Anemias iron deficiency causing

Although EPO deficiency is the primary cause of CKD anemia, iron deficiency is often present, and it is essential to assess and monitor the CKD patient s iron status (NKF-K/DOQI guidelines). Iron stores in patients with CKD should be maintained so that transferrin saturation (TSAT) is greater than 20% and serum ferritin is greater than 100 ng/mL (100 mcg/L or 225 pmol/L). If iron stores are not maintained appropriately, epoetin or darbepoetin will not be effective, and most CKD patients will require iron supplementation. Oral iron therapy can be used, but it is often ineffective, particularly in CKD patients on dialysis. Therefore, intravenous iron therapy is used extensively in these patients. Details of the pharmacology, pharmacokinetics, adverse effects, interactions, dose, and administration of erythropoietin and iron products have been discussed previously. 

Iron deficiency is usually due to blood loss, or more rarely to inadequate iron uptake. During pregnancy, increased demand can also cause iron deficiency states. In severe cases, reduced hemoglobin synthesis can lead to anemia ( iron-deficiency anemia ). In these patients, the erythrocytes are smaller and have less hemoglobin. As their membrane is also altered, they are prematurely eliminated in the spleen. 

Iron deficiency is the most common cause of chronic anemia. Like other forms of chronic anemia, iron deficiency anemia leads to pallor, fatigue, dizziness, exertional dyspnea, and other generalized symptoms of tissue hypoxia. The cardiovascular adaptations to chronic anemia—tachycardia, increased cardiac output, vasodilation—can worsen the condition of patients with underlying cardiovascular disease. 

Iron is used to regenerate hemoglobin. Iron is absorbed in the intestine and enters plasma as heme. Iron is stored as ferritin in the liver, spleen, and bone marrow. Five to twenty milligrams of iron are required daily. Iron deficiency causes anemia. Iron is found in liver, lean meats, egg yolks, dried beans, green vegetables (i.e., spinach), and fruit. Women who are pregnant should increase their iron intake as specified by the healthcare provider. Large doses of iron are prescribed in the second and third trimesters. The patient must adhere to the... 

Iron (ferrous sulfate, gluconate, or fumarate) is used for the regeneration of hemoglobin. Iron deficiency causes anemia. The patient requires 5 to 20 mg of iron each day from eating liver, lean meats, egg yolks, dried beans, green vegetables (such as spinach), and fruit. 

Anemia is a decrease in the number of red blood cells (RBCs), a decrease in die amount of hemoglobin in RBCs, or bodi a decrease in die number of RBCs and hemoglobin. When diere is an insufficient amount of hemoglobin to deliver oxygen to die tissues, anemia exists. There are various types and causes of anemia For example, anemia can be die result of blood loss, excessive destruction of RBCs, inadequate production of RBCs, and deficits in various nutrients, such as in iron deficiency anemia Once the type and cause have been identified, die primary health care provider selects a method of treatment. 

Iron-deficiency anemia in chronic PN patients may be due to underlying clinical conditions and the lack of iron supplementation in PN. Parenteral iron therapy becomes necessary in iron-deficient patients who cannot absorb or tolerate oral iron. Parenteral iron should be used with caution owing to infusion-related adverse effects. A test dose of 25 mg of iron dextran should be administered first, and the patient should be monitored for adverse effects for at least 60 minutes. Intravenous iron dextran then may be added to lipid-free PN at a daily dose of 100 mg until the total iron dose is given. Iron dextran is not compatible with intravenous lipid emulsions at therapeutic doses and can cause oiling out of the emulsion. Other parenteral iron formulations (e.g., iron sucrose and ferric gluconate) have not been evaluated for compounding in PN and should not be added to PN formulations. 

Anemia of chronic kidney disease A decline in red blood cell production caused by a decrease in erythropoietin production by the progenitor cells of the kidney. As kidney function declines in chronic kidney disease, erythropoietin production also declines, resulting in decreased red blood cell production. Other contributing factors include iron deficiency and decreased red blood cell lifespan, caused by uremia. 

Iron-deficiency anemia can be caused by inadequate dietary intake, inadequate GI absorption, increased iron demand (e.g., pregnancy), blood loss, and chronic diseases. 

In iron-deficiency anemia, iron therapy should cause reticulocytosis in 5 to 7 days and raise Hb by 2 to 4 g/dL every 3 weeks. The patient should be reevaluated if reticulocytosis does not occur or if Hb does not increase by 2 g/dL within 3 weeks. Iron therapy is continued until iron stores are replenished, which usually requires at least 3 to 6 months. 

