Clinical pathology Flashcards

1
Q

Hepatocellular enzymes small animals

A

ALT - liver specific

AST - not liver specific - also found in muscles & rbcs

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2
Q

ALP is found in

A

liver, bone, placenta, intestinal mucosa, renal tubules

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3
Q

Muscle damage

A
Increased AST (but no increase ALT)
Increased creatinine kinase
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4
Q

Increased ALP in cats

A

Small rise significant following liver damage. Insensitive for choleostasis.

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5
Q

Increased ALP in dogs

A

Indicates choleostasis

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6
Q

Increased GGT

A

choleostasis & biliary hyperplasia
(+ due to steroids & anti-convulsants in dogs)
more sensitive marker than ALP in cats.

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7
Q

Hepatic lipidosis in cats

A

Marked increase ALP + normal GGT

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8
Q

Bile acid production

A

Produced from cholesterol in hepatocytes.
- conjugated to taurine or lysine
- released into biliary system
- stored in gall bladder
- released into SI - aid fat absorption
Continually circulate between liver and intestine, small amounts lost in faeces

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9
Q

Increased fasting serum bile acid concentration

A
  1. disruption of the enterohepatic circuit - cholestasis/bile duct obstruction or PSS
  2. reduced uptake/excretion by hepatocytes - damage or reduced mass
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10
Q

Bilirubin production

A

RBCs degraded by macrophages in liver/spleen/BM - unconjugated bilirubin - binds albumin - taken up by hepatocytes - conjugated bilirubin - biliary system - intestines

  • converted to faecal pigment by intestinal bacteria
  • reabsorbed - excreted in urine
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11
Q

Hyperbilirubinaemia causes

A

(jaundice)

  1. pre-hepatic - haemolytic anaemia - also see severe regenerative anaemia.
  2. hepatic dz - abnormal uptake, conjugation & release
  3. post-hepatic biliary obstruction
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12
Q

Increased ammonia levels

A
  • hepatic insufficiency
  • PSS
  • increased production - excessive protein diet, GI bleeding, urea cycle failure
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13
Q

Ammonia processing

A

produced in intestines as a by product of protein metabolism - detoxified to urea in hepatocytes

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