| Drug
Information
Alternative Medicines *Diet *Yoga Disease and Managements Drug Information Sites *FDA *CDC *NIH *DSEA Health Extra
|
Anemia
(Aplastic, Hemolytic, Iron Deficiency, Pernicious, Posthemorrhagic)
--An inadequate number of circulating red blood cells and an insufficient amount of hemoglobin to deliver oxygen to tissues, resulting in pallor, fatigue, shortness of breath, and predisposition to cardiac complications. The type and cause dictate manifestations and treatment; various types are addressed below.
Aplastic Anemia
--A reduction in the number of circulating red blood cells resulting from bone marrow failure and generally accompanied by agranulocytosis and/or thrombocytopenia.
Causes and Incidence The etiology is unknown in half of diagnosed cases; the other half are induced by chemicals, drugs, viruses, or radiation. The incidence is low.
Disease Process Exposure to a known or unknown toxin depresses production of erythrocytes, platelets, and granulocytes in the bone marrow. Common toxins include ionizing radiation, chemical agents (e.g., benzene, DDT, carbon tetrachloride), and drugs (e.g., antitumor or antimicrobial agents).
Symptoms The onset is usually insidious, occurring weeks or months after exposure to the toxin. Fatigue, weakness, dyspnea, and waxy pallor of the skin and mucous membranes are characteristic. Thrombocytopenia causes hemorrhage into mucous membranes, skin, and optic fundi. Agranulocytosis leads to severe infection.
Potential Complications Chronic anemia leads to increasing hemorrhage and repeated infections, which result in death in about half of those diagnosed.
Diagnostic Tests
Complete blood count (CBC)
Decreased RBCs (normochromic, normocytic), WBCs, and hemoglobin (Hgb)
Platelet count
Decreased
Serum iron
Increased
Bone marrow biopsy
Hypocellular/hypoplastic; fatty, fibrous tissue
Reticulocyte count
Markedly decreased
Treatments
Surgery
None
Drugs
Corticosteroids to stimulate granulocyte production; antibiotics for infection; androgens to stimulate bone marrow
General
Removal of causative agent; bone marrow transplant from a human leukocyte antigen (HLA)-matched donor (sibling); blood transfusions; hemorrhage precautions
Hemolytic Anemia
--Abnormal or premature destruction of red blood cells and the inability of the bone marrow to produce sufficient RBCs to compensate.
Causes and Incidence The etiology is typically related to an extracorpuscular factor (e.g., trauma, burns, surgery, chemical agents, drugs, infectious organisms, systemic diseases). Less common are intracorpuscular causes, such as a glucose-6-phosphate dehydrogenase (G6PD) deficiency.
Disease Process The precipitating factor results in a shortened life span for erythrocytes and an increase in erythrocyte destruction by the reticuloendothelial system. The bone marrow is unable to produce sufficient replacement cells to keep pace with the destruction, and anemia ensues.
Symptoms Hemolysis can be acute or chronic. The symptoms of chronic hemolysis resemble those of other anemias: fatigue, weakness, dyspnea, and pallor. Individuals with chronic symptoms may suffer from a physiologic or emotional stressor that triggers a hemolytic crisis. Acute hemolytic crisis, which is rare, is characterized by chills; fever; headache; pain in the back, abdomen, and joints; splenomegaly; hepatomegaly; lymphadenopathy; and reduced urinary output.
Potential Complications Chronic symptoms can lead to jaundice, arthritis, renal failure, and other organ failure. Crisis can lead to paresthesia, paralysis, chills, vomiting, shock, and organ failure.
Diagnostic Tests
Sickle cell test
To rule out sickle cell anemia
CBC
Decreased Hgb and hematocrit (Hct)
Serum tests
Elevated lactate dehydrogenase and bilirubin
Bone marrow aspiration
Hyperplasia
Reticulocyte count
Elevated
Urine/fecal urobilinogen
Elevated
Treatments
Surgery
Splenectomy
Drugs
Corticosteroids to depress extracorpuscular factors and diminish inflammatory response; diuretics to prevent tubular necrosis; folic acid to increase RBC production
General
Elimination of causative agent; erythrocytopheresis (RBC exchange); transfusion; oxygen therapy for hypoxemia; fluid and electrolyte management
Iron Deficiency Anemia
--A chronic anemia characterized by depleted iron stores and small, pale red blood cells lacking in hemoglobin.
Causes and Incidence Iron deficiency anemia is usually caused by chronic blood loss or by an increased need for or decreased intake of iron. It is the most common of the anemias, with a high worldwide incidence. It occurs most often in women, children, and the elderly in underdeveloped countries.
