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Hematology is the branch of medicine that studies blood and blood-forming tissues. It includes the study of blood cells, hemostasis, and diseases of the blood. The document discusses the anatomy and physiology of the hematologic system, the composition and function of blood components such as plasma, red blood cells, white blood cells, and platelets. It also covers hematologic tests, blood groups, common types of anemia such as iron deficiency anemia and anemia of chronic disease, and their causes and symptoms.

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Hematology By Mr. Mwandalesa M.(BSc.CS)
Hematology • Branch of medicine that studies blood cells and blood-forming tissue • Includes hemostasis (the process of stopping bleeding) • Tests can detect diseases such as • Anemia • Leukemia • Hemophilia
Anatomy and physiology • Hematologic system consists of the blood and the sites where the blood is produced. • Blood consists of plasma and blood cells. • Because blood cells have a short lifespan, hematopoiesis (production od blood cells in the bone marrow) is needed. 3
Function of Blood • Transporting fluids such as: • Nutrients from digestive tract • O2 from lungs • Waste from cells • Hormones • Aids in heat distribution • Regulates acid-base balance
Composition of Blood • Plasma: liquid portion of blood w/out cells • Contains all of the following • Water Nutrients • Electrolytes Metabolic waste product • Hormones Vitamins and enzymes • Plasma proteins such as fibrinogen, albumin and globulin
Composition of Blood: Erythrocytes • Red blood cells are responsible for: • Transport of oxygen and nutrients • Removal of waste and CO2 from the cells • Distribution of heat • Hemoglobin: • The O2 carrying potential. • Has 4 subunits, each contains a hem attached to a globin chain. • Iron is present in the hem, hem is bind to the oxygen •
Composition of Blood: Leukocytes • WBC are responsible for: • Phagocytosis – to engulf and absorb waste material and harmful microorganisms in the blood stream and tissues • Synthesis of antibody molecules • Inflammation process • Production of heparin – component found in lung and liver tissue which have the ability to prevent clotting of blood.
Composition of Blood: Leukocytes (cont.) • Types of Leukocytes • Granulocytes • Neutrophils • Eosinophils • Basophils • Agranulocytes • Lymphocytes • Monocytes
Composition of Blood: Thrombocytes • Platelets – the smallest of the solid components of the blood • Responsible for the clotting process • Coagulation: term for clotting • Embolism: a blood clot which is moving through the body
INTEPRETATION OF A HEMOGRAM • The 8 parameter cell counter will give the following: 1. WBC count: white blood cell count 2. RBC count: red blood cell count 3. Hb: Hemoglobin 4. Hct: Hematocrit / Packed cell volume (PCV) 5. MCV: Mean cell volume 6. MCH: Mean cell hemoglobin 7. MCHC: Mean cell hemoglobin concentration 8. RDWt: red blood cell distribution width • In addition to these above parameters the 18 parameter cell counter also has White blood cell Differentials: Neutrophils count and percentage, Lymphocyte count and percentage, Monocytes count and percentage, Eosinophil count and percentage, Basophils count and percentage and Pct: Plateletcrit
WHITE BLOOD CELL COUNT • This is the number of white blood cells in 1 cubic mm of whole blood. • The normal value is 4.0-11.0 million cells per microliter. • On its own is not a useful parameter RED BLOOD CELL COUNT • This is the number of erythrocytes in 1 cubic mm of whole blood. • The normal values include: Men= 4.5-6.0 million cells per microliter and Women= 3.9-5.0 million cells per microliter HEMOGLOBIN • Normal hemoglobin values: Men= 13.5-17.5 g/dl and Women= 11.5- 16.0 g/dl HEMATOCRIT/ PACKED CELL VOLUME (PCV) • Normal PCV is Men= 0.4-0.54 L/L and Women= 0.36-0.47 L/L MEAN CELL VOLUME (MCV) • Indicates the average volume of a single RBC. • It is expressed in cubic microns. • The normal value is 80-96 fL
MEAN CELL HEMOGLOBIN (MCH) • This gives an idea about the average hemoglobin content in a single red cell. • Normal range varies between 27 and 32 pico grams. RED BLOOD CELL DISTRIBUTION WIDTH (RDW) • This shows the variation in red cell size • The normal value is 11-15% • In iron deficiency there is increased RDW. • In beta-Thalassaemia trait,the RDW is usually normal. PLATELETS • The normal platelet count is 150-400 (109/L) DIFFERENTIAL COUNT • Neutrophils= 3-6 (109/L),Lymphocytes= 1.5- 4 (109/L), Monocytes= 0.3- 0.6 (109/L), Eosinophils= 0.15-0.30 (109/L) and Basophils= 0-0.1 (109/L) •
Definitions • Anticoagulant: an agent that prevents the clotting of blood. • Examples are EDTA, Citrate and Heparin • Capillary: small blood vessel that connects arterioles and venules • Hematoma: a subcutaneous mass of blood at a venipuncture site • Hemoglobin: the oxygen carrying molecule of red blood cells • Hemolysis: the breakdown of red blood cells, with the release of hemoglobin into the plasma or serum. Cannot use hemolyzed samples in lab tests
• THROMBOCYTOPENIA - Decrease in platelet count below 150 000/cu mm of blood • Thrombocytosis - Increase in platelet count over 450 000/cu mm of blood • Leukocytopenia – wbc less than the normal range in the blood • Leukocytosis - wbc above the normal range in the blood • PANCYTOPENIA – it is combination of anemia, thrombocytopenia and leukocytopenia
BLOOD GROUPS
Blood Types • Four Major Groups • A B AB O • Blood types are inherited from your parents • Antigen is present on the red blood cell; typing is done w/rbc • Antibody is present in the plasma; antibody screening done on plasma
Blood Types • O negative • Universal donor • It carries no antigen • AB positive • Universal recipient • It carries no antibodies in the plasma • 43% of population are O, 42% A, 12% B and 3% AB
ABO & Rh compatibility • Blood is classified according to the presence of these antigens: • Group A contains antigen A • Group AB contains both antigens • Group O contains neither antigen • Blood plasma contains antibodies against the opposite antigen: • A person with Type A blood has antibodies against the B antigen • A person with Type AB blood has no antibodies (Universal Recipient) • A person with Type O blood has antibodies against the A, B & AB antigens (Universal Donor)
ABO & Rh compatibility • People with Rhesus factors in their blood are classified as "Rh positive" • People without the factors are classified as "Rh negative" • Rh negative persons form antibodies against the Rh factor if they are exposed to Rh positive blood • Conclusion: • Blood transfusion between incompatible groups causes an immune response against the cells carrying the antigen, resulting in transfusion reaction
ANEMIA
Anemia • Is a condition in which the hemoglobin concentration is lower than normal (low RBCs). • As a result, the amount of oxygen delivered to the tissue is lower than normal. • It is not a disease but a sign of underlying disorders.
