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Pharm > NSAIDS & such > Flashcards

NSAIDS & such Flashcards

1
Q

five categories of anti-inflammatory and analgesics

A

1) . NSAIDS
2) . acetaminophen
3) . Adjunctive analgesics
4) . neuropathic pain relievers
5) . topical pain relievers

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2
Q

how are eicosanoids made?

A

these signaling molecules are made by oxidation of fatty acids (from membrane layers)

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3
Q

what are the main eicosanoid products we are concerned about?

A

EETs
Prostanoids
HETEs/Leukotrienes/Lipoxins

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4
Q

what are the three prostanoids?

A

prostaglandin, prostacyclin (PGI2), thromboxane (TXA2)

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5
Q

which enzyme converts membrane phospholipid to arachidonic acid?

A

phospholipase A2

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6
Q

which two enzymes convert arachidonic acid to prostanoids?

A

COX 1 and 2

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7
Q

which enzyme converts arachidonic acid to leukotrienes?

A

LOX

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8
Q

corticosteroids work on what enzyme?

A

phospholipase A2

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9
Q

Aspirin and NSAIDs work on what two enzymes?

A

COX 1 and 2

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10
Q

zileuton (an allergy med) works on what enzyme?

A

LOX

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11
Q

Montelukast and zofirlukast works on what eicosanoid?

A

leukotrienes

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12
Q

EETs are used for synthesis of what?

A

cholesterol (they are omega 3’s)

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13
Q

Prostaglandin E2 works on what three tissues?

A

brain, kidney, smooth muscle

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14
Q

Prostacyclin (PGI2) works on what three tissues?

A

brain, kidney, endothelium

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15
Q

Thromboxane A2 works on what four tissues?

A

platelets, macrophages, kidney, smooth muscle

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16
Q

physiologic process of inflammation

A

cyclooxygenase allows prostaglandin formation which modulates inflammation with cytokines

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17
Q

physiologic process of pain

A

prostaglandin E2 sensitizes nerve endings to the action of bradykinin, histamine, and other mediators

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18
Q

physiologic process of fever

A

anterior hypothalamic center becomes elevated; infection triggers WBC, leads to cytokine production and PGE2 production

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19
Q

Non selective COX inhibitors

A 
Ibuprofen
Flurbiprofen
Ketoprofen
Naproxen
Diclofenac
Etodolac
Ketolorac
Diflunisal
Indomethacin
Nabumetone
Oxaprozin
Piroxicam
Sulindac
Tolmetin
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20
Q

what are the two nonacetylated salicylate drugs?

A 
Doans pills (mag salicylate)
and salsalate (salicylsalicylic acid)
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21
Q

what are the two COX 2 selective inhibitors?

A

Celebrex and Mobic (Mobic not classified as selective by FDA)

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22
Q

which enzyme is targeted to prevent inflammation?

A

COX 2 (also gives analgesic effect)

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23
Q

which enzymes are targeted to prevent CNS cytokine effect (antipyretic)?

A

COX 1 and 2 (also analgesic)

24
Q

which enzyme is targeted to prevent lung bronchoconstriction and asthma complications?

A

LOX

25
Q

Inflammation causes COX 2 to effect what two eicosanoids? what do these eicosanoids do?

A

PGE2 and PGI2

-vasodilate, inc vascular permeability, inc cytokine release, inc leukocyte migration, pain

26
Q

CNS cytokines causes COX 1 and 2 to effect what eicosanoid? what does this eicosanoid do?

A

PGE2

-fever and pain neurotransmission

27
Q

COX 2 expression is induced by immune response to what two things?

A

injury or infection

28
Q

LOX usually stimulates leukotrienes to do what four things in the lung?

A

bronchoconstriction, mucus secretion, edema, eosinophil migration

29
Q

NSAIDS: absorption, volume of distribution, protein binding?, metabolism, excretion, half life

A

rapidly absorbed (food delays absorption)
highly protein bound to albumin
large volume of distribution
liver metabolism/renal excretion
Half life varies per group- ibuprofen (1-4 hrs), naproxen (lasts about 12 hrs, 9-25 hr HL), piroxicam: 50 hrs

30
Q

where does diclofenac accumulate?

