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Pharm Exm 4 > Non-opioid Analgesics > Flashcards

Non-opioid Analgesics Flashcards

1
Q

NSAIDs - Arylpropionic acids

A

Ibuprofen

Naproxen

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2
Q

NSAIDs- Arylacetic Acids

A

Indomethacin

Diclofenac

Ketorelac

Etodolac

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3
Q

For myalgias, arthralgias, sprains, strains

A

Ibuprofen

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4
Q

For Dysmenorrhea

A

Ibuprofen

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5
Q

For Headache

A

Tylenol

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6
Q

May potentially inhibit bone healing (post-ortho)

A

Tylenol

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7
Q

Three therapeutic applications of NSAIDs

A

Analgesic

Antipyretic

Anti-inflammatory

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8
Q

Three phases of inflammation

A

Acute (vasodil)

Subacute (infiltration)

Chronic (proliferation)

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9
Q

___ and ___ protect the stomach lining

–what is the enzyme?

A

PGE2 and PGI2

(inhibit acid, promote mucus)

COX1

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10
Q

COX1 is ___

COX2 is ___

A

1 = constitutive

2 = Inducible

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11
Q

COX2 is present constitutively in..

A

the brain and spinal cord

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12
Q

Aspirin MOA

A

Acetylates COX (ser529)

Irreversibly Inhibits COX1/2

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13
Q

NSAIDs (except aspirin) are ______

A

competitive, reversible inhibitors of COX1/2

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14
Q

These NSAIDs also inhibit LT synthesis

A

Indomethacin

Dicclofenac

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15
Q

Aspirin mainly absorbed here

A

Jejunum

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16
Q

Aspirin distribution

A

Most tissues/fluids

Crosses placenta

17
Q

Aspirin T1/2

A

15 minutes

(but metabolite salicylate half life = 12 hr)

18
Q

Is aspirin secreted or reabsorbed in tubule

A

Yes

Active secretion, Passive reabsorption

19
Q

Non-salicylate NSAID’s show little

A

first pass metabolism

(Multiple routes of metabolism – Oxidation, Demethylation, Conjugation)

20
Q

Timeline for aspirin analgesic tolerance

A

no tolerance with analgesic effects!

21
Q

Arylpropionic acids T1/2

A

Ibuprofen = 2h

Naproxen = 14h

22
Q

_____ is safest Arylpropionic in coronary artery disease

A

Naproxen

23
Q

Acetic acid derivatives and their risks

A

Diclofenac (peptic ulcer/kidney dysfxn if prolonged use)

Indomethacin (Gout, ankylosing spond. pericarditis)

Ketorolac (Less than 5 days, low GI effect)

(also etodolac?)

24
Q

Meloxicam at low doses is..

A

COX-2 selective

(long T1/2 = 20hrs)

25
Q

Has a half life of 57 hours!

A

Piroxicam

26
Q

Advantages of APAP

A

No GI tox

Liver dz patients ok

No platelet effect

No Reye’s

27
Q

APAP overdose leads to

A

hepatic necrosis

28
Q

Salicylates - ____ given for GI distress

A

Misoprostol

(PGE1 analog – also labor induction)

29
Q

Metabolic derangement on overdose

A

Metabolic acidosis (kids) and Resp alkalosis (adults)

MAcid = Early decrease in ATP, Late Increase in Lactate and pyruvate

RAlk = Direct stimulation of medullary respiratory centers

30
Q

Sakucylism effects

A

Mild = vertigo, tinnitus, hearing loss

Moderate/Severe = N/V, sweating, fever, delirium/psychosis, stupor, coma

31
Q

Tx for aspirin poisoning

A
  1. Increase urinary excretion (dextrose, sodium bicarb)
  2. Hemodialysis
  3. Charcoal
  4. Correct metabolic imbalance
32
Q

Non-salicates labor use

A

Delay preterm labor by inhibiting uterine motility

33
Q

APAP AE’s (kidney and liver)

A
  • Papillary necrosis, Vasoconstriction by inhibition of PGE2
  • Dose dependent hepatic necrosis (increased with Alcohol’s induction of CYP450)
34
Q

Selective COX2 inhibitors

A

Rofecoxib (Vioxx - withdrawn!)

Celecoxib (Celebrex)

35
Q

All NSAID’s CI’d in…

A

CKD

Peptic Ulcer Dz

GI bleeding Hx

36
Q

NSAID Cardiovascular risk is highest in ____ and lowest in _____

A

Highest = Diclofenac

Lowest = Naproxen

37
Q

NSAIDs that interfere with bone healing

A

All of ‘em

(in high doses)

38
Q

____ less likely to cause NSAID-induced asthma exacerbations

A

COX2-specific

39
Q

Antiproliferative DMARD’s

A

MTX

Cyclophosphamide

Azathioprine

Suppress B and T cell proliferation and function

Pharm Exm 4 (7 decks)

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