Question

Which drug produces transient muscle fasciculations followed by muscle paralysis that is not reversed by neostigmine? (A) rocuronium (B) hyoscyamine (C) cisatracurium (D) succinylcholine (E) pancuronium

Short answer

The drug is succinylcholine (D).

Step-by-step solution

Understanding the Question

The question asks which drug initially causes muscle fasciculations before leading to muscle paralysis, and importantly, this paralysis is not reversed by the drug neostigmine. We need to find the drug with these specific properties.

Identify Drug Mechanism

To solve this, we need to understand the mechanism of action of each option. Neostigmine is an acetylcholinesterase inhibitor used to reverse non-depolarizing neuromuscular blockers but does not affect depolarizing agents.

Analyze Each Option

Rocuronium, cisatracurium, and pancuronium are non-depolarizing neuromuscular blockers, while hyoscyamine is an anticholinergic, thus none of these fit the pattern of initial fasciculations. Succinylcholine is a depolarizing muscle relaxant causing fasciculations followed by paralysis, and neostigmine cannot reverse its effects.

Conclusion

Based on the pharmacological profiles, succinylcholine causes the initial muscle fasciculations and leads to paralysis that cannot be reversed by neostigmine, as it is a depolarizing blocker.

Key concepts

Neuromuscular Blockers

Neuromuscular blockers are drugs that disrupt communication between nerves and muscles, leading to muscle relaxation and paralysis. These agents are commonly used in surgical procedures when muscle relaxation is essential. They work by interfering with the normal transmission of nerve impulses in the neuromuscular junction, where neurons communicate with muscle fibers.

There are two main types of neuromuscular blockers:

• **Depolarizing blockers:** Cause initial muscle contraction or fasciculations followed by relaxation or paralysis.
• **Non-depolarizing blockers:** Prevent muscle contractions by blocking neurotransmitter transmission without causing initial contraction.

This classification is crucial for understanding how different neuromuscular blocking drugs work and their clinical implications. Some blockers, like rocuronium and cisatracurium, can have their effects reversed by anticholinesterase agents such as neostigmine.

However, depolarizing agents behave differently, as we'll see in the next section.

Depolarizing Agents

Depolarizing agents, such as succinylcholine, are a type of neuromuscular blocker with a unique mechanism of action. These agents lead to muscle contraction, known as fasciculations, before causing sustained muscle paralysis. Here is how they work:

• These drugs mimic the neurotransmitter acetylcholine and bind to the acetylcholine receptors on the muscle cell membrane.
• This binding initially causes the muscle to contract (fasciculation), which is a brief period of twitching or jerking.
• Following this, the drug keeps the receptor in a state where it cannot depolarize again, leading to paralysis.

This sequence makes depolarizing agents distinct from non-depolarizing ones, which do not cause fasciculations. An important note to remember is that the effects of depolarizing blockers are not easily reversed by drugs like neostigmine, which is often used to counteract the effects of non-depolarizing neuromuscular blockers.

Understanding the behavior of depolarizing agents is vital in clinical settings to anticipate and manage muscle paralysis.

Drug Mechanism

The drug mechanism of neuromuscular blockers, especially focusing on depolarizing agents like succinylcholine, provides insights into their unique effects. The mechanism involves complex interactions at the neuromuscular junction.

• Succinylcholine binds to acetylcholine receptors at the neuromuscular junction, leading to continuous stimulation.
• This continuous stimulation, unlike the brief pulses of neurotransmitter release, causes sustained depolarization of the muscle cell membrane.
• As a result, the muscle is unable to contract again until the drug is metabolized by plasma cholinesterase.

The paralysis induced by succinylcholine is not reversed by neostigmine because neostigmine increases acetylcholine levels, which does not mitigate the continuous occupation of receptors by succinylcholine.

Knowing the drug mechanism helps medical professionals choose the right neuromuscular blocker for various clinical applications and informs them on how to manage their effects effectively.