1/19
Comprehensive vocabulary flashcards covering drug principles, psychostimulants, nicotine, caffeine, psychedelics, and opioids based on lecture notes.
Therapeutic Index (TI)
A quantitative measure of relative drug safety calculated as the ratio of the median lethal dose to the median effective dose (LD50/ED50).
Margin of Safety
A conservative clinical index of drug safety calculated as the ratio of TD1/ED99 or LD1/ED99.
Cocaethylene
A biologically active metabolite formed exclusively during the co-consumption of cocaine and ethanol, exhibiting similar pharmacodynamics to cocaine but with greater reinforcing efficacy.
Benzoylecgonine
The primary inactive metabolite of cocaine formed via esterase hydrolysis, which possesses an elimination half-life of approximately 1hour (30–90minutes) and remains detectable in urine for multiple days.
Methylphenidate (Ritalin)
A psychostimulant used to treat ADHD that inhibits monoamine reuptake with a rank-order affinity of NET>DAT≫SERT, lacking cocaine's inhibitory effect on voltage-gated Na+ channels.
Exchange Diffusion (Reverse Transport)
A primary mechanism by which amphetamine compounds elevate synaptic monoamines, involving substrate action at plasma membrane transporters and reversal of the normal inward transporter flux.
Behavioral Sensitization
A progressive escalation in a drug's behavioral efficacy following intermittent, repeated administration, which increases in magnitude over time via an incubation effect.
Amphetamine-Induced Stereotypy
Repetitive, perseverative, non-goal-directed motor behaviors induced by amphetamine administration in rodents, including intensive sniffing, head movements, and rearing.
Cotinine
The principal active metabolite of nicotine formed in the liver by the CYP2A6 enzyme, characterized by a plasma half-life of approximately 18hours that serves as a biomarker for tobacco and nicotine exposure.
Nicotinic Acetylcholine Receptor (nAChR)
A ligand-gated, pentameric ionotropic receptor that gates influx of Na+ and Ca2+ to elicit rapid excitatory postsynaptic potentials (EPSPs), but undergoes rapid desensitization upon prolonged agonist exposure.
Theophylline
A methylxanthine compound found in tea leaves and generated as an active metabolite of caffeine by CYP1A2, functioning clinically as a potent respiratory stimulant.
Adenosine
An endogenous constituent of ATP and neuromodulator that accumulates during prolonged wakefulness to promote drowsiness via inhibitory A1 receptors and excitatory A2A receptors, whose sedative actions are competitively blocked by caffeine.
Caffeinism
A toxic clinical syndrome caused by very high doses of caffeine characterized by tremors, agitation, anxiety, rapid breathing, confusion, and incoherent speech.
Bufotenine (5-HO-DMT)
An indolealkylamine psychedelic compound found in the skin and parotoid gland secretions of the Colorado River toad (Bufo alvarius).
Salvinorin A
The active non-nitrogenous diterpenoid constituent of Salvia divinorum (mint family) that acts pharmacodynamically as an agonist at kappa opioid and dopamine receptors.
Ketanserin
A selective 5-HT2A receptor antagonist that blocks the visual restructuring, perceptual distortions, and dramatic psychoactive effects produced by classical psychedelics like psilocybin and LSD.
Morphine-6-Glucuronide (M6G)
A principal active metabolite produced by hepatic glucuronidation of morphine that possesses a half-life of 2–4hours and mediates a substantial proportion of morphine's analgesic efficacy.
Nociceptin Receptor (NOP / ORL1)
A non-classical, metabotropic opioid-like receptor identified in 1994 that couples to second-messenger signaling systems to promote membrane hyperpolarization through K+ channel opening and Ca2+ channel closure.
Opioid Triad
The classic pathognomonic diagnostic grouping of signs indicating acute opioid toxicity: pinpoint pupils (miosis), severe respiratory depression, and coma or unconsciousness.
Conditioned Compensatory Response
A Pavlovian physiological counter-adaptation described by Shepard Siegel in which drug-associated environmental cues trigger anticipatory homeostatic responses that offset drug impact, mediating conditioned tolerance and overdose vulnerability in novel settings.