Hematology Picture

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<p>HEMATOLOGY AND ONCOLOGY</p> <p>CELLULAR ELEMENTS</p> <p>THE RED CELLS</p> <p>Erythropoiesis stem cell proerthroblast basophilic polychromat ophilic</p> <p>orthocromatophil ic</p> <p>reticulocy te</p> <p>Mature RBCs</p> <p>Monocyte Development</p> <p>stem cell</p> <p>monoblast</p> <p>promonocyte</p> <p>Monocyte</p> <p>Lymphocyte Development</p> <p>Stem cell</p> <p>lymphoblast</p> <p>prolymphocyte Lymphocyte</p> <p>The production of platelets is THROMBOPOIESIS</p> <p>Plasma</p> <p>Plasma</p> <p>Sites of formation of hematopoietic cells</p> <p>Differentiation pathway of hematopoietic cells</p> <p>) HEMOGLOBIN ) Hb</p> <p>Different Hemoglobin TypesHb type Embryonic type % at birth % After 2 years Major embryonic Hb are not present after 3rd month of gestation. 3% 95% 1.5-3.5% Embryonic Hb may be present at birth in small percentage. Fetal type(2 2) 45-90% Adult type A1 (2 2) A2 ( ) 10-55% 0-1.5%</p> <p>Proportions of the various human hemoglobin polypeptide chains .through early life</p> <p>valueHematocrit</p> <p>IRON DEFICIENCYANEMIA</p> <p>Iron Metabolism</p> <p>Spooning of the nails</p> <p>Atrophic glossitis</p> <p>HEMOLYTIC ANEMIA</p> <p>BILIRUBIN METBOLISM</p> <p>HEMOGLOBIN</p> <p>GLOBIN</p> <p>HEME</p> <p>AMINOACIDS</p> <p>IRON</p> <p>PROTOPORPHYRIN</p> <p>HEME OXYGENASE BILIVERDIN BILIVIRDIN REDUCTASE UNCONGUGATED BILIRUBIN</p> <p>UNCONGUGATED BILIRUBIN</p> <p>FREE UNCONGUGATED BILIRUBIN</p> <p>ALBUMIN BOUND BILIRUBIN</p> <p>ALBUMIN BOUND BILIRUBIN</p> <p>DETACHED FROM ALBUMIN</p> <p>LIGAND Y&amp;Z PROTEIN SMOOTH ENDOPLASMIC R</p> <p>URIDINE DIPHOSPHATEGLUCORYL TRANSFERASE E CONGUGATED BILIRUBIN</p> <p>INTESTINE</p> <p>URINE</p> <p>CONGUGATED BILIRUBIN</p> <p>B-GLUCURONIDASE E UNCONGUGATED BILIRUBIN</p> <p>INTESTINAL BACTERIAL FLORA E-COLI STECOBILINOGEN</p> <p>OXYDIZED ENTEROHEPATIC CIRCULATION STERCOBILIN</p> <p>]G6PD deficiency[</p> <p>]G6PD deficiency[</p> <p>fava beans</p> <p>SICKLE CELL ANEMIA</p> <p>INHERITANCE</p> <p>PATHOPHYSIOLOGY</p> <p>)Bone infarction)head necrosis</p> <p>THALASSEMIA SYNDROMES</p> <p>Geographical distribution</p> <p>MODE OF TRANSMISSION</p> <p>PATHOPHYSIOLOGY OF THALASSEMIA MAJOR</p> <p>CLINICAL MANIFESTATION OF - THALASSEMIA MAJOR</p> <p>Target cells</p> <p>RADIOLOGIC INVESTIGATIONPlain x ray skull There is maxillary over growth, prominent widening of the diploic spaces, with hair standing on end appearance.</p> <p>Desferal pump</p> <p>HEMORRHAGIC DISEASES</p> <p>Introduction</p> <p>Blood within the vascular tree remains fluid throughout life</p> <p>If a blood vessel is damaged a rapid localized</p> <p>RESPONSE OF BLOOB CLOT FORMATION will occur.</p> <p>Introduction</p> <p>Failure of clotting leads to</p> <p>MECHNISMIS OF HEMOSTASIS</p> <p>Formation of a haemostatic plugPrimary homeostasis Aggregation adhesion fibrinogen GPIIB,IIIA</p> <p>activation</p> <p>release</p> <p>Secondary homeostasisFIBRIN CLOT FORMATION</p> <p>Dr:Mohamed El-shanshory</p> <p>Factor level activity &amp;severitytype severe moderate mild Activity Type of hemorrhage % </p>