Master Succinylcholine with Picmonic for Medicine

Succincylcholine exerts its action by binding to the motor nicotinic receptor, which typically accepts endogenous acetylcholine.

This drug mimics ACh action at nicotinic receptor, opening sodium channels and causing membrane depolarization.

Succinylcholine keeps cells in sustained depolarization, and prevents muscle contraction. This happens because the cells are unable to repolarize and contract again. This can be observed immediately after IV administration of this drug, as patients fasciculate (contract), and are unable to contract again, even after electrical stimulation.

Phase I blocking of this drug is described as maintaining the muscle cell's membrane potential above threshold. The cells are kept in a depolarized state (as succinylcholine is bound to the receptor), as succinylcholine is not broken down quickly. This period of paralysis cannot be overcome, as there is nowhere for acetylcholine to bind.

Phase II blocking of this drug is described by the cells being repolarized but blocked. The myocytes become sensitized to their receptor activity and eventually repolarize. ACh receptors are now available but are less sensitive to acetylcholine; they are desensitized. This paralysis is reversible, but needs a larger acetylcholine stimulus to cause contraction.

Neostigmine is an acetylcholinesterase inhibitor and prevents the breakdown of acetylcholine in the plasma. This leads to an increase in acetylcholine concentration. It is often used to overcome the desensitization experience by paralyzed patients in a Phase II block of succinylcholine.