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MSK Pharm > NSAIDS > Flashcards

NSAIDS Flashcards

1
Q

biosyn of prostaglandins

A
  • cell membrane phospholipids
  • phospholipase A2 (PLA2)
  • AA
  • Cyclooxygenase (COX)
  • prostaglandin (PG) H2
  • tissue-specific isomerases
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2
Q

tissue specific isomerases- uterus, GI, renal a, BVs, platelets, CT

A
  • uterus- PGF2alpha, PGE2
  • GI- PGE2
  • renal a- PGE2
  • BVs- PGI2
  • platelets- TxA2
  • CT- PGE2
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3
Q

excess of PGs in inflamed tissue causes what?

A
  • heat
  • redness
  • swelling
  • pain
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4
Q

prostaglandins- effects on vasculature, CNS, PNS

A
  • PGI2- vasodilation
  • PGE2- permeability
  • PGE2 in CNS- Temp (Fever)
  • PGE2 in PNS- pain sensitization
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5
Q

aspirin and salicylate- anti-infl effects at?

A

higher doses (2-3 g/day)

  • aspirin metabolized to salicylate by liver
  • high dose ASA- pro-drug for anti-infl doses of salicylate
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6
Q

aspirin and salicylate- toxicities

A

COX-indep:

  • acid-base disturbance
  • tinnitus
  • hypersensitivity
  • Reye’s syndrome
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7
Q

aspirin and salicylate- 6-20 g- toxicity

A
  • early- resp alkalosis
  • later- metabolic acidosis
  • fever, dehydratino
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8
Q

progression of aspirin/salicylate toxicity

A
  • salicylates uncouple mitochondrial ox phos in CNS
  • resp center registers dec in ATP fas hypoxemia- responds with hyperventilation
  • hyperventilation blows off CO2- causes resp alkalosis- prompts kidney to deplete bicarbonate
  • organic acids accum b/c ATP is no longer generated thru Krebs cycle
  • metabolic acidosis- life-threatening
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9
Q

Aspirin- contraindications

A

Fever in children/adolescents!!!

  • anyone < 19 yo with a fever- risk of Reye’s syndrome!!!
  • alternative- acetaminophen
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10
Q

traditional NSAIDs- drugs

A
  • Ibuprofen
  • Indomethacin
  • Naproxen
  • Diclofenac
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11
Q

Coxibs- drugs

A

-Celecoxib

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12
Q

Salicylates- drugs

A
  • Salicylate
  • Aspirin
  • Diflunisal
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13
Q

NSAIDS- moa

A
  • inhibit COX- inhibit prostaglandin syn- reduce local edema, vascular permeability (swelling), and pain
  • anti-infl, analgesic, and anti-pyretic
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14
Q

COX-1 and 2- similarities

A
  • use same substrates (AA)
  • make same products (PGs)
  • role in infl
  • role in renal fxn
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15
Q

COX-1

A
  • constitutive- in all tissues
  • PROMINENT role responding to physiological stimuli
  • also has a role in responding to pathological stimuli that release AA from cells
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16
Q

COX-2

A
  • distinctive physiological role in kidney!!

- COX-2 expression is induced- PROMINENT role responding to pathological stimuli

17
Q

COX1, PGs, and inflammation

A
  • infl stim AA release
  • COX-1 converts AA into PGE2
  • PGE2 causes sx’s- erythema, edema, pain
18
Q

COX-2 induction in inflammation

A
  • infl induces COX-2 expression
  • COX-2 converts AA into PGE2
  • COX-2 derived PGE2 amplifies sx’s!!! (worse erythema, edema, pain)
19
Q

tNSAIDS and salicylate- do what

A
  • inhibit COX
  • lower PG formation
  • relieve sx’s
20
Q

traditional NSAIDs and salicylates- moa

A

-competitive, reversible, non-selective!!! (COX-1 and 2)

21
Q

NSAIDS- anti infl indications

A
  • MSK- osteoarthritis, other arthritides, bursitis, gout flare, ankylosing spondylitis
  • other- dysmenorrhea, headache
22
Q

traditional NSAIDs- complications

A
  • ulcer (inhibits mucosal integrity- PGE2)
  • bleeding (inhibits homeostasis- blood platelets- TxA2)
  • peripheral edema, inc BP (inhibits Na, H20 excretion- PGE2 and PGI2-)
23
Q

NSAIDs- not indicated when?

A
  • asthma
  • gut infl (gastritis, colitis, pancreatitis, hepatitis)
  • infectious infl/fever
24
Q

COXIBs- moa

A

(celecoxib)

-selective inhibition of COX-2

25
Q

Coxibs- are they gastric sparing?

A

-COX-1 sparing- yes!!

26
Q

Coxibs- contraindications

A

hypersensitivity to sulfonamides!!!

-Stevens-Johnson Syndrome

27
Q

Coxibs- complications

A

-peripheral edema, inc BP

28
Q

low-aspirin- does what

A
  • acts on platelets- antithrombotic effect
  • not anti-infl- dose is too low
  • irreversible COX inhibition persists days after ASA is metabolized
  • duration of actoin depends on cells ability/rate of COX regeneration- t1/2 of COX protein trumps t1/2 aspirin!!!
  • plts cant regenerate COX
29
Q

aspirin vs tNSAIDs

A
  • aspirin- at anti-infl doses, is a pro-drug- salicylate (reversible COX inhibitor)
  • aspirin- irreversible inhibitor!!!
  • tNSAIDs- reversible COX inhibitors
30
Q

Do Coxibs confer risk of CV toxicity?

A

COX-2 selective inhibitors

  • inhibit prostacyclin (antithrombotic)
  • COX-1- blood plts- thromboxane- thrombotic!!!- COX-1 sparing in platelets!!!
31
Q

NSAIDs- black box warning for?

MSK Pharm (10 decks)

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