2 Anemia is a decrease in the normal number of red blood cells (RBCs) or less than the normal quantity of hemoglobin in the blood. However, it can include decreased oxygen-binding ability of each hemoglobin molecule due to deformity or lack in numerical development as in some other types of hemoglobin deficiency. Because anemia has multiple causes (etiologies) a work-up must be performed to identify the specific cause or in some cases causes.
3 SymptomsMost commonly, people with anemia report non-specific symptoms of a feeling of weakness, or fatigue, general malaise and sometimes poor concentration. They may also report shortness of breath, dyspnea, on exertion. In very severe anemia, the body may compensate for the lack of oxygen carrying capability of the blood by increasing cardiac output. The patient may have symptoms related to this, such as palpitations, angina (if preexisting heart disease is present), intermittent claudication of the legs, and symptoms of heart failure
4 SignsOn examination, the signs exhibited may include pallor (pale skin, mucosal linings and nail beds) but this is not a reliable sign. There may be signs of specific causes of anemia, e.g., koilonychia (in iron deficiency), jaundice (when anemia results from abnormal break down of red blood cells — in hemolytic anemia), bone deformities (found in thalassemia major) or leg ulcers (seen in sickle cell disease).
6 History and PhysicalAs a result of the non-specific signs and symptoms a history and physical examination is performed.
7 Two main causes of anemia Decreased Production of red blood cells and/or hemoglobinIncreased destruction of red blood cells and/or hemoglobinMain test to distinguish the difference is the reticulocyte count. Normal count is .5 – 2%Generally a low normal to low reticulocyte count is caused by decreased production and high one is caused by increased destruction
8 Decreased Production Causes Reduction in red blood cells or subnormal level of hemoglobinInadequate production of red cellsInsufficient raw materialsIron deficiencyVitamin B12 deficiencyFolic acid deficiencyInability to deliver adequate red cells into circulation due to marrow damage or destruction (aplastic anemia), replacement of marrow by foreign or abnormal cells
9 Increased Destruction Causes Excessive loss of red cellsExternal blood loss (hemorrhage)Shortened survival of red cells in circulationDefective red cells: hereditary hemolytic anemiaAccelerated destruction of cells from antibodies to red blood cell or by mechanical trauma to circulating red cells
11 Diagnostic Evaluation of Anemia 1. History and physical examination2. Complete blood count: to assess degree of anemia, leukopenia, and thrombocytopenia3. Blood smear: determine if normocytic, macrocytic, or hypochromic microcytic4. Reticulocyte count: assess rate of production of new red cells5. Lab tests: determine iron, B12, folic acid6. Bone marrow study: study characteristic abnormalities in marrow cells7. Evaluation of blood loss from gastrointestinal tract to localize site of bleeding
12 CBC indices regarding red blood cells Red Blood Cell Count – 5.4 million per microliterHematocrit ( 30 – 60) generally 45% to 52% for men and 37% to 48% for womenHemoglobin ( 13 to 18 grams per deciliter for men and 12 to 16 for women)MCV (Mean Corpuscular Volume) - 80 to 100MCH (Mean Corpuscular Hemoglobin) –this is the average amount of Hgb. in a the typical red blood cell. 27 to 32 picogramsMCHC (Mean Corpuscular Hemoglobin Conc.) - the average concentration of hemoglobin in a given volume of red cells (32 – 36%)RDW – (Red Cell Distribution Width) – a measurement of the variability of red cell size and shape. Higher numbers indicate greater variation in size
13 Peripheral Smear Look at size – 6 – 9 micromillimeters Too small – microcyticToo big – macrocyticNormal size – normocyticLook at colorToo pale – hypochromicToo dark – hyperchromicNormal color - normochromic
14 Anemia: Morphologic Classification Classification based on red cell appearance suggests the etiology of the anemia:Normocytic anemia: normal size and appearanceMacrocytic anemia: cells larger than normalFolic acid deficiencyVitamin B12 deficiencyMicrocytic anemia: cells smaller than normal
15 Anemia: Morphologic Classification Hypochromic anemia: reduced hemoglobin contentHypochromic microcytic anemia: smaller than normal and reduced hemoglobin content
16 Increased Destruction (Peripheral) Too extensive destruction after cells have been formed and released from bone marrowGenerally find a high reticulocyte count – because more and more immature red blood cells are being released from bone marrow to compensate for the shortage in the peripheral circulation
17 Possible Causes of Increased Destruction Acquired hemolytic anemiaNormal red cells but unable to survive due to a “hostile environment”Attacked and destroyed by antibodiesDestruction of red cells by mechanical traumaPassing through enlarged spleen (splenomegaly)In contact with some part of artificial heart valve
18 Possible Causes of Increased Destruction Hemolytic Anemia (Genetic) Hereditary hemolytic anemiaGenetic abnormality prevent normal survival1. Abnormal shape: hereditary spherocytosis2. Abnormal hemoglobin: hemoglobin S (sickle hemoglobin); hemoglobin C; both found predominantly in persons of African descent3. Defective hemoglobin synthesis: thalassemia minor and major; globin chains are normal but synthesis is defective (Greek and Italian ancestry)4. Enzyme defects: glucose-6-phosphatase dehydrogenase deficiency predisposes to episodes of acute hemolysis
