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Anemia
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Anemia means deficiency of hemoglobin in blood either due to few RBCs in blood or too little hemoglobin in the cells.
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Anemia anemia is a functional inability of the blood to supply the tissue with adequate O2 for proper metabolic function. anemia is not a disease, but rather the expression of an underlying disorder or disease.
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Anemia Quantitative and/or qualitative deficiency of RBC ↓ No of RBCs
↓ Amount of Hb ↓ O2 carrying capacity
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Anemia Anemia may develop:
When RBC loss or destruction exceeds the maximal capacity of bone marrow RBC production When bone marrow production is impaired
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Anemia Various diseases and disorders are associated with anemia include: Nutritional deficiencies External or internal blood loss Increased destruction of RBCs Ineffective or decreased production of RBCs Abnormal hemoglobin synthesis Bone marrow suppression by toxins, chemicals, radiation, Infection Bone marrow replacement by malignant cells
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Normal RBCs
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Types of Anemia Blood loss anemia Aplastic anemia Megaloblastic anemia
Hemolytic anemia
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Classification of Anemia
Nutritional anemia Pernicious anemia Aplastic anemia Renal anemia Blood loss anemia Hemolytic anemia Congenital anemia
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Classification of anemias
Anemias may be classified morphologically based on the average size of the cells and the hemoglobin concentration into: Macrocytic Normochromic, normocytic Hypochromic, microcytic
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Nutritional Anemia Iron deficiency anemia ↓ intake of iron
↓ absorption of iron Chronic blood loss ↑ demand of iron (e.g. pregnancy) No of cells may be normal ↓ iron → ↓ Hb → ↓ size of cells (microcytic) ↓ iron → ↓ Hb → ↓ colour (Hypo chromic) (brittle spoon shaped nails- koilonychias- is a common feature)
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Microcytic RBC
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Micocytic Hypochromic anemia
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Nutritional Anemia Magaloblastic anemia ↓ dietary Vitamin B12
↓ intrinsic factor ↓Folic acid Maturation failure Cells- bigger ( megaloblasts) Cell membrane – fragile → easy rupture Hb contents - normal
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Pernicious Anemia Maturation failure anemia
↓ Vit. B12 due to poor absorption from GIT ↓ intrinsic factor in the stomach Autoimmune destruction of parietal cells Atrophy of gastric mucosa Gastrectomy Megaloblastic anemia Cell membrane fragile → easy rupture
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Macro ovalocyte
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Aplastic Anemia Failure of bone marrow to produce RBCs
Aplasia of the bone marrow Bone marrow may be destroyed Radiation e.g X-rays, gamma rays, nuclear bomb explosion Chemicals e.g.benzene, arsenic, chloramphenicol. quinine, gold salts, benzene, radium etc Bacterial toxins Tuberculous invasion HIV infections Invasion of bone marrow by cancer cells Chemotherapy for cancer
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Renal Anemia Renal diseases (CRF) → ↓ Erythropoietin
↓ Erythropoietin → → ↓ Production of erythrocytes
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Hemorrhagic Anemia Acute blood loss anemia Chronic blood loss anemia
Normocytic Normochromic ↓ RBC count ↓ Hb/cmm of blood Chronic blood loss anemia Microcytic Hypochromic
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Normocytic RBC
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Normochromic & Hypochromic cells
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Hemolytic Anemia Erythroblastosis Fetalis Sickle cell anemia
Congenital spherocytosis Hemolysis due to Infections like malaria, septicemia Chemicals like lead, hemolysins Agglutinins (Jaundice is common feature in hemolytic anemia)
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Erythroblastosis fetalis
Rh negative mother Rh positive fetus Mother exposed to positive cells during first delivery Antibodies formed against positive cells Severe anemia in subsequent fetus Blast cells in the blood
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Erythroblastosis fetalis
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Erythroblastosis fetalis
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Sickle cell anemia Sickle-cell anemia – results from a defective gene coding for an abnormal hemoglobin called hemoglobin S (Hb S) Alpha chains are normal, beta chain is defective Hb S has a single amino acid substitution in the beta chain Valine is substituted for Glutamic acid at position 6 Low oxygen → Precipitation and crystallization of Hb S → Sickling & hemolysis of RBC Sickle cell disease crises – a vicious cycle Hb S precipitate and cells aggregate may block small blood vessels leading to necrosis
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Sickle cells
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Hereditary spherocytosis
One of the congenital anemia RBC are spherical instead of being biconcave Decreased deformability Cannot withstand compression Hemolysis in tight vascular beds
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Spherocytes
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Thalassemia Cooley’s anemia or Mediterranean anemia
Impaired α or β chain synthesis due to genetic abnormality α thalassemia Decreased, defective or absent α chain β thalassemia (more common) Decreased, defective or absent β chain
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Effects of anemia ↓ viscosity Easy flow of blood
↑ blood flow in all the tissues ↓O2 →vasodilatation ↑ COP ↑ work load on heart May → cardiac failure
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Common clinical features in anemia
Pale skin, lips, conjunctiva, mucous membrane, koilonychias etc Increased HR, COP, murmurs Increased Respiration rate, breathlessness Anorexia, nausea , vomiting, Headache, lack of concentration, irritability, lethargy, lack of energy, fatigue Menstrual disturbances, menorrhagia, oligomenorrhea, amenorrhea
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Polycythemia An increase in RBC mass is called polycythemia and it may lead to an increase in blood viscosity. Polycythemia Relative polycythemia due to decreased plasma volume e.g. in dehydration. Absolute polycythemia due to actual increase in RBC mass. This may occur in disorders that prevent adequate tissue oxygenation
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Polycythemia Secondary polycythemia
Individuals living at high altitudes have increased RBC levels because of the decreased partial pressure of O2 at high altitudes which leads to decreased O2 saturation. Polycythemia vera Uncontrolled proliferation/production/cancer of RBC
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Choose the best response, During the middle trimester of gestation, which is the main organ for production of RBCs a)Bone marrow b)Spleen c)Liver d)Lymph nodes
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Each gram of pure hemoglobin combines with a)15 ml of oxygen 2)1
Each gram of pure hemoglobin combines with a)15 ml of oxygen 2)1.34 ml of oxygen 3)20 ml of oxygen 4)2.24 ml of oxygen
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Among Plasma proteins 80% of osmotic pressure is exerted by
Albumin Globulin fibrinogen
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After 20 years of age, red cells are produced in the
Marrow of long bones Liver Vertebrae, sternum and ribs
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Chronic blood loss leads to which type of anemia a) megaloblastic anemia b)microcytic hypochromic anemia c) normocytic, normochromic anemia
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Megaloblastic anemia is due to which of the following a) folic acid deficiency b) Iron deficiency c)Vitamin C deficiency
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In sickle cell anemia, a)Alpha chains are faulty b)Beta chains are faulty c)Gamma chains are faulty
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