Causes of Anemia • Iron deficiency • Vitamin B12 deficiency • Infections*: HIV, tuberculosis, malaria, schistosomiasis, hookworm, hepatitis • Drugs: isoniazid, chloramphenicol, alcohol, zidovudine, hydroxyurea • Chronic disease*: renal and liver disease, rheumatologic diseases, hypothyroidism  These are common causes of anemia in adults in Africa.
Common signs and symptoms of anemia • Easy fatigue and loss of energy • Unusually rapid heart beat, particularly with exercise • Shortness of breath and headache, particularly with exercise • Difficulty concentrating • Dizziness • pale skin • Leg cramps • Insomnia
Classifications of Anemia • Etiological clarification • Morphological clarification • Anemia severity classification
Etiological classification 1.Nutrition deficiency anemia • Iron deficiency anemia • Vitamin B12 deficiency anemia 2.Increased RBC destruction • Hemolytic anemia 3.Increased Blood loss • Hemorrhagic anemia 4.Bone marrow suppression (aplastic anemia ) • Anemia of chronic disease • Drug induced Anemia 5.Hereditary classification • Sickle cell Anemia • Thalassemia
Morphological Classification • Microcytic Anemia • Normocytic Anemia • Macrocytic Anemia
Morphological Classification Normochromic, normocytic anemia (normal MCHC, normal MCV). • These include: 1. hemolytic anemias (those characterized by accelerated destruction of rbc's) 2. anemia of acute hemorrhage 3. aplastic anemias (those characterized by disappearance of rbc precursors from the marrow) Hypochromic, microcytic anemia (low MCHC, low MCV). • These include: 1. iron deficiency anemia 2. thalassemias 3. anemia of chronic diseases Normochromic, macrocytic anemia (normal MCHC, high MCV). • These include: 1. vitamin B12 deficiency 2. folate deficiency
Anemia severity classification Populations Mild Moderate Severe Pregnant women 10 – 10.9 7- 9.9 <7 Non pregnant women 11 -11.9 8 – 10.9 <8 Men 11 – 12.9 8 -10.9 <8
TYPES OF ANEMIA
1. IRON DEFICIENCY ANEMIA • This is the most common type of anemia worldwide. • Iron deficiency anemia occurs when the body iron stores become inadequate for the need of normal RBC production. • It is due to decreased levels of iron. • Decreased iron leads to decreased heme and hemoglobin thus resulting in a microcytic anemia. • Iron deficiency anemia is a manifestation of disease, not by itself a complete diagnosis Anemia People with an iron deficiency may experience these symptoms: • A hunger for strange substances such as paper, ice, or dirt (a condition called pica) • Upward curvature of the nails, referred to as koilonychias • Soreness of the mouth with cracks at the corners
IRON METABOLISM Irons is consumed in heme (meatderived) and non-heme (vegetablederived) forms. • Absorption of heme occurs in the duodenum while that of non-heme occurs in the proximal jejunum • Enterocytes have heme and non-heme (DMT1) transports. The heme form is more readily absorbed. • Absorption is facilitated by: stomach acidity (keeps iron in reduced ferrous state Fe2+ and not ferric state Fe3+), Vitamin C (Ascorbic acid), Citrates. • Absorption is limited by: phosphates, oxalates, tannates (tea) and pyrates (plant food) • Enterocytes transport iron across the cell membrane into blood via ferroportin. • Transferrin transports iron in the blood and delivers it to liver and bone marrow macrophages for storage.
2. ANEMIA OF CHRONIC DISEASE • This is associated with chronic inflammation (e.g. endocarditis or autoimmune conditions) or malignant disease. • It is the most common type of anemia in hospitalized patients. • Etiologies: Infectious: TB, lung abscess, osteomyelitis, pneumonia, bacterial endocarditis. Non-infectious: rheumatoid arthritis, lupus, connective tissue disease, sarcoidosis, Crohn’s disease, malignancy (carcinoma, lymphoma, sarcoma).
PATHOGENESIS • Chronic disease results in production of acute phase reactants from the liver, including hepcidin • Hepcidin sequesters iron in storage sites by (1) limiting iron transfer from macrophages to erythroid precursors  (2) suppressing erythropoietin (EPO) production. • The aim is to prevent bacteria from accessing iron, which is necessary for their survival. • Decreased availability of iron results in microcytic anemia. • Other cytokines produced during inflammation reduce life span of RBC (80 days) rendering erythropoietin inadequate.
