Nsaids

Front 1

Analgesic effect:

Back 1

relief of pain, minor aches

Front 2

Inflammatory responses:

Back 2

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.

Front 3

post op pain
Fever regulated by:

Back 3

nsaid > opiods
hypothalamus regulates the set point.

Front 4

ASA is acetyl group binding to the enzyme covalently.

Back 4

non-selective
irreversible
inhibits both COX 1 AND 2 (prostaglandins and thromboxanes)

Front 5

ASA IS USED FOR:

Back 5

1. inhibit granulocyte adherence.
2. stabilize lysosomes
3. inhibit chemotaxis of macrophages & leukocytes.

Front 6

Pharmacokinetics of ASA

Back 6

1. EXTENSIVELY PROTEIN-BOUND.
2. Cross placenta not brain.
3. absorbed in small intestine
4. oral admini.

Front 7

A.E. of ASA

Back 7

Urate Excretion
(>5 g has uricosuric property)

Front 8

A.E. of ASA
GI, HEPATIC, RENAL

Back 8

HEPATIC: increase enzyme level
Renal: NaCl and H20 retention.
Reduction of renal function w/ CHF, renal disease, hypovolemia.

Front 9

A.E. OF ASA FOR GI

Back 9

GI:
1. epigastric distress
2. erosive gastritis
3. ulceration
4. exacerbation of peptic ulcers
5. g i bleeding.
6. n/v

Front 10

DRUG - ASA interactions

Back 10

Enhances warfarin effect.
ANTAGONIZE EFFECTS OF URICOSURICS
Increases methotrexate conc.

Front 11

TX OF SALICYLATE INTOXICATION

Back 11

1. activated charcoal
2. I.V. Na bicarbonate

Front 12

NON-ACETLYATED SALICYLATES:

less effect analgesic than ASA.

Back 12

1. Choline salicylate (arthropan)
2. Na salicylate
3. Mg salicylate
4. Salicysalicyate

Front 13

APAP and pharmacokinetics

Back 13

- active metabolite of phenacetin
- 20-50% bound- binding of drug to plasma protein is variable.

Front 14

APAP USED FOR:

Back 14

- WEAK ANTI-INFLAMMATORY EFFECT
- ANAGLESIC AND ANTIPYRETIC EFFECT (INHIBIT COX IN BRAIN)