different effectiveness of codeincodein is prodrug with basically no effects by itself
it instead must be ☆metabolized (by the liver via CYP2D6) into morphine in order to provide analgesia anesthesiologypharmacologyfree120 HirotoShishido
halothane
toxicity→ histology, labs(remains one of the most commonly used inhaled anesthetics worldwide)
hepatotoxicity (fulminant hepatitis with a 50% fatality rate)
→ causes the liver to rapidly atrophy and appears ☆shrunken on autopsy
(histologically, centrilobular necrosis is indistinguishable from acute viral hepatitis)
prolonged muscular paralysis by succinylcholinepseudocholinesterase deficiency(AR)
(genetic polymorphism in the BCHE gene)
☆decreased plasma hydrolysis
heterozogotes may experience double the normal duration of paralysis, homozygotes have persistent paralysis for several hours anesthesiologyUWorld HirotoShishido
which channels are involved in opiate binding to mu receptorclosure of voltage-gated Ca channels, reduced calcium influx, and decreased excitatory neurotransmitter release (eg, acetylcholine, norepinephrine, serotonin, glutamate, substance P) from the presynaptic terminal
Opiates also bind to mu receptors on the postsynaptic membrane, which opens ☆K channels and leads to membrane hyperpolarization due to potassium efflux neurologyanesthesiologyUWorld HirotoShishido