• The term AA is first used by Ehrlich in 1888 • Describes a disorder of unknown etiology characterized by • pancytopenia with • hypo or acellular bone marrow. • It is one of the stem cell disorders. 3. Aplastic Anemia (AA)
Classification of AA Acquired AA 1. Idiopathic 2. Radiation 3. Drugs/chemicals • Chloramphenicol • NSAID: (phenylbutasone,indomethacin,gold etc) • Oral hypoglycemic drugs (chlorpropamide,tolbutamide) • Antithyroid drugs, phenothiazines, antimalarials, diuretics,antiepileptics – Rubella – CMV – HIV – Parvovirus – Brucellosis – Tbc – Toxoplasmosis
Infections • Hepatitis • E.Barr virus • Rubella • CMV • HIV • Parvovirus • Brucellosis • Tbc • Toxoplasmosis Immunologic disorders • SLE, eosinophilic fasciitis • Graft- versus- Host Disease • Hypoimmunoglobulinemia • Thymoma
Clinical Features of AA • History: • Bleeding • Symptoms of anemia • Infections • Drugs, chemicals or other etiologically important exposures have to be questioned. • Physical exam: • Petechiae, ecchymosis • Retinal bleeding • Pallor • Fever and other signs of infection • Presence of lymphadenomegaly and /or splenomegaly are unusual (indicate other diagnoses).
• LAB: • Pancytopenia • Reticulocytes: Low or absent • RBC: normochrome-normocytic,or slight macrocytosis • Neutropenia and relative lymphocytosis • Red and white cell precursors are almost neverseen in the peripheral smear • Serum iron is increased • Bone marrow : • Aspiration; Dry tap • Biopsy; all three cell lines are reduced or absent, raplaced by fatty tissue, residual lymphocytes, increased iron stores,rarely hot spots of hematopoesis
4. HEMOLYTIC ANEMIA • Due to red cell destruction and increased red cell turnover. Bone marrow is able to compensate 5 times the normal rate. • Clinical features: jaundice, hepatosplenomegaly, dark urine. • Etiology can be classified as: 1. Congenital Hemoglobinopathies: sickle cell disease*, thalassemia Enzymopathies: G6PD deficiency*, Pyruvate kinase deficiency Membranopathies: hereditary spherocytosis, eliptocytosis In born errors of metabolism 2. Acquired Microangiopathic hemolytic anemia: TTP, HUS, DIC, eclampsia, HELLP syndrome Autoimmune hemolytic anemia Infections: Malaria
SICKLE CELL DISEASE • A severe hemolytic anemia caused by a point mutation resulting in the substitution of glutamate for valine on the 6th position of the beta globin chain forming HbS. • When deoxygenated, HbS molecules polymerize into long fibers and cause the red blood cells to sickle
Normal  Disc-Shaped  Deformable  Life span of 120 days Sickle  Sickle-Shaped  Rigid  Lives for 20 days or less
SICKLE CELL DISEASE Symptoms may not appear until 6 months of age Mortality rate children < 3 Years old is 15-35% Early Diagnosis: Amniocentesis, Newborn Screen
Signs & Symptoms Initially: fever & anemia at 6 mos  Pallor  Fatigue  SOB  Irritability  Jaundice
severe anemia causes crises • Vasocclussive crisis • Aplastic crisis • Splenic sequestration • Hemolytic crisis
1. VASO-OCCLUSIVE CRISES • An early presentation may be acute pain in the hands and feet: dactylitis due to vaso-occlusion of the small vessels. • (hand-foot syndrome) • Severe pain in other bones e.g. femur, humerus, vertebrae, ribs, pelvis occurs in older children/adults. • Attacks vary from person to person. Fever often accompanies the pain. • Triggers of vaso-occlusive crisis include: Hypoxemia: may be due to acute chest syndrome or respiratory complications, Dehydration: acidosis results in a shift of the oxygen dissociation curve and Changes in body temperature
dactylitis priapism
Priapism • Prolonged erection of the penis, usually without sexual arousal • Commonly occurs in children and adolescents with SS or SC ( • Treatment is difficult 1. Opioid pain medication 2. Intravenous fluids 3. Aspiration and irrigation of the corpus cavernosum 4. Surgery 5. Blood Transfusions 6. Impotence with severe disease or recurrent episodes
2. BONE MARROW APLASIA (APLASTIC CRISIS) • This most commonly occurs following infection with erythrovirus B19 (previously called Parvovirus B19) which invades proliferating erythroid progenitors. • There is a rapid fall in hemoglobin with no reticulocytes in the peripheral blood, because of the failure of erythropoiesis in the marrow
3. SPLENIC SEQUESTRATION • Vaso-occlusion produces an acute painful enlargement of the spleen. • There is a splenic pooling of red cells and hypovolemia, leading in some to circulatory collapse and death. • There will be severe hemolysis, rapid splenomegaly and a high reticulocyte count. • The condition occurs in childhood before multiple infarctions have occurred. • Multiple infarctions lead to a fibrotic non-functioning spleen
SPLENIC SEQUESTRATION  Sudden trapping of blood within the spleen  Usually occurs in infants under 2 years of age with SS  Spleen enlarged on physical exam, may not be associated with fever, pain, respiratory, or other symptoms  Circulatory collapse and death can occur in less than thirty minutes
Treatments For Splenic Sequestration • Intravenous fluids • Maintain vascular volume • Cautious blood transfusion • Treat anemia, sequestered blood can be released from spleen • Spleen removal or splenectomy • If indicated
4. HEMOLYTIC CRISIS • Red cell half life is reduced to 10 – 20 • This results into rapid destruction rbc leading anemia CLINICAL FEATURES • Anaemia • Jaundice • Gallstones • Cardiomegaly:CHF • Leg ulcers • Marrow hyperplasia • Poor physical development • Delayed maturation • Subjective symptoms
Chronic Complications  Anemia/Jaundice  Brain Damage/Stroke  Kidney failure  Decreased lung function  Eye disease (bleeding, retinal detachment)  Leg ulcers  Chronic pain management  Stroke
Thalassemia • Heterogenous group of genetic disorders which results from a reduced rate of synthesis of alpha (coded for by 4 genes) or beta chains (coded for by 2 genes) of hemoglobin. • Changes in normal ratio results in each of the disorders. • Due to inherited mutations carriers are protected against Plasmodium falciparum malaria. • Thalassemia are divided into alpha and beta thalassemia. • Normally there are 3 types of hem HbA (2 alpha, 2 beta) HbA2 (2 alpha and 2 delta). HbF (2alpha, 2 gamma)
ALPHA THALASSEMIA • Alpha thalassemia is usually due to gene deletion, normally 4 alpha genes are present on chromosome 16. • One gene deleted- asymptomatic • Two gen deleted- mild anemia with slightly increased RBC count BETA THALASEMMIA • Usually due to gene mutations (point mutations in promoter or splicing sites) seen in individuals of African and Mediterranean descent. • Two beta genes are present on chromosome 11, mutations result in absent or diminished production of the beta-globin chain. • Beta thalassemia minor is the mildest form of the disease and is usually asymptomatic with an increased RBC count
Leukemia Definition It is a group of malignant disorder, affecting the blood and blood –forming tissue of the bone marrow lymph system and spleen. A etiology Combination of predisposing factors including genetic and environmental influences. Chronic exposure to chemical such as benzene Radiation exposure. Cytotoxic therapy of breast, lung and testicular cancer.
