Myasthenia Gravis Mandy VanBibber posted Dec 16, 2020 1:44 AM Subscribe Previous Next This page automatically marks posts as read as you scroll. Adjust automatic marking as read setting A 30 year old female presents with muscle weakness and fatigue. Abnormal electromyography testing and a positive increase in ACTH receptor test is reported. Her final diagnosis is Myasthenia Gravis. Myasthenia gravis is a type of autoimmune disorder. Antibodies are proteins made by the body’s immune system when it finds harmful substances. Antibodies in this case is produce when the immune system mistakes healthy tissues to be a harmful substance. In people with myasthenia gravis, the body produces antibodies that block the muscle cells from receiving the neurotransmitters from the nerve cells. Myasthenia gravis can affect people at any age but is most common in young women and older men (Myasthenia gravis, 2019). Describe the normal synaptic transmission at the Neuromuscular Junction (NMJ). Neuromuscular transmission depends on the blend, storage, and release of acetylcholine from the presynaptic motor nerve ending at the neuromuscular junction, binding of acetylcholine to nicotinic receptors on the postsynaptic region of the muscle cell membrane, with simultaneously generating of the action potential and rapid influx of acetylcholine by the acetylcholinesterase enzyme present in the synaptic cleft (Naguib, 2007). 2. Why is the ACTH level increased? If adrenal glands are healthy and functioning normally, cortisol level will rise in response to ACTH you are given in the ACTH receptor test. This test was done to rule out primary adrenal insufficiency (Montes-Villarreal, 2020) Explain why the patient with myasthenia gravis cannot generate consistent action potentials in the muscle fiber. Acetylcholine receptor antibodies bind to the acetylcholine receptors and block many of the receptors, so the action or activity of this acetylcholine neurotransmitter results in a reduced movement of the voluntary muscle (Myasthenia gravis, 2019). Treatment for the patient involves pyridostigmine—what does this drug do and how would it benefit our patient? Pyridostigmine inhibits acetylcholinesterase in the synaptic cleft by competing with acetylcholine for attachment to acetylcholinesterase and slows down the hydrolysis of the acetylcholine effectively increasing the efficiency of the cholinergic transmission in the neuromuscular junction, prolonging the effects of acetylcholine (Apinyawasisuk, Chongpison, Thitisaksakul, & Jariyakosol,2020). Reference Apinyawasisuk, S., Chongpison, Y., Thitisaksakul, C., & Jariyakosol, S. (2020). Factors Affecting Generalization of Ocular Myasthenia Gravis in Patients With Positive Acetylcholine Receptor Antibody. American Journal of Ophthalmology, 209, 10-17. http://dx.doi.org/10.1016/j.ajo.2019.09.019 Montes-Villarreal, J., Perez-Arredondo, L., Rodriguez-Gutierrez, R., Alejandro Diaz Gonzalez-Colmenero, Solis, R. C., González-González, J. G., & Mancillas-Adame, L. (2020). SERUM MORNING CORTISOL AS A SCREENING TEST FOR ADRENAL INSUFFICIENCY. Endocrine Practice, 26(1), 30-35. http://dx.doi.org/10.4158/EP-2019-0327 Myasthenia gravis (2019). Johns Creek: Ebix Inc. Retrieved from https://search.proquest.com/other-sources/myasthenia-gravis/docview/2085179337/se-2?accountid=100141 Naguib, M., W.B. Saunders, (2007). Complications in Anesthesia (Second Edition),Chapter 116 – Myasthenic Disorders, pages 448-449, (http://www.sciencedirect.com/science/article/pii/B9781416022152501216)
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