can someone explain how morphine is degraded into active metabolites that accumulate? I couldn't find any sources that state this fact. Isn't it metabolized through the P450 system and excreted in urine?
Unfortunately, I chose (C) thinking that the down-regulation of receptors would lead to needing higher doses for efficacy (patient is using a patient controlled pump), however tolerance to miosis does not develop, and thus eventually this side effect would occur.
Could anyone point out where my train of thought is incorrect? I suspect that my assumption of the patient increasing their dose is not warranted?
submitted by โmoloko270(77)
Morphine is metabolized in the liver to morphine-6-glucuronide and morphine-3-glucuronide, both of which are excreted by the kidneys. In the setting of renal failure, these metabolites can accumulate, resulting in a lowering of the seizure threshold. Morphine should therefore be used with caution with mild renal impairment and be avoided in the setting of renal failure.
source: https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/morphine-6-glucuronide
they gave a hint of increased creatinine level, plus older age can give a slowed down metabolism and CNS symptoms