Anemias

Core Concepts

The RBC life cycle and the three mechanisms

RBCs are produced in the bone marrow from hematopoietic stem cells under the influence of erythropoietin, a hormone released mainly by the kidneys when they sense low oxygen. Mature RBCs live about 120 days and are then removed by the spleen, which recycles their iron. Against that backdrop, the three mechanisms of anemia make sense:

• Decreased production — the marrow makes too few cells. Causes include iron, B12, or folate deficiency; chronic inflammation; kidney disease (too little erythropoietin); marrow damage from chemotherapy, radiation, or disease; and aplastic anemia.
• Increased destruction (hemolysis) — cells are destroyed faster than they are replaced, either because the cell itself is abnormal (hereditary disorders, covered in the next topic) or because something outside attacks it (autoimmune hemolysis, some medications, mechanical damage).
• Blood loss — acute loss (trauma, surgery, bleeding ulcer) or chronic loss (heavy menstruation, slow gastrointestinal bleeding). Chronic loss matters because it quietly depletes iron stores over months.

Reading the CBC clues: cell size and the marrow response

The CBC reports hemoglobin, hematocrit (the proportion of blood made of cells), and the MCV. Cell size narrows the diagnosis: small cells suggest trouble making hemoglobin (iron deficiency, thalassemia); large cells suggest trouble making DNA (B12 or folate deficiency); normal-sized cells fit blood loss, chronic disease, kidney disease, or early iron deficiency. The reticulocyte count answers the second question — is the marrow trying? A high count means the marrow is responding, pointing toward destruction or recent blood loss; a low count points toward a production problem. These are patterns, not absolute rules, and the clinician reads them with the full history.

Iron-deficiency anemia: the most common anemia

Iron is the core of the hemoglobin molecule — without it, the marrow makes small, pale cells. Iron deficiency develops when intake is inadequate (common in restrictive diets), absorption is impaired (after gastric surgery, in celiac disease), or — most important in adults — iron is being lost through bleeding. Heavy menstrual bleeding is a leading cause in women; in men and in postmenopausal women, gastrointestinal blood loss is suspected until proven otherwise, which is why a new diagnosis of iron-deficiency anemia often triggers a gastrointestinal evaluation. Features include fatigue, pale skin and conjunctivae, and sometimes cravings for non-food items such as ice or dirt (pica) or a sore tongue. Treatment is directed by the provider — typically iron replacement plus correction of the cause — and the nurse teaches how to take iron (constipation and dark stools are common, expected effects), dietary sources, and the importance of the follow-up workup.

B12 and folate deficiency: the macrocytic anemias

Vitamin B12 and folate are needed to build DNA, so when either is lacking, the marrow's dividing cells grow abnormally large — producing macrocytic anemia. Pernicious anemia is an autoimmune condition in which the stomach stops making intrinsic factor, the protein needed to absorb dietary B12; without it, B12 cannot get in no matter how much is eaten. B12 deficiency deserves special attention because it can cause neurologic symptoms — numbness, tingling, balance problems, cognitive changes — that can appear before the anemia does and may not fully reverse if treatment is delayed. Folate deficiency produces the same blood picture without the neurologic component, so the two are always distinguished before treatment. Vegans and people with gastric surgery are at higher risk and are often advised to monitor their B12 levels.

Anemia of chronic disease and kidney disease

Chronic inflammation — from conditions like rheumatoid arthritis, cancer, chronic infection, or kidney failure — disrupts iron use: iron is present but trapped in storage, and erythropoietin production falls. The result is usually a mild, slowly developing anemia that does not improve with iron supplements alone. In kidney disease the problem is more direct: damaged kidneys make too little erythropoietin, so the marrow is under-stimulated. Management targets the underlying condition, sometimes with provider-ordered erythropoiesis-stimulating therapy and iron — a good example of why mechanism thinking matters: giving iron to someone whose problem is hormone deficiency will not fix it.

Nursing care of the person with anemia

Assessment focuses on the body's response to reduced oxygen delivery: fatigue, pallor of the skin and mucous membranes, dyspnea on exertion, palpitations, dizziness, and — in severe anemia — chest pain, confusion, or dyspnea at rest. Orthostatic vital signs (lying, sitting, standing) identify volume and perfusion changes that raise fall risk. Falls are the practical danger, so call-light teaching, a low bed, and assistance with ambulation are standard. Energy-conservation teaching helps patients pace activity and rest. Dietary teaching covers iron-rich foods and the fact that vitamin C enhances iron absorption while tea, coffee, and calcium can reduce it — general educational points, with specifics deferred to the dietitian and provider. When transfusion is ordered, the nurse follows the institution's policy, monitors during the infusion, and knows the signs of a transfusion reaction (see the Blood Products and Transfusion Principles topic). Scope note: assessment, monitoring, safety, and education are core nursing work; iron studies, transfusions, and erythropoietin therapy require provider orders, and exact thresholds vary by institution.

Common Confusions