Alterations in Oxygen Transport Deb Smith, age fifty-six, came to her nurse practitioner (NP) with fatigue, pallor, dyspnea on exertion, and palpitations. Her laboratory report indicates that her hematocrit, hemoglobin, and reticulocyte counts are low; that her MCV is high; and that her MCH and MCHC are normal. Her diagnosis is pernicious anemia. Answer the following questions regarding Deb’s anemia and provide the pathophysiology associated with the body’s response to this disease process.
Pernicious anemia is a type of vitamin B12 deficiency anemia characterized by a decreased production of red blood cells due to a lack of intrinsic factor, a substance required for the absorption of vitamin B12 in the intestines. This deficiency can occur due to an autoimmune destruction of the gastric parietal cells, which produce intrinsic factor. Without intrinsic factor, the body is unable to properly absorb vitamin B12 from the diet, leading to impaired DNA synthesis and ultimately affecting the production of red blood cells.
Deb Smith’s symptoms of fatigue, pallor, dyspnea on exertion, and palpitations are characteristic of anemia, which is a condition that results from a decreased number of red blood cells or a decreased amount of hemoglobin. Hematocrit, hemoglobin, and reticulocyte counts are all measures of the red blood cell count, and in Deb’s case, they are low. This suggests that she has a reduced number of red blood cells circulating in her bloodstream.
The mean corpuscular volume (MCV) is a measure of the average size of red blood cells. In Deb’s case, her MCV is high, indicating that her red blood cells are larger than normal. This is a common characteristic of vitamin B12 deficiency anemia.
The mean corpuscular hemoglobin (MCH) and mean corpuscular hemoglobin concentration (MCHC) are measures of the amount and concentration of hemoglobin within the red blood cells, respectively. In Deb’s case, her MCH and MCHC are normal, suggesting that the amount and concentration of hemoglobin within her red blood cells are within the expected range.
The pathophysiology of pernicious anemia begins with the autoimmune destruction of gastric parietal cells. These cells are responsible for producing intrinsic factor, a glycoprotein that binds to vitamin B12 in the stomach and facilitates its absorption in the intestines. Without intrinsic factor, vitamin B12 cannot be absorbed from the diet.
Vitamin B12 is essential for the production of DNA and the maturation of red blood cells in the bone marrow. It acts as a coenzyme for the conversion of methylmalonyl-CoA to succinyl-CoA and for the conversion of homocysteine to methionine. These processes are necessary for the synthesis of DNA and the production of red blood cells.
In pernicious anemia, the lack of vitamin B12 affects the production of red blood cells in the bone marrow. Immature red blood cells, known as megaloblasts, are formed due to impaired DNA synthesis. These megaloblasts have a larger size, hence the high MCV observed in Deb’s case.
Due to the insufficient number of red blood cells and the larger size of the existing cells, oxygen transport in the body is compromised. Red blood cells are responsible for carrying oxygen from the lungs to the tissues and removing carbon dioxide from the tissues to the lungs. In pernicious anemia, the decreased production of red blood cells results in a reduced capacity to carry oxygen.
The lack of oxygen transport leads to a variety of symptoms, such as fatigue, pallor, dyspnea on exertion, and palpitations, all of which Deb Smith is experiencing. Fatigue occurs because the tissues are not receiving enough oxygen to support their metabolic demands. Pallor is caused by a decreased number of red blood cells, which are responsible for the red color of blood. Dyspnea on exertion is a result of the body’s increased effort to compensate for the reduced oxygen-carrying capacity. Palpitations, or a racing heart, can occur because the heart is working harder to pump a decreased amount of oxygenated blood.
In summary, Deb Smith’s diagnosis of pernicious anemia is characterized by a lack of intrinsic factor, resulting in impaired absorption of vitamin B12. The deficiency of vitamin B12 leads to decreased red blood cell production, increased production of megaloblasts, and impaired oxygen transport. This leads to symptoms such as fatigue, pallor, dyspnea on exertion, and palpitations. Understanding the pathophysiology of pernicious anemia helps to explain the body’s response to this disease process.