Classification of leukaemia 1. 1. Acute lymphatic leukaemia (ALL) Usually occurs before 14 years of age peak incidence is between 2-9 years of age, older adult Pathophysiology It arising from a single lymphoid stem cell, with impaired maturation and accumulation of the malignant cells in the bone marrow.
Acute lymphatic leukaemia Cont. Signs and symptoms Anaemia, bleeding, lymphadenopathy, infection Clinical manifestation Clinical manifestation Fever Pallor Bleeding Anorexia Fatigue Weakness Bone, joint and abdominal pain Increase intracranial press. Generalized lymphadenopathy Infection of respiratory tract Anaemia and bleeding of mucus membrane Ecchymoses Weight loss Hepatomegaly Mouth sore
Acute lymphatic leukaemia Cont. Management Diagnosis Low RBCs count, Hb, Hct, low platelet count , low normal or high WBC count. Blood smear show immature lymph blasts. Treatment Chemotherapeutic agent, it involve three phases 1. Induction: Using vincristine and prednisone. 2. Consolidation: Using modified course of intensive therapy to eradicate any remaining. 3. Maintenance
Acute lymphatic leukaemia Cont. Treatment Cont. Prophylactic treatment of the CNS , intrathecal administration and /or craniospinal radiation with eradicate leukemic cells. Eat diet that contains high in protein, fibres and fluids.
Acute lymphatic leukaemia Cont. Treatment Cont. Avoid infection (hand washing, avoid crowds),injury Take measure to decrease nausea and to promote appetite, smoking and spicy and hot foods. Maintain oral hygiene.
Acute Myelogenous Leukaemia (AML) It occurs at any age but occurs most often at adolescence and after age of 55 Pathophysiology Characterized by the development of immature myeloblasts in the bone marrow. Clinical manifestation Similar to ALL plus sternal tenderness. Management Diagnosis Low RBC, Hb, Hct, low platelet count, low to high WBC count with myeloblasts.
Acute Myelogenous Leukaemia (AML) Cont. Treatment Use of cytarabine, 6-thioquanine, and doxorubic The same care of client as All, plus give adequate amounts of fluids(2000 to 3000 ml per day.) Instruct client about medication, effects, side effects and nursing measures
Chronic lymphocytic Leukaemia (CLL) The incidence of CLincreases with age and is rare under the age of 35.It is common in men. Pathophysiology It is characterized by proliferation of small, abnormal , mature B lymphocytes, often leading to decreased synthesis of immunoglobulin and depressed antibody response. The number of mature lymphocytes in peripheral blood smear and bone marrow are greatly increased
Chronic lymphocytic Leukaemia (CLL) Cont Clinical Manifestation Usually there is no symptoms. Chronic fatigue , weakness , anorexia, splenomegaly , lymphadenopathy, hepatomegaly. Signs and Symptoms  Pruritic vesicular skin lesions .  Anaemia  Thrombocytopenia.  The WBC count is elevated to a level between 20,000 to 100,000.  Increase blood viscosity and clotting episode.
Chronic lymphocytic Leukaemia (CLL) Cont Management I. Persons are treated only when symptoms, particular anaemia , thrombocytopenia , enlarged lymph nodes and spleen appear. I. Chemotherapy agents such as chlorambucil , and the glucocorticoids. I. Client and family education is that describe for AML.
Chronic Myelogenous Leukaemia(CML) Occurs between 25-60 years of age. Peak 45 year It is caused by benzene exposure and high doses of radiation. Clinical Manifestation There is no symptoms in disease. The classic symptoms of chronic types of leukaemia, include: Fatigue, weakness, fever, sternal tenderness. Weight loss, joint & bone pain.
Chronic Myelogenous Leukaemia(CML) Cont. Clinical Manifestation Cont. Massive splenomegaly and increase in sweating.  The accelerated phase of disease(blostic phase) is characterized by increasing number of granulocytes in the peripheral blood. There is a corresponding anaemia and thrombocytopenia.
BLOOD TRANSFUSION
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hematology.pptx

  • 1.
  • 2.
    Hematology • Branch ofmedicine that studies blood cells and blood-forming tissue • Includes hemostasis (the process of stopping bleeding) • Tests can detect diseases such as • Anemia • Leukemia • Hemophilia
  • 3.
