Pharm - Nsaids

Front 1

Autocoids most involved in increasing vascular permeability

Back 1

Histamine and leukotrienes

Front 2

Autocoids most involved in chemotaxis

Back 2

Prostaglandins and leukotrienes

Front 3

Autocoids most involved in pain mediation

Back 3

Bradykinin (and to a lesser extent, prostaglandins)

Front 4

Autocoids most involved in vasodilation

Back 4

Bradykinin and prostaglandins (also histamine, and lastly serotonin)

Front 5

10-20% of pts taking NSAIDs experience what?

Back 5

Dyspepsia

Front 6

Prostaglandins produced in gut epithelia

Back 6

PGE2 and PGI2

Front 7

PGE2 and PGI2 act how to limit proton pumps in the gut?

Back 7

Via a GPCR

Front 8

Which is present in plts, Cox-1 or Cox-2?

Back 8

Cox-1 only (the plt lacks a nucleus, so it cannot induce cox-2 expression)

Front 9

Production of TxA2 by plts does what?

Back 9

Promotes clotting

Front 10

Cox-1 functions in the kidney

Back 10

Control of hemodynamics and GFR

Front 11

Cox-2 functions in the kidney

Back 11

Salt and water excretion

Front 12

PGE2 and PGI2 do what in the kidney?

Back 12

Regulate blood flow

Front 13

Renal effects of decreased PGE2

Back 13

Sodium retention, increased BP, and in rare cases, CHF

Front 14

Renal effects of decreased PGI2

Back 14

Hyperkalemia and ARF

Front 15

The primary mediator of swelling a/w inflammation

Back 15

PGE2 and PGI2

Front 16

Why are NSAIDs anti-pyretic?

Back 16

Prostaglandin signaling at the hypothalamus contributes to fever; NSAIDs also inhibit IL-1

Front 17

Cox-2 expression is induced by what inflammatory mediators?

Back 17

IL-1, TNF, LPS, mitogens, and ROS

Front 18

Aspirin is the prototype of what NSAID class?

Back 18

Salicylic acid derivatives

Front 19

Acetaminophen is the prototype of what NSAID class?

Back 19

Para-aminophenol derivatives

Front 20

Indomethacin is the prototype of what NSAID class?

Back 20

Indole and indene acetic acids

Front 21

What is the largest and most prescribed NSAID class?

Back 21

Arylproprionic acids (e.g. ibuprofen, naproxen)

Front 22

Ibuprofen and naproxen are prototypes for what NSAID class?

Back 22

Arylproprionic acids

Front 23

Sulindac is a pro-drug of what class of NSAID?

Back 23

Arylproprionic acids

Front 24

Diclofenac is the prototype of what class of NSAID?

Back 24

Heteroaryl acetic acids

Front 25

Ketorolac is part of what class of NSAID?

Back 25

It is a heteroaryl acetic acid approved for IV

Front 26

Diclofenac may be given alone, or combined with what?

Back 26

Misoprostol

Front 27

Meclofenamic acid is the prototype for what class of NSAID?

Back 27

Anthranilic acids (fenamates)

Front 28

Piroxicam and meloxicam are prototypes of what NSAID class?

Back 28

Enolic acids

Front 29

What is the difference between piroxicam and meloxicam?

Back 29

Meloxicam is Cox-2 selective

Front 30

Nambumetone is the prototype of what class of NAID?

Back 30

Alkanones

Front 31

The metabolite of this alkanone is Cox-2 selective

Back 31

Nambumetone

Front 32

These NSAIDs have no platelet effects

Back 32

Celecoxib, rofecoxib (Cox-2 selective)

Front 33

Which NSAIDs reversibly inhibit cyclooxygenase?

Back 33

All except aspirin.

Front 34

How do NSAIDs generally work?

Back 34

They are organic acids that competitively inhibit the binding of arachidonic acid by Cox.

Front 35

Do NSAIDs inhibit leukotriene synthesis (lipoxygenase pathway?)

Back 35

No - this is why pts may have mild anaphylaxis or allergy-like sx (not true NSAID allergies)

Front 36

What is the most important difference between NSAIDs?

Back 36

Cox-1 : Cox-2 selectivity

Front 37

The only NSAID approved for IV and IM use

Back 37

Ketorolac (a heteroaryl acetatic acid)

Front 38

The only NSAID approved for injection to close the ductus arteriosus in neonates

Back 38

Indomethacin

Front 39

Salicylates may have this additional anti-inflammatory effect

Back 39

ROS scavengers

Front 40

Metabolism of NSAIDs

Back 40

Hepatic (CYP3A or CYP2C)

Front 41

Excretion of NSAIDs

Back 41

Renal; some biliary excretion and reabsorption (correlates w/ lower GI irritation)

Front 42

NSAIDs are contraindicated in whom?

