Regarding the pathophysiology of myasthenia gravis, in its most common form it is:
ExplanationC. In over 80% to 85% of patients with myasthenia gravis, the pathophysiology relates to the presence of circulating antiacetylcholine receptor antibodies, which have an affinity to the postsynaptic acetylcholine receptor and can be binding, blocking, or modulating. The most commonly detected are the binding type. These antibodies cause complement-mediated destruction of the junctional folds that contain dense concentrations of this receptor, and a higher rate of internalization and destruction of acetylcholine receptors. Blocking antibodies might block binding of acetylcholine to its receptor at the neuromuscular junction, while modulating bind to a site on the receptor other than the acetylcholine binding site and alter the structure of the active site. Antibodies against presynaptic voltage-gated calcium channels occur in Lambert– Eaton myasthenic syndrome. Botulinum toxin inhibits exocytosis of presynaptic vesicles containing acetylcholine . Rarely, myasthenia results from mutations in the acetylcholine receptor gene
