Sections View Full Chapter Figures Tables Videos Annotate Full Chapter Figures Tables Videos Supplementary Content +++ INTRODUCTION ++ Anemia is a group of diseases characterized by a decrease in either hemoglobin (Hb) or the volume of red blood cells (RBCs), resulting in decreased oxygen-carrying capacity of blood. The World Health Organization defines anemia as Hb less than 13 g/dL (<130 g/L; <8.07 mmol/L) in men or less than 12 g/dL (<120 g/L; <7.45 mmol/L) in women. +++ PATHOPHYSIOLOGY ++ The functional classification of anemias is found in Fig. 33–1. The most common anemias are included in this chapter. Morphologic classifications are based on cell size. Macrocytic cells are larger than normal and are associated with deficiencies of vitamin B12 or folic acid. Microcytic cells are smaller than normal and are associated with iron deficiency, whereas normocytic anemia may be associated with recent blood loss or chronic disease. Iron-deficiency anemia (IDA) can be caused by inadequate dietary intake, inadequate gastrointestinal (GI) absorption, increased iron demand (eg, pregnancy), blood loss, and chronic diseases. Vitamin B12– and folic acid–deficiency anemias can be caused by inadequate dietary intake, decreased absorption, and inadequate utilization. Deficiency of intrinsic factor causes decreased absorption of vitamin B12 (ie, pernicious anemia). Folic acid–deficiency anemia can be caused by hyperutilization due to pregnancy, hemolytic anemia, myelofibrosis, malignancy, chronic inflammatory disorders, long-term dialysis, or growth spurt. Drugs can cause anemia by reducing absorption of folate (eg, phenytoin) or through folate antagonism (eg, methotrexate). Anemia of inflammation (AI) is a newer term used to describe both anemia of chronic disease and anemia of critical illness. AI is an anemia that traditionally has been associated with infectious or inflammatory processes, tissue injury, and conditions associated with release of proinflammatory cytokines. See Table 33–1 for diseases associated with AI. For information on anemia of chronic kidney disease, see Chapter 74. Age-related reductions in bone marrow reserve can render elderly patients more susceptible to anemia caused by multiple minor and often unrecognized diseases (eg, nutritional deficiencies) that negatively affect erythropoiesis. Pediatric anemias are often due to a primary hematologic abnormality. The risk of IDA is increased by rapid growth spurts and dietary deficiency. ++ FIGURE 33–1. Functional classification of anemia. Each of the major categories of anemia (hypoproliferative, maturation disorders, and hemorrhage/hemolysis) can be further subclassified according to the functional defect in the several components of normal erythropoiesis. Graphic Jump LocationView Full Size||Download Slide (.ppt) ++Table Graphic Jump LocationTABLE 33–1Diseases Causing Anemia of InflammationView Table||Download (.pdf) TABLE 33–1 Diseases Causing Anemia of Inflammation Common causes Chronic infections Tuberculosis Other chronic lung infections (eg, lung abscess, bronchiectasis) Human immunodeficiency virus Subacute bacterial endocarditis Osteomyelitis Chronic urinary tract infections Chronic inflammation Rheumatoid arthritis Systemic lupus erythematosus Inflammatory bowel disease Inflammatory osteoarthritis Gout Other (collagen vascular) diseases Chronic inflammatory liver diseases Malignancies Carcinoma Lymphoma Leukemia Multiple myeloma Less common causes Alcoholic liver disease Congestive heart failure Thrombophlebitis Chronic obstructive pulmonary ... Your MyAccess profile is currently affiliated with '[InstitutionA]' and is in the process of switching affiliations to '[InstitutionB]'. Please click ‘Continue’ to continue the affiliation switch, otherwise click ‘Cancel’ to cancel signing in. Get Free Access Through Your Institution Learn how to see if your library subscribes to McGraw Hill Medical products. Subscribe: Institutional or Individual Sign In Username Error: Please enter User Name Password Error: Please enter Password Forgot Username? Forgot Password? Sign in via OpenAthens Sign in via Shibboleth