Disease Process Some factor (e.g., chronic blood loss, a decrease in iron intake) leads to iron deficiency. This occurs in orderly steps. Initially, iron loss exceeds intake, and the iron stores in the bone marrow are used and depleted. A compensatory mechanism increases absorption of dietary iron but depletion continues, and insufficient iron is available for RBC formation. This leads to a decrease in Hgb production, microcytosis, and a decrease in oxygenation of the tissues.
Symptoms Usual signs and symptoms associated with anemia (pallor, fatigue, weakness) plus symptoms specific to the iron deficiency, such as glossitis, cheilosis, koilonychia (spoon-shaped fingernails), and pica.
Potential Complications Exhaustion, infection, and respiratory and cardiac complications are possible if the condition goes untreated.
Diagnostic Tests
CBC
Decreased RBCs, Hgb, and Hct
Peripheral blood smear
Decreased mean corpuscular volume and mean corpuscular Hgb concentration; microcytosis; hypochromia
Iron capacities
Decreased serum iron, serum ferritin, and iron ferritin; increased iron-binding capacity
Bone marrow aspiration
Erythrocyte:granulocyte ratio 1:1 (normal, 1:3-1:5); lack of marrow iron; ringed sideroblasts
Treatments
Surgery
None
Drugs
Iron replacement PO or parenterally
General
Correction of underlying cause (e.g., treatment of bleeding, increased dietary intake of iron); nutritional education
Pernicious Anemia
--A chronic, progressive anemia characterized by the production of megaloblasts, which are enlarged red blood cells with an immature nucleus.
Causes and Incidence Pernicious anemia usually is caused by a deficiency in or underutilization of vitamin B12. It is a fairly common anemia in adults over 50 years of age who are of Scandinavian origin.
Disease Process Most commonly, the gastric mucosa develops a defect caused by an unknown factor and atrophies. This inhibits the secretion of intrinsic factor (IF), which binds and transports dietary vitamin B12 to the ileum for absorption. The lack of IF prevents vitamin B12 from entering the body, and existing stores of the vitamin are depleted, leading to the production of enlarged, immature RBCs.
Symptoms Usual signs and symptoms associated with anemia (pallor, fatigue, weakness, dyspnea) plus symptoms that stem from the physiologic changes in the gastrointestinal tract (e.g., glossitis, gingivitis, indigestion, epigastric pain, loss of appetite, diarrhea, constipation, weight loss). Peripheral neurologic changes occur, with paresthesia in the hands and feet.
Potential Complications If the condition goes untreated, the neurologic changes become more profound, with involvement of the spinal cord and loss of vibratory sense, ataxia, spasticity, and disturbances in bowel and bladder function. Depression, paranoia, and delirium may follow. Splenomegaly and hepatomegaly occur, as well as organ failure, neurologic degeneration, or infection, eventually causing death.
Diagnostic Tests
Peripheral blood smear
Oval macrocytes, hypersegmented neutrophils, enlarged platelets
Schilling test
Radioactive-tagged vitamin B12 is not excreted in urine
Complete blood count
Decreased Hgb, leukocytes, erythrocytes, and thrombocytes
Bone marrow aspiration
Hyperplasia; increased large-cell megaloblasts
Gastric analysis
Lack of free hydrochloric acid
Treatments
Surgery
None
Drugs
Lifelong parenteral vitamin B12 replacement (dietary vitamin B12 replacement is not effective); oral iron if Hgb does not rise
General
Treatment of underlying cause of gastric atrophy, if possible; oxygen to increase arterial levels; oral hygiene; orientation if confused; safety precautions for neurologic effects; instruction about vitamin B12 replacement as a life change
Posthemorrhagic Anemia
--An anemia characterized by a decrease in hemoglobin in the blood related to rapid, massive hemorrhage
Causes and Incidence Rapid blood loss may be caused by traumatic rupture or incision or erosion of a large blood vessel (ulcer, tumor). The prognosis depends on the rate and site of bleeding and the total blood loss.
Disease Process With blood loss, blood volume diminishes, hemodilution occurs, and oxygenation of the tissues declines.
Symptoms The rate of blood loss determines the signs and symptoms, which may include dizziness; faintness; weakness; pallor; thirst; sweating; rapid, weak pulse; rapid respiration; and orthostatic hypotension.
Potential Complications Lack of prompt treatment or failure to control the bleeding results in shock, coma, and death.
Diagnostic Tests
Complete blood count
RBCs, Hgb, and Hct are deceptively high during initial period of hemorrhage because of vasoconstriction; values begin to decline within hours of the onset of bleeding if hemorrhage is not controlled
Peripheral smear
Normocytic cells, agranulocytosis
Coagulation time
Reduced
Treatments
Surgery
If indicated to control hemorrhage
Drugs
Iron replacement
General
Control of bleeding; blood transfusions; IV fluids, oral fluids as tolerated; oxygen; absolute bed rest; diet high in protein and iron
