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A patient is admitted for electroconvulsive treatment (ECT). The physician orders the neuromuscular blocking agent metocurine iodide (metubine) to reduce trauma by relaxing skeletal muscles. Explain the process of muscle contraction and how a neuromuscular blocking agent, such as metubine, would interfere with muscle contraction.

Aaron arrived at the hospital with the following symptoms: drooping eyelids; fatigue and weakness of his muscles; and difficulty talking, breathing, and swallowing. What is his diagnosis? Explain.
Aaron displays the classic symptoms of myasthenia gravis. This disorder is caused by insufficient binding of acetylcholine (ACh) neurotransmitters due to antibodies blocking their receptors at the postsynaptic neuron. Because ACh cannot bind, there is no chemical signal to begin depolarization, therefore a graded potential is not generated. Without the graded potential, there is certainly no action potential which can cause the muscle fiber to contract. This causes a fluctuation in muscle strength that can affect varying parts of the body, and eventually leads to the degradation of the ACh receptors. Aaron is experiencing these symptoms because his muscles are not correctly responding to the neural transmitters movement signals. There are a few treatments to consider for myasthenia gravis. To limit antibody interference at the neuromuscular junction, immunosuppressants are used to prevent immune system activity and antibody production by lymphocytes. Although this will allow ACh to gain access back to its receptor, suppressing the immune system makes the body extremely susceptible to infection. Another alternative is treating the disease with acetylcholinesterase inhibitors. After binding, acetylcholinesterase normally breaks ACh down to stop further muscle contraction. This medication works to inhibit enzymatic activity, allowing ACh more time for stimulation at the receptor. Being an autoimmune disease, myasthenia gravis is difficult to treat without damaging other body systems as well as putting the patient at risk for delayed healing and infection. The process of skeletal muscle contraction begins with excitation from motor neurons in the nervous system. Neurons extend out to muscle cells where their axon endings meet muscle fibers at the neuromuscular junction. At the axon terminal, there are synaptic vesicles, little sacs filled with acetylcholine (ACh). ACh is a

neurotransmitter that travels across the synaptic cleft to bind with its appropriate receptors at the motor end plate to induce an excitatory response within the sarcolemma. This electrical signal triggers contraction of the muscle fibers. Metocurine iodide, commonly known as metubine, is a neuromuscular blocking agent that competitively inhibits the binding of ACh at the postsynaptic synapse. Through this chemical antagonism, ACh is unable to bind to its receptor at the motor end plate, preventing the ligand-gated channel from allowing Na+ and K+ to pass. Without this generated graded potential, there is certainly no action potential to stimulate the muscle fibers to contact. Metubine is an effective anesthetic that works to induce muscle relaxation and lessens the intensity of contractions during electroconvulsive treatment for patients with psychotic disorders. -The somatic nervous system is responsible for the process of skeletal muscle contraction -nerve impulse reaches axon terminal -causes vesicles containing ACh to burst, allowing the neurotransmitter to diffuse across the synaptic cleft -ACh binds to its receptors -ACh initiates a conformational change allowing Na+ to diffuse into the membrane and K+ out -this depolarization generates a graded potential -graded potential acts to open the voltage-gated ion channels -this change produces an action potential which tells the muscle fiber to contract