N: Nsaids And Migraine Drugs

Front 1

What types of agents are used as prophylaxis against Migraines?

Back 1

B-blockers (propranolol, timolol)
TCA (Amitriptyline)
Anticonvulsants (divalproex)
CCB (verapamil)

Front 2

What types of agents are used to treat acute migrane attacks?

Back 2

Triptans, Dihydroergotamine, analgesics

Front 3

Dihydroergotamine
- vasodilator/vasconstrictor?
- mechanism?
- tx for what?
- most effective when given during which phase?
- contraindications?
- common side effect? Way to prevent it?

Back 3

- vasoconstrictor
- 5HT1d agonist (inhib trigeminal nerve actv and this inhibits meningeal vasodilation) --> meningeal vasoCONSTRICTION
- acute migraine attacks
- prodromal phase
- CAD, PVD, preg
- nausea; antiemetics

Front 4

Triptans
- mechanism?
- prototype?
- Major side effect?
- drug interactions?

Back 4

- 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

Front 5

Celebrex
- mech of action
- more or less GI SE than other NSAIDs?
- cardioprotective?
- negative associations?

Back 5

- inhib prostaglandin synth via selective COX-2 inhib.
- less
- no, v. little effect on platelets
- higher than normal stroke incidence

Front 6

ASA
- mech?
- indications?
- any help in tx'ing completed strokes?
- most common SE at therapeutic doses?
- higher doses?
- HUGE doses?
- OD?

Back 6

- 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

Front 7

Can ASA be used to tx the pain associated w/ gout?

Can ASA affect a diabetic's insulin requirements?

Back 7

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.

Front 8

Acetaminophen
- mechanism?
- inhib COX 1/2?
- major toxicity?
+ how long can this take to appear?
+ tx?

Back 8

- 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
+ NAC

Front 9

Ibuprofen
- mechanism?
- uses
- effects of concomittant ASA tx?
- effects on furosemide and thiazide diuretics?
- ix w/ Li?
- ix w/ACE inhib?

Back 9

- 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

Front 10

Naproxen
- SE wrt Ibuprofen?

Back 10

- GI sidefx still low, but DOUBLE that of ibuprofen.

Front 11

Nabumetone
- what is this?
- advantage?

Back 11

- prodrug that is converted into a naproxen-like drug in the body.
- hl permits once-daily dosing.

Front 12

Diclofenac
- mech?
- indications?
- accumulates where?
- SE?

Back 12

- 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.

Front 13

What are the prototypic sensitizing agents in the acute inflammatory process?

What types of pain are NSADs mainly effective against?

Back 13

Prostaglandins (PGs)

the types in which PG amplify the basic pain mechanism.

Front 14

indomethacin, sulindac, and phenylbutazone are the most potent what? When are they used?

Back 14

NSAIDS
used only when other agents are unsatisfactory.

Front 15

What are the three overarching basic toxicities of NSAIDS?

Back 15

GI irritation, HyperS, and renal Tox

Front 16

How do NSAIDs cause their antipyretic effect?

Back 16

NSAIDs block
PGE synthesis in the hypothalamus, reset the hypothalamic “thermostat”, reduce fever.

Front 17

Salicylate acid (SA)
- does it have acetylating capacity? inhib PG synth?
- uses?
- SE?

Back 17

- no and no.
- effective analgesic thru a non-PG mech
- corrosive non-PG effect on GI

Front 18

What is Reyes' syndrome?

Back 18

Aspiring is contraindicated in children because of Reye's syndrome (caused if you give ASA to kids with flu/chix pox)

Front 19

Many of the unwanted rxn's of nonselective COX inhib are due to inhib of what?

Back 19

COX-1 inhib.

Front 20

What can induce closure of the ductus arteriosus in the fetus?

Back 20

COX-1 inhibition --> PG inhibition

Front 21

Why can selective COX-2 inhibition lead to Thrombotic events?

Back 21

COX-2 inhibitor blocks the formation ofendothelium-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