C. Hallmark symptoms and characterization
The hallmark symptoms for MG include: fatigued muscle weakness, a fluctuation of symptoms, and overly sensitive reactions to environmental stressors (Spillane et al. 2012; Gilhus et al. 2011). Patients usually have worsening symptoms near the end of the day, and about 10% of patients have another autoimmune disorder (Gilhus et al. 2011). Often the most severe cases of MG lead to myasthenia crisis, an acute respiratory failure requiring mechanical ventilation of the patient, though any patient can go into crisis (Spillane et al. 2012; Mao et al. 2010). One of the most common symptoms is drooping of the eyes, ptosis.
D. Treatment and Prognosis
MG is occasionally treated with acetylcholinesterase
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inhibitors (a drug class that inhibits the binding of acetylcholine to remove it from the synaptic cleft) that can cause short-term relief for patients but are generally ineffective in the long-term (Spillane et al., 2012). Other drugs such as corticosteroids have been seen to be helpful in the most severe cases (Gilhus et al., 2011). A thymectomy, removal of the thymus gland, is done in patients with a high risk for a tumor on the gland, who are young, without antibodies for muscle specific tyrosine kinase, and/or have a generalized response(Spillane et al., 2012). A third approach is with immunosuppressive therapies that reduce the signals given by the thymus gland to acetylcholine receptors as antigens (Spillane et al., 2012; Conti-Fine et al., 2006). The prognosis seems largely positive for patients who receive treatment early in the onset of the disease (Spillane et al., 2012; Conti-Fine et al., 2006; Gilhus et al., 2011; Mao et al. 2010). Treatment is more difficult in patients with a specific antibody response to tyrosine kinases (a class of kinases that work on the amino acid tyrosine) in the acetylcholine pathway. Prognosis has been correlated with age of onset and time of onset before treatment (Mao et al., 2010). It is necessary, then, for this rare disease to be caught early by physicians. E. Relation to case study Dwight Jameson seemed to have a fairly straightforward case of MG.
His symptoms were strongly aligned with the hallmark characteristics of the disease, and his reception to treatment was largely without complication. It seems like the age of diagnosis, I am assuming in his mid- to late-twenties, was a strong factor in his full recovery. The issues with the case study that may have been simplified were that he required less than a year of immunosuppressant therapy. Spillane explained that immunosuppressant therapy was not always straight-forward, but that it required constant monitoring and adjustments. Continuing a career in football after such invasive surgery and therapies is somewhat unlikely, based on the discussion on recovery times and complications in both Gilhus et al. and Spillane et al. Also, Conti-Fine et al. explained that there are antibodies that interact with different parts of the pathway, making treatment more nuanced than simply addressing one antibody that has high affinity for the “acetylcholine receptor …show more content…
protein.” F. Information learned about normal brain function These literature reviews were helpful in understanding the specific pathway of acetylcholine at NMJs, but also in understanding in a broader sense neurotransmitter activity. Neurotransmitters must be targeted to the postsynaptic cleft, while this seems relatively straight-forward, cells are highly complex and simply having a receptor on one membrane does not mean that the neurotransmitter will make it to the receptor. Neurotransmitters are released then bound (causing conformational change in the receptor protein) to the receptor proteins, allowing for a change in the membrane structure (gates open or close). Part III. I’m interested in the prognosis of the disease, and how early diagnosis leads to higher survival rates and less severe symptoms in the long run. Presumably, if the antibodies are inhibited sooner and steps are taken to alter the immunoresponse, the disease will be less severe. It is also interesting how as the disease progresses, the symptoms take longer to recover (this is of course in the untreated cases). Analysis of acetylcholine receptors in individuals may help gain an understanding of what actually results in this increased recovery time; if antibodies are being generated for different parts of the receptor (for example one antibody binds to the N-terminus, and another to the C-terminus, etc) over time, then drug therapies that target one antibody will be ineffective for the others. I hypothesize that as the disease progresses, antibodies are being made for different antigen-binding sites within the acetylcholine pathway, leading to more nuanced and severe symptoms in older patients or patients who had early onset but late diagnosis. To study this, isolating acetylcholine receptors and antibodies from diseased individuals would be effective. It would be necessary to purify a known antibody for the receptor, and then analyze where in the protein the antibody is binding. With a large population, patterns of antibody binding sites may become clear. It would be crucial to have a good understanding of the patient clinically in order to understand the relationship between antibody binding sites and symptoms. IV.
Works cited
Conti-fine, B. M., Milani, M., & Kaminski, H. J. (2006). Science in medicine Myasthenia gravis : past , present , and future, 116(11), 2843–2854. doi:10.1172/JCI29894.which
Gilhus, N. E., Owe, J. F., Hoff, J. M., Romi, F., Skeie, G. O., & Aarli, J. a. (2011). Myasthenia gravis: a review of available treatment approaches. Autoimmune Diseases, 2011, 847393. doi:10.4061/2011/847393
Mao, Z.-F., Mo, X., Qin, C., Lai, Y.-R., & Olde Hartman, T. C. (2010). Course and prognosis of myasthenia gravis: a systematic review. European Journal of Neurology : The Official Journal of the European Federation of Neurological Societies, 17(7), 913–21. doi:10.1111/j.1468-1331.2010.03017.x
Spillane, J. Highan, E. Kullman, D.M. (2012) Myasthenia gravis, 8497(December), 1–4.
doi:10.1136/bmj.e8497
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