Marga created. Back to Myasthenia Gravis, the receptor

Marga David

BIOS: 487 Medical
Physiology

Your time is important. Let us write you an essay from scratch
100% plagiarism free
Sources and citations are provided


Get essay help

Dr. Sumitra Miriyala  

 

1.      The
patient’s condition is referred to as Myasthenia Gravis.

2.    
Pathology of the neuromuscular junction
could result in a progressive muscle paralysis. The neuromuscular junction is
composed of the synaptic trough, cleft, and sub neural cleft. As an action potential
is created, it then travels along the nerve and then arrives at the NMJ. A
neurotransmitter, acetylcholine, is released in many, little vesicles when the
nerve impulse arrives at the terminal. They are released to the synaptic space.
In reference to Myasthenia Gravis, the auto antibodies would be considered the
cause of the illness (Mehndiratta, Pandey, & Kuntzer, 2014). This disease not only causes fatigue,
but muscle weakness as well. Acetylcholine is a neurotransmitter that excites
the muscle fiber membrane. It then, activates the Ach receptors and the muscle
action potential is created. The muscle cell contracts as a result of the
action potential created. Back to Myasthenia Gravis, the receptor site of the
muscle is either blocked or destroyed by the antibodies, which are produced by
the immune system (Mehndiratta et al., 2014). This receptor site is
designated for the acetylcholine. When this occurs, the nerve signals are
reduced or none occur at all, causing weakness of the muscle. Eventually, the
end plate potential will become extremely weak and as it progresses, the Ach
receptors will result in hindered binding of the acetylcholine and progressive muscle
paralysis will occur. Depending on
what acts or stimulates the Ach receptor can directly or indirectly effect the
receptors.

 

References

Mehndiratta,
M. M., Pandey, S., & Kuntzer, T. (2014, October 13). Acetylcholinesterase inhibitor treatment for myasthenia gravis. Retrieved
January 27, 2018, from      https://www.ncbi.nlm.nih.gov/pubmed/25310725