Back 42

Women in their 3rd trimester of pregnancy

Front 43

What maintains the PDA during pregnancy?

Back 43

PGE2 and PGI2

Front 44

NSAIDs reduce the effectiveness of which drugs?

Back 44

Diuretics, some antihypertensives

Front 45

This drug accelerates NSAID metabolism

Back 45

Cimetidine (use famotidine or a PPI instead)

Front 46

NSAIDs should be discontinued before administering what?

Back 46

Anti-virals (e.g. ciclofovir) - increased potential for nephrotoxicity if used concurrently

Front 47

NSAIDs interfere w/ excretion of what?

Back 47

Lithium

Front 48

These drugs upregulate a wide variety of P450s, and decrease NSAID efficacy

Back 48

Steroids

Front 49

Do Cox-2 inhibitors cause as many renal complications as non-selectives?

Back 49

Yes

Front 50

Why do Cox-2 inhibitors enhance cardiac events?

Back 50

They block PGI2 synthesis, but do NOT inhibit platelet aggregation

Front 51

Actions of PGI2 in vascular endothelium

Back 51

Relaxation, and prevention of adhesion molecule synthesis

Front 52

Why aren't Cox-2 inhibitors anti-thrombotic?

Back 52

Platelets have only Cox-1.

Front 53

How do the analgesic and antipyretic activities of acetaminophen compare to those of NSAIDs?

Back 53

Equal

Front 54

Why isn't acetaminophen as effective as NSAIDs in reducing pain?

Back 54

It is destroyed in inflamed tissue

Front 55

This NSAID reduces the risk of colorectal cancer

Back 55

Aspirin

Front 56

This NSAID may decrease the progression of atherosclerosis

Back 56

Aspirin

Front 57

How selective an NSAID is aspirin?

Back 57

Aspirin is 170x as potent in inhibiting Cox-1 than Cox-2

Front 58

This NSAID is easier on the GI, but harder on the liver

Back 58

Acetaminophen

Front 59

The preferred analgesic/antipyretic for pts in whom aspirin is contraindicated

Back 59

Acetaminophen

Front 60

Acute acetaminophen overdose leads to what?

Back 60

Hepatotoxicity and ARF

Front 61

Chronic acetaminophen overdose leads to what?

Back 61

Hepatotoxicity, chronic analgesic nephropathy

Front 62

Used primarily for the treatment of RA and OA

Back 62

Indomethacin

Front 63

Indomethacin administration routes

Back 63

PO, rectal, or IV

Front 64

Indicated for tx of RA, OA, and dysmenorrhea

Back 64

Ibuprofen

Front 65

Ibuprofen pharmacokinetics

Back 65

PO administration; 80% absorption; T1/2 3 hrs

Front 66

Ibuprofen elimination is significantly prolonged in pts w/ what?

Back 66

Cirrhosis

Front 67

Rapid-release form of the potassium salt indicated for treating pain and dysmenorrhea

Back 67

Diclofenac

Front 68

Delayed-release form approved for OA, RA, and AS

Back 68

Diclofenac

Front 69

A 3% topical gel exists for actinic keratosis tx

Back 69

Diclofenac

Front 70

Effective in cases of hyperalgesia

Back 70

Diclofenac

Front 71

Inhibits miosis when applied topically, but does not affect intraocular pressure

Back 71

Diclofenac

Front 72

Advantage of piroxicam

Back 72

Long T1/2 - can be administed once a day

Front 73

Piroxicam is indicated for tx for what?

Back 73

RA and OA

Front 74

Piroxicam is not recommended for pts w/ what?

Back 74

Severe renal impairment

Front 75

A prodrug that is converted to 6-MNA, which at low doses is Cox-2 selective

Back 75

Nabumetone

Front 76

Nabumetone should be used cautiously in pts w/ what?

Back 76

Hepatic dysfunction

Front 77

Used as adjuvant treatment for pts w/ FAP to reduce colorectal polyps

Back 77

Celecoxib

Front 78

Darvocet

Back 78

Prophoxyphene and acetaminophen

Front 79

Percocet

Back 79

Oxycodone and acetaminophen

Front 80

Percodan

Back 80

Oxycodone and aspirin

Front 81

Vicodin

Back 81

Hydrocodone and acetaminophen

Front 82

Caffeine affects NSAIDs how?

Back 82

It enhances the analgesic effects