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14 Cards in this Set

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Analgesic effect:
relief of pain, minor aches
Inflammatory responses:
1. Acute phase: Local vasodilation and increased capillary permeability.
2. Subacute phase: infiltration of leukocytes and phagocytic cells
3. Chronic proliferative phase: tissue degeneration and fibrosis.
post op pain
Fever regulated by:
nsaid > opiods
hypothalamus regulates the set point.
ASA is acetyl group binding to the enzyme covalently.
non-selective
irreversible
inhibits both COX 1 AND 2 (prostaglandins and thromboxanes)
ASA IS USED FOR:
1. inhibit granulocyte adherence.
2. stabilize lysosomes
3. inhibit chemotaxis of macrophages & leukocytes.
Pharmacokinetics of ASA
1. EXTENSIVELY PROTEIN-BOUND.
2. Cross placenta not brain.
3. absorbed in small intestine
4. oral admini.
A.E. of ASA
Urate Excretion
(>5 g has uricosuric property)
A.E. of ASA
GI, HEPATIC, RENAL
HEPATIC: increase enzyme level
Renal: NaCl and H20 retention.
Reduction of renal function w/ CHF, renal disease, hypovolemia.
A.E. OF ASA FOR GI
GI:
1. epigastric distress
2. erosive gastritis
3. ulceration
4. exacerbation of peptic ulcers
5. g i bleeding.
6. n/v
DRUG - ASA interactions
Enhances warfarin effect.
ANTAGONIZE EFFECTS OF URICOSURICS
Increases methotrexate conc.
TX OF SALICYLATE INTOXICATION
1. activated charcoal
2. I.V. Na bicarbonate
NON-ACETLYATED SALICYLATES:

less effect analgesic than ASA.
1. Choline salicylate (arthropan)
2. Na salicylate
3. Mg salicylate
4. Salicysalicyate
APAP and pharmacokinetics
- active metabolite of phenacetin
- 20-50% bound- binding of drug to plasma protein is variable.
APAP USED FOR:
- WEAK ANTI-INFLAMMATORY EFFECT
- ANAGLESIC AND ANTIPYRETIC EFFECT (INHIBIT COX IN BRAIN)