Anemia etiology

Respiratory alkalosis is characterized by an increased arterial pH, a primary decrease in the arterial PaC02 and, when present for sufficient time, a compensatory fall in the HCOf concentration. Respiratory alkalosis represents hyperventilation and is remarkably common. The most common etiologies of respiratory acidosis are listed in Table 25-7 and range from benign (anxiety) to life-threatening (pulmonary embolism). Some causes of hyperventilation and respiratory acidosis are remarkably common (hypoxemia or anemia). 

Table 63-1 describes common tests used to determine the etiology of anemia. A diagnostic and treatment algorithm for anemia is outlined in Fig. 63-3. 

The underlying cause of anemia (e.g., blood loss iron, folic acid, or vitamin B12 deficiency or chronic disease) must be determined and used to guide therapy. As discussed previously, patients should be evaluated initially based on laboratory parameters to determine the etiology of the anemia (see Fig. 63-3). Subsequently, the appropriate pharmacologic treatment should be initiated based on the cause of anemia. 

The first step in managing chronic HF is to determine the etiology or precipitating factors. Treatment of underlying disorders (e.g., anemia, hyperthyroidism) may obviate the need for treating HF. 

Anemias can be classified on the basis of RBC morphology, etiology, or pathophysiology (Table 33-1). The most common anemias are included in this chapter. 

Hemolytic anemia results from decreased RBC survival time due to destruction in the spleen or circulation. The most common etiologies are RBC membrane defects (e.g., hereditary spherocytosis), altered Hb solubility or stability (e.g., sickle cell anemia [see Chap. 34] and thalassemias), and changes in intracellular metabolism (e.g., glucose-6-phosphate dehydrogenase deficiency). Some drugs cause direct oxidative damage to RBCs (see Appendix 3). 

Elderly patients with symptoms of anemia should undergo a complete blood cell count with peripheral smear and reticulocyte count, and other laboratory studies as needed to determine the etiology of anemia. 

The ultimate goals of treatment in the anemic patient are to alleviate signs and symptoms, correct the underlying etiology (e.g., restore substrates needed for RBC production), and prevent recurrence of anemia. 

Oral folate 1 mg daily for 4 months is usually sufficient for treatment of folate-deficiency anemia, unless the etiology cannot be corrected. If malabsorption is present, the daily dose should be increased to 5 mg. 

Patients with other types of anemias require appropriate supplementation depending on the etiology of anemia. 

Treatment of aplastic crisis is primarily supportive. Blood transfusions may be indicated for severe or symptomatic anemia. Antibiotic therapy is not warranted because the most common etiology is viral, not bacterial, infection. 

Nutritional deficiency diseases are relatively rare in the temperate zone. The etiology of numerous other clinical conditions involve vitamin deficiencies, due to faults in absorption, transfer, or utilization. Because of the central position of the vitamins as sources of coenzymes, such functional deficiencies are important in malabsorption, where the picture is often complicated by multiple deficiencies, in anemias where the defect is in general highly specific, and in many other diseases where the deficiency is secondary to other pathologic events, but nevertheless of grave consequences. 

A vitamin is often the etiological center of a disease as vitamin Bi2 and folic acid in macrocytic anemias. Here, because of the obvious implications for diagnosis and therapy the determination of the nucleo-genic vitamins, Bi2 and folic acid, is imperative in the routine of clinical hematology. 

Reports of Stoddard solvent as an etiologic agent in the development of aplastic anemia are of questionable validity. Skin exposure may cause dermatitis and sensitization. ... 

Fischer B. 1955. Significance of Heinz bodies in anemia of obscure etiology.Am J Med Sci 230 143-146. 

Radium was also used as a "rejuvenating" tonic in the 1920s and was available to the general public in bottled water. Gettler and Norris (1933) described a case of a 52-year-old man who drank about 1,400 bottles of "Radithor", containing radium at 2 pg/60 ml bottle, over a 5-year period (total dose approximately 2,800 pCi or 56 pCi/kg or 2,074 kBq/kg for a 50-kg man). The cause of death was stated to be a combination of necrosis of the jaw, abscess of the brain, secondary anemia and terminal bronchopneumonia. However, it is important to note that each of these effects can also be attributed to other etiologies. 

The first step in managing chronic HF is to determine the etiology or precipitating factors. Treatment of underlying disorders (e.g., anemia, hyperthyroidism) may obviate the need for treating HF. Nonpharmacologic interventions include cardiac rehabflitation and restriction of fluid intake (maximum 2 L/day from all sources) and dietary sodium (approximately 2 to 3 g of sodium per day). 

Treatment of aplastic crisis is primarily supportive. Blood transfusions may be indicated for severe or symptomatic anemia. Antibiotic therapy is not warranted because the most common etiology is viral, not bacterial, infection. Treatment options for splenic sequestration include observation alone, especially for adults because they tend to have milder episodes chronic transfusion to delay splenectomy and splenectomy after a hfe-threatening crisis, after repetitive episodes, or for chronic hypersplenism. 

Complete blood cell count with differential In cases of uveitis a complete blood cell coimt can help identify an underlying bacterial or viral etiology based on the white cell differential. Additionally, this test may assist in the detection of a white blood cell malignancy, such as leukemia or lymphoma. A complete blood cell count should also accompany an erythrocyte sedimentation rate (ESR) analysis, because the complete blood cell count identifies anemia that may affect the results of the ESR. 

C5. Castle, W. B., Observations on the etiologic relationship of achylia gastrica to pernicious anemia. I. The effect of the administration in patients with pernicious anemia of the contents of the normal human stomach recovered after the ingestion of beef muscle. Am. J. Med. Sci. 178, 748-764 (1929). 

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