    Anatomy and physiology •Hematologic system consists of the blood and the sites where the blood is produced. • Blood consists of plasma and blood cells. • Because blood cells have a short lifespan, hematopoiesis (production od blood cells in the bone marrow) is needed. 3
  • 4.
    Function of Blood •Transporting fluids such as: • Nutrients from digestive tract • O2 from lungs • Waste from cells • Hormones • Aids in heat distribution • Regulates acid-base balance
  • 5.
    Composition of Blood •Plasma: liquid portion of blood w/out cells • Contains all of the following • Water Nutrients • Electrolytes Metabolic waste product • Hormones Vitamins and enzymes • Plasma proteins such as fibrinogen, albumin and globulin
  • 6.
    Composition of Blood: Erythrocytes •Red blood cells are responsible for: • Transport of oxygen and nutrients • Removal of waste and CO2 from the cells • Distribution of heat • Hemoglobin: • The O2 carrying potential. • Has 4 subunits, each contains a hem attached to a globin chain. • Iron is present in the hem, hem is bind to the oxygen •
  • 7.
    Composition of Blood:Leukocytes • WBC are responsible for: • Phagocytosis – to engulf and absorb waste material and harmful microorganisms in the blood stream and tissues • Synthesis of antibody molecules • Inflammation process • Production of heparin – component found in lung and liver tissue which have the ability to prevent clotting of blood.
  • 8.
    Composition of Blood:Leukocytes (cont.) • Types of Leukocytes • Granulocytes • Neutrophils • Eosinophils • Basophils • Agranulocytes • Lymphocytes • Monocytes
  • 9.
    Composition of Blood:Thrombocytes • Platelets – the smallest of the solid components of the blood • Responsible for the clotting process • Coagulation: term for clotting • Embolism: a blood clot which is moving through the body
  • 10.
    INTEPRETATION OF AHEMOGRAM • The 8 parameter cell counter will give the following: 1. WBC count: white blood cell count 2. RBC count: red blood cell count 3. Hb: Hemoglobin 4. Hct: Hematocrit / Packed cell volume (PCV) 5. MCV: Mean cell volume 6. MCH: Mean cell hemoglobin 7. MCHC: Mean cell hemoglobin concentration 8. RDWt: red blood cell distribution width • In addition to these above parameters the 18 parameter cell counter also has White blood cell Differentials: Neutrophils count and percentage, Lymphocyte count and percentage, Monocytes count and percentage, Eosinophil count and percentage, Basophils count and percentage and Pct: Plateletcrit
  • 11.
    WHITE BLOOD CELLCOUNT • This is the number of white blood cells in 1 cubic mm of whole blood. • The normal value is 4.0-11.0 million cells per microliter. • On its own is not a useful parameter RED BLOOD CELL COUNT • This is the number of erythrocytes in 1 cubic mm of whole blood. • The normal values include: Men= 4.5-6.0 million cells per microliter and Women= 3.9-5.0 million cells per microliter HEMOGLOBIN • Normal hemoglobin values: Men= 13.5-17.5 g/dl and Women= 11.5- 16.0 g/dl HEMATOCRIT/ PACKED CELL VOLUME (PCV) • Normal PCV is Men= 0.4-0.54 L/L and Women= 0.36-0.47 L/L MEAN CELL VOLUME (MCV) • Indicates the average volume of a single RBC. • It is expressed in cubic microns. • The normal value is 80-96 fL
  • 12.
    MEAN CELL HEMOGLOBIN(MCH) • This gives an idea about the average hemoglobin content in a single red cell. • Normal range varies between 27 and 32 pico grams. RED BLOOD CELL DISTRIBUTION WIDTH (RDW) • This shows the variation in red cell size • The normal value is 11-15% • In iron deficiency there is increased RDW. • In beta-Thalassaemia trait,the RDW is usually normal. PLATELETS • The normal platelet count is 150-400 (109/L) DIFFERENTIAL COUNT • Neutrophils= 3-6 (109/L),Lymphocytes= 1.5- 4 (109/L), Monocytes= 0.3- 0.6 (109/L), Eosinophils= 0.15-0.30 (109/L) and Basophils= 0-0.1 (109/L) •
  • 13.
    Definitions • Anticoagulant: anagent that prevents the clotting of blood. • Examples are EDTA, Citrate and Heparin • Capillary: small blood vessel that connects arterioles and venules • Hematoma: a subcutaneous mass of blood at a venipuncture site • Hemoglobin: the oxygen carrying molecule of red blood cells • Hemolysis: the breakdown of red blood cells, with the release of hemoglobin into the plasma or serum. Cannot use hemolyzed samples in lab tests
  • 14.
    • THROMBOCYTOPENIA -Decrease in platelet count below 150 000/cu mm of blood • Thrombocytosis - Increase in platelet count over 450 000/cu mm of blood • Leukocytopenia – wbc less than the normal range in the blood • Leukocytosis - wbc above the normal range in the blood • PANCYTOPENIA – it is combination of anemia, thrombocytopenia and leukocytopenia
  • 15.
  • 16.
    Blood Types • FourMajor Groups • A B AB O • Blood types are inherited from your parents • Antigen is present on the red blood cell; typing is done w/rbc • Antibody is present in the plasma; antibody screening done on plasma
  • 17.
    Blood Types • Onegative • Universal donor • It carries no antigen • AB positive • Universal recipient • It carries no antibodies in the plasma • 43% of population are O, 42% A, 12% B and 3% AB
  • 18.
    ABO & Rhcompatibility • Blood is classified according to the presence of these antigens: • Group A contains antigen A • Group AB contains both antigens • Group O contains neither antigen • Blood plasma contains antibodies against the opposite antigen: • A person with Type A blood has antibodies against the B antigen • A person with Type AB blood has no antibodies (Universal Recipient) • A person with Type O blood has antibodies against the A, B & AB antigens (Universal Donor)
  • 19.
