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Mrs. A is a 48-year-old white woman who has had 2 months of fatigue due to anemia.

Image not available.What is the differential diagnosis of anemia? How would you frame the differential?

The framework for organizing the differential diagnosis of anemia is a combination of pathophysiologic and morphologic. The first step in determining the cause of an anemia is to determine the general mechanism of the anemia, using a pathophysiologic framework. Anemia is caused by 1 of 3 processes:

  1. Acute or chronic blood loss is clinically obvious. Chronic blood loss leads to iron deficiency and consequent underproduction.

  2. Underproduction of RBCs by the bone marrow.

  3. Increased destruction of RBCs, known as hemolysis.

After determining the general mechanism, the next step is to determine the cause of the underproduction or increased destruction. (This chapter will not discuss the approach to acute blood loss.) The framework for underproduction anemia is morphologic:

  1. Microcytic anemias (mean corpuscular volume [MCV] < 80 mcm3)

    1. Iron deficiency

    1. Thalassemia

    1. Anemia of inflammation (formerly called anemia of chronic disease)

    1. Sideroblastic anemia

    1. Lead exposure

  2. Macrocytic anemias (MCV > 100 mcm3)

    1. Megaloblastic anemias (due to abnormalities in DNA synthesis; hypersegmented neutrophils also occur)

      1. Vitamin B12 deficiency

      1. Folate deficiency

      1. Antimetabolite drugs, such as methotrexate or zidovudine

    1. Nonmegaloblastic anemias (no hypersegmented neutrophils)

      1. Alcohol abuse

      1. Liver disease

      1. Hypothyroidism

  3. Normocytic anemias

    1. Anemia of inflammation

    1. Early iron deficiency

    1. Infiltration of bone marrow due to malignancy or granulomas

    1. RBC aplasia

      1. Aplastic anemia

      1. Suppression by parvovirus B19 or medications

The framework for hemolytic anemias is pathophysiologic:

  1. Hereditary

    1. Enzyme defects, such as pyruvate kinase or glucose-6-phosphate dehydrogenase (G6PD) deficiency

    1. Hemoglobinopathies, such as sickle cell anemia

    1. RBC membrane abnormalities, such as spherocytosis

  2. Acquired

    1. Hypersplenism

    1. Immune

      1. Autoimmune: warm IgG, cold IgM, cold IgG

      1. Drug induced: autoimmune or hapten

    1. Traumatic

      1. Impact

      1. Macrovascular: shearing due to prosthetic valves

      1. Microvascular: disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura (TTP), and hemolytic uremic syndrome (HUS)

    1. Infections, such as malaria

    1. Toxins, such as snake venom and aniline dyes

    1. Paroxysmal nocturnal hemoglobinuria

Figure 6–1 outlines the approach to evaluating anemia caused by underproduction and increased destruction of RBCs.

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Mrs. A has a past medical history of obesity, reflux, depression, asthma, and arthritis. She comes to your office complaining of feeling down with progressive fatigue for the last 2 months. She has no chest pain, cough, fever, weight loss, or edema. Her only GI symptoms are poor appetite and her usual reflux symptoms; she has had no vomiting, melena, or rectal bleeding. She still has regular menses that are occasionally heavy. She brought in her medication bottles, which include ranitidine, sertraline, tramadol, cetirizine, and a fluticasone inhaler. Her physical exam shows a depressed affect, clear lungs, a normal cardiac exam, a nontender abdomen, guaiac-negative stool, no edema, and no pallor.

Image not available.How reliable is the history ...

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