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Brain and Behavior 2 > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

common mechanisms of NSAIDs

A

inhibit COX, which blocks formation of prostaglandins, thromboxane A2

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2
Q

function of PGI2

A

vasodilation, inhibits platelet aggregation

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3
Q

function of TXA2

A

vasoconstriction, platelet aggregation

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4
Q

function of PGI2 and PGE2

A

decrease gastric acid secretion; lower pain threshold

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5
Q

function of PGE2 and PGF2

A

contract uterine smooth muscle

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6
Q

major sites of COX1 expression (which could result in toxicity of NSAIDs)

A

platelets, kidneys, blood vessels, stomach

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7
Q

when is COX2 expressed vs when COX1 is expressed?

A

COX2 expression is induced during inflammation; COX1 expression on nearly every cell

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8
Q

how do NSAIDs produce analgesia?

A

by blocking production of prostaglandins, which lower pain threshold. effective against mild to moderate dull, aching pain; act synergistically with opiates

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9
Q

how do NSAIDs produce anti-inflammatory effects?

A

reduce edema by bocking PGE2, PGI2; reduce pain; high concs of NSAIDs reduce neutrophil migration

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10
Q

how are NSAIDs antipyretic?

A

PGE2 alters body temp set point, so it blocks production of PGE2

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11
Q

clinical uses of NSAIDs

A

pain, primary dysmenorrhea, joint inflammation, fever

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12
Q

why is GI distress, damage, bleeding a common side effect of NSAIDs?

A

PGs help secrete mucous, bicardonate, H+ to protect the stomach from acid. NSAIDs decrease PG levels, so overtime the stomach acid causes pain and bleeding ulcers

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13
Q

common renal side effects of NSAIDs

A

fluid retention (increased AHD activity), decreased sodium excretion, decrease GFR, interstitial nephritis

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14
Q

common vascular side effects of NSAIDs

A

prolonged bleeding time and hypertension in sensitive patients.

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15
Q

contraindications of NSAIDs

A

px with reduced clotting factors, where TXA2 plays an important role in clotting; px with atheroschlerosis, where PGI2 plays an important role in opposing constriction (because NSAIDs increase bleeding and blood pressure)

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16
Q

salicylate NSAIDs

A

aspirin, diflunisal

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17
Q

acetic acid derivative NSAIDs

A

indomethacin, ketorolac

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18
Q

proprionic acid derivative NSAIDs

A

ibuprofen, naproxen

19
Q

enolic acid derivative NSAIDs

A

meloxicam

20
Q

COX2 selective NSAID

A

celecoxib

21
Q

mechanism of action of salicylates (aspirin)

A

binds to COX irreversibly!; alters ratio of PGI2:TXA2 in the vasculature (decreases TX over time)

22
Q

describe what happens to TXA2 and PGI2 in an endothelial cell after a dose of aspirin

A

inhibits endothelial and platelet COX; level of TX decreases permanently for the 21 day life of the platelets. endothelial cells regenerate AA and PGI in a couple hours.

23
Q

to reduce the chance of a 2nd MI, a px must..

A

take a low dose aspirin once every day

24
Q

PCKNs of aspirin/salicylates

A

rapidly metabolized to salicylic acid (T1/2=15 mins); salicylic acid is active/has T1/2 of 3-4 hours

1st order at low dises, 0 order at high doses

decrease of pH increases distribution

25
Q

symptoms of mild intoxication of aspirin (and how many grams?)

A

6-7 g: tinnitus, vomiting, vertigo, hyperventilation (resp alkalosis)

26
Q

symptoms/dose of moderate aspirin toxicity

A

8-10 g; increased metabolic rate, fever, metabolic acidosis

27
Q

symptoms/dose of severe aspirin toxicity

A

20-50 g: respiratory depression, higher free conc of drug, acid/base probs, dehydration, loss of electrolytes, coma, renal and resp failure

28
Q

treatment for salicylate intoxication

A

cool, rehydrate, correct electrolyte imbalance, prevent further absorption (emesis), alkalinize the urine to increase excretion (bicarb, or sodium citrate), hemodialysis, diazepam for convulsions

29
Q

contraindications of aspirin

A

px w/ renal disease, bleeding disorders, hypersensitivity, gout, young child after viral infection (reyes syndrome), use w/ caution during 3rd trimester

30
Q

properties of ibuprofen (proprionic acid derivative) at low doses vs high doses

A

low dose: more effective analgesic

high dose: anti-inflammatory activity as effective as aspirin

31
Q

half life of naproxen (proprionic acid deriv)?; potency?

A

long T1/2: 13 hr

intermediate potency

32
Q

most potent NSAID

A

indomethacin (acetic acid deriv)

33
Q

clinical uses of indomethacin

A

acute gout, spondylitis, osteoarthritis, ductus arteriosus

34
Q

NSAID that can be given IM or IV (orally and IV)/ clinical use?

A

ketorolac; short-term pain management

35
Q

half life of meloxicam/ what’s its more selective for / clinical uses

A

20 hr

COX2

osteoarthritis, RA

36
Q

why do selective COX2 inhibitors (celecoxib) have a health advisory?

A

they also have some selective inhibitor activity against PGI2 synthase; increased incidence of CV events

37
Q

studies show that non-aspirin NSAID use..

A

increases the incidence of arial fib and increases recurrent MI; even short-term use is not advised in px with known CV disease

38
Q

what is gout caused by? what triggers the inflammation?

A

metabolic disorder characterized by hyperuricemia and deposition of monosodium urate in joints; inflammation triggered by action of granulocytes trying to remove the urate crystals

39
Q

drugs for acute treatment of gout

A

colchicine, indomethacin

colchicine-highly toxic but good for acute attacks; nausea, vomiting, diarrhea

40
Q

drugs for prevention of gout

A

probenecid (urate diuretic) inhibits renal tubular reabsorption of urate

allopurinol (XO inhibitor) blocks urate synthesis by suicide inhibition of XO

41
Q

side effect of uricosuric agents and XO inhibitors

A

can cause acute gout attack when crystal begin to break up

to avoid this, use 1-2 weeks after an acute attack and combine with colchicine or NSAID (not aspirin)

42
Q

*site of inhibition of PGE2 production by NSAIDs

A

hypothalamus

43
Q

characteristic of mild intox of aspirin

A

tinnitus

Brain and Behavior 2 (25 decks)

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