Promotes inflammation and sensitize receptors to painful stimuli PGE2 and PGI2

Promotes inflammation and sensitize receptors to

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Promotes inflammation and sensitize receptors to painful stimuli (PGE2 and PGI2) Protection of the gastric mucosa (PGE2 and PGI2) Reduces secretion of gastric acid Increases secretion of bicarbonate and cytoprotective mucus Maintenance of submucosal blood flow Stimulates platelet aggregation with synthesis of TXA2 Vasodilation with synthesis of prostacyclin Promotes vasodilation and maintain renal blood flow in the kidney (PGE2, and PGI2) Mediates fever and contributes to perception of pain in the brain Promotes contraction of uterus at term COX-1: Housekeeping. Protects gastric mucosa, supports renal function, and promotes platelet aggregation Inhibition of COX-1 can cause harmful effects: Gastric erosion and ulceration Bleeding tendencies Renal impairment Beneficial Effect from inhibition: Protection against MI and stroke COX-2: Produced mainly at sites of tissue injury Mediates inflammation and sensitizes receptors to painful stimuli Found in brain to mediate fever and perception of pain, kidneys to support renal function, blood vessels to promote vasodilation, and colon where it can contribute to
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colon cancer Inhibition of COX-2 can provide the following benefits: Suppress inflammation Alleviates pain Reduces fever Protection against colorectal cancers Inhibition of COX-2 has the following adverse effects: Renal impairment Promotion of MI and stroke Drug Class: First-Generation Nonsteroidal Anti inflammatory Drugs (NSAIDs) Page number: p. 605 Prototype drug: Aspirin (ASA) Other Drugs in class: Indications for use: Mild to moderate pain (joint, muscle, and HA pain), reduces fever, protects against thrombotic disorders, drug of choice for rheumatoid arthritis and other inflammatory conditions, dysmenorrhea Mechanism of Action: IRREVERSIBLE nonselective inhibitor of cyclooxygenase (Inhibition of COX2= reduction of inflammation, pain, and fever and inhibition of COX1= protection against MI and ischemic stroke. Duration of action depends on how quickly specific tissues can synthesize new molecules of COX1 and COX2 Relieves pain through actions in the periphery by inhibiting COX2 which suppresses prostanoid production and also works in the CNS for pain relief. Inhibiting prostaglandin synthesis in uterine smooth muscle alleviates dysmenorrhea Suppresses platelet aggregation by causing irreversible inhibition of COX1, the enzyme that makes TXA2. Recommended daily for ischemic stroke, TIA, primary prevention of MI, acute MI, previous MI, chronic stable angina, unstable angina, and angioplasty or other revascularization procedures Protects against colorectal cancer by inhibiting COX2 Pharmacokinetics: Absorption: Small Intestine. If given rectally, absorbed slowly and blood levels are lower. Half-life: 15-20 mins d/t rapid conversion to salicylic acid Distribution: All body tissues and fluids including breast milk, fetal tissues, and CNS Excretion of salicylic acid depends on urinary pH. The higher the pH, the increased rate of excretion Adverse Reactions: Common: Gastric distress, heartburn, and nausea Occult GI Bleeding, gastric ulceration, perforation, and bleeding. Ulcers result from:
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