19 Distortion of red cells containing sickle hemoglobin when incubated under reduced oxygen tension.
20 Distortion of red calls containing sickle hemoglobin when incubated under reduced oxygen tension. Higher magnification view.
22 Decreased ProductionSomething is causing red blood cells not to be produced fast enoughGenerally the reticulocyte count is low or low normal. The reason is that if production is bad –reticulocytes (immature red blood cells) also cannot be produced adequately.
23 Classification of anemia based on the “bone marrow factory” concept
24 Iron-Deficiency Anemia Characteristic laboratory profileLow serum ferritin and serum ironHigher than normal serum iron-binding proteinLower than normal percent iron saturationTreatmentPrimary focus: learn cause of anemiaDirect treatment towards cause than symptomsAdminister supplementary ironExamplesInfant with a history of poor dietAdults: common cause is chronic blood loss from GIT (bleeding ulcer or ulcerated colon carcinoma)Women: excessive menstrual blood lossToo-frequent blood donations
27 Vitamin B12 Deficiency Anemia Vitamin B12: meat, liver, and foods rich in animal proteinFolic acid: green leafy vegetables and animal protein foodsBoth required for normal hematopoiesis and normal maturation of many other types of cellsVitamin B12: for structural and functional integrity of nervous system; deficiency may lead to neurologic disturbances
28 Vitamin B12 Deficiency Anemia Absence or deficiency of vitamin B12 or folic acidAbnormal red cell maturation or megaloblastic erythropoiesis with formation of large cells called megaloblastsMature red cells formed are larger than normal or macrocytes; corresponding anemia is called macrocytic anemiaAbnormal development of white cell precursors and megakaryocytes: leukopenia, thrombocytopenia
29 Most vitamin B12 deficiency symptoms are actually folate deficiency symptoms, since they include all the effects of pernicious anemia and megaloblastosis, which are due to poor synthesis of DNA when the body does not have a proper supply of folic acid for the production of thymine. When sufficient folic acid is available, all known B12 related deficiency syndromes normalize, save those narrowly connected with the vitamin B12-dependent enzymes
30 The total amount of vitamin B12 stored in body is about 2–5 mg in adults. Around 50% of this is stored in the liver. Approximately 0.1% of this is lost per day by secretions into the gut as not all these secretions are reabsorbed. Bile is the main form of B12 excretion, however, most of the B12 that is secreted in the bile is recycled via enterohepatic circulation
32 Pernicious AnemiaLack of intrinsic factor results in macrocytic anemiaVitamin B12 in food combines with intrinsic factor in gastric juiceVitamin B12 intrinsic factor complex absorbed in ileumCausesGastric mucosal atrophy; also causes lack of secretion of acid and digestive enzymesGastric resection and bypass: vitamin B12 not absorbedDistal bowel resection or disease: impaired absorption of vitamin B12 intrinsic factor complexMay develop among middle-aged and elderlyAssociated with autoantibodies against gastric mucosal cells and intrinsic factor
34 (b) Enlarged view of gastric pits and gastric glands Surface epithelium(mucous cells)GastricpitMucous neck cellsParietal cellChief cellGastricglandEnteroendocrine cell(b) Enlarged view of gastric pits and gastric glandsFigure 23.15b
35 Folic Acid Deficiency Anemia Relatively commonThe body has very limited stores, which rapidly become depleted if not replenished continuallyPathogenesisInadequate diet: encountered frequently in chronic alcoholicsPoor absorption caused by intestinal diseaseOccasionally occurs in pregnancy with increased demand for folic acid
36 Polycythemia Secondary polycythemia Primary/Polycythemia vera Reduced arterial O2 saturation leads to compensatory increase in red blood cells (increased erythropoietin production)Emphysema, pulmonary fibrosis, congenital heart disease; increased erythropoietin production by renal tumorPrimary/Polycythemia veraManifestation of diffuse marrow hyperplasia of unknown etiologyOverproduction of red cells, white cells, and plateletsSome cases evolve into granulocytic leukemia
37 Polycythemia Complications Treatment Clot formation due to increased blood viscosity and platelet countTreatmentPrimary polycythemia: treated by drugs that suppress marrow functionSecondary polycythemia: periodic removal of excess blood
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