Anemia decreased-production

MANAGING HONE MARROW SUPPRESSION. Bone marrow suppression is a potentially dangerous adverse reaction resulting in decreased production of blood cells. Bone marrow suppression is manifested by abnormal laboratory test results and clinical evidence of leukopenia, thrombocytopenia, or anemia For example, there is a decrease in the white blood cells or leukocytes (leukopenia), a decrease in the thrombocytes (thrombocytopenia), and a decrease in the red blood cells, resulting in anemia Fhtients with leukopenia have a decreased resistance to infection, and the nurse must monitor them closely for any signs of infection. 

Anemia occurs as the result of a decreased production of red blood cells in the bone marrow and is characterized by fatigue, dizziness, shortness of breath, and palpitations. On occasion, the administration of blood transfusions may be necessary to correct the anemia... 

Anemia (decreased hemoglobin and hematocrit) occurs as a result of variceal bleeding, decreased erythrocyte production, and hypersplenism. 

The causes of anemia can be divided into three main categories decreased production, increased destruction, and blood loss. Drug therapy is the mainstay of treatment for anemias caused by reduced production of erythrocytes and will be the focus of this chapter. 

The anemia of hyperthyroidism is usually normochromic and caused by increased red blood cell turnover. The anemia of hypothyroidism may be normochromic, hyperchromic, or hypochromic and may be due to decreased production rate, decreased iron absorption, decreased folic acid absorption, or to autoimmune pernicious anemia. LDH, lactic dehydrogenase AST, aspartate aminotransferase. 

Aphytic zone Parts of the lake floor where vegetation is not available Aplastic anemia Bone marrow failure with markedly decreased production of white blood cells, red blood cells, and platelets, leading to increased risk of infection and bleeding... 

Any of several basic disorders may account for decreased production. These may include congenital disorders such as hypoplastic anemia, hypoplastic thrombocytopenia, acquired conditions such as nutritional deficiency, toxic depression of the bone marrow, or the replacement of the bone marrow as in leukemia, carcinoma, granuloma, or fibrosis. Increased platelet destruction may include congenital disorders or such acquired disorders as chronic infections, portal hypertension, lymphomas, or thrombotic thrombocytopenia. 

Deficiency of pyruvate kinase causes decreased production of ATP from glycolysis. Red blood cells have insufficient ATP for their sodium pumps their membranes lyse, and a hemolytic anemia results. 

The pathophysiology of isoimmune hemolysis is the same for all antigens. The differences in severity of disease are due to differences in the expression of the antigen on the surface of the cells, the intrinsic immunogenicity of the antigen, and peculiarities of the immune response of the mother. Destruction of the fetal erythrocytes, which is the central problem, produces several other problems. Fetal anemia imposes an extra burden on the fetal heart to provide adequate oxygen supply to fetal tissues. Anemia stimulates the fetal marrow and extramedullary erythropoiesis in the liver and spleen to replace the destroyed erythrocytes. Extramedullary erythropoiesis destroys hepatocytes and leads to decreased production of serum albumin and decreased oncotic pressure in tire intravascular space. 

Hypochromic, normocytic anemia is usual with C-AMB and reverses slowly following cessation of therapy. It likely reflects decreased production of erythropoietin and often responds to... 

ACUTE HEALTH RISKS gastrointestinal effects abdominal pain nausea diarrhea vomiting headaches weakness delirium anemia leukopenia decreased production of red and white blood cells cardiovascular system effects abnormal heart rhythm blood vessel damage hypotension liver, kidney and blood effects shock death. 

Anemia resulting from decreased production of erythropoietin (renal system) and decreased vitamin absorption (gastrointestinal system) can result in decreased oxygenation and tissue hypoxia (lactic acidosis). 

Gastric and intestinal mucosae atrophy with decreased production of acid and intrinsic factor needed for absorption of vitamin Bj. These changes result in acid-base imbalance and potential circulatory/respiratory problems related to anemia (i.e., hypoxia). 

The production of monoclonal antibodies in vivo, using mice (or other laboratory animals) has come under increasing criticism because of the ethical issues posed by the use of laboratory animals. In Europe, regulatory approval of this method has been withdrawn except for cases were alternative methods are shown not to be available. Mice generating Mabs typically exhibit abdominal distention, anorexia, anemia, decreased activity, and body mass, dehydration, difficulty in walking, respiratory distress, shock, hunched posture, peritonitis, immunosuppression, and possibly death. 

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. 

In homozygotes, the synthesis of 3-chains is greatly decreased and as a result a severe anemia may develop after birth when the y-chain production ceases, 3-Thalassemla, like thalassemia, is a heterogeneous condition which can be concluded ftom the differences in suppression of 3-chain synthesis. In some cases 3-chain production is completely absent (the 3 type) wher. as, in others, a considerable 3-chain synthesis can be observed (the 3 type). The severe anemia will lead, by a mechanism which is still not completely understood, to an increased production of y-chains. Both types ( -and -chains) are present and are produced in heterozygotes in either one of two distinct ratios, namely 7 3 as in the newborn or 2 3 as in the normal adult (for a summary see ). 

The progenitor cells of the kidney produce 90% of the hormone erythropoietin (EPO), which stimulates red blood cell (RBC) production. Reduction in nephron mass decreases renal production of EPO, which is the primary cause of anemia in patients with CKD. The development of anemia of CKD results in decreased oxygen delivery and utilization, leading to increased cardiac output and left ventricular hypertrophy (LVH), which increase the cardiovascular risk and mortality in patients with CKD. 

The primary cause of anemia in patients with CKD is a decrease in EPO production. With normal kidney function, as Hgb, hematocrit (Hct), and tissue oxygenation decrease, the... 

A decrease in erythrocyte production can be multifactorial. A deficiency in nutrients (such as iron, vitamin B12, and folic acid) is a common cause that often is easily treatable. In addition, patients with cancer and CKD are at risk for developing a hypoproductive anemia. Furthermore, patients with chronic immune-related diseases (such as rheumatoid arthritis and systemic lupus erythematosus) can develop anemia as a complication of their disease. Anemia related to these chronic inflammatory conditions is typically termed anemia of chronic disease. 

Patients with CKD suffer from a decrease in erythropoietin production because erythropoietin is produced mainly in the kidneys.4,5 Finally, in patients with anemia of chronic disease, there is a blunted erythropoietin production as well as a diminished response to erythropoietin.9 Anemia of chronic disease also affects iron homeostasis, causing iron sequestration into storage sites and decreasing the amount available to the rest of the body.9... 

Studies have shown that in patients with chemotherapy-related anemia, therapy with erythropoietin products (epoetin-alfa and darbepoetin) can increase hemoglobin, decrease transfusion requirements, and improve quality of life.12 Epoetin is recombinant human erythropoietin, and darbepoetin is structurally similar to endogenous erythropoietin. Both bind to the same receptor to stimulate red blood cell production. Darbepoetin differs from epoetin in that it is a glycosylated form and exhibits a longer half-life in the body. The half-lives of a single subcutaneous injection of epoetin or darbepoetin in patients are roughly 27 and 43 hours, respectively. 

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. 

A marked interference with heme synthesis results in a reduction of the hemoglobin concentration in blood. Decreased hemoglobin production, coupled with an increase in erythrocyte destruction, results in a hypochromic, normocytic anemia with associated reticulocytosis. Decreased hemoglobin and anemia have been observed in lead workers and in children with prolonged exposure at higher PbB levels than those noted as threshold levels for inhibition or stimulation of enzyme activities involved in heme synthesis (EPA 1986a). 

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