Lecture 3 - Asparin (Effects and Toxicities) Flashcards
What are some characteristics of non-opioid analgesics and NSAIDs?
(analgesic effects, body temperature, inflammation)
- Analgesic
- Antipyretic (reduces body temperature)
- anti-inflammatory (NSAID), except aceaminophen
- inhibit prostoglandin synthesis, by inhibiting prostaglandin synthetase, (i.e. COX enzyme)
What are the uses and toxicities of Asparin and salicylates?
- analgesic, anti-pyretic, anti-inflammatory
Toxocity: ASA inhibits platelet aggregation
What is the analgesic MOA for ASA?
What is the effect on prostoglandins?
- inhibit prostoglandin synthesis by cyclooxgenase (COX1)
- prostoglandins cause hyperalgesia (increase response to painful stimuli) therefore inhibit decreases pain response
- inhibit has peripheral and central actions
What is the antipyretic MOA for ASA?
(What is the effect on temperature in fever and normal conditions, how does it dissipate heat, how are prostoglandins affected in the hypothalamus)
- decreases fever
- no effect on normal temperatures
- heat dissipation, vasodilation and sweating
- PG increase body temp by increase cAMP
- ASA centrally inhibits PG in hypothalamus, thus decreasing rising body temperature
What is the anti-inflammatory MOA for ASA?
What receptors to PG affect to stimulate inflammation, waht effect that GP inhibitors have on phagocytes?
- PG sensitize receptors to 5-HT, bradykinin, histamine (inflammatory mediators)
- inhibiting PG inhibit inflammation
- Phagocytes cause release of lysozymes that contribute to inflammation (not blocked by PG inhibitors)
What is the platelet aggregation effect and MOA for ASA?
What enzymes to PG inhibit relaxed to platelet aggregation
- ASA most effective
- irreversible acetylation of COX enzyme, inhibits synthesis
- PG (thromboxane A2) stimulate platelet aggregation
- Mechanism that increase ADP will cause agrregation
- Can decrease risk on certain thrombolytic diseases
What is the GI effect and MOA for ASA?
What secretion is affected and what is the result, what drug can be prescribed to prevent NSAID induced ulceration
- salicylates and NSAID cause GI disturbances
- PG may stimulate mucous and HCO3 secretion to protect stomach
- ulcers, bleeding, anemia and perforation
- Misoprostol prevents NSAID induced ulcers
What is the respiration and metabolic effects for ASA?
(Increase/decrease respiration? Respiratory acid/base balance, Increase/decrease oxygen consumption, metabolic acid/base balance)
- Respiration: high doses increase respiration (respiratory alkalosis)
- Metabolism: Uncouples oxidative phosophorylation, increases O2 consumption and heat production
(See Metabolic acidosis)
What are the pharmacokinetics of ASA?
rapid absorption?, ASA half life versus salicylic acid half life
- ASA rapidly absorbed after oral administration
- ASA hydrolyzes to salicyclic acid, half life of 30 minutes
- salicyclic acid half life 6-30 hours (increased dosage = slower elimination)
What are the GI tract toxicities of ASA?
Think about how ASA inhibit mucous and HCO3 secretion
- upset, nausea, vomiting, ulceration and bleeding
- tarry stools (Ocult blood loss)
What is the mechanism that makes overdose of ASA the most serious toxicity?
(Think about metabolism)
- Overdose (especially in children) can cause electrolyte imbalance, fever and metabolic acidosis.
What is the hypersensitivity toxicity of ASA?
What effects does hypersensitivity have on heat and leukotriene effects?
- anaphylaxis (cross reactive with NSAID)
- patient has enhanced sensitivity to heat and leukotriene effects
What are the toxicities of ASA and intoxication?
low doses, higher doses
- Low dose: tinnitus, dizzinss, headache, confusion
- higher dose: vomiting, diarrhea, hyperpnea (increased breathing), acid/base problems, hemorrhage
What are the toxicities of ASA when giving to a kid with undiagnosed fever?
- Reye’s Syndrome: ASA after viral disease can cause nerve damage and liver problems