    ABO & Rhcompatibility • People with Rhesus factors in their blood are classified as "Rh positive" • People without the factors are classified as "Rh negative" • Rh negative persons form antibodies against the Rh factor if they are exposed to Rh positive blood • Conclusion: • Blood transfusion between incompatible groups causes an immune response against the cells carrying the antigen, resulting in transfusion reaction
  • 20.
  • 21.
    Anemia • Is acondition in which the hemoglobin concentration is lower than normal (low RBCs). • As a result, the amount of oxygen delivered to the tissue is lower than normal. • It is not a disease but a sign of underlying disorders.
  • 22.
    Causes of Anemia •Iron deficiency • Vitamin B12 deficiency • Infections*: HIV, tuberculosis, malaria, schistosomiasis, hookworm, hepatitis • Drugs: isoniazid, chloramphenicol, alcohol, zidovudine, hydroxyurea • Chronic disease*: renal and liver disease, rheumatologic diseases, hypothyroidism  These are common causes of anemia in adults in Africa.
  • 23.
    Common signs andsymptoms of anemia • Easy fatigue and loss of energy • Unusually rapid heart beat, particularly with exercise • Shortness of breath and headache, particularly with exercise • Difficulty concentrating • Dizziness • pale skin • Leg cramps • Insomnia
  • 24.
    Classifications of Anemia •Etiological clarification • Morphological clarification • Anemia severity classification
  • 25.
    Etiological classification 1.Nutrition deficiencyanemia • Iron deficiency anemia • Vitamin B12 deficiency anemia 2.Increased RBC destruction • Hemolytic anemia 3.Increased Blood loss • Hemorrhagic anemia 4.Bone marrow suppression (aplastic anemia ) • Anemia of chronic disease • Drug induced Anemia 5.Hereditary classification • Sickle cell Anemia • Thalassemia
  • 26.
    Morphological Classification • MicrocyticAnemia • Normocytic Anemia • Macrocytic Anemia
  • 27.
    Morphological Classification Normochromic, normocyticanemia (normal MCHC, normal MCV). • These include: 1. hemolytic anemias (those characterized by accelerated destruction of rbc's) 2. anemia of acute hemorrhage 3. aplastic anemias (those characterized by disappearance of rbc precursors from the marrow) Hypochromic, microcytic anemia (low MCHC, low MCV). • These include: 1. iron deficiency anemia 2. thalassemias 3. anemia of chronic diseases Normochromic, macrocytic anemia (normal MCHC, high MCV). • These include: 1. vitamin B12 deficiency 2. folate deficiency
  • 28.
    Anemia severity classification PopulationsMild Moderate Severe Pregnant women 10 – 10.9 7- 9.9 <7 Non pregnant women 11 -11.9 8 – 10.9 <8 Men 11 – 12.9 8 -10.9 <8
  • 29.
  • 30.
    1. IRON DEFICIENCYANEMIA • This is the most common type of anemia worldwide. • Iron deficiency anemia occurs when the body iron stores become inadequate for the need of normal RBC production. • It is due to decreased levels of iron. • Decreased iron leads to decreased heme and hemoglobin thus resulting in a microcytic anemia. • Iron deficiency anemia is a manifestation of disease, not by itself a complete diagnosis Anemia People with an iron deficiency may experience these symptoms: • A hunger for strange substances such as paper, ice, or dirt (a condition called pica) • Upward curvature of the nails, referred to as koilonychias • Soreness of the mouth with cracks at the corners
  • 31.
    IRON METABOLISM Irons isconsumed in heme (meatderived) and non-heme (vegetablederived) forms. • Absorption of heme occurs in the duodenum while that of non-heme occurs in the proximal jejunum • Enterocytes have heme and non-heme (DMT1) transports. The heme form is more readily absorbed. • Absorption is facilitated by: stomach acidity (keeps iron in reduced ferrous state Fe2+ and not ferric state Fe3+), Vitamin C (Ascorbic acid), Citrates. • Absorption is limited by: phosphates, oxalates, tannates (tea) and pyrates (plant food) • Enterocytes transport iron across the cell membrane into blood via ferroportin. • Transferrin transports iron in the blood and delivers it to liver and bone marrow macrophages for storage.
  • 32.
    2. ANEMIA OFCHRONIC DISEASE • This is associated with chronic inflammation (e.g. endocarditis or autoimmune conditions) or malignant disease. • It is the most common type of anemia in hospitalized patients. • Etiologies: Infectious: TB, lung abscess, osteomyelitis, pneumonia, bacterial endocarditis. Non-infectious: rheumatoid arthritis, lupus, connective tissue disease, sarcoidosis, Crohn’s disease, malignancy (carcinoma, lymphoma, sarcoma).
  • 33.
    PATHOGENESIS • Chronic diseaseresults in production of acute phase reactants from the liver, including hepcidin • Hepcidin sequesters iron in storage sites by (1) limiting iron transfer from macrophages to erythroid precursors  (2) suppressing erythropoietin (EPO) production. • The aim is to prevent bacteria from accessing iron, which is necessary for their survival. • Decreased availability of iron results in microcytic anemia. • Other cytokines produced during inflammation reduce life span of RBC (80 days) rendering erythropoietin inadequate.
  • 34.
    • The termAA is first used by Ehrlich in 1888 • Describes a disorder of unknown etiology characterized by • pancytopenia with • hypo or acellular bone marrow. • It is one of the stem cell disorders. 3. Aplastic Anemia (AA)
  • 35.
