Chapter 116 - hepatic failure Flashcards

1
Q

Hepatic encephalopathy typically occurs with the loss of how much hepatic function?

A

70%

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2
Q

List compounds found in excess in circulation in HE

A
ammonia
aromatic amino acids
bile acids
endogenous benzodiazepines
false neurotransmitters (tyrosine, phenylalanine, methionine)
GABA
glutamine
manganese
phenol
short-chain fatty acids
tryptophan
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3
Q

Which major excitatory neurotransmitter is increased with increased levels of ammonia?

A

Glutamate

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4
Q

What is ammonia converted to in the urea cycle in the healthy liver?

A

Glutamine, urea

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5
Q

What percentage of humans with hepatic failure have cerebral edema?

A

up to 80%

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6
Q

Mechanisms of coagulopathy in liver failure?

A
decreased factor synthesis
increased factor utilisation
decreased factor turnover
increased fibrinolysis & tissue thromboplastin release
dysfibrinogenemia
decreased platelet function & numbers
vitamin K def (esp with bile duct obstruction)
increased production of anticoagulants
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7
Q

mechanisms of pulmonary oedema in liver failure?

A

altered pulmonary capillary permeability
decreased albumin/COP
vasodilation
+/- endotoxemia

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8
Q

mechanism of PU/PD in liver failure?

A
  • decreased urea production so defective renal medullary concentration gradient
  • decreased release of ADH
  • decreased responsiveness of collecting ducts to ADH
    +/- primary polydipsia from central effects of hepatotoxins
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9
Q

possible RBC morphology changes in liver failure

A
target cells
acanthocytes
anisocytosis
(nonregen anaemia of chronic disease, chronic GI bleeding, shunting)
(regen anaemia if GI bleeding)
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10
Q

how does GGT sensitivity/specificity compare with ALP in cats with cholestatic disease?

A

more specific, less sensitive

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11
Q

why can small amounts of bilirubin in urine be normal in dogs but not in cats?

A

dogs can produce and conjugate bilirubin in renal tubules

cats cannot, and also have a higher threshold for bilirubin reabsorption (x9)

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12
Q

why is hypophosphatemia sometimes seen in hepatic encephalopathy?

A

centrally induced hyperventilation –> hypocapnia –> shift of intracellular carbon dioxide into the extracellular space –> increased intracellular pH –> accelerates the use of phosphate to phosphorylate glucose –> hypophosphatemia

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13
Q

why is fresh whole blood preferred to stored whole blood in HE patients requiring transfusion?

A

not as much ammonia

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14
Q

why are milk and vegetable proteins preferred over meat proteins for animals with HE?

A

lower in aromatic amino acids, higher in branched chain amino acids (valine, leucine, isoleucine), less likely to potentiate HE

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15
Q

MOA of vitamin E

A

antioxidant, prevents the action of lipid peroxidase on unsaturated bonds in hepatocyte cell membranes

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16
Q

MOA of silymarin

A

antioxidant and free radical scavenging properties. Inhibits lipid peroxidase and beta-glucoronidase. Inhibits the cytotoxic, inflammatory and apoptotic effects of TNF. Inhibits hepatic glutathione content and retards hepatic collagen formation.