LFTs Flashcards

1
Q

components assessed

A
  • AST - aspartate aminotransferase
  • ALT ananine aminotransferase
  • ALP alkaline phosphatase
  • GGT - gamma-glutamyl transferase
  • bilirubin - total and direct
  • albumin
  • PT / INR (prothrombin time / international normalized ratio)
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2
Q

alanine aminotransferase

A

RAISED - HEPATOCELLULAR
- Involved in amino acid metabolism
- mostly found in liver - making it more of a specific marker of liver injury than AST
- found in hepatocytes
- almost entirely in cytoplasm and not mitochondria

levels;
- normal - 7-56

pathology:
- hepatocyte distress - leaks into blood
- because its in the cytoplasm it leaks more readily and earlier

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3
Q

aspartate aminotransferase

A

RAISED = HEPATOCELLULAR
- enzyme involved in amino acid megtabolism
- key role in krebs

found in:
- liver
- heart
- skeletal muscles
- kidneys
- brain
- RBC

levels:
- normal 10-40
- mostly found inside cells - abnormal to be in blood

when liver is injured cell membranes become damaged, causing AST to leak into the bloodstream
- this is because its released during necrosis
- in severe cases mitochondrial AST is released

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4
Q

alkaline phosphatase

A

RAISED = CHOLESTATIC
- removes phosphate groups from molecules
- functions best in alkaline conditions

found in:
- liver in bile ducts
- bone
- placenta
- kidneys and intestines

physiology:
- in liver - helps in bile secretion and production

levels:
- 30-120 normal
- found in bile ducts so if high in blood - biliary disease eg gallstones

if present with high GGT - liver disease
if present with normal GGT - bone disease

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5
Q

gamma-glutamyl transferase

A

RAISED = CHOLESTATIC
- enzyme involved in glutathione metabolism and amino acid transfer
- Involved in detoxification
- prominent in alcohol-related liver damage
- normal level 8-61
- higher in men
- naturally inc with age

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6
Q

bilirubin

A
  • yellow pigment from Hb breakdown

levels:
- total - 0.3-1.2
- unconjugated - 0.1-0.7
- conjugated - 0-0.3

why it increases:
- inc rbc destruction eg bleeding and hemolytic anaemia
- impaired liver uptake or conjugation of bilirubin eg hepatitis
- bile duct obstruction eg gallstones

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7
Q

how is bilirubin formed?

A
  • rbc breakdown and produce heme
  • heme is converted into biliverdin (green)
  • this is then reduced to bilirubin
  • this is unconjugated and bound to albumin
  • transferred to liver where it is conjugated
  • then is secreted into bile, stored in the gallbladder, and released into the intestines for excretion in stool
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8
Q

albumin

A

functions:
- maintains oncotic pressure
- transports substances
- detoxification
- buffers blood PH

levels:
- 35-50

pathology:
- liver diseases can cause decreased slbumin synthesis
- low levels in liver disease - poor prognosis

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9
Q

Prothrombin Time (PT) / International Normalized Ratio (INR) in Liver Disease

A
  • Clotting factors are produced by the liver
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10
Q

investigating Ascites

A

serum albumin
low - liver cirrhosis, heart failure, portal vein thrombosis, alcoholic hepatitis

high - TB, pancreatitis, infection, peritoneal cancer, nephrotic syndrome

High neutrophil count seen in spontaneous bacterial peritonitis

High lymphocyte count seen in TB

Bloody fluid could be malignancy or trauma

Milk coloured (chylous) could be lymphoma, TB, malignancy

Cloudy could be SBP, perforated bowel, pancreatitis
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