Aspirin vs other NSAIDS - ANSWERaspirin- orginal NSAID- others were developed to improve efficacy and decrease toxicity/ ADEs
aspirin causes IRREVERSIBLE inactivation of COX-1 = production of thromboxane for the LIFE of the platelet k
others: have reversible inactivation of cyclooxyrgenase (l...
Pharmacology- Neuropharmacology
Questions & Answers
Aspirin vs other NSAIDS - ANSWERaspirin- orginal NSAID- others were developed to
improve efficacy and decrease toxicity/ ADEs
aspirin causes IRREVERSIBLE inactivation of COX-1 = production of thromboxane for
the LIFE of the platelet k
others: have reversible inactivation of cyclooxyrgenase (lasting only for duration of drug
activity)
NSAID Cox 1 & 2 MOA - ANSWERNSAIDS: decrease sensitivity of vessels to
bradykinin and histamine, affect T lymphocytes and reverse vasodilation of inflammation
all (except COX 2 selective agents) inhibit platelet aggregation
COX 2 selective inhibitors (coxibs) inhibit prostaglandin synthensis at sight of
inflammation w/o affecting COX1
NSAID effects - ANSWERanalgesic, anti inflammatory, and antipyretic
NSAID indications - ANSWERmild-mod pain secondary to soft tissue injury, athletic
injury, dental pain, minor surgery, OA, RA, dysmenorrhea, Gout
-not all indicated for all rheumatic diseases- most likely effective in rheumatic arthritis,
psoriatic arthritis and arthritis assoc w/ inflammatory bowel disease
Osteoarthritis pathophysiology - ANSWERdegeneration of articular cartilge
body attempts to repair, compensates, hypertrophy at articular margins, forms spurs,
thickening of synovial membranes
low levels of inflamation
nonpharm: proper exercise w/ rest periods, weight loss in overweight pts
Gout Pathophysiology - ANSWERinflammatory response to monosodium urate crysatls
in tissues. Distal joints usually affected, crystals can be any size in any tissue and
, present as otphaceous gout or urate neuropathy if crystalization is localized in renal
medulla
tophi- crystals of urate precipitate in joints
Gout pharm treatment - ANSWERpreventative: 1st line: colchicine; 2nd line: urocosuric
drug if uric acid under excreted, allopurinol or febuxostate if uric acid overproduced
acute attack: NSAIDS (indomethacin most frequently, naproxen), corticosteroids,
colcichine
Colchicine - ANSWER1st line treatment for prevention of gout-
exact MOA Unknown- decreases deposition of uric crystals, reduction of inflammatory
response- does NOT affect uric acid metabolism, NOT an analgesic
ADEs: N/V, abd pain, diarrhea
- geriatrics: GI toxicities in up to 80% of geriatrics, bone marrow suppression, bloody
dyscrasisis, hepatic necrosis, and seizures possible
-preg category C
Drug interactions: enhanced effects of CNS depressants and sympathomimetic agents;
may interfere w/ vit. B12 absorption(concern if using chronically), increased toxicity if
used w/ clarithomycin, erythromycin and grapefruit juice; cyclosporine levels are
increased
monitoring-
-1st time users: monitor weekly for signs of toxicity
-3-6month blood counts if long-term therapy
-may cause reversible malabsorption of B12- periodic monitoring recommended
-LFTs q 2-3 months
Xanthine Oxidase Inhibitors - ANSWERAllopurinol and Febuxostat(newer, more
expensive)
used in chronic gout (not in acute attack)
MOA: decrease concentration of less soluble uric acid: decreases precipitation of uric
acid crystals in joints and tissues
contraindications: not given during an acute attack- usually w/held for 1-2 after acute
attack and given w/ colchicine or NSAID to avoid an attack
allopurinol - ANSWERa xanthine oxidase inhibitor-see that term
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