Muscular+Case+Study

Answer the following questions before doing the case study: 1. What functions does the skeletal muscle system perform for us?

2. What makes the three kinds of muscle tissues different from each other in terms of:

3. Arrange these terms in order, going from largest to smallest: 4. What are the names of the proteins that are involved with muscle cell contraction?
 * || * types of cells ||
 * || * location of tissue types ||
 * * || * muscle ||
 * * || * myofilament ||
 * * || * muscle fiber ||
 * * || * myofibril ||

5. Are these proteins located inside or outside of the sarcomere?

6. What creates the banding pattern (the striated appearance) on skeletal muscle tissue?

7. What is the importance of the neuromuscular junction (NMJ)? What chemical is released to trigger contraction at the NMJ?

8. Put the events of muscle contraction in order: On physical examination, she has notable ptosis ("drooping") of both eyelids after repeated blinking exercises. When smiling, she appears to be snarling. Electromyographic testing revealed progressive weakness and decreased amplitude of contraction of the distal arm muscles upon repeated mild shocks (5 shocks per second) of the ulnar and median nerves. Both her symptoms and electromyographic findings were reversed within 40 seconds of intravenous administration of edrophonium (Tensilon), an acetylcholinesterase inhibitor (i.e. an "anticholinesterase"). Blood testing revealed high levels of an anti-acetylcholine receptor antibody in her plasma, and a diagnosis of myasthenia gravis was made. Myasthenis gravis is an autoimmune disorder causing improper functioning of the neuromuscular junction. The immune system produces antibodies that damage the acetylcholine receptors on the sarcolemma. Jill was treated with pyridostigmine bromide, which is a long-acting anticholinesterase drug, and was also started on prednisone, which is a corticosteroid drug. She also underwent occasional plasmapheresis when her symptoms became especially severe. She was given a prescription of atropine as needed to reduce the nausea, abdominal cramps, diarrhea, and excessive salivation she experienced as side effects of the anticholinesterase drug. Acetylcholinerase is an enzyme that normally will break down acetylcholine in the synaptic cleft at the end of a muscle cell contraction. Anticholinsesterase drugs block the effect of acetylcholinersterase. 1. Why is this young woman experiencing difficulty chewing and double vision?
 * Cross bridges form between myosin heads and actin filaments
 * Nerve impulse reaches synaptic cleft
 * Acetycholine binds with receptors on the sarcolemma
 * Calcium is released from sarcoplasmic reticulum
 * Actin filaments slide towards the middle of the sarcomere
 * Acetylcholine is released into the synaptic cleft and diffuses across it
 * Z lines are pulled towards each other
 * Case Study **
 * Chief Complaint: ** A 26-year-old woman with muscle weakness in the face.
 * History: ** Jill Rothman, a 26-year-old gymnastics instructor, presents with complaints of muscle weakness in her face that comes and goes, but has been getting worse over the past two months. Most notably, she complains that her "jaw gets tired" as she chews and that swallowing has become difficult. She also notes diplopia ("double vision") which seems to come on late in the evening, particularly after reading for a few minutes. At work, it has become increasingly difficult to "spot" her gymnasts during acrobatic moves because of upper arm weakness.
 * Questions ** :

2. How are the anti-acetylcholine receptor antibodies interfering with her normal skeletal muscle activity?

3. How do the anticholinesterase drugs act to improve Jill's skeletal muscle function?

4. Why are nausea, abdominal cramps, diarrhea, and excessive salivation all side effects of the anticholinesterase drug she is taking?

5. Why does repetitive nerve stimulation result in decreased amplitude of the muscle contractions?

6. The corticosteroid prednisone is a drug that suppresses the immune system. How will prednisone benefit this patient?

7. Plasmapheresis involves removing the patient’s plasma with an alternative plasma solution that has no antibodies against acetylocholine receptors. Why must Jill undergo plasmapheresis when her symptoms become especially severe?

8. Jill's doctor advises her that she is at increased risk for respiratory failure. Explain why this is so.

KEY

Answer the following questions before doing the case study: 1. What functions does the skeletal muscle system perform for us?

// Protection, movement, generation of body heat //

2. What makes the three kinds of muscle tissues different from each other in terms of:

//cardiac muscle cells: multinucleate, branched, striated// // smooth muscle cells: uninucleate, fibers, not striated // // skeletal muscle cells: multinucleate, fibers, striated // || //cardiac muscle tissue: heart// // smooth muscle tissue: in walls of hollow internal organs // // skeletal muscle tissue: external to hollow organs // || 3. Arrange these terms in order, going from largest to smallest: 4. What are the names of the proteins that are involved with muscle cell contraction? // Actin and myosin //
 * || * types of cells
 * * || * location of tissue types
 * * || * Muscle (1) ||
 * * || * Myofilament (4) ||
 * * || * muscle fiber (2) ||
 * * || * Myofibril (3) ||

