Nursing Elites

1. What is the etiology and most likely treatment for myasthenia gravis in a 22-year-old female college student?

• A. Autoimmune destruction of skeletal muscle cells; treatment with intensive physical therapy and anabolic steroids.
• B. A decline in functioning acetylcholine receptors; treatment with corticosteroids and intravenous immunoglobulins.
• C. Cerebellar lesions; surgical and immunosuppressive treatment.
• D. Excess acetylcholinesterase production; treatment with thymectomy.

Correct answer: B

Rationale: Myasthenia gravis is characterized by a decline in functioning acetylcholine receptors rather than autoimmune destruction of skeletal muscle cells (Choice A), cerebellar lesions (Choice C), or excess acetylcholinesterase production (Choice D). The most likely treatment for myasthenia gravis involves corticosteroids to reduce inflammation and intravenous immunoglobulins to block the antibodies attacking acetylcholine receptors. Intensive physical therapy and anabolic steroids are not primary treatments for myasthenia gravis.

2. A staff member asks what leukocytosis means. How should the nurse respond? Leukocytosis can be defined as:

• A. A normal leukocyte count
• B. A high leukocyte count
• C. A low leukocyte count
• D. Another term for leukopenia

Correct answer: B

Rationale: Leukocytosis refers to an abnormally high leukocyte count. This condition is characterized by an elevated number of white blood cells in the bloodstream. Choice A is incorrect because leukocytosis does not refer to a normal leukocyte count. Choice C is incorrect as leukocytosis is not related to a low leukocyte count. Choice D is incorrect as leukopenia is the opposite of leukocytosis, indicating a low white blood cell count.

3. Why is a beta-blocker prescribed to a client with a history of myocardial infarction?

• A. To reduce myocardial oxygen demand.
• B. To increase cardiac output.
• C. To prevent arrhythmias.
• D. To prevent the development of angina.

Correct answer: A

Rationale: The primary reason for administering a beta-blocker to a client with a history of myocardial infarction is to reduce myocardial oxygen demand. By reducing myocardial oxygen demand, beta-blockers help decrease the workload on the heart, making it easier for the heart to function effectively. This is crucial for clients with a history of myocardial infarction to prevent further damage to the heart. Choice B is incorrect because beta-blockers do not aim to increase cardiac output; instead, they help improve cardiac function by reducing workload. Choice C is incorrect because while beta-blockers can help prevent certain arrhythmias, the primary reason for their use in this case is to reduce myocardial oxygen demand. Choice D is incorrect as preventing angina is not the primary purpose of administering beta-blockers to a client with a history of myocardial infarction.

4. How can a colony-stimulating factor affect the patient's erythrocyte count?

• A. It stimulates the growth of red blood cells.
• B. It suppresses T-cell production.
• C. It inhibits protein synthesis.
• D. It stimulates antibody production.

Correct answer: A

Rationale: Colony-stimulating factors are substances that stimulate the production of blood cells in the bone marrow. Erythrocytes are red blood cells, so a colony-stimulating factor would specifically stimulate the growth of red blood cells, leading to an increase in the patient's erythrocyte count. Choice B is incorrect because colony-stimulating factors do not suppress T-cell production. Choice C is incorrect because colony-stimulating factors do not inhibit protein synthesis. Choice D is incorrect because colony-stimulating factors do not stimulate antibody production; they primarily affect the production of blood cells.

5. Which of the following mediators of inflammation causes increased capillary permeability and pain?

• A. Serotonin
• B. Histamine
• C. Bradykinin
• D. Nitric oxide

Correct answer: C

Rationale: Bradykinin is the correct answer. It is a potent mediator of inflammation that causes increased capillary permeability and is responsible for the pain associated with inflammation. Serotonin and histamine are also mediators of inflammation, but they are not primarily known for increasing capillary permeability or inducing pain. Nitric oxide is involved in various physiological processes but is not a primary mediator of inflammation that causes increased capillary permeability and pain.

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