ANEMIAS

Anemia: Deficiency of hemoglobin in the blood. Causes: Too few RBCs. Too little hemoglobin in cells Decreased packed cell volume. This may be due to: decreased production of RBCs. increased destruction.

Classification of anemia: Morphological classification. 1. normocytic normochromic anemia. 2. macrocytic normochromic anemia. 3. macrocytic hypochromic anemia. 4. Microcytic hypochromic anemia. Etiological classification. 1. hemorrhagic anemia. 2. hemolytic anemia. 3. nutritional deficiency anemia. 4. aplastic anemia. 5. anemia of chronic disease.

Morphological classification: Depending upon size, color volume and number of cells. 1.Normocytic normochromic anemia: Size and colour are normal. Less in number. 2. Macrocytic normochromic anemia: Larger in size. Normal color. RBC count is less 3. Macrocytic hypochromic anemia: Larger pale RBCs. 4. Microcytic hypochromic anemia: Smaller pale RBCs.

Etiological classification:

1.Hemorrhagic anemia: Occurs in both acute and chronic hemorrhagic conditions. After acute hemorrhage: Plasma replaced in 24 hours. Low concentration of RBCs. RBC concentration return to normal in 4-6 weeks. Less RBCs -> hemodilution. Normochromic normocytic RBCs. Hypoxia stimulates RBCs production. Chronic hemorrhage: Loss of blood by internal/ external bleeding. Enough iron can not be absorbed from intestines. Small RBCs with little hemoglobin. Microcytic hypochromic RBCs.

2. Hemolytic anemia: Fragile cells rupture easily while passing through spleen and capillaries. Number of cells might be normal or greater than normal but short life span. Destruction faster than formation. Classification: A. extrinsic hemolytic anemia. B. intrinsic hemolytic anemia. Types: Hereditary spherocytosis. Sickle cell anemia. Erythroblastosis fetalis. Thalassemia.

A: Extrinsic hemolytic anemia. Destruction of RBCs by external factors. Antibodies, chemicals and drugs. Autoimmune hemolytic anemia. Hereditary spherocytosis and Erythroblastosis fetalis. B: Intrinsic hemolytic anemia. Destruction due to defective RBCs. Unhealthy short lived RBCs Often inherited E.g sickle cell anemia, thalassemia. Cells are fragile and susceptible for hemolysis.

Sickle cell anemia: Have abnormal Hb S. with faulty beta chains. Inherited blood disorder. Exposure to low oxygen precipitates it into crystals. They elongate the cells into sickle. Damage cell membrane and cause serious anemia. In children, sickled cells block blood vessels and cause infarction. Hand and foot syndrome. Sickle cell disease crisis: Low oxygen tension in tissues causes sickling rupturing RBCs and further causing oxygen tension. Serious decrease in RBCs and eventually death.

Thalassemia: Inherited disorder characterised by abnormal hemoglobin. Types: Alpha thalassemia Beta thalassemia. (commom) Defective globin gene with imbalanced chains. Disturbed erythropoisis.

Alpha thalassemia: Beta thalassemia: Fetal life or infancy. Alpha chains are less, absent or abnormal. Children= gama chains excess. Adults= beta chains are in excess. Defective erythropoiesis and haemolysis. Infants are stillborn or die immediately. Beta thalassemia: Beta chains are less, absent or abnormal. Excess alpha chains. Defective erythropoiesis and hemolysis.

Hereditary spherocytosis: Small, spherical cells lacking normal, loose baglike cell membrane. Ruptured while passing through sphlenic pulp and tight vascular beds.

Erythroblastosis fetalis: Rh-positive RBCs of fetus attacked by Rh- negative antibodies of mother. Rh-positive cells become fragile and rupture making child seriously anaemic.

3:Nutritional deficiency anemia: Substances necessary for erythropoiesis are deficient. Iron, proteins, vitamins c and B12 and folic acid. Types: A: Protein deficiency anemia: Synthesis of hemoglobin is reduced. Macrocytic hypochromic RBCs. B: Iron deficiency anemia. Microcytic hypochromic RBCs. Symptoms: Brittle nails, atrophy of papillas in tongue and dysphagia.

C: pernicious anemia/ Addison's disease Deficiency of Vit B 12. Atrophy of gastric mucosa due to autoimmune destruction of parietal cells. Decreased production of intrinsic factor and poor absorption of Vit B12. Macrocytic normochromic/ hypochromic RBCs. Associated with Addison's disease or thyroid disorders. Symptoms: Paresthesia Progressive weakness. Ataxia. Lemon yellow color of skin. Red sore tongue.

D: Megaloblastic anemia: Folic acid. Slow reproduction of erythroblasts in bone marrow. Defective DNA synthesis. Large, odd shaped cells. Megaloblastic hypochromic RBCs. Neurological disorders are not present.

4: Aplastic anemia: Bone marrow aplasia means lack of functioning bone marrow. Bone marrow reduced and replaced by fatty tissues. Gama ray radiation after nuclear blast can cause complete destruction of bone marrow. X-ray treatment. Industrial chemicals. Drugs. Lethal anemia. Tuberculosis. Viral infections like hepatitis and HIV infections. Normocytic normochromic RBCs.

5. Anemia of chronic disease: Second most common type. Disturbed iron metabolism or resistance to erythropoietin action. Develops after few months of sustained disease. Normocytic normochromic RBCs. Causes: Non infectious inflammatory diseases e.g rheumatoid arthritis. Tuberculosis. Renal failure. Neoplastic disorders.

Effects on circulation: Viscosity of blood falls to 1.5 times that of water in severe anemia. Blood flow through the capillaries and heart increases thus increasing cardiac output. Hypoxia due to diminished transport of oxygen causes dilation of peripheral vessels. Increase in blood return to heart and cardiac output and increased pumping workload on heart. Increased cardiac output overcomes reduced oxygen supply. Exercise-> extreme hypoxia -> acute cardiac failure.

Signs and symptoms: Skin and mucous membrane. Cardiovascular system. Pale thin and dry skin. Early greyness of hair. Brittle easily breakable nails. Cardiovascular system. Tachcardia, heart is hypertrophied,velocity of blood flow is increased. Respiration. Increased ratee and flow of respiration.SOB and dyspnea. Digestion Anorexia, nausea, vomiting, abnormal discomfort, constipation. Metabolism Rate is increased. Kidney Albuminuria. Reproductive system Menstural cycle s distured. Neuromuscular system. Increased sensitivity to cold, headache, lack of concentration, Restlessness, irritability, dizziness and vertigo. Weakness and fatigue

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