Anaemia

  • June 2020
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ANAEMIA Background: Anemia, like a fever, is a symptom of disease that requires investigation to determine the underlying etiology Anemia is strictly defined as a decrease in red blood cell (RBC) mass. In practice however; anemia is usually discovered and quantified by measurement of the RBC count, hemoglobin (Hb) concentration, and hematocrit (Hct).In kenya defined as Hb below 10g/dl.WHO definition Hb below 12g/dl. Changes in plasma volume. eg, dehydration elevates these values, and increased plasma volume in pregnancy can diminish them without affecting the RBC mass. Pathophysiology: Erythroid precursors develop in bone marrow at rates usually determined by the requirement for sufficient circulating Hb to oxygenate tissues adequately. Erythroid precursors differentiate sequentially from stem cells to progenitor cells to erythroblasts to normoblasts in a process requiring growth factors and cytokines. This process of differentiation requires several days. Normally, erythroid precursors are released into circulation as reticulocytes. -Reticulocytes remain in the circulation for approx. 1 day before reticulin is excised by reticuloendothelial cells with the delivery of the mature erythrocyte into circulation. -The mature erythrocyte remains in circulation for about 120 days before being engulfed and destroyed by phagocytic cells of the reticuloendothelial system. -Because erythrocytes have no nucleus, they lack a Krebs cycle and rely on glycolysis via the Embden-Meyerhof and pentose pathways for energy -Basically, only 3 causes of anemia exist: 1) Blood loss 2) Increased RBC destruction (hemolysis)

3) Decreased production of RBCs. -Each of these 3 causes includes a number of etiologies that require specific and appropriate therapy. -Often, the etiology can be determined if the RBCs are altered in either size or shape or if they contain certain inclusion bodies. For example, Plasmodium falciparum malaria is suggested by the presence of more than one ring form in an RBC and produces pan-hemolysis of RBCs of all ages. Prevalance Although geographic diseases, such as  sickle cell anemia  Thalassemia  malaria  Hookworm 

Chronic infections, are responsible for a portion of the increase - nutritional factors with iron deficiency and, to a lesser extent, folic acid deficiency play major roles in the increased prevalence of anemia. Populations with little meat in the diet have a high incidence of iron deficiency anemia because heme iron is better absorbed from food than inorganic iron

History: Primary symptoms result from tissue hypoxia and might include the following: Fatigue, weakness, irritability - Headache, Dizziness, especially postural

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Vertigo ,Tinnitus ,Syncope Dyspnea, especially with increased physical activity (exercise intolerance) Chest pain, palpitations Difficulty sleeping or concentrating Thirst ,Anorexia, Decreased urine output/bowel irregularity

Mortality/Morbidity: -The morbidity and mortality of anemias vary greatly depending on the etiology. -Acute hemorrhage has variable mortality depending on the site of bleeding (80% with aortic rupture, 30-50% with bleeding esophageal varices, approximately 1% with benign peptic ulcers). -Anemia from gastrointestinal bleeding may be the first evidence of an intestinal malignancy. -Sickle cell disease may be associated with frequent painful crises and a shortened lifespan, or patients with sickle cell disease may remain relatively asymptomatic with a nearly normal lifespan. -Most patients with beta-0 homozygous thalassemia die during the second or third decade of life unless they undergo bone marrow transplantation. -Hereditary spherocytosis either may present with a severe hemolytic anemia or may be asymptomatic with compensated hemolysis. -Similarly, glucose-6-phosphate dehydrogenase (G-6-PD) deficiency may manifest as chronic hemolytic anemia or exist without anemia until the patient receives an oxidant medication. -The 2-year fatality rate for severe aplastic anemia is 70% without bone marrow transplantation or a response to immunosuppressive therapy. -In addition, tolerance of anemia is proportional to the anemia's rate of development. Symptoms and mortality associated with rapidly developing anemia are more profound than in slowly developing anemia. Sex: Overall, anemia is twice as prevalent in females as in males. -This difference is significantly greater during the childbearing years due to pregnancies and menses. -Approximately 65% of body iron is incorporated into circulating Hb. -Women have a markedly lower incidence of anemia from X-linked anemias, such as G-6-PD deficiency and sexlinked sideroblastic anemias. Age: -Severe genetically acquired anemias (eg sickle cell disease, thalassemia, Fanconi syndrome) are more commonly found in children because they do not survive to adulthood. -During the childbearing years, women are more likely to become iron deficient. -Neoplasia increases in prevalence with each decade of life and can produce anemia from bleeding, from the replacement of bone marrow with tumor, or from the development of anemia associated with chronic disorders. -Use of aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), and Coumadin increases with age and can produce gastrointestinal bleeding.

-Folate deficiencies may have a sore tongue, cheilosis, and symptoms associated with steatorrhea -Color, bulk, frequency, and odor of stools and whether the feces float -malabsorption. In steatorrhea whether the toilet needs to be flushed more than once to rid it of stool and whether an oily substance is floating on the water surface after the first flush. -Fever because infections, neoplasm, and collagen vascular disease can cause anemia. -Occurrence of purpura, ecchymoses, and petechiae suggest the occurrence of either thrombocytopenia or other bleeding disorders; this may be an indication either that more than one bone marrow lineage is involved or that coagulopathy is a cause of the anemia because of bleeding

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