    Classification of AA AcquiredAA 1. Idiopathic 2. Radiation 3. Drugs/chemicals • Chloramphenicol • NSAID: (phenylbutasone,indomethacin,gold etc) • Oral hypoglycemic drugs (chlorpropamide,tolbutamide) • Antithyroid drugs, phenothiazines, antimalarials, diuretics,antiepileptics – Rubella – CMV – HIV – Parvovirus – Brucellosis – Tbc – Toxoplasmosis
  • 36.
    Infections • Hepatitis • E.Barrvirus • Rubella • CMV • HIV • Parvovirus • Brucellosis • Tbc • Toxoplasmosis Immunologic disorders • SLE, eosinophilic fasciitis • Graft- versus- Host Disease • Hypoimmunoglobulinemia • Thymoma
  • 37.
    Clinical Features ofAA • History: • Bleeding • Symptoms of anemia • Infections • Drugs, chemicals or other etiologically important exposures have to be questioned. • Physical exam: • Petechiae, ecchymosis • Retinal bleeding • Pallor • Fever and other signs of infection • Presence of lymphadenomegaly and /or splenomegaly are unusual (indicate other diagnoses).
  • 38.
    • LAB: • Pancytopenia •Reticulocytes: Low or absent • RBC: normochrome-normocytic,or slight macrocytosis • Neutropenia and relative lymphocytosis • Red and white cell precursors are almost neverseen in the peripheral smear • Serum iron is increased • Bone marrow : • Aspiration; Dry tap • Biopsy; all three cell lines are reduced or absent, raplaced by fatty tissue, residual lymphocytes, increased iron stores,rarely hot spots of hematopoesis
  • 39.
    4. HEMOLYTIC ANEMIA •Due to red cell destruction and increased red cell turnover. Bone marrow is able to compensate 5 times the normal rate. • Clinical features: jaundice, hepatosplenomegaly, dark urine. • Etiology can be classified as: 1. Congenital Hemoglobinopathies: sickle cell disease*, thalassemia Enzymopathies: G6PD deficiency*, Pyruvate kinase deficiency Membranopathies: hereditary spherocytosis, eliptocytosis In born errors of metabolism 2. Acquired Microangiopathic hemolytic anemia: TTP, HUS, DIC, eclampsia, HELLP syndrome Autoimmune hemolytic anemia Infections: Malaria
  • 40.
    SICKLE CELL DISEASE •A severe hemolytic anemia caused by a point mutation resulting in the substitution of glutamate for valine on the 6th position of the beta globin chain forming HbS. • When deoxygenated, HbS molecules polymerize into long fibers and cause the red blood cells to sickle
  • 41.
    Normal  Disc-Shaped  Deformable Life span of 120 days Sickle  Sickle-Shaped  Rigid  Lives for 20 days or less
  • 42.
    SICKLE CELL DISEASE Symptomsmay not appear until 6 months of age Mortality rate children < 3 Years old is 15-35% Early Diagnosis: Amniocentesis, Newborn Screen
  • 43.
    Signs & Symptoms Initially:fever & anemia at 6 mos  Pallor  Fatigue  SOB  Irritability  Jaundice
  • 44.
    severe anemia causescrises • Vasocclussive crisis • Aplastic crisis • Splenic sequestration • Hemolytic crisis
  • 45.
    1. VASO-OCCLUSIVE CRISES •An early presentation may be acute pain in the hands and feet: dactylitis due to vaso-occlusion of the small vessels. • (hand-foot syndrome) • Severe pain in other bones e.g. femur, humerus, vertebrae, ribs, pelvis occurs in older children/adults. • Attacks vary from person to person. Fever often accompanies the pain. • Triggers of vaso-occlusive crisis include: Hypoxemia: may be due to acute chest syndrome or respiratory complications, Dehydration: acidosis results in a shift of the oxygen dissociation curve and Changes in body temperature
  • 46.
  • 47.
    Priapism • Prolonged erectionof the penis, usually without sexual arousal • Commonly occurs in children and adolescents with SS or SC ( • Treatment is difficult 1. Opioid pain medication 2. Intravenous fluids 3. Aspiration and irrigation of the corpus cavernosum 4. Surgery 5. Blood Transfusions 6. Impotence with severe disease or recurrent episodes
  • 48.
    2. BONE MARROWAPLASIA (APLASTIC CRISIS) • This most commonly occurs following infection with erythrovirus B19 (previously called Parvovirus B19) which invades proliferating erythroid progenitors. • There is a rapid fall in hemoglobin with no reticulocytes in the peripheral blood, because of the failure of erythropoiesis in the marrow
  • 49.
    3. SPLENIC SEQUESTRATION •Vaso-occlusion produces an acute painful enlargement of the spleen. • There is a splenic pooling of red cells and hypovolemia, leading in some to circulatory collapse and death. • There will be severe hemolysis, rapid splenomegaly and a high reticulocyte count. • The condition occurs in childhood before multiple infarctions have occurred. • Multiple infarctions lead to a fibrotic non-functioning spleen
  • 50.
    SPLENIC SEQUESTRATION  Suddentrapping of blood within the spleen  Usually occurs in infants under 2 years of age with SS  Spleen enlarged on physical exam, may not be associated with fever, pain, respiratory, or other symptoms  Circulatory collapse and death can occur in less than thirty minutes
  • 51.
    Treatments For SplenicSequestration • Intravenous fluids • Maintain vascular volume • Cautious blood transfusion • Treat anemia, sequestered blood can be released from spleen • Spleen removal or splenectomy • If indicated
  • 52.
    4. HEMOLYTIC CRISIS •Red cell half life is reduced to 10 – 20 • This results into rapid destruction rbc leading anemia CLINICAL FEATURES • Anaemia • Jaundice • Gallstones • Cardiomegaly:CHF • Leg ulcers • Marrow hyperplasia • Poor physical development • Delayed maturation • Subjective symptoms
  • 53.
