The basis of treatment for myasthenia gravis with _____ involves the binding of a molecule to acetylcholinesterase to decrease its activity. This enables more acetylcholine to be available for binding to the receptors on the sarcolemma.

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Question restatement: The basis of treatment for myasthenia gravis with _____ involves the binding of a molecule to acetylcholinesterase to decrease its activity. This enables more acetylcholine to be available for binding to the receptors on the sarcolemma.

Option 1: immunosuppressants. While immunosuppressants can be used in myasthenia gravis to reduce immune activity against acetylcholine receptors, they do not work by binding to acetylcholinesterase or directly increasing acetylcholine availability at the neuromuscular junction. Their mechanism is broader immune system suppression rather than enzyme inhibition at the synapse.

Option 2: corticosteroids. Similar to other immunosuppressive strategies, corticosteroids help modulate the immune response and may reduce disease activity, but they do not inhibit acetylcholinesterase or specifically elevate acetylcholine levels at the motor endplate. Their primary action is anti-inflammatory and immunosuppressive, not enzymatic inhibition at the NMJ.

Option 3: anti-inflammatories. General anti-inflammatory drugs reduce inflammation and immune-mediated damage in various conditions, yet they do not target acetylcholinesterase nor increase acetylcholine availability at the sarcolemma. This choice misses the molecular mechanism described in the stem.

Option 4: cholinesterase inhibitors. This category of drugs binds to acetylcholinesterase and decreases its activity, slowing acetylcholine breakdown. The resulting higher acetylcholine concentration at the neuromuscular junction improves transmission by promoting binding to nicotinic receptors on the sarcolemma, which aligns precisely with the described treatment basis for myasthenia gravis.

Conceptual check: The stem emphasizes a mechanism that directly modulates acetylcholine availability at the NMJ via enzyme inhibition. Among the options, only cholinesterase inhibitors fit this exact mechanism, providing a targeted pharmacologic approach for MG symptoms by sustaining acetylcholine signaling at the receptor sites. The other choices involve immune modulation or non-specific anti-inflammatory effects, which do not match the described enzymatic target or the pathophysiology described in the stem.

BIOL 251 Clinical Connections 5: A Muscle Mystery

The basis of treatment for myasthenia gravis with _____ involves the binding of a molecule to acetylcholinesterase to decrease its activity. This enables more acetylcholine to be available for binding to the receptors on the sarcolemma.

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