exam 2 Flashcards
(172 cards)
T/F
Sedative/hypnotic agents possess good analgesic properties
false
chronic pain
difficult to identify source
assoc. with a complicated set of behavioral issues
pharm approach is only one comp. of management of chronic pain
acute pain
- tissue injury and inflammation
- mediated by biochemical mediators: histamine, prostaglandins, bradykinin
- PGE2 causes hyperalgesia by sensitizing afferent nociceptive receptors to histamine and bradykinin
- CNS A delta and C fibers of cranial nuclei V, VII, IX, X to nucleus caudalis of medulla and then to higher brain centers
pharmacological management as adjunct to treatment of _______ is appropriate
acute pain
Non-narcotic analgesics
- salicylates (aspirin)
- acetaminophen
- Non-steroidal anti-inflammatory drugs (NSAIDs)
- COX 2 inhibitors
examples of NSAIDs
- ibuprofen
- naproxen
- naproxen sodium
- diflunsial
- flurbiprofen
- ketorolac
- etodolac
ibuprofen
best in dentistry Non-selective NSAID adverse GI effects COX inhibitor ( 1--regulates homeostasis; 2--inducable
COX 2 inhibitors
celebcoxib
Rofecoxib (withdrawn)
better for GI tract
selective
what do corticosteroids inhibit?
Phospholipase A 2
antiinflammatory
what does aspirin & NSAID inhibit?
cyclooxygenase (non-selective)
PGI2
prostacyclin (endothelium)
- vasodilation; decreased platelet aggregation
PGE2/PGF2e
prostaglandin smooth muscles vasodilation, edema - sensitizes free nerve endings - mediates pain and inflammation
TXA2
thrombozanes
platelets
vasoconstriction; increased platelet aggregation
aspirin made of
salicylic acid, sodium salicylate, acetylsalicylic acid
antipyretic action of apsirin
occurs centrally (ibhibition of PGE2)
effective in febrile pts
little effect on normal body temp
IL1 (endogenous pyrogen) triggers synthesis of CNS Prostaglandins
analgesic action of aspirin
mediated thru central and peripheral mechanisms:
- salicylates inhibit synthesis of prostaglandins in inflamed tissues–> prevent sensitization of pain receptors
- analgesic site close to antipyretic region in hypothalamus (doesn’t cause sedation)
- max effect–> 650-1000 mg
antiinflammatory effects of aspirin
inhibition of PG synthesis
also inhibition of leukocyte phagocytosis, suppression of immulogical process and stabilization of lysosomal membranes
hematologic effects of aspirin
- products of PG path (thromboxane A2, prostacycline, ,PGI2) have major influence on initiation and inhibition of platelet aggregration
- platelet agg. related to clot formation and bleeding time
- aspirin decreases platelet aggregation (more bleeding)
- **effect of aspirin on platelets due to irreversible inhibition (acetylation) of enzyme cyclooxygenase
- inhibition of platelet TXA2 synthesis –> over activity of vascular PGI2
at high doses, aspirin decreases ______and impairs _____
decreases plasma prothrombin and impairs coagulation
sodium salicylate has much less effect on prolonging bleeding time
maximum dose of aspirin’s effect on respiratory system
- partial uncoupling of oxidative phosphorylation
- increased CO2 production
- compensatory increase in ventilation prevents changes in plasma pH
toxic dose of aspirin effect on resp system
stimuates ventilation by effects on receptors in medulla
- –> respiratory alkalosis (due to increased CO2)
- compensated by renal elimination of bicarbonate, sodium, and potassium
- reduction in bicarbonate impairs bicarbonate buffering capacity
therapeutic dose of aspirin on resp system
minimal effect
what happens as aspirin doing increases?
metabolic acidosis due to uncoupling of oxidative phosphorlyation
- other factors that contribute: acidity depression of resp center, loss of bicarbonate buffering capacity, changes in carb met
- *fatal metabolic/respiratory acidosis and respiratory paralysis
effects of aspirin on cardio system
little effect at therapeutic doses