A

has short half life but accumulates in synovial fluid to inhibit inflammation for RA pts

31
Q

which enzymes are blocked by NSAIDs in the GI mucosa?

A

Cox 1

32
Q

which enzymes are blocked by NSAIDs in the kidney?

A

COX 1 and 2

33
Q

which enzymes are blocked by NSAIDs in the CV system?

A

Cox 1 and 2

34
Q

gastric/duodenal ulcers occur in ___% of people who take NSAIDs

A

10%

35
Q

complications of ulcers when taking NSAIDs occur in what pt populations? (4)

A

elderly, hx of ulcers, multiple NSAID use, anticoag/steroid use

36
Q

How to use Ketorolac and risk if not used appropriately

A

Give IM loading dose, 40 mg max daily, use max for 5 days only in a 21 day period; ulcers form

37
Q

besides ketorolac, what three other NSAIDs are associated with significant GI risk?

A

oxaprozin, piroxicam, flurbiprofen

38
Q

NSAIDS cause retention of ______ and _______

A

salt and fluid

39
Q

irreversible COX 1 inhibition has been shown to be ___________

A

cardioprotective

40
Q

spectrum of NSAID selectivity

A

High COX 2 selectivity - moderate COX 2 selectivity- low COX 2 selectivity - non selective

41
Q

Celebrex use puts pts at increased risk for what?

A

serious thrombotic events, MI and stroke (because COX 2 selective and leaving COX 1 uninhibited)

42
Q

general use guidelines for celebrex

A

lowest effective dose for shortest amount of time

43
Q

aspirin does what at low doses vs what at high doses?

A

low doses- irreversible inhibitor of COX 1

high doses- non selective inhibitor

44
Q

Mobic/Meloxicam should be used with caution in what patients? describe GI effects compared to ibuprofen

A

caution in pts with inc CV risk; not as much GI irritation/bleeding compared to ibuprofen

45
Q

NSAIDs do what to kidney afferent arteriole? ACE/ARBs do what to kidney perfusion?

A

NSAIDs constrict afferent; ACE/ARB dilate efferent

**BAD for kidney perfusion- AVOID combo

46
Q

if patient is on chronic NSAID, what are two things to do to monitor for AKI?

A

avoid dehydration and check SCr frequently

47
Q

how do other NSAIDs’ antiplatelet effects compared to aspirin?

A

they reversibly bind to COX enzyme in platelets so effects aren’t as long lasting as aspirin

48
Q

_______ enhances platelet aggregation; _______ decreases it

A

TXA2; PGI2

49
Q

what two things besides Aspirin have zero order kinetics?

A

alcohol and phentoynin (anti-seizure med)

50
Q

what is the specific COX 1 enzyme blocked by aspirin?

A

SER 529

51
Q

when to used nonacetylated salicylate NSAIDs?

A

when you need an NSAID but don’t want an increased risk of bleeding (better than aspirin); also asthma patient
**NOT HELPFUL FOR ANTIPLATELET EFFECT

52
Q

which NSAID is not effective for gout?

A

tolmentin

53
Q

Avoid NSAID use in these pts: (5)

A

HF, CKD, active peptic ulcer dz, uncontrolled HTN, any atherosclerotic disease (MI, bypass surgery, unstable angina)

54
Q

what do you give pt for Tylenol overdose

A

n-acetyl cysteine (also used in COPD pts to break disulfide bonds)

55
Q

Use of acetaminophen

A

MILD pain reliever- doesnt help much if inflammation is source of pain tho

56
Q

Tylenol can be added to _______ or ________ to increase analgesia

A

NSAIDs, narcs

57
Q

Capsaicin works best for what specific neuropathic pain?

A

post herpetic neuralgia- complication of shingles (arthritis too)

Pharm (10 decks)

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