What is the underlying pathophysiology of Myasthenia Gravis?

What is the underlying pathophysiology of Myasthenia Gravis?

• A. Inflammation of peripheral nerves
• B. Autoantibodies that bind to pre-synaptic ACh receptors
• C. Autoantibodies that bind to postsynaptic ACh receptors
• D. Deficiency of neurotransmitters

Answer: (C)

Myasthenia Gravis is primarily characterized by the presence of autoantibodies that bind to postsynaptic acetylcholine (ACh) receptors at the neuromuscular junction. This binding disrupts the normal communication between nerves and muscles, leading to muscle weakness and fatigue. In a healthy neuromuscular junction, acetylcholine is released from the nerve terminals and binds to specific receptors on the muscle membrane, which triggers muscle contraction. However, in Myasthenia Gravis, the autoantibodies block, alter, or destroy these receptors, resulting in decreased sensitivity to acetylcholine and impaired neuromuscular transmission. The pathophysiological process also induces complement-mediated damage to the postsynaptic membrane, further reducing the number of functional ACh receptors and exacerbating muscle weakness. Symptoms can vary widely among individuals, often worsening with activity due to the depletion of available ACh receptors. Other options describe different pathological mechanisms that do not specifically pertain to Myasthenia Gravis. For example, inflammation of peripheral nerves could relate to other neuropathic conditions but does not represent the mechanism at play in Myasthenia Gravis. Similarly, the concept of autoantibodies binding to presynaptic

Myasthenia Gravis is primarily characterized by the presence of autoantibodies that bind to postsynaptic acetylcholine (ACh) receptors at the neuromuscular junction. This binding disrupts the normal communication between nerves and muscles, leading to muscle weakness and fatigue. In a healthy neuromuscular junction, acetylcholine is released from the nerve terminals and binds to specific receptors on the muscle membrane, which triggers muscle contraction. However, in Myasthenia Gravis, the autoantibodies block, alter, or destroy these receptors, resulting in decreased sensitivity to acetylcholine and impaired neuromuscular transmission.

The pathophysiological process also induces complement-mediated damage to the postsynaptic membrane, further reducing the number of functional ACh receptors and exacerbating muscle weakness. Symptoms can vary widely among individuals, often worsening with activity due to the depletion of available ACh receptors.

Other options describe different pathological mechanisms that do not specifically pertain to Myasthenia Gravis. For example, inflammation of peripheral nerves could relate to other neuropathic conditions but does not represent the mechanism at play in Myasthenia Gravis. Similarly, the concept of autoantibodies binding to presynaptic