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Dentistry at Helwan National University

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hematology blood pathophysiology anemia blood

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This document provides a detailed explanation of blood pathophysiology, including its components, functions, and different types of anemia. It covers topics like blood cells, their roles, and various conditions, along with their causes and symptoms.

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Pathophysiology of Hematologic system Components of the Hematologic System All the blood elements Plasma Lymphoid Organs Blood cells Plasma – clotting factors = Serum e.g. Spleen and the bone marrow. Blood Components  Plasma -55% of t...

Pathophysiology of Hematologic system Components of the Hematologic System All the blood elements Plasma Lymphoid Organs Blood cells Plasma – clotting factors = Serum e.g. Spleen and the bone marrow. Blood Components  Plasma -55% of total blood  Blood elements -45% of volume. total blood volume. Mostly water 91% Red blood cells Soluble blood proteins 7% White blood cells Hormones Blood platelets Nutrients 2% Electrolytes Plasma  Liquid part of blood  Pale yellow made up of 91% water,9% other.  Colloid: liquid containing suspended substances that don’t settle out.  Albumin: Important in regulation of water movement between tissue.  Globulin: Immune system or transport molecules.  Fibrinogen: Responsible for formation of blood cell. Blood Cells  Erythrocytes: RBC  Leukocytes: WBC  Neutrophil  Monocyte  Eosinophil  Basophil  Lymphocytes: T lymphocytes, B lymphocytes.  Thrombocyte: Platelet Functions of the Hematologic System 1) Transport Medium: -Transports gases , nutrients, vitamins , hormones and waste products. This is achieved by RBCs and plasma 2) Defensive Function: -This function is achieved by white blood cells through phagocytosis of the invading microorganisms or formation of antibodies and sensitized T lymphocytes against those invading pathogens. 3) Hemostatic Function: -Hemostasis means stoppage of extravasation of blood caused by injury of a blood vessels. This function is achieved by the platelets and the coagulation factors present in blood. 4) Homeostatic Function: -Homeostasis means to keep the composition of internal environment constant. This is achieved by the whole blood. Fate of Erythrocytes  Unable to divide, grow, or synthesis protiens.  Wear out in 100 to 120 days.  Removed by phagocytosis in the spleen or liver.  New RBCs are made by stem cells in bone marrow.  Production increases when oxygen level decreases or during pregnancy. Hemoglobin is the protein molecule in red blood cells that carries oxygen from the lungs to the body's tissues and returns carbon dioxide from the tissues back to the lungs. Hemoglobin is made up of four protein molecules (globulin chains) that are connected together. Types f hemoglobin: HBA1: The major hemoglobin in humans. First appears 12 weeks after birth (minor component of normal adult HB). HBF: Normally synthesized only during fetal development in fetus and newborn infants. HbF is replaced by HbA during the first few months of life. HBA1C: Has glucose residues attached to β-globin chains–increased amounts in diabetes, so HbA1c could be used as a monitor for the control of the blood glucose level for diabetic patients. HBS: Contains two mutant b-globin chains. In mutant chains, glutamate at position 6 is replaced with valine resulting in RBCs of HBS have shorter life span than normal RBCs (less than 20 days, compared to 120 of normal) Hence, anemia is a consequence of HBS. Normal values related to RBCs Red blood cell count: 4.0 to 5.5 million/mL of blood Hemoglobin: 14.0 to 17.5 grams/100 mL for males; 12.0 to 16.0 grams/100 mL for females Hematocrit (% of red blood cells): 42% to 52% for males; 36% to 48% for females Normal values related to WBCs  Total leukocyte count: 4000 - 1 l,000/mm3. * Classification: differential leukocyte count: I. Granular leucocytes : Neutrophils: 60-70%. Eosinophils: 2 - 4%. Basophils: 0 - 1%. II. Agranular leucocytes : Lymphocytes: 20 - 30%. Monocytes: 2 - 8%. Normal values related to hemostatic function (platelets and coagulation factors) 1) Platelet count: 1/4 - 1/2 millions/mm3 (average 300,000/mm3). 2) Bleeding Time: normally after 1 - 6 minutes. 3) Tests For Coagulation Function: I-The Whole Blood Coagulation Time: is from 6 - 10 minutes 2- The Activated Partial Thromboplastin Time: is 30- 40 seconds. 3- Prothrombin Time: is from10 - 14 seconds ANEMIA Definition: decreased red blood cell count or decreased hemoglobin % or both. So, there is decreased O2 transport to tissues General manifestation of anemia: 1-Pale or yellowish skin 2-Fatigue 3-Cold hands and feet 4-Headache 6-Shortness of breath & Irregular heartbeat Types of anemia Based on red cell morphology, anemia is classified into: I) Microcytic: small size and smaller Hg content of each RBC II) Macrocytic: increased size of each RBC III) Hypochromic means that the RBC have less hemoglobin than normal. Normocytic normochromic anemia Results from: A) Decreased production of RBCs: caused by depression of bone marrow → decreased all blood elements including RBCs (aplastic anemia) Causes of aplastic anemia 1-Radiation 2-Chemicals 3-Chemotherapy 4-Certain antibiotics 5- infection 6- Toxins B) Very rapid loss of RBCs: due to 1- Massive hemorrhage → hemorrhagic anemia 2-Hemolysis of RBCs → hemolytic anemia Hemolytic anemia This group of anemia develops when red blood cells are destroyed faster than bone marrow can replace them either in the blood vessels or elsewhere in the human body. Hemolysis of RBCs may be: *Acquired: caused by :  chemical toxins, bacterial toxins,  Drugs  Snake venom  Autoimmune: incompatible blood transfusion  Cancers.  