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Advanced Biochemistry > Liver Function 11/11 > Flashcards

Liver Function 11/11 Flashcards

1
Q

What are the 2 types of liver cells?

A

Hepatocytes and Kuppfer cells

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2
Q

What is the function of hepatocytes?

A

Protein synthesis

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3
Q

What is the function of Kupffer Cells?

A

Macrophages lining sinusoids that act as phagocytes and engulf bacteria, toxins and debris

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4
Q

What are the 5 major functions of the liver?

A
  1. Metabolism
  2. Synthesis
  3. Storage
  4. Detoxification
  5. Excretion/digestion
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5
Q

Describe the metabolic function of the liver.

A

Carbohydrate metabolism (storage of glycogen/release of glucose)
Protein metabolism
Lipid/cholesterol metabolism

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6
Q

Describe the synthesis function of the liver.

A

The liver synthesises plasma proteins such as albumin, clotting factors and c-reactive proteins

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7
Q

Describe the storage function of the liver.

A

Stores iron, glycogen, amino acids, some vitamins (A, D, B12), temporary lipid storage

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8
Q

Describe the detoxification function of the liver.

A

Detoxifies alcohol, paracetemol, drugs, GIT metabolites

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9
Q

Describe the excretory/digestive function of the liver.

A

Removes waste eg degrades bilirubin and excretes excess cholesterol in bile

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10
Q

Define jaundice.

A

A clinical condition associated with increased serum bilirubin and its deposition in the skin, mucous membranes and white of the eye (sclera) giving a characteristic yellow colouring known as icterus

= problems with heme degredation

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11
Q

What causes prehepatic jaundice?

A

anything which causes an increased rate of haemolysis (breakdown of red blood cells) (eg malaria, sickle cell disease, haemolytic disease of the newborn)

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12
Q

What biochemical changes will you see in prehepatic jaundice?

A

Increase in unconjugated bilirubin
Increase in plasma total bilirubin
Increase in urine urobilinogen

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13
Q

What are the 3 types of hepatic/intrahepatic jaundice?

A
  1. Hepatocellular damage
  2. Disorders of bilirubin metabolism and transport
  3. Transient immaturity of the liver - neonatal physiological jaundice
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14
Q

What are the 4 different causes of hepatocellular damage?

A
  1. Hepatitis
  2. Drug induced hepatic damage
  3. Wilson’s disease
  4. Liver tumors
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15
Q

Describe Wilson’s disease.

A

Low levels of caeruloplasmin (copper transport protein) resulting in deposition of copper in the liver causing cirrhotic damage (scarring of liver cells)

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16
Q

What biochemical changes will you see in hepatic/intrahepatic jaundice?

A 
Increased conjugated bilirubin
Increased total plasma bilirubin
Increased urine bilirubin
Decreased urine urobilinogen
Increased plasma AST and ALT
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17
Q

What are the 3 disorders of bilirubin metabolism and transport?

A
  1. Gilbert’s disease
  2. Crigler-Najjar disease
  3. Dublin-johnson syndrome
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18
Q

Describe Gilbert’s disease.

A

Defective transport of bilirubin into the hepatocytes = causes an increase in unconjugated bilirubin

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19
Q

Describe Crigler-Najjar disease.

A

Hereditary deficiency of the UDPG-transferase enzyme (can’t convert unconjugated bilirubin to conjugated)

20
Q

Describe Dublin-Johnson syndrome.

A

Deficiency of canalicular multidrug transporter protein = defective removal of conjugated bilirubin = accumulation in blood

21
Q

Describe transient immaturity of the liver - neonatal physiological jaundice

A

Short term delay in the ability to produce UDPG-transferase enzyme resulting in rapid buildup of unconjugated bilirubin

22
Q

What are the possible treatment options for neonatal physiological jaundice?

A

Phototherapy (UV light) to isomerise bilirubin into a non-toxic form
Exchange blood transfusion to prevent damage to the brain (kernicterus)

23
Q

What causes posthepatic jaundice?

A

Partial or complete obstruction of the biliary tree that prevents flow of conjugated bilirubin into the bile canaliculi (stools become clay coloured since it doesn’t reach the gut)

e.g gall stones or pancreatic cancer

24
Q

What biochemical changes will you see in posthepatic jaundice?

A 
Increased conjugated bilirubin
Increased total plasma bilirubin
Positive urine bilirubin
Decreased urine urobilinogen
Increased plasma GGT and ALP
25
Q

What are the 3 types of liver function tests?

A
  1. Tests measuring synthetic ability
  2. Tests measuring nitrogen metabolism
  3. Tests measuring bilirubin metabolism
26
Q

What are the 3 things you could measure when testing for synthetic ability of the liver?

A
  1. Albumin - major plasma protein produced by the liver, decreased in chronic liver disease
  2. Prothrombonin time - commonly increases in liver disease due to inadequate production of clotting factors and inadequate absorption of vitamin K from intestine due to disrupted bile flow
  3. Lipids - hepatic disorders cause derangements in lipoproteins metabolism but this is not specific for liver
27
Q

Why is albumin testing not useful for acute liver disease?

A

Because it has a long half life there will still be albumin levels circulating

28
Q

Describe tests measuring nitrogen metabolism.

A

Protein metabolism produces ammonia NH4+ which is toxic so is converted to urea by the liver

In liver failure plasma ammonia levels are increased and are responsible for neurological signs of hepatic encephalopathy (decline in brain function), transient hyperammonaemia in newborn due to liver immaturity, or urea cycle enzyme deficiencies

29
Q

What are the 3 main types of liver function tests (broad)?

A
  1. Liver function
  2. Liver damage tests
  3. Cholestasis
30
Q

What do tests measuring bilirubin metabolism measure for?

A

Total plasma bilirubin
Conjugated/unconjugated bilirubin
Urine bilirubin
Urine urobilinogen

31
Q

What enzymes are measured in liver damage tests and why?

A

Plasma AST and ALT - released into circulation after an injury that results in cytolysis or necrosis

32
Q

What is measuring AST and ALT used for?

A

Used to differentiate hepatocelluar damage from obstructive liver disease

33
Q

Where is AST produced?

A

By hepatocytes and many other tissues such as cardiac muscle, skeletal muscle and erythrocytes

34
Q

Where is ALT produced?

A

Primarily by hepatocytes (more specific than AST)

35
Q

In acute hepatitis, what biochemical response would you see?

A

Early and dramatic rise in AST and ALT

36
Q

In hepatic necrosis why would you see a sudden decrease in AST and ALT?

A

Due to total liver cell destruction - bad prognostic sign

37
Q

In chronic hepatits what levels of AST and ALT would you see?

A

Mildly elevated levels of AST and ALT

38
Q

From alcohol, drugs, cirrhosis, what levels of AST and ALT would you see.

A

AST higher than ALT

39
Q

What is cholestasis?

A

Blockage of the bile duct = no bile can flow from the liver to the intestine

40
Q

What causes intrahepatic cholestasis?

A

Liver cancer, biliary cirrhosis

41
Q

What causes extrahepatic cholestasis?

A

Gallstone or tumor blocking

42
Q

What enzyme is more specific to blockage of bile duct?

A

GGT

ALP is produced by hepatocytes but also bone, intestine and placenta

43
Q

How are GGT levels used to monitor alcohol intake?

A

Levels decline with abstention of alcohol intake

44
Q

What is the limitation of liver enzymes in acute disease?

A

They don’t correlate with severity/prognosis

45
Q

What is the limitation of liver enzymes in chronic liver disease?

A

They can only tell us something is wrong with the liver - not useful in addressing severity or progression

Advanced Biochemistry (18 decks)

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