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Myasthenia Gravis: Case Study Analysis

The issue under analysis features the case of a 45-year-old woman, who has been experiencing consisted fatigue, particularly, after making a physical effort such as a walk or any kind of physical activity. In addition, her speaking skills seem to be impaired as her speech turned unintelligible after a few minutes of conversation. After a visit to the neurologist, the issues such as a bilateral ptosis, medial strabismus, facial paralysis and swallowing issues are apart from the problems listed above.

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Based on the symptoms listed above, one may conclude that the woman suffers from myasthenia gravis, a medical condition characterized by fatigue and progressive speech impairment (Acetylcholinesterase inhibitor treatment for myasthenia gravis, 2014). The condition involves the development of progressive muscle weakness, which aggravates as the patient engages in any form of physical activities, including exercises (Bhatnagar, 2013). Moreover, the specified disorder manifests itself in patients with an ocular motor dysfunction (Acetylcholinesterase inhibitor treatment for myasthenia gravis, 2014), as the case in point shows quite graphically.

The mechanism of the myasthenia gravis development is rather basic. According to the existing definition of the phenomenon, the disorder occurs as a result of the postsynaptic membrane destruction. To be more exact, the junctions that are created as an axon reaches the muscle fiber neuron and that is identified as a postsynaptic membrane can no longer release acetylcholine so that the nerve impulse could be transformed into the muscular fiber contraction. The muscle weakness mentioned above, therefore, can be viewed as the effect of the antibodies preventing the acetylcholine receptors from creating a junction with the axon (Myasthenia gravis, 2015). The problem above can occur as a result of a defect that prevents the successful contraction of the membrane. Particularly, the process of the disorder development must have been reinforced after the introduction of the patient to an acetylcholinesterase (AChE) drug. The latter is typically known as the inhibitor that blocks the operation of certain neurotransmitters in the human body (Bhatnagar, 2013).

The fact that the patient is in her forties should not be viewed as an argument either against or in favor of the diagnosis, as the instance of myasthenia gravis may occur at any age, according to the existing information (NINDS congenital myasthenia information page, 2016). More importantly, the specified disorder is claimed to occur at a genetic level; herein the necessity to track the patient’s family history down lies. Indeed, the identified problem can be an instance of a congenital myasthenic syndrome (Bhatnagar, 2013), which, in its turn, triggers a genetic mutation of cells and contributes to the development of MG prerequisites in a patient. It should be borne in mind, though, that there is a tangible difference between MG and the congenital myasthenic syndrome. While the former is caused by gene mutation, the development of the latter is enhanced by antibodies (Acetylcholinesterase inhibitor treatment for myasthenia gravis, 2014).

To address the specified instance of MG, a nurse must consider running the tests that will help identify the type of the disorder. To be more exact, the tests such as RAPSN, CHAT, and COLQ) (NINDS congenital myasthenia information page, 2016) must be considered as the first choice tools. Afterward, the nurse must identify the tools that will help address the lack of response to the signal between the nerve and the muscle (Bhatnagar, 2013). It is suggested that the medications such as fluoxetine, ephedrine, 3,4-diaminopyridine, etc. (NINDS congenital myasthenia information page, 2016) should be prescribed. In case of a timely management of the issue, a recovery is likely to become a possibility.

Reference List

Acetylcholinesterase inhibitor treatment for myasthenia gravis. (2014). Web.

Bhatnagar, A. (2013). Neuroscience for the study of communicative disorders (4th ed.). Philadelphia, PA: Lippincott, Williams, & Wilkins.

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Myasthenia gravis. (2015). Web.

NINDS congenital myasthenia information page. (2016). Web.

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