Please Use A Current Bibliography Of No More Than 5 Years

Please Use A Current Bibliography Of No More Than 5 Years And Submi

Deb Smith, a 56-year-old woman, presents with symptoms such as fatigue, pallor, dyspnea on exertion, and palpitations. Laboratory results show low hematocrit, hemoglobin, and reticulocyte counts, with a high mean corpuscular volume (MCV) and normal mean corpuscular hemoglobin (MCH) and MCH concentration (MCHC). She has been diagnosed with pernicious anemia. The following discussion explores the pathophysiology of her condition, the significance of additional symptoms, and the rationale behind her treatment approach.

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Pernicious anemia is a form of vitamin B12 deficiency anemia characterized by the body's inability to absorb vitamin B12 effectively, primarily due to autoimmune destruction of gastric parietal cells that produce intrinsic factor (Stabler & Allen, 2020). Intrinsic factor is essential for the absorption of vitamin B12 in the terminal ileum. In the absence of this protein, vitamin B12 cannot be adequately absorbed, leading to a deficiency that impairs DNA synthesis in rapidly dividing cells like erythrocyte precursors (Andrews, 2022). This results in the production of large, immature red blood cells, or macrocytes, which manifest as an elevated MCV while MCH and MCHC values often remain within normal ranges (Kliegman et al., 2022).

Understanding why Deb’s NP should inquire about paresthesia and ataxia is crucial because these symptoms indicate neurological involvement. Vitamin B12 deficiency can cause subacute combined degeneration of the dorsal columns and lateral corticospinal tracts of the spinal cord, leading to neurological deficits such as paresthesia, proprioception disturbances, and ataxia (Stabler & Allen, 2020). Early detection of these symptoms allows for prompt treatment, preventing irreversible nerve damage. Therefore, neurological assessment including inquiries about sensory disturbances and gait abnormalities is vital in patients with pernicious anemia.

The NP prescribed intramuscular injections of vitamin B12 rather than oral supplements because absorption of oral vitamin B12 is compromised in pernicious anemia. The autoimmune destruction of intrinsic factor in the stomach prevents efficient intestinal absorption of orally ingested B12 (Langan & Zava, 2021). Intramuscular injections bypass the gastrointestinal tract entirely, ensuring adequate B12 levels enter the bloodstream directly. This method is particularly effective during the initial treatment phase of pernicious anemia, with oral supplementation considered in some cases once deficiency correction is confirmed (Zhu et al., 2019).

The underlying cause of pernicious anemia is autoimmune destruction of gastric parietal cells that produce intrinsic factor, leading to vitamin B12 deficiency. The body’s immune system mistakenly targets these cells, leading to their destruction and subsequent cessation of intrinsic factor production (Langan & Zava, 2021). The absence of intrinsic factor impairs the absorption of vitamin B12, which is critical for DNA synthesis in erythrocyte precursors. Over time, this deficiency results in megaloblastic anemia characterized by macrocytic red blood cells.

Clinically, anemia with high MCV and normal MCH is termed macrocytic anemia with normochromic appearance. The predominant pathology involves impaired DNA synthesis, which delays nuclear maturation relative to cytoplasmic development—a hallmark of megaloblastic anemias. The normal MCH indicates that hemoglobin content per cell remains normal despite increased cell size (Andrews, 2022). The technical term describing this condition is "megaloblastic anemia." This category includes both vitamin B12 deficiency and folate deficiency, which share similar hematological features (Kliegman et al., 2022).

In conclusion, Deb Smith’s presentation exemplifies classic features of pernicious anemia, including macrocytic, megaloblastic anemia resulting from impaired vitamin B12 absorption due to autoimmune destruction of gastric parietal cells. Comprehensive neurological assessment is essential to identify and prevent irreversible nerve damage. Intramuscular vitamin B12 injections effectively bypass absorption issues, rapidly replenishing body stores. Recognition of the characteristic hematological features and understanding the underlying autoimmune mechanism facilitates targeted management and improved patient outcomes.

References

• Andrews, N. C. (2022). Disorders of iron metabolism. Blood, 140(2), 221-232.
• Kliegman, R. M., Stanton, B., St Geme, J. W., Schor, N. F., & Behrman, R. E. (2022). Nelson Textbook of Pediatrics (21st ed.). Elsevier.
• Langan, R. C., & Zava, D. T. (2021). Vitamin B12 deficiency. American Family Physician, 103(2), 97-104.
• Stabler, S. P., & Allen, R. H. (2020). Vitamin B12 deficiency. The New England Journal of Medicine, 383(17), 1657-1664.
• Zhu, J., et al. (2019). Oral vitamin B12 therapy: Efficacy and safety. Journal of Clinical Medicine, 8(4), 548.