Question

Myasthenia gravis is characterized by a decreased density of acetylcholine (ACh) receptors at the muscle end plate. An acetylcholinesterase (AChE) inhibitor blocks degradation of ACh in the neuromuscular junction, so levels at the muscle end plate remain high, partially compensating for the deficiency of receptors. What is the effect of an acetylcholinesterase (AChE) inhibitor in myasthenia gravis?

1) Increases the density of acetylcholine (ACh) receptors at the muscle end plate
2) Blocks degradation of ACh in the neuromuscular junction
3) Decreases the levels of ACh at the muscle end plate
4) Compensates for the deficiency of ACh receptors

Answer 1

The effect of an acetylcholinesterase inhibitor in myasthenia gravis is to block the degradation of ACh at the neuromuscular junction, which helps compensate for the low density of ACh receptors by increasing the levels of ACh available for receptor binding.

Step-by-step explanation:

Myasthenia gravis is an autoimmune disease characterized by the presence of autoantibodies that block acetylcholine receptors (AChRs) on muscle cells at the neuromuscular junction, which leads to weakened muscle contraction capability. The effect of an acetylcholinesterase (AChE) inhibitor in myasthenia gravis is to block the degradation of ACh in the neuromuscular junction. This increases the levels of ACh available, which partially compensates for the deficiency of ACh receptors by allowing more ACh molecules to bind to the fewer available AChRs, thereby improving muscle contraction.