Discuss The Defect Of Gastric Secretion Of Intrinsic Factor

Discuss The Defect Of Gastric Secretion Of Intrinsic Factor If That

Discuss the defect of gastric secretion of intrinsic factor (IF) that leads to anemia. Identify the type of anemia this defect can cause and the risk factors that can lead to this anemia to develop. Briefly discuss the treatment options for this type of anemia.

Paper For Above instruction

Intrinsic factor (IF), a glycoprotein produced predominantly by the parietal cells in the lining of the stomach, plays a critical role in the absorption of vitamin B12 (cobalamin), which is essential for DNA synthesis and red blood cell formation (McCance & Huether, 2019). When there is a defect or absence of gastric secretion of intrinsic factor, the body cannot effectively absorb vitamin B12 from dietary sources, leading to a specific form of anemia known as pernicious anemia. This essay explores the pathophysiology of intrinsic factor deficiency, the consequent development of pernicious anemia, associated risk factors, and possible treatment strategies.

The production of intrinsic factor is a normal physiological process involving parietal cells within the stomach's mucosal lining. When this process is disrupted—either due to autoimmune destruction of the parietal cells, congenital absence, or atrophic gastritis—the secretion of intrinsic factor diminishes significantly or ceases altogether. The most common cause of intrinsic factor deficiency is autoimmune gastritis, which results from the immune system mistakenly targeting and destroying gastric parietal cells (Harvard Health, 2019). This autoimmune response impairs the secretion of both hydrochloric acid and intrinsic factor, and over time, this leads to the loss of gastric mucosa and the subsequent deficiency of intrinsic factor necessary for vitamin B12 absorption (McCance & Huether, 2019).

Pernicious anemia, a form of megaloblastic anemia characterized by the presence of large, immature red blood cells (megaloblasts), arises when vitamin B12 absorption is impaired due to the lack of intrinsic factor. The deficiency of vitamin B12 hampers DNA synthesis, especially in rapidly dividing cells like red blood cell precursors in the bone marrow, leading to ineffective erythropoiesis and anemia (McCance & Huether, 2019). Moreover, neurological manifestations such as paresthesia, memory disturbances, and cognitive decline can occur because vitamin B12 is vital for neurologic health (Lindenbaum et al., 1990).

Several risk factors predispose individuals to intrinsic factor deficiency and pernicious anemia. Autoimmune disorders, including autoimmune gastritis, are primary drivers of IF deficiency. These conditions are more prevalent among individuals with other autoimmune diseases such as autoimmune thyroiditis, vitiligo, Addison’s disease, and Type 1 diabetes mellitus (Harvard Health, 2019). Genetic predisposition can play a role, with a higher incidence observed in individuals of Northern European descent (Lindenbaum et al., 1990). Additionally, surgical removal of parts of the stomach or resection of the ileum—where vitamin B12 is absorbed—can lead to vitamin B12 deficiency, although these are secondary causes rather than primary intrinsic factor defects (McCance & Huether, 2019). Risk factors that increase the body’s demand for vitamin B12, including pregnancy and chronic infections, can exacerbate the deficiency."

Diagnosis of pernicious anemia involves a combination of clinical evaluation and laboratory investigations. Typical laboratory findings include macrocytic anemia, low serum vitamin B12 levels, elevated serum methylmalonic acid (MMA), and homocysteine levels, which reflect B12 deficiency at the cellular level. Presence of anti-intrinsic factor or anti-parietal cell antibodies strongly supports the diagnosis of autoimmune-mediated pernicious anemia (Gilbert, 2017). Additional diagnostic tests include gastric biopsy showing atrophic gastritis and decreased parietal cell mass, further confirming the autoimmune process (McCance & Huether, 2019).

Effective treatment of pernicious anemia focuses on replenishing vitamin B12 levels through parenteral administration, as oral supplementation is often insufficient due to impaired absorption. The primary treatment involves intramuscular injections of vitamin B12 (cyanocobalamin or hydroxocobalamin), initially administered weekly until hematologic normalization, followed by monthly maintenance doses for life (McCance & Huether, 2019; Gilbert, 2017). This approach bypasses the need for intrinsic factor in absorption. In some cases, high-dose oral vitamin B12 supplements may be effective if absorption through passive diffusion is adequate, but injectable therapy remains the standard in severe cases. Treating the underlying autoimmune process may involve monitoring and managing other autoimmune conditions, although it does not reverse the gastric atrophy or the deficiency once established (Harvard Health, 2019). The timely correction of B12 deficiency can resolve anemia and prevent neurologic damage if initiated early.

In summary, the defect in gastric secretion of intrinsic factor, often due to autoimmune destruction of parietal cells, impairs vitamin B12 absorption, leading to pernicious anemia. Recognizing risk factors, early diagnosis, and prompt treatment with vitamin B12 supplementation are crucial in preventing serious hematological and neurological complications associated with this condition.

References

  • Gilbert, L. (2017). Diagnosis and treatment of pernicious anemia. Practice Nurse, 47(4), 20-23.
  • Harvard Health. (2019). Vitamin B12 deficiency. Harvard Health Publishing. Retrieved from https://www.health.harvard.edu
  • Lindenbaum, J., et al. (1990). Neuropsychiatric and hematologic aspects of vitamin B12 deficiency. Annals of Internal Medicine, 112(4), 543-550.
  • McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The Biological Basis for Disease in Adults and Children (8th ed.). Elsevier.

Related Assignments