrypsin deficiency?

A

Alpha 1 antitrypsin and genetic testing

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14
Q

What LFTs are done to look for hepatocellular cancer?

A

AFP as is a primary liver tumour marker

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15
Q

What test is more specific for liver disease - ALT or AST?

A

ALT as only released by cellular damage of the liver and AST is also released from red cells

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16
Q

What are common causes of acute hepatitis?

A

Paracetamol
Viral - hep B&E

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17
Q

How is acute hepatitis defined?

A

As severe hepatic dysfunction developing within 6 months of the first onset of liver disease and in the absence of pre existing liver disease.

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18
Q

How do patients with acute hepatitis present?

A

Hepatic encephalopathy (impaired brain function due to liver failure)
Prolonged and persistent prothrombin time and international normalised ratio
Grossly hepatic picture
Deep jaundice
Potentially hypoglycaemia

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19
Q

What commonly causes chronic hepatitis?

A

Virus - B and C
Alcohol
Wilson’s disease
Alpha 1 antitrypsin
Autoimmune hepatitis

20
Q

How is chronic hepatitis defined?

A

When there is clinical or biochemical features of liver disease perspiring for more than 6 months. This disease is graded according to necroinflammatory activity and degree of fibrosis.

21
Q

What are the 3 stages of alcoholic liver disease?

A

Fatty liver (steatosis)
Alcoholic hepatitis
Cirrhosis

22
Q

What results in LFTs are seen as a result of biliary tract damage?

A

Increased conjugated bilirubin (due to impaired excretory function)
Increased ALP and gammaGT (due to increased synthesis of enzymes by cells lining the bile canaliculi)

23
Q

What can cause increased production of ALP by cells lining the bile canaliculi?

A

Cholestasis (intra or extra hepatic)
Infiltrative disease
Space occupying lesions (tumours)
Cirrhosis

24
Q

Where is ALP produced?

A

Liver
Bone
Intestine
Placenta

25
Q

What can be used to look at ALP isoenzymes?

A

Electrophoresis

26
Q

What can cause elevated gamma glutamyltransferase?

A

Structural damage of liver by:
Alcohol
Enzyme inducing agents like anti-epileptics
Fatty liver
Heart failure
Prostatic disease
Pancreatic disease
Kidney damage

27
Q

How can you determine if a raised ALP is of liver origin?

A

By checking gamma GT levels

28
Q

What is primary biliary cirrhosis?

A

Chronic cholestatic condition with destruction of bile ducts associated with an isolated raised ALP, raised IgM and anti-mitochondrial antibodies presenting mainly in females with pruritus,jaundice and non-specific tiredness.

29
Q

What is primary sclerosing cholangitis?

A

A progressive disease of diffuse inflammation and fibrosis of the biliary system which is progressive and autoimmune - associated with IBD- appearing mainly in men. Starts with minor ALP elevations which progressively become more severe until patients have deep jaundice.

30
Q

What biochemical marker score can be used to asses fibrosis if the liver?

A

ELF (enhanced level fibrosis) score - which looks at PIINP, TIMP-1 and hyaluronic acid

31
Q

What is bilirubin a marker of?

A

The excretory capacity of the liver and free flow of bile

32
Q

What types of bilirubin are measured?

A

Total
Unconjugated
Conjugated

33
Q

At what level of bilirubin is jaundice seen?

A

When serum bilirubin > 40-50 micromoles per litre

34
Q

What does unconjugated bilirubin measure?

A

Pre hepatic and hepatic bilirubin levels

35
Q

What does conjugated bilirubin measure?

A

Post-hepatic (obstructive) and hepatic bilirubin

36
Q

What are normal bilirubin levels?

A

<20 micromoles per litre

37
Q

Is bilirubin soluble or insoluble in water?

A

Insoluble in water

38
Q

How is bilirubin transported in the blood?

A

Bound to albumin

39
Q

How is bilirubin metabolised?

A

Haemoglobin —> bilirubin <==> albumin bound bilirubin
/
/
Ligandin in liver conjugates bilirubin into bilirubin glucuroinde via UDP glucuronyl transferase —> excreted into bile for fat digestion and absorption

Bilirubin at kidney forms urobilinogen and is oxidised into urobilin and excreted in urine

40
Q

What are 2 pre-hepatic causes of hyperbilirubinaemia?

A

Haemolysis e.g. due to rhesus incompatibility
Ineffective erythropoiesis e.g. due to spherocytosis

41
Q

What are 4 causes of post-hepatic/obstructive hyperbilirubinaemia?

A

Gallstones
Biliary stricture
Cancer e.g. cholangiocarcinoma
Cholangitis

42
Q

What are some hepatic causes of hyperbilirubinaemia?

A

Unconjugated = pre-microsomal and microsomal causes + inherited disorders of conjugation like Gilbert’s
Conjugated = post-microsomal/impaired excretion, intrahepatic obstructions + inherited disorders of excretion like Dubin-Johnson

43
Q

What are some inborn errors of bilirubin metabolism?

A

Decreased activity of UDP glucuronyl transferase
Reduced ability to extreme bilirubin glucoronide

44
Q

What does an elevated AST/ALT and normal ALP suggest about a patients diagnosis?

A

Likely to have hepatitis (90%)

45
Q

What does a normal AST/ALT and an elevated ALP suggest about a patient’s diagnosis?

A

Likely to have obstructive jaundice (90%)

46
Q

Continue lecture at 34:20

A

Clinical Pathology (65 decks)

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