    Chronic Complications  Anemia/Jaundice Brain Damage/Stroke  Kidney failure  Decreased lung function  Eye disease (bleeding, retinal detachment)  Leg ulcers  Chronic pain management  Stroke
  • 54.
    Thalassemia • Heterogenous groupof genetic disorders which results from a reduced rate of synthesis of alpha (coded for by 4 genes) or beta chains (coded for by 2 genes) of hemoglobin. • Changes in normal ratio results in each of the disorders. • Due to inherited mutations carriers are protected against Plasmodium falciparum malaria. • Thalassemia are divided into alpha and beta thalassemia. • Normally there are 3 types of hem HbA (2 alpha, 2 beta) HbA2 (2 alpha and 2 delta). HbF (2alpha, 2 gamma)
  • 55.
    ALPHA THALASSEMIA • Alphathalassemia is usually due to gene deletion, normally 4 alpha genes are present on chromosome 16. • One gene deleted- asymptomatic • Two gen deleted- mild anemia with slightly increased RBC count BETA THALASEMMIA • Usually due to gene mutations (point mutations in promoter or splicing sites) seen in individuals of African and Mediterranean descent. • Two beta genes are present on chromosome 11, mutations result in absent or diminished production of the beta-globin chain. • Beta thalassemia minor is the mildest form of the disease and is usually asymptomatic with an increased RBC count
  • 56.
    Leukemia Definition It is agroup of malignant disorder, affecting the blood and blood –forming tissue of the bone marrow lymph system and spleen. A etiology Combination of predisposing factors including genetic and environmental influences. Chronic exposure to chemical such as benzene Radiation exposure. Cytotoxic therapy of breast, lung and testicular cancer.
  • 57.
    Classification of leukaemia 1.1. Acute lymphatic leukaemia (ALL) Usually occurs before 14 years of age peak incidence is between 2-9 years of age, older adult Pathophysiology It arising from a single lymphoid stem cell, with impaired maturation and accumulation of the malignant cells in the bone marrow.
  • 58.
    Acute lymphatic leukaemiaCont. Signs and symptoms Anaemia, bleeding, lymphadenopathy, infection Clinical manifestation Clinical manifestation Fever Pallor Bleeding Anorexia Fatigue Weakness Bone, joint and abdominal pain Increase intracranial press. Generalized lymphadenopathy Infection of respiratory tract Anaemia and bleeding of mucus membrane Ecchymoses Weight loss Hepatomegaly Mouth sore
  • 59.
    Acute lymphatic leukaemiaCont. Management Diagnosis Low RBCs count, Hb, Hct, low platelet count , low normal or high WBC count. Blood smear show immature lymph blasts. Treatment Chemotherapeutic agent, it involve three phases 1. Induction: Using vincristine and prednisone. 2. Consolidation: Using modified course of intensive therapy to eradicate any remaining. 3. Maintenance
  • 60.
    Acute lymphatic leukaemiaCont. Treatment Cont. Prophylactic treatment of the CNS , intrathecal administration and /or craniospinal radiation with eradicate leukemic cells. Eat diet that contains high in protein, fibres and fluids.
  • 61.
    Acute lymphatic leukaemiaCont. Treatment Cont. Avoid infection (hand washing, avoid crowds),injury Take measure to decrease nausea and to promote appetite, smoking and spicy and hot foods. Maintain oral hygiene.
  • 62.
    Acute Myelogenous Leukaemia(AML) It occurs at any age but occurs most often at adolescence and after age of 55 Pathophysiology Characterized by the development of immature myeloblasts in the bone marrow. Clinical manifestation Similar to ALL plus sternal tenderness. Management Diagnosis Low RBC, Hb, Hct, low platelet count, low to high WBC count with myeloblasts.
  • 63.
    Acute Myelogenous Leukaemia(AML) Cont. Treatment Use of cytarabine, 6-thioquanine, and doxorubic The same care of client as All, plus give adequate amounts of fluids(2000 to 3000 ml per day.) Instruct client about medication, effects, side effects and nursing measures
  • 64.
    Chronic lymphocytic Leukaemia(CLL) The incidence of CLincreases with age and is rare under the age of 35.It is common in men. Pathophysiology It is characterized by proliferation of small, abnormal , mature B lymphocytes, often leading to decreased synthesis of immunoglobulin and depressed antibody response. The number of mature lymphocytes in peripheral blood smear and bone marrow are greatly increased
  • 65.
    Chronic lymphocytic Leukaemia(CLL) Cont Clinical Manifestation Usually there is no symptoms. Chronic fatigue , weakness , anorexia, splenomegaly , lymphadenopathy, hepatomegaly. Signs and Symptoms  Pruritic vesicular skin lesions .  Anaemia  Thrombocytopenia.  The WBC count is elevated to a level between 20,000 to 100,000.  Increase blood viscosity and clotting episode.
  • 66.
    Chronic lymphocytic Leukaemia(CLL) Cont Management I. Persons are treated only when symptoms, particular anaemia , thrombocytopenia , enlarged lymph nodes and spleen appear. I. Chemotherapy agents such as chlorambucil , and the glucocorticoids. I. Client and family education is that describe for AML.
  • 67.
    Chronic Myelogenous Leukaemia(CML) Occursbetween 25-60 years of age. Peak 45 year It is caused by benzene exposure and high doses of radiation. Clinical Manifestation There is no symptoms in disease. The classic symptoms of chronic types of leukaemia, include: Fatigue, weakness, fever, sternal tenderness. Weight loss, joint & bone pain.
  • 68.
    Chronic Myelogenous Leukaemia(CML)Cont. Clinical Manifestation Cont. Massive splenomegaly and increase in sweating.  The accelerated phase of disease(blostic phase) is characterized by increasing number of granulocytes in the peripheral blood. There is a corresponding anaemia and thrombocytopenia.
  • 69.
  • 70.