Blood Testing 1

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    Blood Testing

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    Objectives:

    Define blood testing Significance of blood testing

    What is CBC?

    Normal Ranges

    Direct measurements

    Indirect measurements

    Anemias

    Classification

    Brief description

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    Blood Testing

    Blood Sample

    Complete Blood Count (CBC) WBCs (4000-10800 cells/mm3 )

    Plateltes (150,000-400,000 cells/mm3)

    RBCs (Male: 4.65.9, Female: 4.25.4 million cells/mm3 )

    Direct measurements RCC (Red cells Count)

    Hb Concentration (g/dl)

    Hematocrit (Hct) (Vol of RBCs / Vol of whole blood)

    Calculated from direct measurements MCH (Mean Corpuscular Hb Mass / RBC)

    MCV (Mean Corpuscular volume/RBC)

    MCHC (Mean Corpuscular Hb Conc. per Liter (RBC)

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    Blood Testing

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    Anemias

    Diagnostic Classification

    1. Kinetic Approach Production vs. destruction or loss

    Reticulocyte Production Index (RPI)

    2. Morphological Approach Red blood cell size

    Microcytic (Cells Smaller than normal size i.e. MCV< 80 fl)

    Normocytic (Cells Normal sized i.e. MCV = 80-100 fl)

    Macrocytic (Cells bigger than normal size i.e. > 100 fl)

    Concentration of Hb Hyperchromic (Increased Hb Concentration)

    Normochromic (Normal Hb Concentration)

    Hypochromic (Decreased Hb Concentration- cells palerthan normal)

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    Anemia Anemia means deficiency of hemoglobin in the blood

    Cause Too few red blood cells or Too little hemoglobin in the cells.

    Classification

    1. Aplastic or Hypoplastic Anemia

    2. Nutritional Anemia

    3. Hemolytic Anemia

    Aplastic or Hypoplastic Anemia Aplastic Loss of bone marrow function Hypoplastic Reduced bone marrow function

    Anemia due to lack of functioning of Bone Marrow or bonemarrow aplasia. Aplastic anemia patients have lower counts of all

    three blood cell types: termedpancytopenia. Characterstics:

    Decreased Red blood cells

    Diminished immunity Tendency to bleed

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    Aplastic Anemia

    Causes

    Drugs e.g. (Cytotoxic drugs, some anti convulscent drugs etc)

    Radiations (X-Rays)

    Chemicals (Benzene and its derivatives)

    Viral diseases

    Invasion of bone marrow (fibrosis or Leukemia)

    Hereditary Congenital hypoplastic anemia (or constitutional aplastic anemia) a

    type of aplastic anemia which is primarily due to a congenitaldisorder(defects or damage to a developing fetus). Examples include:

    Fanconi anemia (Caused by short Stature, Skeletal Abnormalities) Diamond-Blackfan anemia (Congenital Erythroid Aplasia- Characterized by anemia

    with decreased erythroid progenitors in bone marrow)

    Acquired Pure Red cell Aplasia (PRCA)

    Sideroblastic anemia (Sideroachrestic anemia)1 The body has iron available, butcannot incorporate it into hemoglobin

    Myelophthisic anemia2 (Normal marrow space is replaced by nonhematopoietic orabnormal cells). Cause e.g. tumors

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    Nutritional Anemia

    1. Nutritional Anemia Type of anemia that can be directly attributed to nutritional

    disorders Iron Deficiency Anemia (Microcytic) Megaloblastic Anemia (Macrocytic)

    Iron Deficiency Anemia (Microcytic) Sideropenic Anemia, cells are smaller in size and paler in colour

    Causes: Parasitic Infections

    e.g. Hook worms Normal Requirement, Deficient intake

    Weight reducing diets, Vegetarian diets High Requirements, Normal or deficient intake

    Pregnancy Chronic blood loss (peptic ulcers, menorrhagia,

    haemorrhoids, GI carcinoma) Low iron absorption or malabsorption

    GI abnormalities Increase in pH (removal of part of stomach)

    Loss of absorbing surface area (intestine removal)

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    Nutritional Anemia

    Megaloblastic Anemia (Macrocytic) Inhibition of DNA synthesis during erythropoiesis

    Large, immature RBCs (Megaloblasts)

    Characterstics: Immature, fragile cells,

    Life span b/w 40-50 days

    Size larger than normal cells,

    Might contain nucleus

    Causes: Hypovitminosis (B12, B9)

    Antimetabolites that inhibit DNA synthesis e.g.

    Purine & Pyrimidine Antagonists (6-Mercaptopurine,

    Cytosine)

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    Nutritional Anemia Vitamin B12 deficiency Anemias

    Deficient intake in diet (vegetarians)

    Deficient intrinsic factor (Gestractomy & Pernicious Anemia) Selective B-12 malabsorption (removal of Terminal ileum) Increased needs: pregnancy, infant, rapid cellular proliferation.

    Pernicious Anemia Most common form of Vitamin B12 deficiency Anemias Occurs more often in females

    Cause: Autoimmune disease results in production of antibodies

    directed against Intrinsic Factor (IF)*andparietal cells instomach.

    Impaired absorption of vitamin B-12 due to the absence ofintrinsic factor as a result of loss of gastric parietal cells.

    Treatment IV injections of Vitamin B-12

    Complications of B-12 deficiency anemia Appear before the signs of anemia Includes Irreversible neurological damage commonly in spinal

    cord (B-12 needed for formation and maintenance of Myelin byschwann cells)

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    Nutritional Anemia

    Vitamin B9 (Folic Acid) deficiency Anemias

    Deficiency causes megaloblastic anemia but notassociated with neurological damage

    Causes Dietary Deficiency e.g. in infants absence or delay of

    establishing mix diets. Alcoholism Anorexia (Loss of appetite) Pregnancy (Raised requirement)

    Malabsorption from jejunum (tropical sprue) Interference with Folate metabolism

    Folic acid Antagonists (Methotrexate)

    Trimethoprim (Antimicrobial agent)

    Deficiency Causes neural tube defects duringpregnancy*

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    Folic acid Metabolism

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    Hemolytic Anemias

    1. Hemolytic Anemias

    Occur when RBCs are destroyed in circulation or removedprematurely from circulation because of abnormal cells oroveractive spleen

    Hereditary or Congenital hemolytic AnemiasHereditary or Congenital hemolytic Anemias Hemolytic anemia which is primarily due to congenital

    disorders Types include:

    Genetic conditions of RBC Membrane Hereditary spherocytosis (Sphere shaped RBCs)

    Hereditary elliptocytosis (Elliptical RBCs) (Also known as ovalocytosis)

    Genetic conditions of RBC metabolism (enzyme defects) Glucose-6-phosphate dehydrogenase deficiency (G-6-PD)

    Pyruvate kinase deficiency (No energy)

    Hemoglobinopathies / genetic conditions of hemoglobin Sickle cell anemia

    Thalassaemia

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    Hemolytic Anemias

    Acquired hemolytic anemia

    No familial or racial factors have been identified Causes:

    Chemical Agents: These agents may cause excessive or early hemolysis

    Some Drugs, if taken for long time & in large doses e.g.

    Sulphonamides

    Chemicals faced in general or work environment e.g.

    lead, arsenic compounds

    Toxins produced by certain microbes.

    e.g. streptococcus pyogenes

    Autoimmunity Production of antibodies against self antigens

    Blood transfusion Reactions Parasitic Disease e.g. malaria

    Physical damage to cells by e.g. artificial heart valves, dialysismachines.