NSAIDS

Question 1

Aspirin

Answer 1

1. NSAID: analgesic, antipyretic, anti-inflammatory, antiplatelets
2. Irreversible COX1/2 inhibitor,
3. Biphasic effects on respiration (stim then depress), uric acid excretion (prevent secretion then reabsorption). GI issues, asthma, Reyes syndrome, nephrotoxicity.
4. Lots of interactions, big ones are anticoagulants or anything that binds to plasma proteins.
5. Can have hypersensitivity
6. CI in gastric ulcers, hypoprothrominemia, vit k def, hemophilia. Stop 1wk prior to surgery.

Question 2

Sodium salicylate, methyl salicylate (oil of wintergreen), Diflunisal

Answer 2

Sodium salicylate: nonacetylated salicylate; no platelet effects, no irreversible cox inhibition, effective anti-inflammatory, less analgesic than ASA.
Methyl Salicylate (Oil of wintergreen): irritating to skin/mucosa, fatal dose is 4-5 mL in children
Diflunisal: little antipyretic effects (poor CNS penetration), less GI irritation than ASA, not metabolized to salicylic acid but is a derivative of it.

Question 3

Analgesics and PUD

Answer 3

No history of PUD: any NSAID
PUD history but not active: celecoxib w/ or w/out antacid or some NSAIDs w/misoprostal or “prazols” (but not aripiprazole)
Active PUD: acetaminophen and/or opioids (codeine) only!

Question 4

Celecoxib

Answer 4

1. Reversible Cox2 inhibitor
2. No inhibitory effects on platelet aggregation
3. Inc risk of CV disease. GI disease, asthma, renal failure
4. CI in pregnancy/breast feeding, GI disease, asthma, renal fialure
5. Less risk of GI bleeding/gastropathy

Question 5

Indomethacin

Answer 5

1. Inhibits Phospholipase A
2. Very potent, reduces PMN migration, used to close PDA
3. Worst side effects of NSAIDs, particularly upper GI/CNS effects

Question 6

Sulindac

Answer 6

1. NSAID
2. Long t1/2, less nephrotoxic
3. Severe GI effects including pancreatitis

Question 7

Meclofenamate

Answer 7

1. NSAID
2. No advantages over other drugs
3. Frequent SE, DIARRHEA

Question 8

Diclofenac

Answer 8

1. NSAID, potent COX inhibitor, also dec arachidonic acid availability.
2. Oral admin, liver metabolism
3. GI side effects (combined with misoprostol (arthrotec is the combination drug) to avoid GI SE)

Question 9

Ketorlac

Answer 9

1. NSAID: highest potency NSAID
2. Analgesic post op, often combined w/opiates
3. Get GI SE after 5 days of use, dont use longer than 5 days

Question 10

Ibuprofen

Answer 10

1. NSAID DOC: best SE profile, probably least potent
2. Anti-inflammatory, antipyretic, analgesic. Better tolerated than ASA –> less SE. Less platelet effects than ASA.
3. GI SE common, inc in alkaline phosphatse (indicates liver damage). Hyperuricemia possible.
4. If combined with ASA the effects will decrease.
5. Used in RA and osteoarthrits

Question 11

Naproxen

Answer 11

1. NSAID: longest t1/2, used in RA, osteoarthritis
2. Extensively bound to plasma proteins
3. Crosses placenta (CI in pregnancy), typical GI effects, bleeding not as bad as w/ASA

Question 12

Piroxicam

Answer 12

1. Inhibits PMN migration/lymphocyte function-dec radical production
2. long t1/2
3. GI effects very common

Question 13

Nabumetone

Answer 13

1. NSAID
2. Prodrug: must be metabolized to active form, long t1/2, once daily dosing
3. fewer GI SE

Question 14

Acetaminophen

Answer 14

1. Antipyretic and analgesic, not anti-inflammatory
2. Not a COX inhibitor, tolerated better than ASA
3. Fatal hepatic necrosis at high doses (if all reduced glutathione is used up), elevated serum transaminase and LDH indicate hepatic damage. No blood clotting defects, acid-base intolerance or auditory toxicity.
4. Chronic EtOH consumption inc toxicity due to induction of CYP2E1.
5. Tx of toxicity: gastric lavage (if w/in 4 hrs), forced dialysis (furosemide), admin antagonist (n-acetylcysteine (mucomyst)-paraenteral) hemodialysis. Preffered over ASA for those with ASA allergies, coagulation disorders, peptic ulcers, gout, children (reye’s). Not anti-rheumatic.