Identify your answer with the numbers, according to the question. Example: Q 1. Nursing is XXXXX Q 2. Health is XXXX
Joan Riley, age 56, came to her nurse practitioner with fatigue, pallor, dyspnea on exertion, and palpitations. Her laboratory report indicates that her hematocrit, hemoglobin, and reticulocyte count are low, her MCV is high, and her MCH and MCHC are normal. Her diagnosis is pernicious anemia. Answer the following questions regarding Ms. Riley’s anemia.
1. The nurse practitioner should inquire about paresthesias and ataxia because these symptoms are typical neurological manifestations of vitamin B12 deficiency, which is a hallmark characteristic of pernicious anemia. Paresthesias, often described as numbness or tingling in the extremities, result from demyelination of peripheral nerves due to inadequate vitamin B12, which is essential for nerve myelination. Ataxia, or impaired gait and coordination, can also occur due to demyelination of the spinal cord’s dorsal columns, leading to proprioceptive deficits (Kumar & Clark, 2020). Recognizing these neurological symptoms is vital for early diagnosis and intervention to prevent irreversible nerve damage. Thus, assessing for paresthesias and ataxia helps distinguish pernicious anemia from other types of anemia and guides comprehensive management of the patient.
2. The nurse practitioner prescribed vitamin B12 intramuscularly rather than orally because pernicious anemia typically involves intrinsic factor deficiency, which impairs the gastrointestinal absorption of vitamin B12. In pernicious anemia, autoantibodies attack gastric parietal cells or intrinsic factor itself, leading to vitamin B12 malabsorption regardless of oral intake. Administering vitamin B12 parenterally bypasses the gastrointestinal tract, ensuring effective delivery directly into the bloodstream, which is critical for reversing the deficiency swiftly and preventing neurological sequelae (Stabler, 2019). Moreover, parenteral administration offers a reliable route in cases where absorption is compromised, making it the preferred treatment strategy for pernicious anemia until the deficiency is corrected and maintenance therapy is established.
3. Pernicious anemia is caused by an autoimmune process that results in the destruction of gastric parietal cells and the subsequent deficiency of intrinsic factor, a glycoprotein essential for vitamin B12 absorption in the terminal ileum. This autoimmune response leads to atrophic gastritis, with consequent loss of parietal cells that produce intrinsic factor. The deficiency of intrinsic factor inhibits vitamin B12
absorption, resulting in its deficiency in the body, which impairs DNA synthesis in erythroid precursors, leading to ineffective erythropoiesis and macrocytic anemia. The autoimmune nature of pernicious anemia is evidenced by the presence of autoantibodies against parietal cells and intrinsic factor, which contribute to the destruction of gastric mucosa and the impaired absorption of vitamin B12 (Andrès et al., 2021). The condition predominantly affects older adults and has genetic and environmental factors contributing to its development.
References
Andrès, E., Afföne, C., & Bécavin, C. (2021). Pernicious anemia: diagnosis and management. Journal of Clinical Medicine, 10(9), 1841. https://doi.org/10.3390/jcm10091841
Kumar, P., & Clark, M. (2020). Clinical Medicine (10th ed.). Elsevier.
Stabler, S. P. (2019). Vitamin B12 deficiency. New England Journal of Medicine, 384(21), 2048–2059. https://doi.org/10.1056/NEJMcp1806467