Pharm 3

Front 1

Mechanism of NSAIDS

Back 1

- inhibition of COX (cyclo-oxygenase)
- this enzyme ultimatley used in the formation of prostaglandins

Front 2

COX-1

Back 2

- found in a variety of tissues
- involved in many housekeeping functions of prostaglandins

Front 3

COX-2

Back 3

- involvedi n the inflammatory responses, fever, and algesia
- also expressed in vessels, kidney, heart, brain

Front 4

Actions of prostoglandins

Back 4

- vasodilation
- vasoconstriction
- contracts other smooth muscle**
- INHIBIT MAST CELL SECRETION
- PYROGENIC
- Sensitize nerve endings to other algesic mediators

Front 5

Actions of Leukotrienes

Back 5

- aids in the migration of leukocytes
- long lasting BRONCHIOLAR CONSTRICTION
- increased capillary permeability

Front 6

NSAIDS and INFLAMMATION

Back 6

- reduce vasodiations, edema, and pain associated with inflammation
- MAINLY ACUTE PHASE
- require high dose of NSAID
- ion trapping
-

Front 7

NSAIDS and Analgesia

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- inhibition of COX-2
- classified as mild analgesics
-

Front 8

NSAIDS and ANTI-PYRESIS

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- centrally mediated effect via resetting of temp control center of the hypothalamus
- INHIBIT THE COX-2 and block production of prostaglandins in the brain

Front 9

NSAIDS AND PLATELET AGGREGATION

Back 9

- inhibit COX-1
- this is involved with TxA2 (thromboxane)
- SO... increase bleed time
- inhibition of platelet aggregation

Front 10

ASPRIN

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- covalently madifies and IRREVERSIBLY INHIBITS PLATELET CYCLO-OXYGENASE
- achieved at low dose

Front 11

NSAIDS and Cardiovascular effects

Back 11

- COX-2 protects from reperfusion injury

Front 12

NSAIDS renal effects

Back 12

- Prostaglandins not involved in maintaining normal renal blood flow, but become inmportant in the compromised kidney
- Pts that are volume depleted are at risk of renal ischemia when on NSAIDS

Front 13

NSAIDS AND GI effects

Back 13

- gastric distress
- gastric bleeding
- sudden acute hemorrhage
can see too much acit secretion