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14 Cards in this Set
- Front
- Back
why is therapeutic drug monitoring (TDM) needed?
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some drugs have a very low therapeutic index (LD50/ED50) hence can easily OD. sometimes there can be a poor correlation between dose and circulation concentration, and therapeutic and toxic effects
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how do you work out TDM and what samples do you need?
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usually need 6 intervals to get steady state and multiply by the half life of the drug to work out how long to monitor for (normally about 2 weeks). with repeated dosing, a steady plasma concentration is attained (Cmax and Cmin unchanged). need venous blood for plasma or serum
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in what stage of inflammation to NSAIDS have their greatest effect?
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In the acute transient phase when there is local vasodilation, and increased capillary permeability
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What are the main effects of NSAIDS? what are their benefits?
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analgesic, anti inflammatory, anti pyretic, used for pain and inflammation in chronic osteoarthritis, post trauma and perioperatively.
they are non-narcotic, non sedating, not ataxia inducing and can be used with narcotics. |
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what are some other uses of NSAIDS?
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anti-tumour effects via COX-2 inhibition for transitional cell carcinomas (-oxicam family)
antithrombotic (reduce risk of thromboembolism) ophthalmic (keratitis and scleritis) immune modulating (decrease autoantibody producing B cells) ie rheumatoid arthritis antipyretic is cattle, endotoxic shock |
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how to NSAIDS work:
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Inhibit COX 1 and COX 2 and also LOX.
cell damage→ phospholipids→ phospholipase(inhibited by corticosteroids)→ arachidonic acid→ COX 1 and 2 to produce thromboxane and prostaglandins or LOX to produce leukotrienes |
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describe the differences between COX 1 and 2
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COX 1 is constitutively produced and has many protective roles, present in BV, GI, mucosa and kidney, produces PGE2 and PGI2.
COX 2 is induced after an injury (ie ischaemia, infec, trauma) to produce mediators of pain, inflammation and pyrexia. |
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what can NSAIDS have adverse effects on?
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GI tract (ulceration)
kidneys blood liver toxicity inhibit proteoglycan synthesis |
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describe how NSAIDS cause gastric ulceration
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prostaglandins (PGI2 and PGE2)have protective function by inhibiting mucous secretion, increasing mucosal blood flow and production. to alleviate the side effects, omeprazole (H2 blocker) can reduce acid secretion, misoprostal is a PGE analogue hence prevents ulceration. USE COX-2 inhibitors
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describe how NSAIDS have adverse effects on kidneys
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normally PGE2 and PGI2 increase salt and water excretion and increase renal vasodilation. increased water retention→ hypertension→ decreased renal blood flow→ interstitial necrosis and nephritis. Animals with heart dis (hence lower CO) at increased risk.
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why should you not use NSAIDS in volume depleted animals?
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can lead to renal compromise, failure and death
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describe how NSAIDs can have an adverse reaction on blood
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thromboxane is a proaggregator of platelets needed for thrombus formation and haemostasis. older drugs inhibit hence cause prolonged bleeding time. (Not COX2 specific drugs)
removal of PGI2 inhibits platelet aggregation, hence can cause abnormal bleeding. |
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how to NSAIDS cause liver toxicity?
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accumulation of toxic metabolites?
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when would you use NSAIDS in cats and when would you not?
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if severe inflammation ok, give with IV fluid is dehydrated. Not if has kidney or bleeding problems. Moderate pain relief may be ok to give, but not to replace antinflammatory. meloxicam is the only NSAID safe to use in cats.
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