Essay On Myasthenia Gravis

Myasthenia gravis is an autoimmune disease that effects the skeletal muscles of the body at the neuromuscular junction. The 40th Edition of Gray’s Anatomy defines it as, “myasthenia gravis is essentially an autoimmune disease in which acetylcholine receptor proteins of neuromuscular junctions are attacked by autoantibodies.” (Gray’s). This chronic disease is characterized by muscles that fatigue quickly activity and gets better after rest. The muscles that are most often effected are those that control facial expressions, eyelids, chewing, swallowing, and talking, but sometimes those that control breathing, and movement in the neck and limbs are also impacted (“Myasthenia Gravis Fact Sheet,” 2010).

Cellular and histological component of the condition comparing normal to abnormal:

The exact cause of myasthenia gravis is still not completely proven; however, there have been many correlations linked between certain autoantibodies as well as thymus abnormalities in 80-90 percent of people affected by the disease (Bird, 2016). Normal function of a muscle at the neuromuscular junction involves a neurotransmitter called Acetylcholine and its receptor. When an action potential is sent from the neuron and arrives at the axon terminal,

Further research has revealed that 40-70 percent of Caucasian patients contain an antibody that effects a different protein on the muscle membrane called the muscle-specific receptor tyrosine kinase (MuSK). In normal muscle tissue, MuSK plays a role in the recruitment of AChR binding proteins to stimulate the clustering of AChRs. The exact process of how these antibodies effect MuSK to cause myasthenia gravis is still not fully understood. However, the distinction between AChR and MuSK antibody positive myasthenia gravis is important because there is a difference between symptoms and treatments for the two categories of myasthenia gravis (Bird,