Muscle Weakness In The Face Case Study Assignment

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Muscle Weakness In The Face Case Study Assignment

APA format, three references, at least 300 words

Review the following case study:

Chief Complaint:

A 23-year-old woman presents with complaints of muscle weakness in the face.


The patient is a 23-year-old administrative assistant who complains of intermittent muscle weakness in her face that has been getting worse over the past 3 months. She also states that as she chews, her jaws feel tired. Swallowing has also become difficult. She reports episodes of double vision (diplopia), which seems to occur after reading for a few minutes in the late evening. With certain strenuous activities or after typing for long periods of time at work, she reports problems with bilateral arm weakness.

Physical Examination:

Notable ptosis (drooping) of the eyelids after repeated blinking exercises. When asked to smile, she appears to be snarling. Reflexes and sensation are normal in both upper and lower extremities. There is considerable weakness of the arms noted bilaterally after exercise.

Case Questions:

  1. Is the patient’s condition neurological, musculoskeletal, or both? Explain why and support your thoughts with evidence-based literature. What would be a possible neurologic or musculoskeletal condition causing the symptoms?
  2. Explain the pathophysiology behind the condition.
  3. What pharmacological agent(s) are commonly used to treat the disorder and how do the agent(s) alter the pathophysiology of the condition?
  4. What would be your educational plan for the patient?

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.

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.

Case Study Critical Thinking Questions

1.Why is this young woman experiencing difficulty chewing and double vision? In your answer, state the name of the disease and provide its definition.

2. How are the anti-acetylcholine receptor antibodies interfering with her normal skeletal muscle activity? In your answer, describe the NORMAL mechanism beginning with the presynaptic motor neuron and contrast this to the PATHOPHYSIOLOGY occurring in the MG patient.

3. How do the anticholinesterase drugs act to improve Jill’s skeletal muscle function? Describe the mechanism behind how pyridostigmine bromide functions and how this helps the MG patient.

Name of the disease is Myasthenia gravis, It is an autoimmune disease that causes chronic, progressive damage of the neuromuscular junction. It is caused, when immune system inappropriately produces antibodies that bind to and block acetylcholin………

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