Nsaids 1 And 2

Front 1

General reasons to choose and NSAID

Back 1

Inflammation like RA, gout, or osteoarthritis
musculoskeletal problems, strains, sprains, and lower back pain
fever reduction common cold and flu
dysmennorhea
prophylactic treatment of colon cancer
low dose aspirin for prevention of MI or stroke

Front 2

General reasons to choose acetominophen

Back 2

Non-anti-inflam
Non anti-platelet analesic
good for fever

Front 3

GI adverse events associated with NSAIDS

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caused by inhibition of COX-1 (so not prob w/Coxibs) in the stomach, which decreases cytoprotective PGs, bicarb & mucous production. Patients have: ulcers & bleeding, diarrhea, nausea, dyspepsia.

Front 4

Renal adverse events associated with NSAIDS

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NSAID induced vasoconstriction (most common); caused in part by COX-2 constitutive expression in kidney. Rarer: NSAID-induced acute interstitial nephritis & nephrotic syndrome; occurs after several months of exposure, seen in elderly and women. Chronic daily overuse can lead to ESRD!

Front 5

CV adverse events associated with NSAIDS

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Worsening of UNDERLYING HYPERTENSION. Can worsen PRE-EXISTING heart dx due to inc. afterload from systemic vasoconstriction

Front 6

Liver adverse events with NSAID uses

Back 6

elevated liver enzymes (common); liver failure is rare. ( In OD of non-NSAID acetominophen, cause of death is liver failure)

Front 7

Platelet adverse events associated with NSAIDs

Back 7

increased RISK OF BLEEDING due to COX-1 inhibitions (not seen in Coxibs)

Front 8

Other adverse events associated with NSAID

Back 8

Hypersensitivity (allergy); CNS-tinnitus, Skin rxns (Stevens-Johnson), Photosensitivity, issues w/pregnancy. Note traditional NSAIDS are highly protein bound and could interact w/warfarin, etc.

Front 9

When you want Simple fever releif choose?

Back 9

Want: Rapid onset, short duration. Try: Aspirin, Ibuprofen, Naproxen

Front 10

When you want management of long term pain choose

Back 10

Want: longer duration. Try: Sulindac, Naproxen, Oxaprozin

Front 11

Clinically impt NSAID drug interactions

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NSAIDS & oral anti-coagulants (warfarin); antihypertensives or diuretics (reduced effectiveness, can inc. BP). Salicylates & oral hypoglycemics (potentiate hypoglycemia)

Front 12

Why use aspirin

Back 12

simple fever, anti-inflammatory, analgesic, Rheumatoid Arthritis…

Front 13

Mechanism of action of aspirin

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IRREVERSIBLE COX-1 inhibitor; acetylates COX-2 but active site is very large.

Front 14

PK of aspirin

Back 14

can be zero-order kinetics at increasing doses! (highest doses used for anti-inflam)

Front 15

Adverse events associated with aspirin

Back 15

see above. In pregnancy: delayed onset of labor, early closing of ductus arteriosus in fetus!

Front 16

When not to use Aspirin

Back 16

Pt hx of: GI Ulcers; Bleeding Disorders or on Anti-Coagulants, Renal Disorders, Hypersensitivity to any NSAIDS, pregnant patients, elderly patients, NO aspirin for children due to RISK of REYE's SYNDROME. Note in 20% of people aspirin can cause serious airway hypersensitivity and an asthma attack!! No salicylates for gout patients.

Front 17

Common use of aspirin

Back 17

baby aspirin dose of (81 mg) is given for MI and stroke prophylaxis

Front 18

Symptoms of aspirin/salicylates OD

Back 18

aspirin/salicyclate OD: metabolic acidosis, dehydration, hyperthermia, seizures, cerebral edema, coma and death.

Front 19

Mechanism of action of Salicylates

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COX1/COX2 inhibitor (not irreversible, only aspirin is. Everyone else=reversible!)

Front 20

Why use Salicylates

Back 20

better than aspirin for pts w/GI complications or bleeding (hemophiliacs)

Front 21

Adverse events associated with salicylates

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WORSENS GOUT PATIENTS due to decreased uric acid elimination.

Front 22

What can't difulsinal ( a salicylate) be used for and why?

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DIFLUSINAL cannot be used for FEVER (doesn't cross BBB!)

Front 23

Notes about salicylates

Back 23

not acetylated, do not irreversibly inhibit COX-1 like aspirin, all salicylates except diflusinal cross BBB & Placenta!

