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Block 3 Up To Quiz 1 > NSAIDS PT 2 > Flashcards

NSAIDS PT 2 Flashcards

1
Q
A
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2
Q

prostacyclin (PGI2) fx in vessels

A

stimulates vasodilation and inhibit platelet aggregation inhibit this promote clotting (high does aspirin will do this thats why can only give a low dose)

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3
Q

NSAID absorption

A
  • absorbed rapidly and almost completely following oral administration - peak plasma concentration 2-4 hrs after oral administration - absorption mainly in stomach and upper small intestine, influenced by pH - most are weak acids and are un-ionized in highy acidic gastric environment in
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4
Q

NSAID un-ionized state

A

high lipid soluble and easily diffuse into gastric cells where pH is higher and the drug dissociates; NSAIDs highly protein bound (mainly to albumin) only unbound drug is biologically active

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5
Q

NSAID metabolism and excretion

A

metabolized in lier and mainly excreted in urine - eliminated by conduction (glucuronidation, sulfating, glycination), or oxidation (cytochrome p450 enzymes)

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6
Q

carporphen and keotprophen eliminated

A

primarily by conjucation

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7
Q

meloxicam and piroxiacm eliminted

A

clear by oxidation

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8
Q

feline NSAID elimination

A

cats defecting in several drug conjunction pathways -> slow elimination of certain drugs must be careful with dosing or can -> adverse effects - phenolic compounds slow elimination in felines bc lack several enzymes for glucuronidation - certain drugs, piroxicam cleared more rapidly in cats than humans and dogs - slower aspirin clearance bc poor glycine conjugation

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9
Q

adverse effets NSAIDs

A

common: - V+ - D+ - anorexia - lethargy - melena mostly due to gastropathies and renal toxicosis Uncommon: - cardiovascular and hepatic problems possible but rare

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10
Q

gastric epithelium normal

A
  • gastric epithelium normally secretes bicarbonate-rich fluid and forms protective mucosal gel layer providing defense against gastric acid - gel contains phospholipids that make it hydophobic preventing back diffusion of acid from gastric lumen to epithelial cells - surface epithelial cells rapidly migrate and divide to repair small defects - Adequate mucosal blood flow allows epithelium to tolerate wide array insults, reduced mucosal blood flow -> sever mucosal injury
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11
Q

NSAIDs gastric damage

A
  • induce gastric damage through local and systemic effects -NSAIDs slightly acidic can become concentrated in gastric mucosa via ion trapping -> direct cellular injury - inhibition endogenous PG production -> systemic effects bc decreased PG production -> decreased mucin quality and bicarbonate content of mucous gel layer -> more vulnerable mucosa more vulnerable to acid-induced injury - NSAIDs can inhibit endogenous prostanoids which have vasodilatory affect normally-> areas reduced blood flow w/ in mucosa
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12
Q

renal blood flow regulation normally

A
  • PGE2 and PGI2 function normally function as vasodilatory agents to regulate renal blood flow, when there is decreased renal profusion PGs cause afferent arteriolar dilation -> maintain renal blood flow by counteracting the effect of systemic vasoconstrictors
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13
Q

shorter use NSAIDs healthy animal renal function

A

should have little effect on renal hemodynamics and function

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14
Q

Use of NSAIDs during hemodynamic compromise

A

circulating vasoconstrictors released to maintain vascular resistance and blood pressure at expense of organ blood flow, kidneys more dependent on vasodilatory effects of PG to maintain renal blood flow and glomerular filtration rate; use of NSAIDs during this time will prevent this retention of renal blood flow and glomerular filtration rate normally achieved during hemodynamic compromise which: can -> ischemic kidney injury -> acute renal failure

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15
Q

NSAID potential risks in cardiovascular and hepatic systems

A
  • vet patients without cardiovascular or hepatic problems rarely present adverse symptoms in these symptoms with NSAIDS - NSAIDs can generate impabalcne between vasodilatory PGI2/PGE2 and vasoconstrictive TXA2 in endothelium which can -> thrombosis and heart failure - COX2 inhibition by NSAIDs promotes sodium and water retention -> exacerbation heart failure and hypertension and increase adverse ventricular remodeling - acute liver failure possible after prolonged usage or an overdose like any other drug
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16
Q

NSAIDs use for vet pateints

A

-carprophen - meloxicam - flunixin - ketoprophen -aspirin

17
Q

carprophen

A
  • cox2 selective at low dose - at high dose lose selectivity COX-2 and toxicity can result from inhibition COX-1 - mostly used in dogs - oldest of new NSAIDs
18
Q

meloxicam

A
  • mostly for treatment osteoarthritis in dogs - single dose injectable prior to sx use in cats for postoperative pain and inflammation associated with ortho sx, ovariohysterectory, castration - oral pain calves, sheep, goats, pigs - studied in horses
19
Q

flunixin

A
  • large animals - horse soft tissue pain
20
Q

ketoprophen

A
  • large animals and exotics
21
Q

aspirin

A
  • rarely used for analgesia now - anti-thrombotic - dogs tolerate better than cats
22
Q

COX-2 specific inhibitors

A
  • robenacoxib - deracoxib - firocoxib
23
Q

robenacoxib

A

onsior post op pain and inflammation in dogs and cats

24
Q

deracoxib

A

osteoarthritis dogs

25
Q

firocoxib

A

horses and dogs

26
Q

side effects COX2 specific inhibitors

A
  • COX-2 specific NSAIDs “safer” for GI tract but worst side effects seen with COX-2 specific inhibitors probably bc COX2 plays role in healing
27
Q

give cox2 inhibitor to dog with subclinical GI dx

A
  • healing process slows down so potentially leads to perforated stomach or intestine - do not use NSAIDs in patient with GI dx
28
Q

grapiprant

A
  • non-COX-inhibiting prostaglandin receptor antagonist (PRA) - trade name Galliprant - works by blocking EP4 receptor = primary mediator canine OA pain and inflammation
29
Q

why use NSAIDs during sx

A

prevent peripheral sensitization bc peripheral system receiving signals and amplifiers problem when patient wakes up

30
Q

acetyl salicylic acid

A

aspirin

31
Q

COX enzymes=

A

cyclooxygenases

32
Q

what converts phospholipid to arachadonic acid

A

phospholipase A2

33
Q

COX 1 summary

A
  • ubiquitous and constitutive - mucosal defense (PGE2) - Renal perfusion (PGE2 and PGI2) - Platlet aggregation (TXA2)
34
Q

COX2 summary

A
  • inducible - inflammation and tumorigenesis
35
Q

PGE2 modulates peripheral sensation via

A

EP receptors - EP affects K+ channels and makes membrane more excitable by blocking K+ channels and exciting Na+ channels - more Ca2+ release bc potentiates Ca2+ - NSAIDs that block PGE2 suppress pain

36
Q

EP4

A

PGE2 receptor antagonize the EP4 with grapiprant and reduce dog osteoarthritis pain and inflammation with less side effects than NSAIDs

Block 3 Up To Quiz 1 (24 decks)

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