Autonomic Nervous Systems
A patient presents with food poisoning that is attributed to botulism. Which would be a correct or mechanism associated with this toxin? (AIPG 2012)
|A||Complete failure of all cholinergic neurotransmission|
|B||Favorable response to administration of pralidoxime|
|C||Impairment of parasympathetic, but not sympathetic, nervous system activation|
|D||Massive overstimulation of all structures having muscarinic cholinergic receptors|
a. Botulinus (botuhnum) toxin prevents release of acetylcholine (from storage vesicles) by virtually all cholinergic nerves.
b. Thus, there is no activation of any cholinergic receptors, whether nicotinic or muscarinic.
c. Noteworthy findings, then, include an inability to activate all postganglionic neurons (sympathetic and parasympathetic), no physiologic release of epinephrine from the adrenal medulla, and flaccid skeletal muscle paralysis due to failure of ACh release from motor nerves.
d. The cause of death is ventilatory failure because the intercostal muscles and diaphragm are nonfunctional.
e. Pralidoxime is a cholinesterase reactivator, an antidote for poisonings with “irreversible” cholinesterase inhibitors such as soman, sarin (“nerve gases”), and many organophosphorus insecticides.
f. Because no ACh is being released in botulinus poisoning, “reactivation” of the enzyme that normally metabolizes the neurotransmitter is irrelevant (and ineffective).