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Blood Testing

 Define blood testing
 Significance of blood testing
 What is CBC?
 Normal Ranges
 Direct measurements
 Indirect measurements
 Anemias
 Classification
 Brief description
Blood Testing
 Blood Sample
 Complete Blood Count (CBC)
 WBC’s (4000-10800 cells/mm3 )
 Plateltes (150,000-400,000 cells/mm3)
 RBC’s (Male: 4.6–5.9, Female: 4.2–5.4 million cells/mm3 )
 Direct measurements
 RCC (Red cells Count)

 Hb Concentration (g/dl)

 Hematocrit (Hct) (Vol of RBC’s / 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)

Blood Testing

 What is anemia?
 Diagnostic basis of classification
 Types and Classification
 Etiology or Causes of disease
 Compare and contrast different types of
 Polycythemia
 Why polycythemia occurs
 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 paler
than normal)
 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 bone
marrow aplasia. Aplastic anemia patients have lower counts of all
three blood cell types: termed pancytopenia.
 Characterstics:
 Decreased Red blood cells
 Diminished immunity
 Tendency to bleed
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 congenital disorder
(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, but
cannot incorporate it into hemoglobin
 Myelophthisic anemia2 (Normal marrow space is replaced by nonhematopoietic or
abnormal cells). Cause e.g. tumors
Nutritional Anemia
1. Nutritional Anemia
 Type of anemia that can be directly attributed to nutritional
 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)
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,
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)* and parietal cells in
 Impaired absorption of vitamin B-12 due to the absence of
intrinsic 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 by
schwann cells)
Nutritional Anemia
 Vitamin B9 (Folic Acid) deficiency Anemias
 Deficiency causes megaloblastic anemia but not
associated 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 during
Folic acid Metabolism
Hemolytic Anemias
1. Hemolytic Anemias
 Occur when RBCs are destroyed in circulation or removed
prematurely from circulation because of abnormal cells or
overactive spleen
 Hereditary or Congenital hemolytic Anemias
 Hemolytic anemia which is primarily due to congenital
 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
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, dialysis