Problem:

Shirley is a 23 year old female who is going through a progressive muscle weakness, especially in her extremeties. It's becoming more difficult for her to climb the sttairs in her home. Her doctor noticed ptosis and th epresence of diplopia during the examination. A radioimmunoassay detected that there is a presence of acetylcholine receptor antibodies in the Shirley's blood. Anticholinesterase test was performed. Edrophonium, a short-acting acetylcholinesterase inhibitor, was administered intravenously. This drug caused a brief, but dramatic improvement in muscle function. Based on the patient's symptoms and the results of the clinical tests, the patient was diagnosed with myasthenia gravis. Neostigmine, a reversible anticholinesterase agent, was prescribed in tablet form.

Required:

Question 1: What's the acetylcholine mechanism of action at the neuromuscular junction?

Question 2: Why is progressive muscle weakness a hallmark of myasthenia gravis? Explain.

Question 3: What is ptosis and diplopia and why are these symptoms present in Shirley?

Question 4: How does an action potenential's propagation along the muscle fiber ultimately leads to skeletal muscle contraction. What is the source of calcium for skeletal muscle contraction?

Question 5: How is acetylcholine normally removed from the neuromuscular junction? why is immediate removal important?

Question 6: How does the test with edrophonium confirm the diagnosis of myasthenia gravis

Question 7: Short-acting reversible agents such as neostigmine allow for smooth control of skeletal muscle function. What systemic symptoms would be apparent in a patient following an overdose of neostigmine?

Question 8: Organophosphates, including the nerve gas sarin, irreversibly inactivate acetylcholinesterase. Why are these substances extremely toxic and may lead to death?

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