Anticholinergics: Nicotinic ANTAgonist Flashcards
Neuromuscular blocking drugs
-resemble ACh
-succinylcholine and tubocurarine
Tubocurarine
-non-depolarizing blockade
-normal antagonist
Succinylcholine
-depolarizing blockade
-first activates, then blocks
Stimulation of Muscle by nicotine
Normal operation of nicotinic receptors
-rapid degradation of synaptically released ACh
-allows membrane to REpolarize and Na channels (action potential) reset
-next ACh release causes DEpolarization that OPENS Na+ channels and action potential
Depolarizing Blockade of nicotinic receptors
-Na+ channels close but agonist remains bound to receptor
-channels cannot reset to active state
Tubocurarine (Curare) clinical use
-skeletal muscle relaxation during anesthesia esp for intubation
-also poison arrows
Succinylcholine mechanism
-binds nicotinic receptor as AGONIST = depolarization
-persistent depolarization = muscle fiber resists further stimulation by ACh by preventing reset of Na+ channels
-metabolized to choline = increase BP
-muscle fasciculation precedes paralysis
-arm, neck, leg then resp muscles
-rapid onset (secs), short duration (min)
Butyrylcholinesterase
-metabolize succinylcholine to choline in plasma
-slower than AChesterase
Succinylcholine clinical use
-skeletal muscle relaxation during anesthesia esp for intubation
-also used for electro-convulsant therapy
problems with succinylcholine
-muscle soreness
-avoid in hyperkalemia (=heart attack)
-malignant hyperthermia
-prolonged paralysis in people with atypical cholinesterases
Botulinum Toxin
-indirect acting
-inhibit release of ACh
-treat dystonias (spasms), cerebral palsy, anal fissure, hyperhidrosis
Botulinum toxin problems
can spread from injection site
Hexamethonium
-ganglionic nicotinic receptor ANTAgonist
-block all SNS and PSNS activity
hexamethonium use
-originally HTN but bad effects