Front 24

Why use ibuprofen

Back 24

fever and acute pain

Front 25

Mechanism of action of Ibuprofen

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traditional NSAID (-COX)

Front 26

PK of Ibuprofen

Back 26

rapid onset of about 15-30 minutes

Front 27

Aspirin vs Ibupofen potencey

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equipotent

Front 28

How are traditional NSAIDs excreted

Back 28

note traditionals all have liver metab & kidney excreetion

Front 29

Why use Oxaprozin

Back 29

Gout

Front 30

Mechanism of action of Oxaprozin

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traditional NSAID so -COX

Front 31

PK of Oxaprozin

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slow onset about 6 hours
longest half life about 50-60 hrs

Front 32

How does Oxaprozin help Gout

Back 32

increases uric acid excretion

Front 33

Notes about Oxaprozin

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Since it has such a long half live, you can do a daily dose or even less

Front 34

Why ues Nabumetone

Back 34

arthritis, osteoarthritis

Front 35

Mechanism of action of Nabumetone

Back 35

traditional NSAID -COX

Front 36

PK of Nabumetone

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SECOND longest t 1/2 (22-30 hrs) for 1x daily dosing
prodrug synthesized in vivo to its active form

Front 37

What makes Nabumetone different

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very EXPENSIVE

Front 38

Why use Naproxen

Back 38

fever

Front 39

Mechanism of action of Naproxen

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traditional NSAID -COX

Front 40

PK of Naproxen

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THIRD longest 1/2 life 14 hrs, rapid onset 60 min

Front 41

Adverse events withe Naproxen

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one of the safest NSAIDs, see LESS GI bleeding

Front 42

What makes Naproxen different

Back 42

20x more potent than aspirin
Long 1/2 life allows for 2x daily dose

Front 43

Why use Indomethacin

Back 43

anti-inflam 10-40X better than aspirin
also used to close PDA in babies

Front 44

Mech of action of Indomethacin

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traditional NSAID -COX

Front 45

Adverse effects of Indomethacin

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not tolerated as well as ibuprofen, 50% of users have side effects (CNS-dizziness, anxiety, confuse)
toxicity limits its use

Front 46

Why use Ketorolac

Back 46

IV for post surgical pain
weak anti-inflam, mainly for pain

can be used to replace opioids, like morphine

Front 47

Mech of action of Ketorolac

Back 47

traditional NSAID -COX

Front 48

Why use Diclofenac*

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more potent anti-inflam than indometh or naproxen

Front 49

Mech of action of DIclofenac

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traditional NSAID -COX

Front 50

Adverse effects associated with Diclofenac

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increased heart/stroke risk similar to vioxx

Front 51

Mechanism of action of Meloxicam*

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Traditional NSAID -COX
relatively COX2 selective

Front 52

Adverse events with Meloxicam*

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increased heart/stroke risk

Front 53

Mechanism of action of Piroxicam*

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Traditional NSAID -COX
non-selective

Front 54

Adverse events with Piroxicam*

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increased peptic ulcers/bleeding

Front 55

Why use Celecoxib ('Coxibs)

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RA & Osteoarthritis; inflam in pts w/GI bleed

Front 56

Mechanism of action of Celecoxib ('Coxibs)

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selective COX-2 inhibitor

Front 57

Contraindications of Celecoxib ('Coxibs)

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PATIENTS w/ CVD risk , Renal patients (COX2 constitutive in kidney)

Front 58

Adverse events associated with Celecoxib ('Coxibs)

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note COX-2 is constitutively expressed in endothelium, may explain CV effects

Front 59

Notes and Considerations for Celecoxib ('Coxibs)

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do not present w/ COX-1 associated side effects like GI bleeds or platelets

celecoxib does NOT screw up the good effects of low-dose aspirin!

Front 60

Why use Acetominophen (Tylenol, Paracetamol)

Back 60

mild to mod pain NOT from inflammation; analgesia/anti-pyretic in kids or in those with GI bleeds or hemophilia

Front 61

Mechanism of action of Acetominophen (Tylenol, Paracetamol)

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non-NSAID analgesic/anti-pyretic; does not inhibit COX 1 or COX 2 in the periphery

Front 62

PK of Acetominophen (Tylenol, Paracetamol)

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Well absorbed orally, metabolized in the liver

Front 63

Adverse events associated with Acetominophen (Tylenol, Paracetamol)

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FATAL (over 15g ingested) as result of HEPATOTOXICITY b/c of metabolite NAPQI. Slow death in 4-7 days.

Front 64

Contraindications of Acetominophen (Tylenol, Paracetamol)

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DO NOT TAKE WITH ALCOHOL-->risk of serious liver damage

Front 65

Notes and considerations of Acetominophen (Tylenol, Paracetamol)

Back 65

Not an NSAID. No anti-inflammatory actions. No anti-platelet actions. Works mainly in CNS.

treat overdose with N-Acetyl Cysteine (replaces glutathione levels which stops NAPQI formation)