The primary cause of anemia in patients with CKD or ESRD is erythropoietin deficiency. Other contributing factors include decreased lifespan of red blood cells, blood loss, and iron deficiency. 

Vitamin Bg deficiency, iron deficiency, and lead poisoning all can cause anemia. These three conditions are summarized and compared in Ihble 1-17-6. 

A frequent cause of iron deficiency is chronic blood loss due to gastric/in-testinal ulcers or tumors. One liter of blood contains 500 mg of iron. Despite a significant increase in absorption rate (up to 50%), absorption is unable to keep up with losses and the body store of iron falls. Iron deficiency results in impaired synthesis of hemoglobin and anemia (p. 

The length of iron therapy depends upon the cause and severity of the iron deficiency. In general, approximately 4 to 6 months of oral iron therapy is required to reverse uncomplicated iron deficiency anemias. Iron therapy should increase hemoglobin levels by 1 g/week. 

Evidence of iron overload known hypersensitivity to iron sucrose or any of its inactive components anemia not caused by iron deficiency. 

Alcohol indirectly affects hematopoiesis through metabolic and nutritional effects and may also directly inhibit the proliferation of all cellular elements in bone marrow. The most common hematologic disorder seen in chronic drinkers is mild anemia resulting from alcohol-related folic acid deficiency. Iron deficiency anemia may result from gastrointestinal bleeding. Alcohol has also been implicated as a cause of several hemolytic syndromes, some of which are associated with hyperlipidemia and severe liver disease. 

For patients who are unable to tolerate penicillamine, trientine, another chelating agent, may be used in a daily dose of 1-1.5 g. Trientine appears to have few adverse effects other than mild anemia due to iron deficiency in a few patients. Zinc acetate administered orally increases the fecal excretion of copper and is sometimes used for maintenance therapy. The dose is 50 mg three times a day. Zinc sulfate (200 mg/d orally) has also been used to decrease copper absorption. Zinc blocks copper absorption from the gastrointestinal tract by induction of intestinal cell metallothionein. Its main advantage is its low toxicity compared with that of other anticopper agents, although it may cause gastric irritation when introduced. 

Different iron salts provide different amounts of elemental iron, as shown in Table 33-3. In an iron-deficient individual, about 50-100 mg of iron can be incorporated into hemoglobin daily, and about 25% of oral iron given as ferrous salt can be absorbed. Therefore, 200-400 mg of elemental iron should be given daily to correct iron deficiency most rapidly. Patients unable to tolerate such large doses of iron can be given lower daily doses of iron, which results in slower but still complete correction of iron deficiency. Treatment with oral iron should be continued for 3-6 months after correction of the cause of the iron loss. This corrects the anemia and replenishes iron stores. 

Patients with iron deficiency anemia present with fatigue, weakness, and pallor, and possibly also with glossitis, headache, dysphagia, fingernail changes, gastric atrophy, and paresthesias. Inadequate intake of iron, malabsorption, and blood loss from any origin are the principal causes of iron deficiency anemia. 

Iron deficiency is the most common cause of chronic anemia—anemia that develops over time. 

The most common cause of iron deficiency in adults is blood loss. Menstruating women lose about 30 mg of iron with each menstrual period women with heavy menstrual bleeding may lose much more. Thus, many premenopausal women have low iron stores or even iron deficiency. In men and postmenopausal women, the most common site of blood loss is the gastrointestinal tract. Patients with unexplained iron deficiency anemia should be evaluated for occult gastrointestinal bleeding. 

Iron is stored in intestinal mucosal cells as ferritin (an iron/protein complex) until needed by the body. Iron deficiency results from acute or chronic blood loss, from insufficient intake during periods of accelerated growth in children, or in heavily menstruating or pregnant women. Therefore it essentially results from a negative iron balance due to depletion of iron stores and inadequate intake, culminating in hypochromic microcytic anemia. Supplementation with ferrous sulfate is required to correct the deficiency. Gastrointestinal disturbances caused by local irritation are the most common adverse effects caused by iron supplements. 

Erythropoietin [ery throw PO eetin] is a glycoprotein, normally made by the kidney, that regulates red cell proliferation and differentiation in bone marrow. Human erythropoietin, produced by recombinant DNA technology, is effective in the treatment of anemia caused by end-stage renal disease, anemia associated with HIV-infected patients, and anemia in some cancer patients. Supplementation with iron may be required to assure an adequate response. The protein is usually administered intravenously in renal dialysis patients, but in others the subcutaneous route is preferred. Side effects such as iron deficiency and an elevation in blood pressure occur. [Note The latter may be due to increases in peripheral vascular resistance and/or blood viscosity.]... 

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