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29 Cards in this Set

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Bradykinin
Causes the synthesis and release of prostaglandin
Prostaglandin
Sensitizes nociceptors and increases the likelihood that other inflammatory agents will come to the site
Prostaglandin Synthesis
Bradykinin activates Phospholipase A2
Phospholipase A2 cleaves phospholipids into Arachodonic Acid
Arachodonic Acid can then be converted to prostaglandin
Inhibition of Prostaglandin Synthesis
Glucocorticoids
Nonsteroidal Anti-Inflammatory Agents (NSAIDs)
Glucocorticoids
-Inhibit Phospholipase A2
-Inhibit COX pathway, preventing synethesis of prosta's from Arachidonic Acid
**Glucocorticoids are potent anti-inflammatory agents and not typically used as analgesics b/c there are so many glucocorticoid receptors throughout the body.
Nonsteroidal Anti-Inflammatory Agents (NSAIDs)
Inhibit cyclooxygenase which prevents prostaglandin synthesis
-Blockage of prosta pathway may also increase leukotriene synthesis
Normal Physiological Functions of Prostaglandins
Smooth muscle contraction/relaxation
Renal electrolyte and water transport
CNS activity
Bone Absorption
Inflammation
Vascular Permeability
GI Secretion
Hormone Release
Platelet Aggregation
Nociception
COX 1
Constitutive (Always around)
Smooth Muscle Contraction/Relaxation
Renal Electrolyte and Water tranport
CNS Activity
Bone Absorption
Hormone Release
GI Secretion
Platlet Aggregation
COX 2
Inducible
Some preceding event produces COX 2
Inflammation
Renal Functions
CV Function
Aspirin
Covalently modifies COX 1&2 resulting in irreversible inhibition of cyclooxygenase activity-->duration depends on rate of cyclooxygenase turnover (body size)
-More selective for COX 1
Therapeutic Uses for Salicylates
Analgesia
Antipyresis
Anti-Inflammatory Agents
Prophylaxis of Coronary Artery Disease
Salicylates Analgesic Effects
Relieve mild-moderate nociceptive pain
*Advantages
-Can be used to treat neurogenic pain
-Lack the unwanted effects of opiods (tolerance, dependence, abuse potential)
Salicylates Antipyretic Effects
NSAIDs promote return of set point to normal
Salicylates as Anti-Inflammatory Agents
Inhibit prostaglandin synthesis
Tx of musculoskeletal disorders such as rheumatoid arthritis, osteoarthritis
*Anti-Inflammatory effects can take days to appear and must use high doses
Salicylates & Prophylaxis of Coronary Artery Disease
Inhibit platelet aggregation
low doses are used (<325mg/day)
Hemostatis
Vascular Injury
-Exposes subendothelial matrix providing a substrate for platelet adhesion/aggregation
Platelet Aggregation
-Thromboxane A2 (COX1) aggregate nearby platelets forming a hemostatic plug
ASPIRIN BLOCKS FORMATION OF THIS PLUG BY INHIBITING COX 1
Inhibition of Platelet Aggregation
Prostacyclin (COX2) are released and inhibit platelet aggregation and vasoconstriction
ASPIRIN IS LESS LIKELY TO AFFECT THIS B/C IT IS MORE SELECTIVE FOR COX1
Shared Side Effects of Salicylates
--Gastric Ulceration and Intolerance
--Impaired renal function
--Hypersensitivity Reactions
--Toxicity
GI Effects from Salicylates
-->prostaglandins normally have a protective effect on gastric mucosa so inhibition of prosta synthesis can be bad
--GI Effects can also be due to inhibition of COX2 which increases luekotriene synthesis
Renal Impairment from Salicylates
Prosta's normally reduce water and sodium reabsorbtoin-->NSAIDs can lead to increased retention-->increased BP, renal artery vasoconstriction
Hypersensitivity Reactions associated with Salicylates
Cross reaction occurs to all NSAIDs
Salicylates: Contraindications
Ulcer, Gout, Diabetes, Influenza/Chickenpox, Hypocoagulation states
Propionic Acid
Aspirin alternatives
less likely to produce GI side effects than aspirin
less effective in reducing platelet aggregation
EX. Ibuprofen & Ketoprofen
COX 2 Inhibitors
Bextra, Celebrex, Vioxx (Rofecoxib)
--50-60% decrease in serious GI complications
Mechanism of Action Acetominophen
Effective antipyretic due to inhibition of COX in the brain
Clinical Uses of Acetominophen
Analgesia & Antipyretic
DOES NOT inhibit inflammation
DOES NOT inhibit platelet aggregation
Adverse Effects of Acetominophen
Largely confined to acute overdose
Acetominophen Overdose
Overdose depletes glutathione levels which leads to a dangerous increase in NAPQI levels. NAPQI is a toxic metabolite which can be fatal to cells
Chronic Alcohol and Acetominophen
Chronic booze results in increase in CYP2D1 which leads to depletion of glutathione
Combo Therapy: Opiods and NSAIDs
Periphereal analgesics act to reduce inflammatory reponse
Opioids alter reaction to pain
-->Can increase analgesia wile decreasing dose of opioiods