Pathophysiological Mechanism of Myasthenia Gravis

Pathophysiological Mechanism of Myasthenia Gravis

Introduction

Myasthenia is a disease in which patient suffers weakness of voluntary muscles. This condition occurs due to lack of communication between voluntary muscles and nerves. It is an autoimmune disease, body's own immune system starts making antibodies against it (Christadoss, 2000).Antibodies that provides protection against the harms caused by foreign antigen, start acting against the receptors of muscles by destroying or blocking the receptor sites. So the whole phenomenon of muscle contraction become disturbed and makes the muscles weak.

Major symptoms faced by the patients are drooping eyelids and problem in the movement of eyelids, facial expression become problem and there is difficulty in swallowing. But other body muscles can also be affected. Patient feels muscle weakness more when utilizing voluntary muscle while performing work.

The medicines use for myasthenia gravis act by making muscles stronger and improving message conduction from nerve to muscle. Other drugs restrict the body to make abnormal antibodies from the blood.

Discussion

Normal Anatomy/Physiology of Muscle Contraction

Muscles contraction occurs when the motor neurons send signals. Muscle cells and motor neurons meet at a point known as Neuromuscular Junction abbreviated as NMJ. Neurotransmitter chemicals are released by the motor neurons at the neuromuscular junction that bond to the motor end plate, a special part of the sarcolemma. There are various ion channels present on the motor end plate that activated and open in response to the neurotransmitters (Matthews, 2009). These ions channels then allow the positive ions to enter the muscle fiber. The electrochemical gradient formed by the positive ions spreads throughout the T-tubules and sarcolemma by activating or opening even more ion channels. Ca2+ ions are released and flow into the myofibrils, when positive ions reach the sarcoplasmic reticulum. This Calcium ion (Ca2+) bind with the troponin, that causes the transformation of ...