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Laboratory 13: Skeletal Muscle Histology Myasthenia Gravis An autoimmune disease

ID: 3515606 • Letter: L

Question

Laboratory 13: Skeletal Muscle Histology Myasthenia Gravis An autoimmune disease occurs when antibodies produced by the immune system mistakenly attack body tissues. In the case of myasthenia gravis, the antibodies damage or destroy the acetylcholine receptors at the motor e a Latin term meaning 'serious muscle weakness" (my/o- serious). The prima The most commonly affected muscles are the extrinsic eye, eyelid, facial expression, chewing, talking nd plate of a neuromuscular junction. Myasthenia gravisis muscle, -asthenia weakness, y symptom is muscle weakness that worsens with activity and improves with rest. and swallowing muscles Women between 20-40 and men over 60 are most commonly affected, but this condition is found in all age groups, all ethnic groups, and both genders Figure 13.7illustrates the neuromuscular junction. Complete the following activities using this figure Label the structures labeled with capital letters. The numbers 1-4 indicate the chain of events that occur at the neuromuscular junction. Put these events in chronological order by placing a 1 in the blank before the first event, etc. Refer back to Figure 12.5 for information. Acetylcholine diffuses across the synaptic cleft. Nerve impulse reaches the axon terminal. _ Synaptic vesicles release acetylcholine into the synaptic cleft. Acetylcholine binds to receptors at the motor end plate. Answer the following questions. 1. Which event listed above is the point at which myasthenia gravis interrupts the process? Explain why 2. One treatment for myasthenia gravis is a medication that blocks the activity of acetylcholinesterase. Suggest why this might be a successful treatment.

Explanation / Answer

A. Presynaptic neuron

B. Synaptic cleft

C. Receptors

D. Motor end plate

1. Nerve impulse reaches the axon terminal

2. Synaptic vesicles release acetylcholine into the synaptic cleft

3. Acetylcholine diffuses across the synaptic cleft

4. Acetylcholine binds to receptors at the motor end plate

1. Acetylcholine binds to the receptor at the motor end plate

The above event is the point in which myasthenia gravis interrupts the process. In this disease the receptors of the motor end plates are destroyed. This disease causes due to destruction or damage of the receptors of motor end plate which binds the acetylcholine and thus unable to transmit the nerve impulse from neuron to muscles. The receptors of the motor end plate is destroyed due to the antibodies which is released from the immune system and attacks the connection between the nerves and muscles.

2. Acetylcholinesterase is the enzyme which helps to degrade the acetylcholine. The drugs which acts as the inhibitor of acetylcholinesterase helps the acetylcholine not to degrade and thus to prevent it from release into the synaptic cleft from the vesicles and as a results the amount of acetylcholine increases. This increase in amount increase the muscle activation and contraction.