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21 Cards in this Set

  • Front
  • Back
What types of agents are used as prophylaxis against Migraines?
B-blockers (propranolol, timolol)
TCA (Amitriptyline)
Anticonvulsants (divalproex)
CCB (verapamil)
What types of agents are used to treat acute migrane attacks?
Triptans, Dihydroergotamine, analgesics
- vasodilator/vasconstrictor?
- mechanism?
- tx for what?
- most effective when given during which phase?
- contraindications?
- common side effect? Way to prevent it?
- vasoconstrictor
- 5HT1d agonist (inhib trigeminal nerve actv and this inhibits meningeal vasodilation) --> meningeal vasoCONSTRICTION
- acute migraine attacks
- prodromal phase
- CAD, PVD, preg
- nausea; antiemetics
- mechanism?
- prototype?
- Major side effect?
- drug interactions?
- serotonin agonists, acting @ 5-HT-1d receptors
---> vasoconstriction!
- sumatriptan
- possibility of MI and HTN. Don't give to pts with CAD, PVD w/o a thorough eval first.
- don't give to pts on MAOI
- mech of action
- more or less GI SE than other NSAIDs?
- cardioprotective?
- negative associations?
- inhib prostaglandin synth via selective COX-2 inhib.
- less
- no, v. little effect on platelets
- higher than normal stroke incidence
- mech?
- indications?
- any help in tx'ing completed strokes?
- most common SE at therapeutic doses?
- higher doses?
- HUGE doses?
- OD?
- irreversibly inhibits COX 1 and 2 & inhib platelet aggregation via TRANS-acetylation rxn. Also inhibits granulocyte adherance to damaged vasculature, as well as chemotaxis of PMNs and other things to injury sites.

- antiinflammatory, analgesia, antipyretic, antiplatelet, MI prophylaxis, TIA attacks (i/ men
- no current evidence for this
- GI upset, gastic and duodenal ulcers
- salicylism: vomiting, tinnitus, decreased hearing, vertigo
- hyperpnea
- respiratory alkalosis followed by metabolic acidosis --> respiratory depression --> cardiotoxicity
Can ASA be used to tx the pain associated w/ gout?

Can ASA affect a diabetic's insulin requirements?
no, smaller amounts ay decrease the uricosuric effects of probenecid, sulfinpyrazone, and phenylbutazone.

large doses have a hypoglycemic action that can enhance the effect of oral hypoglycemic drugs.
- mechanism?
- inhib COX 1/2?
- major toxicity?
+ how long can this take to appear?
+ tx?
- peripherally elevates pain threshold; antipyresis thru action on the hypothalamic heat regulating center
- 1 and 2 both weakly. **NOT ANTIINFLAMMATORY**
- hepatotoxicity w/ as little as 15g
+ 48 to 72 hrs after injestion
- mechanism?
- uses
- effects of concomittant ASA tx?
- effects on furosemide and thiazide diuretics?
- ix w/ Li?
- ix w/ACE inhib?
- nonselective COX inhib (reversible)
- analgesic, antipyretic, antiinflammatory
- may interfere with platelet inhib of ASA, and may blunt cardioprotective effects.
- reduce the natriuretic effect in some pts.
- raise lvls
- may potentiate renal dz
- SE wrt Ibuprofen?
- GI sidefx still low, but DOUBLE that of ibuprofen.
- what is this?
- advantage?
- prodrug that is converted into a naproxen-like drug in the body.
- hl permits once-daily dosing.
- mech?
- indications?
- accumulates where?
- SE?
- nonselective COX inhib
- acute and chronic sx of OA and RA; ankylosing spondylitis
- synovial fluid
- SE in up to 20%: GI distress, GI bleeding, gastric ulceration. Can impair RBF and GFR @ 150mg/d and above.
What are the prototypic sensitizing agents in the acute inflammatory process?

What types of pain are NSADs mainly effective against?
Prostaglandins (PGs)

the types in which PG amplify the basic pain mechanism.
indomethacin, sulindac, and phenylbutazone are the most potent what? When are they used?
used only when other agents are unsatisfactory.
What are the three overarching basic toxicities of NSAIDS?
GI irritation, HyperS, and renal Tox
How do NSAIDs cause their antipyretic effect?
NSAIDs block
PGE synthesis in the hypothalamus, reset the hypothalamic “thermostat”, reduce fever.
Salicylate acid (SA)
- does it have acetylating capacity? inhib PG synth?
- uses?
- SE?
- no and no.
- effective analgesic thru a non-PG mech
- corrosive non-PG effect on GI
What is Reyes' syndrome?
Aspiring is contraindicated in children because of Reye's syndrome (caused if you give ASA to kids with flu/chix pox)
Many of the unwanted rxn's of nonselective COX inhib are due to inhib of what?
COX-1 inhib.
What can induce closure of the ductus arteriosus in the fetus?
COX-1 inhibition --> PG inhibition
Why can selective COX-2 inhibition lead to Thrombotic events?
COX-2 inhibitor blocks the formation of endothelium-derived COX-2-dependent prostacyclin (PGI2), a potent inhibitor of platelet aggregation.

COX-2 inhibitor has no effect on the synthesis of
thromboxane A2, a potent activator of platelet aggregation

In the presence of COX-2 inhibitor,
TBA2 >> PGI2, which leads to thrombotic events