NSAIDS & such

Question 1

five categories of anti-inflammatory and analgesics

Answer 1

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

Question 2

how are eicosanoids made?

Answer 2

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

Question 3

what are the main eicosanoid products we are concerned about?

Answer 3

EETs
Prostanoids
HETEs/Leukotrienes/Lipoxins

Question 4

what are the three prostanoids?

Answer 4

prostaglandin, prostacyclin (PGI2), thromboxane (TXA2)

Question 5

which enzyme converts membrane phospholipid to arachidonic acid?

Answer 5

phospholipase A2

Question 6

which two enzymes convert arachidonic acid to prostanoids?

Answer 6

COX 1 and 2

Question 7

which enzyme converts arachidonic acid to leukotrienes?

Answer 7

LOX

Question 8

corticosteroids work on what enzyme?

Answer 8

phospholipase A2

Question 9

Aspirin and NSAIDs work on what two enzymes?

Answer 9

COX 1 and 2

Question 10

zileuton (an allergy med) works on what enzyme?

Answer 10

LOX

Question 11

Montelukast and zofirlukast works on what eicosanoid?

Answer 11

leukotrienes

Question 12

EETs are used for synthesis of what?

Answer 12

cholesterol (they are omega 3’s)

Question 13

Prostaglandin E2 works on what three tissues?

Answer 13

brain, kidney, smooth muscle

Question 14

Prostacyclin (PGI2) works on what three tissues?

Answer 14

brain, kidney, endothelium

Question 15

Thromboxane A2 works on what four tissues?

Answer 15

platelets, macrophages, kidney, smooth muscle

Question 16

physiologic process of inflammation

Answer 16

cyclooxygenase allows prostaglandin formation which modulates inflammation with cytokines

Question 17

physiologic process of pain

Answer 17

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

Question 18

physiologic process of fever

Answer 18

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

Question 19

Non selective COX inhibitors

Answer 19

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

Question 20

what are the two nonacetylated salicylate drugs?

Answer 20

Doans pills (mag salicylate)
and salsalate (salicylsalicylic acid)

Question 21

what are the two COX 2 selective inhibitors?

Answer 21

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

Question 22

which enzyme is targeted to prevent inflammation?

Answer 22

COX 2 (also gives analgesic effect)

Question 23

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

Answer 23

COX 1 and 2 (also analgesic)

Question 24

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

Answer 24

LOX

Question 25

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

Answer 25

PGE2 and PGI2 | -vasodilate, inc vascular permeability, inc cytokine release, inc leukocyte migration, pain

Question 26

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

Answer 26

PGE2 | -fever and pain neurotransmission

Question 27

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

Answer 27

injury or infection

Question 28

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

Answer 28

bronchoconstriction, mucus secretion, edema, eosinophil migration

Question 29

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

Answer 29

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

Question 30

where does diclofenac accumulate?

Answer 30

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

Question 31

which enzymes are blocked by NSAIDs in the GI mucosa?

Answer 31

Cox 1

Question 32

which enzymes are blocked by NSAIDs in the kidney?

Answer 32

COX 1 and 2

Question 33

which enzymes are blocked by NSAIDs in the CV system?

Answer 33

Cox 1 and 2

Question 34

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

Answer 34

10%

Question 35

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

Answer 35

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

Question 36

How to use Ketorolac and risk if not used appropriately

Answer 36

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

Question 37

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

Answer 37

oxaprozin, piroxicam, flurbiprofen

Question 38

NSAIDS cause retention of ______ and _______

Answer 38

salt and fluid

Question 39

irreversible COX 1 inhibition has been shown to be ___________

Answer 39

cardioprotective

Question 40

spectrum of NSAID selectivity

Answer 40

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

Question 41

Celebrex use puts pts at increased risk for what?

Answer 41

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

Question 42

general use guidelines for celebrex

Answer 42

lowest effective dose for shortest amount of time

Question 43

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

Answer 43

low doses- irreversible inhibitor of COX 1 | high doses- non selective inhibitor

Question 44

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

Answer 44

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

Question 45

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

Answer 45

NSAIDs constrict afferent; ACE/ARB dilate efferent | **BAD for kidney perfusion- AVOID combo

Question 46

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

Answer 46

avoid dehydration and check SCr frequently

Question 47

how do other NSAIDs' antiplatelet effects compared to aspirin?

Answer 47

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

Question 48

_______ enhances platelet aggregation; _______ decreases it

Answer 48

TXA2; PGI2

Question 49

what two things besides Aspirin have zero order kinetics?

Answer 49

alcohol and phentoynin (anti-seizure med)

Question 50

what is the specific COX 1 enzyme blocked by aspirin?

Answer 50

SER 529

Question 51

when to used nonacetylated salicylate NSAIDs?

Answer 51

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

Question 52

which NSAID is not effective for gout?

Answer 52

tolmentin

Question 53

Avoid NSAID use in these pts: (5)

Answer 53

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

Question 54

what do you give pt for Tylenol overdose

Answer 54

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

Question 55

Use of acetaminophen

Answer 55

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

Question 56

Tylenol can be added to _______ or ________ to increase analgesia

Answer 56

NSAIDs, narcs

Question 57

Capsaicin works best for what specific neuropathic pain?

Answer 57

post herpetic neuralgia- complication of shingles (arthritis too)