Certain viral infection and parasitic infection (malaria) *Heriditary:e.g, Hereditary spherocytosis, sickle cell anemia and thalassemia Hereditary sperocytosis: RBCs are abnormally sphere shaped → abnormally fragile → hemolysis Sickle cell anemia is an inherited form of anemia, it's caused by a defective form of hemoglobin, the red blood cells become rigid and sticky and are shaped like sickles or crescent. These irregularly shaped cells can get stuck in small blood vessels, which can slow or block blood flow and oxygen to parts of the body. Thalassemia Inherited blood disorders in which the body is not able to make enough hemoglobin,. This causes the body to make fewer healthy red blood cells than normal. → increased RBCs fragility → hemolysis of RBCs Manifestations of hemolytic anemia: 1- Common manifestations of anemia 2- Hemolysis of RBCs → Jaundice, i.e, yellowish coloration of skin and mucous membranes due to increased blood bilirubin 3-Sickling of RBCs in sickle cell anemia → increased blood viscosity → Decreased blood flow to tissues → hypoxia &pain 4-Splenomegally II) Microcytic hypochromic anemia  RBCs are smaller in size and contain smaller amount of Hg than normal RBCs caused by iron deficiency.  Causes of iron deficiency: 1-Decreased iron intake: especially occurs in vegetarians , infants and females in reproductive periods 2-Decreased iron absorption from intestine 3-Chronic blood loss e.g, bleeding and neoplasia (an abnormal growth of tissue). III) Macrocytic anemia  RBCs are larger in size than normal RBCs always associated with insufficient numbers of cells and often also insufficient hemoglobin content per cell due to vitamin B12 or folic acid deficiency. Pathophysiological Effects of Anemia: Decreased blood viscosity in anemia ---> increased rate of blood flow --> increased venous return --> increased cardiac output to compensates the decreased 02 content in the anemic blood. In hemolytic anemia, there is excessive production of bile pigments causing jaundice. In pernicious anemia (is a condition in which the body can't make enough healthy red blood cells because it doesn't have enough vitamin B12), there are sensory disturbances due to degeneration of dorsal column of spinal cord. Polycythemia  Means the RBC count is greatly increased  Types: I)Relative polycythemia: decreased plasma volume → increased concentration of RBCs. II) Primary polycythemia :  Caused by bone marrow makes too many RBCs and may also result in production of too many of the other types of blood cells — white blood cells and platelets. These excess cells thicken your blood and cause complications, such as such as a risk of blood clots or bleeding.  III) Secondary polycythemia: caused by chronic hypoxia, e.g, living at high altitudes. Manifestations of polycythemia: 1- Increased blood volume 2- Increased blood viscosity →  Risk of thrombosis  Occlusion of small blood vessels  Impaired blood flow to tissues (ischemia) 3-Hepatosplenomegally due to pooling of blood. Treatment of polycythemia  1-Giving fluids to dilute blood in relative polycythemia  2-Removal of part of blood to decrease blood volume and blood pressure in secondary polycythemia  3-Use of chemotherapy to kill the hyperactive bone marrow stem cells in primary polycythemia Pathophysiology of hemostasis Definition of hemostasis: stoppage of bleeding when a blood vessel is injured Steps of hemostasis: 1-Vasoconstriction of blood vessel 2-Formation of platelet plug. 3-Formation of blood clot. 4-Growth of fibrous tissue Abnormalities in coagulation process→ increased bleeding tendencies Causes: -Genetic : e.g, hemophilia -Acquired: Vit K deficiency Liver diseases Drug-induced Characteristics: 1-Increased coagulation time 1-Hemophilia  Is a rare bleeding disorder in which the blood doesn't clot normally, caused by deficiency of some clotting factors. Manifestations:  Mild, moderate to severe bleeding disorders  Excessive bleeding with trauma or surgery  Bleeding into soft tissues (muscles and joints) Treatment of hemophilia:  Avoidance of injury and prevention of bleeding  Replacement of the deficient clotting factors 2-Vitamin K deficiency:  Vit K is required for synthesis of clotting factors II,VII,IX & X  Sources of Vit K: Exogenous: from diet Endogenous: from bacteria flora of intestine  Causes of deficiency: 1-Intestinal malabsorption,. 2-Destruction of bacteria flora by antibiotics  Treatment: 1- Vitamin K administration 2-Supplementation of deficient clotting factors 3-Liver diseases: Clotting factors are synthesized in the liver. Liver diseases → decreased production of clotting factors → defect in blood coagulation → increased bleeding tendencies Examples of liver diseases: hepatitis, cirrhosis, liver cancer, liver failure 4-Drug induced : Use of anticoagulants, e.g, Warfarin and heparin Abnormalties in blood platelets→ increased bleeding tendencies  Include: 1-Decreased platelet count. 2-Impaired platelet functions.  Charactrized by: 1-Prolonged bleeding time Increased blood coagulability  Causes: 1-Inherited disorders of coagulation 2- Polycythemia 3-Obesity 4- Prolonged bed rest 5-Cancer 6- Venous stasis 7-Sepsis 8- Trauma or surgery  Danger: Increased risk of thrombosis..

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