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HEMATOLOGIC

QuestionAnswer
CHEIF FUNCTION DELIVERY OF SUBSTANCES FOR CELLULAR METABOLISMMICROOORAGNISMS AND INJURY<BR>MAINTENACE OF ACID BASE BALANCE<BR>REMOVE WASIT<BR>DEFENSE AGAINST
COMPOSIT. OF BLOOD 55% PLASMA, 45% BLOOD CELLS
THREE TYEPS OF BLOOD CELLS RBC, PLATELETS, WBC
RBC 4.2-6.2 MIL
PLATELETS 150,000-400,000
WBC 5000-10,000
ERYTHROCYTES MOST ABUNDANT<BR>TISSUE OXYGENATION<BR>REVERSE DEFORMITY<BR>120 LIFE
LEUKO CYTES WBC<BR>DEFENDS BODY AND REMOVE DEBRIS
GRANULOCYTES MEMBRAIN BOUND<BR>ENZYMES DESTROY MICROORANISMS<BR>INFLAMMATORY AND IMMUNE FUNCTIONS
4GRANULOCYTES NEEUTROPHILS<BR>EOSINOPHILS<BR>MAST CELLS<BR>BASOPHILS
NEUTRO.. PMN<BR>PHAGOCYTES (EARLY)
EOSINOPHILS IGE HYPERSENSITIVITY<BR>INCREASE PARASITIC INFECTIONS<BR>INGEST ANTIGEN-ANTIBODY
MASTCELLS CENTRAL CELL<BR>FOUND IN VASCULARAIZED CONNECTIVE TISSUE
BASOPHILS STRUCTURALLY AND FUNCTIONALLY SIMILAR TO MAST CELLS
ACTIVATION OF PLATELETS LEADS TO CONFORMATIONAL CHANGE IN GP RECEPTORS<BR>BINDS TO PROTEINS<BR>SHAPE CHANGES<BR>PSEUDOPODS<BR>ACTIVATION OF ARACHIDONIC PATHWAY
ADHESION LOSS OF ENDO CELLS
AGGREGATION RELEASE OF TXA<BR>HEPARIN ENHANCES CLOT FORMATION<BR>PLUG IS TABLE<BR>ACTIVATES COAGULATION
ANEMIA DECREASE RBC MASS
WORKING DEF OF ANEMIA DECREASED RBC COUNT HEMOG HEMATO
MECHANISM OF ANEMIA <BR>PRODUCTION DISORDER IRON<BR>V-B12<BR>FOLATE<BR>THALASSEMIAS
HEMATOPOIETIC CELL FAILURE APASTIC, MAY BE DUE TO DRUGS, RADIATION, INFECTIONS, TOXINS
INCREAED CELL LOSS MEHOLYTIC SICKLE CELL, THALASSEMIAS
SICKLE CELL ANEMIA HEREDITARY<BR>HEMOGLOBINOPATHY WITH PARTIAL OR COMPLETE REPLACEMENT OF NORMAL HEMOGLOBIN WITH HEMOG S<BR>S ASSUMES A SICKLED SHAPE AND DERMS RBCS<BR>HEMOLYTIC ANEMIA RESULTS
NORMAL HEMOGLOBIN DISC SHAPED<BR>SOF<BR>EASILY FLOW THROUGH BV<BR>LIVES FOR 120 DAYS
SICKLE SICLES SHAPED<BR>HARD<BR>OFTEN GET STUCK IN SMALL BLOOD VESSELS<BR>LIVES FOR 20 DAYS
POLYCYTHEMIA 3 TYPES VERA, SECONDARY, RELATIVE
VERA NEOPLASTIC TRANSFORMATION OF HEMATOPOETIC STEM CELLS
SECONDARY CHRONIC HYPOXEMIA
RELATIVE DEHYDRATION
POLYCYTHEMIA RESULTS IS INCREASED BLOOD VISCOSITY AND RISK OF THROMBI
TREATMENT OF POLYCYTHEMIA PHLEBOTOMY, BONE MARROW SUPPRESSANTS
INTRINSCI PATHWAY ACTIVATED WHEN FACTOR XII CONTACTS SUBENDOTHELIAL SUBSTANCES EXPOSED BY VASCULAR INJURY
EXTRINSIC PATHWAY ACTIVATED WHEN TISSUE FACTOR IS RELEASED BY DAMAGED ENDOTHELIAL CELLS
TESTS OF BONE MARROW FUNCTION ASPIRATION<BR>BIOPSY<BR>MEASUREMENT OF BONE MARROW IRON STORES<BR>DIFFERENTIAL CELL COUNT
Created by: leah_76
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