The nurse administers vitamin B12 to a patient with pernicious anemia. This patient has the inability to absorb vitamin B12 because of a deficiency in


• Intrinsic factor, released by parietal cells of the stomach, binds to B12 to facilitate absorption in the small bowel. A deficiency of intrinsic factor leads to pernicious anemia.

• Gastrin is a peptide hormone that stimulates gastric acid secretion.

• Folic acid is important in DNA synthesis and the production and maintenance of new cells. A deficiency would cause anemia, but this is unrelated to B12.

Pernicious anemia is a macrocytic anemia that results when vitamin B12 cannot be absorbed in the distal small intestine because there is a lack of the required intrinsic factor (which is normally produced by parietal cells in the stomach) for this absorption to occur. Pernicious anemia may result after surgical removal of parts of the stomach or from chronic gastritis causing decreased secretion of intrinsic factor. Autoimmune conditions may also produce antibodies against gastric parietal cells. When the production of intrinsic factor declines gradually, symptoms may progress over 20+ years, from mild GI effects and mood swings to weakness and fatigue, paresthesias of feet and fingers, and even cognitive effects and memory deficits, as well as difficulty walking. In later stages, these patients may have a beefy, red tongue and an enlarged liver that can lead to right-sided heart failure. The HGB can be 7–8 g/dL. Treatment requires monthly B12 injections for life.

Folate (folic acid) deficiency is another macrocytic anemia. Folate deficiency is dangerous for unborn infants because folic acid prevents neural tube defects. Pregnant women are recommended to have at least 400 ug/day. Folate is absorbed in the small intestine and stored in the liver. Alcoholism or a diet low in vegetables can lead to folate deficiency. Patients with folate deficiency may develop stomatitis and ulcerations on the tongue. They may have dysphagia, flatulence, and watery diarrhea. 

Iron deficiency anemia is a microcytic anemia often caused by chronic blood loss from minor gastrointestinal bleeding or colon cancer. Over time, the demands for iron exceed intake. Even blood loss of 10–20 milliliters of red cells per day is more iron a person can absorb in the diet. Manifestations of iron deficiency anemia include fatigue, pallor, fissures at the corners of the mouth, spooning of fingernails, and reduced exercise tolerance. Anemia is defined as HGB <13 g/dL for men and <12 g/dL for women.

Thalassemia major or Cooley's anemia is a disorder caused by defects in both beta-chains of the hemoglobin molecule, result in a severe microcytic anemia. These patients develop facial deformities from expansion of the marrow of the facial bones, including maxillary hyperplasia and frontal bossing. Thalassemia is found most often in Black, Mediterranean, and Southeast Asian ethnic groups.

Aplastic anemia is a normocytic anemia resulting from a decline in blood cell production related to bone marrow depression. (Pancytopenia is often also be seen with this type of anemia, resulting in the decline of all three types of blood cells.) RBC production declines gradually than WBCs or PLTs, so this anemia appears with a chronic pattern. Aplastic anemia can be either hereditary or acquired after birth. If the onset is sudden, symptoms include hypoxia, pallor, weakness, fever, and dyspnea. The slower onset produces progressive weakness, infections, low-grade fever, cellulitis in the neck, nosebleeds, or waxy and pale skin tones. Aplastic anemia can cause an extremely low HGB of 7 g/dL. 

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