Myasthenia Gravis

Myasthenia Gravis (MG) is by far the most commonly occurring major malady of neuromuscular transmission. An acquired immunological abnormality is the usual cause of MG. However, another reason is a genetic defect at the neuromuscular junction. Several studies have been conducted to uncover the intricacies around Myasthenia Gravis. They dwell on the pathophysiology and immunopathology of MG. Therefore, the paper seeks to discuss the MG pathophysiology, signs and symptoms, lab and diagnostic tests available, medical treatments, nursing assessments diagnosis, and management.

Definition and Pathophysiology

Myasthenia Gravis is an acquired autoimmune disorder initiated by the antibody blockade of neuromuscular transmission, which causes muscle weakness. The attack on the autoimmune transpires by the formation of autoantibodies that act against the nicotinic acetylcholine postsynaptic receptors present at the junction of neuromuscular skeletal muscles (AL-Zwaini, & Ali, 2019). The principal target of the attack is usually nicotinic acetylcholine receptor (nAChR); nevertheless, implications of some other antigenic targets, which are neuromuscular junction components, also occur. The pathophysiology entails a regular release of acetylcholine (Ach) at the neuromuscular junction (NMJ) from the motor nerve. After diffusion of Ach quanta across synaptic left and receptor binding, motor nerve stimulation releases many Ach quanta resulting in depolarization of muscle end-plate, and significant muscle contraction happens.

In Myasthenia Gravis, Ach release occurs typically; nonetheless, the effect it has on postsynaptic membrane reduces. Therefore, the autoantibody acting against AChRs causes damage to the postsynaptic membrane and a significant reduction of Ach receptors present at the binding (the muscle end-plate membrane). This action starts an inconsistency in the generation of potential muscular activity translating into muscle weakness. The postsynaptic membrane-damaging process depends on complement activation. An antigenic target has been found in patients lacking antibodies against AChRs. The antigenic target is a muscle-specific tyrosine, which is dependent on muscle protein (AL-Zwaini, & Ali, 2019).     

Signs and Symptoms

The disorder affects people at any age, specifically among women under 40 years of age and men above 60 years old. In such occurrences, there may be some common signs and symptoms noted. The continued use of an affected muscle only worsens the condition. Some of the signs and symptoms include problems with eye muscles. It is the first sign and symptom where either one or both eyelids droop, a condition called ptosis. A double vision (diplopia) can also occur vertically or horizontally, and usually, a temporary improvement in the closing of one eye happens (Young, & Leavitt, 2016). Other signs and symptoms include weaknesses in the face and throat muscles, neck, and limb muscles. Face and throat signs and symptoms involve impaired speech that sounds nasal or soft, swallowing difficulty, chewing problems and changes in facial expressions. The neck and limbs challenges comprise, impaired walking from weak legs. Patients positive of anti-MuSK have a weakness with bulbar alongside facial and tongue atrophy. They also possess shoulder, neck, and respiratory activity, having an ocular weakness. The patients tend to have a slow response towards acetylcholine esterase inhibitors, which worsens symptoms when administered.   

Laboratory and Diagnostic tests

Serological tests include anti-MuSk (muscle-specific tyrosine kinase) antibody, which usually results in positive results in a good percentage of myasthenic patients having negative anti-AChR. The Anti-acetylcholine receptor antibody test is typically reliable in diagnosing autoimmune MG because of its preciseness. The results frequently occur in almost 90 percent of patients with general MG; however, only 50 to 65 percent in those patients having the ocular MG. Therefore, false negatives results can surface in purely ocular MG cases. Other tests include anti-lipoprotein-related protein 4 (LRP4). This LRP4 exists on the postsynaptic membrane being a receptor for agrin and vital for MuSK activation.

The activation of MuSK leads to rapsyn activation manifesting into the clustering of AChRs through binding to the postsynaptic membrane. Studies show that the prevalence of anti-LRP4 antibodies ranging from 3 percent to 50 percent of MG double seronegative patients varies in several geographic locations. Other tests include anti-striated muscle antibody, tests of rheumatoid factor, and antinuclear antibodies, thyroid function test. Radiological studies include the chest X-ray, MRI, and CT scan to examine patients with speculated thymoma and anterior mediastinal mass (AL-Zwaini, & Ali, 2019).

These act to dismiss brain and orbit mass injuries that trigger cranial nerve palsies in ocular Myasthenia Gravis. Ophthalmologists in assessing improvements in diplopia and ptosis, use the ice pack test (AL-Zwaini, & Ali, 2019). The determination of serum antibody is the universal diagnostic tool for MG. The electromyography (EMG) and response to cholinesterase inhibitors are significant factors for confirmation of diagnosis. Edrophonium injection confirms the diagnosis, and the MRI demonstrates an enlargement of the thymus gland. General, serum analysis for AChR and EMG (electromyography) form the basis of tests in measuring the electrical potential of muscle cells.

Medical Treatments, Management, Nursing Assessment, and Nursing Diagnosis

Treatment of MG depends on the severity, which will entail to some point therapeutic options. The seriousness of MG involves classification into mild, moderate, and severe. Treatments used comprise symptomatic therapies with medication involving cholinesterase inhibitors, thymectomy, intravenous immunoglobulin, and immunosuppressive agents. The management consists of encouraging the patients to sit upright when eating, planning short exercises in line with times of maximal muscle strength, and instructing patients to avoid stress, over-the-counter medications, and fatigue (Tibin, Nandini, & Siji, 2017). The nursing assessments refer to reviewing the priorities for patients affected by MG. The patient weakness assessment, the understanding of treatment and medication, and the awareness of the need for patient support and education form the critical areas for patient care. The primary diagnosis made by nurses is ineffective airway clearance concerning swallowing and aspiration difficulties (Tibin, Nandini, & Siji, 2017). Other assessments include monitoring the respiratory failure of patients, ptosis and diplopia monitoring, assessing patients’ muscle status, and speech monitoring.

Conclusion

The management of Myasthenia Gravis is critical to the betterment of patient health. Several advances in the medical field resulted in patients experiencing average lifespan. The patient caregivers need to do close assessments of their patients for effective medication. MG generally causes muscle weakness, and therapeutic medications are essential in as much as medications with a cholinesterase inhibitor. Therefore, the two types of medication apply to patient recovery.

References

AL-Zwaini, I. J., & Ali, A. M. (2019). Introductory Chapter: Myasthenia Gravis-An Overview. In Selected Topics in Myasthenia Gravis. IntechOpen.

Tibin, J., Nandini, M., & Siji, C. (2017). Myasthenia gravis and the role of nurse. The Journal of Nursing Trendz8(1), 27-31.

Young, J. D., & Leavitt, J. A. (2016). Lambert–Eaton myasthenic syndrome: ocular signs and symptoms. Journal of Neuro-ophthalmology36(1), 20-22.

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