5. Are these proteins located inside or outside of the sarcomere? // These are both inside the sarcomere //

6. What creates the banding pattern (the striated appearance) on skeletal muscle tissue? // The myosin fibers are thick, dark fibers, while the actin fibers are thin and light. The arrangement of the these fibers creates the banding pattern. The actins and myosins are all lined up together down the whole length of the fiber. //

7. What is the importance of the neuromuscular junction (NMJ)? What chemical is released to trigger contraction at the NMJ? // The NMJ is where the impulse to contract is transferred from a motor neuron to a muscle fiber. Acetylcholine is released by the neuron to trigger the contraction in the muscle fiber. // 8. Put the events of muscle contraction in order: ** Case Study ** ** Chief Complaint: ** A 26-year-old woman with muscle weakness in the face. ** History: ** Jill Rothman, a 26-year-old gymnastics instructor, presents with complaints of muscle weakness in her face that comes and goes, but has been getting worse over the past two months. Most notably, she complains that her "jaw gets tired" as she chews and that swallowing has become difficult. She also notes diplopia ("double vision") which seems to come on late in the evening, particularly after reading for a few minutes. At work, it has become increasingly difficult to "spot" her gymnasts during acrobatic moves because of upper arm weakness. On physical examination, she has notable ptosis ("drooping") of both eyelids after repeated blinking exercises. When smiling, she appears to be snarling. Electromyographic testing revealed progressive weakness and decreased amplitude of contraction of the distal arm muscles upon repeated mild shocks (5 shocks per second) of the ulnar and median nerves. Both her symptoms and electromyographic findings were reversed within 40 seconds of intravenous administration of edrophonium (Tensilon), an acetylcholinesterase inhibitor (i.e. an "anticholinesterase"). Blood testing revealed high levels of an anti-acetylcholine receptor antibody in her plasma, and a diagnosis of myasthenia gravis was made. Myasthenis gravis is an autoimmune disorder causing improper functioning of the neuromuscular junction. The immune system produces antibodies that damage the acetylcholine receptors on the sarcolemma. Jill was treated with pyridostigmine bromide, which is a long-acting anticholinesterase drug, and was also started on prednisone, which is a corticosteroid drug. She also underwent occasional plasmapheresis when her symptoms became especially severe. She was given a prescription of atropine as needed to reduce the nausea, abdominal cramps, diarrhea, and excessive salivation she experienced as side effects of the anticholinesterase drug. Anticholinsesterase drugs block the effect of acetylcholinerase, which is an enzyme that normally will break down acetylcholine in the synaptic cleft at the end of a muscle cell contraction.
 * Cross bridges form between myosin heads and actin filaments (5)
 * Nerve impulse reaches synaptic cleft (1)
 * Acetycholine binds with receptors on the sarcolemma (3)
 * Calcium is released from sarcoplasmic reticulum (4)
 * Actin filaments slide towards the middle of the sarcomere (6)
 * Acetylcholine is released into the synaptic cleft and diffuses across it (2)
 * Z lines are pulled towards each other (7)

1. Why is this young woman experiencing difficulty chewing and double vision? The muscles of her face and eyes are weakening due to the lack of impulse transmission. 2. How are the anti-acetylcholine receptor antibodies interfering with her normal skeletal muscle activity? By damaging the acetylcholine receptors on the sarcolemma, these antibodies are causing interference with normal contraction impulse transmission between the motor neurons and muscle fibers. Acetylcholine can’t bind to the muscle cell, so an action potential can’t develop and contraction won’t occur. 3. How do the anticholinesterase drugs act to improve Jill's skeletal muscle function? As mentioned above, acetylcholinersterase is a naturally-occurring chemical that breaks up the acetylcholine in the synaptic cleft after impulse transmission. An anticholinersterase drug will prevent release of acetylcholinesterase, so the acetylcholine in the synaptic cleft will not be broken down. Having the acetylcholine linger in the gap will increase the chance of contraction impulse being transmitted in the presence of fewer functioning acetylcholine receptors on the muscle fiber. 4. Why are nausea, abdominal cramps, diarrhea, and excessive salivation all side effects of the anticholinesterase drug she is taking? The drug will affect all junctions, including junctions between neurons and smooth muscles. These smooth muscles will then be essentially over-stimulated and will contract excessively, leading to the cramps, etc. 5. Why does repetitive nerve stimulation result in decreased amplitude of the muscle contractions? The muscles will become fatigued with repetitive stimulation. 6. The corticosteroid prednisone is a drug that suppresses the immune system. How will prednisone benefit this patient? It should slow down the destruction of the acetylcholine receptors on the sarcolemma. 7. Plasmapheresis involves removing the patient’s plasma with an alternative plasma solution that has no antibodies against acetylocholine receptors. Why must Jill undergo plasmapheresis when her symptoms become especially severe? Replacing part of the patient’s plasma will reduce the concentration of the antibodies that are destroying the acetylcholine receptors. 8. Jill's doctor advises her that she is at increased risk for respiratory failure. Explain why this is so. If the patient’s diaphragm and intercostals muscles are affected the she will experience respiratory failure.
 * Questions ** :