Discuss the condition in the discussion post and critique the post. Citations: A

Discuss the condition in the discussion post and critique the post. Citations: At least one high-level scholarly reference in APA from within the last 5 years
A 30-year-old female presents with muscle weakness and fatigue. Abnormal electromyography testing and a positive acetylcholine receptor antibodies test is reported. Her final diagnosis is Myasthenia Gravis.
Question 1: Describe the normal synaptic transmission at the Neuromuscular Junction (NMJ).
Neurons are the functional unit of nervous system. Neurons communicate with one another at junctions called synapses. At a synapse, one neuron sends a message to a target neuron—another cell. Synapses are chemical and electrical. Electrical synapses occur through flow of ions and chemical synapse occurs through release of neurotransmitters (Omar et al., 2022). At a chemical synapse, an action potential triggers the presynaptic neuron or sending neuron to release neurotransmitters such as serotonin, GABA, Acetylcholine, epinephrine, norepinephrine, dopamine etc., which binds to receptors on the postsynaptic cell and generate an action potential.
Question 2: Why is the ACh level increased?
Ach is the neurotransmitter at the Neuromuscular junction and at synapses at spinal cord autonomic ganglia. Myasthenia gravis is an autoimmune disease with progressive loss of muscle tone, due to damage and antagonism of Ach receptor. In Myasthenia gravis, the weakness of muscles is due to the antibody-mediated process (Sam & Bordoni, 2022). In this autoimmune antibody mediated process, antibodies generated against Ach receptors (AChR), these antibodies have Tropism for Ach receptors or their associated proteins at postsynaptic neurons which cause binding of antibodies on receptor sites instead of ACH which leads to the increased unbound circulating level of ACh and less contraction of muscles (Sam & Bordoni, 2022).
Question 3: Explain why the patient with myasthenia gravis cannot generate consistent action potentials in the muscle fiber.
In myasthenic patients the neuromuscular junction has decreased numbers of acetylcholine receptors, a wider synaptic cleft, and simplified synaptic folds. These changes account for the clinical features of myasthenia gravis. Decreased numbers of acetylcholine receptors result in fewer interactions between acetylcholine and its receptors, leading to decreased activation of action potentials (Phillips & Vincent, 2016). When the transmission of action potentials decreases, the power of the muscle’s contraction is reduced, causing weakness.
Question 4: Treatment for the patient involves pyridostigmine- what does this drug do and how would it benefit our patient?
The pyridostigmine therapy is used as a first-line treatment for all types of MG. In the case of AChR antibodies, AChRs are directly bound and cross-linked, impairing acetylcholine binding and contributing through various mechanisms to receptor degradation. The lack of ACh signaling leads to muscle tone loss, muscle weakness, and fatigue. Pyridostigmine is a reversible ACh inhibitor that increases extracellular acetylcholine levels in the NMJ by impairing its breakdown by acetylcholinesterase. The increased acetylcholine leads to increased neural transmission across the junction, which drastically improves myasthenia gravis symptoms, thereby improving nerve-muscle communication and muscle strength (Farrugia & Goodfellow, 2020).
Farrugia, M., & Goodfellow, J. A. (2020). A practical approach to managing patients with myasthenia gravis—opinions and a review of the literature. Frontiers in Neurology, 11. https://doi.org/10.3389/fneur.2020.00604
Omar, A., Marwaha, K., & Bollu, P. C. (2022). Physiology, Neuromuscular Junction. StatPearls. https://www.ncbi.nlm.nih.gov/books/NBK470413/
Phillips, W. D., & Vincent, A. (2016). Pathogenesis of myasthenia gravis: Update on disease types, models, and mechanisms. F1000Research, 5, 1513. https://doi.org/10.12688/f1000research.8206.1
Sam, C., & Bordoni, B. (2022). Physiology, Acetylcholine. StatPearls. https://www.ncbi.nlm.nih.gov/books/NBK557825/

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