Hematology Picture
Post on 14-Nov-2014
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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&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 &severitytype severe moderate mild Activity Type of hemorrhage % </p>