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Dr Than Kyaw 13 February 2012 Cardiovascular System (CVS) L-2: Hematopoiesis, Blood Groups, & Hemostasis.

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Presentation on theme: "Dr Than Kyaw 13 February 2012 Cardiovascular System (CVS) L-2: Hematopoiesis, Blood Groups, & Hemostasis."— Presentation transcript:

1 Dr Than Kyaw 13 February 2012 Cardiovascular System (CVS) L-2: Hematopoiesis, Blood Groups, & Hemostasis

2 Hematopoiesis Formation of Blood Elements ● Mainly formed in the red marrow of many bones. ● Also can be formed in liver, spleen and lymphatic tissues. Erythropoiesis Leukopoiesis Hematopoiesis

3 All blood cells originate from pluripotent stem cells hemocytoblasts – The mother of all blood stem cells Hemocytoblasts differentiate into myeloid stem cells and lymphoid stem cells – Myeloid stem cells become myeloblasts or monoblasts Granulocytes formed from myeloblasts Monoblasts enlarge and form monocytes – Lymphoid stem cells become lymphoblasts Lymphoblasts develop into lymphocytes Hematopoiesis

4 Pluripotent stem cells (Hemocytoblasts) Myeloid stem cells Lymphoid stem cells Myeloblast Monoblast Granulocytes (Neutrophils, Eosinophils, Basophils Monocytes All blood cells originate from pluripotent stem cell hemocytoblasts Rubriblast Megakaryoblasts Lymphoblast Thrombocytes Erythrocytes Lymphocytes

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7 Hormonal control of erythropoiesis Erythropoietin (glycoprotein produced by kidney) Bone marrow Erythropoiesis Hypoxia (decreased RBCs) Decreased O 2 availability Increased tissue demand for O 2 Adequate supplies of iron, amino acids, and B vitamins Stimulate

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9 Erythropoiesis requires: – Proteins, lipids, and carbohydrates – Iron, vitamin B 12, and folic acid The body stores iron in Hb (65%), the liver, spleen, and bone marrow Intracellular iron is stored in protein-iron complexes such as ferritin and hemosiderin Circulating iron is loosely bound to the transport protein transferrin Erythropoiesis Dietary Requirements

10 Blood Groups and Transfusions Large losses of blood have serious consequences Loss of 15 to 30 % causes weakness Loss of over 30 % causes shock, fatal Transfusions are the only way to replace blood quickly Seldom practiced in animal  Transfused blood must be of the same blood group  Wrong group: dead patient  First done: William Harvey, England (about 1600)

11 Animals and human - a variety of different blood types In human – usually only 4 types of groups used Blood groups in animals and man

12 Blood Groups of some animals Animal sppBlood groups CattleA, B, C, F, J, L, M, R, S, T, Z11 GoatsA, B, C, M, J5 SheepA, B, C, D, M, R and X7 Horse8 major groups (A, C, D, K, P, Q, U, T)Over 30 CatA, B, AB3 Dog DEA 1.1, 1.2, 4, 5, 6,7, 8 8 Human A, B, AB, O 4 DEA=Dog Erythrocyte Antigen

13 RBCs carry genetically determined proteins Called agglutinogens or antigens (Ag) Proteins embedded in cell membrane A foreign protein (Ag) may be attacked by the immune system Two types of antigens Type A Type B Based on presence / absence of antigens A & B Type AB (presence of both antigens - A & B) Type O (absence of both antigens - A & B) Blood groups & blood typing in man

14 Two types of antibodies - Agglutinins (Ab) Anti A and Anti B Blood typing is done based on antigen-antibody reaction Blood groups & blood typing in man When serum containing anti-A or anti-B agglutinins is added to blood, agglutination will occur between the agglutinin and the corresponding agglutinogens Agglutination - Positive reactions

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16 Blood type being testedRBC agglutinogensSerum Reaction Anti-AAnti-B ABA and B++ BB–+ AA+– ONone–– Blood groups & blood typing in man

17 Rh Blood Groups  Depends on presence or absence of Rh antigens (agglutinogen D)  Problems can occur in mixing Rh + blood into a body with Rh – blood  Called hemolytic disease of the newborn or Erythroblastosis fetalis  Danger is only when  the mother is Rh –  the father is Rh +  the child inherits the Rh + factor

18 Rh Dangers During Pregnancy  Mom’s immune system is sensitized  Makes antibodies against Rh +  In a subsequent pregnancy:  Mother’s blood carries antibodies  Anti-Rh antibodies cross placenta  Attack the Rh + blood in the fetus  Because immunity development takes time – the first baby may not be affected. What will happen to the Rh + baby?

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20 Hemostasis and coagulation Hemostasis – stoppage of bleeding Involve 3 basic reactions 1. constriction of smooth m/s of blood vessels to reduce openning 2. Formation platelet plug to occlude the opening 3. Clot formation to complete occlusion of the opening

21 Hemostasis and coagulation Platelets adhere to collagens and other proteins in the damaged C/T, release secretory granules* The surface of damaged blood vessel – losses its smoothness and nonwetatability that attract platelets to be adhered These activated platelets stimulate other platelets to those already present, thus making platelet plug May be sufficient to occlude very small vessels *  granules and dense granules: containing many of the coagulation factors, proteins, calcium, serotonin, ADP, ATP; all assist or potentiate the coagulation process

22 Platelets aggregation – regulated by 2 eicosanoids - Thromboxane A 2 (TXA 2 ) and - Prostacyclin (PGI 2 ) TXA 2 – secreted by adhered platelets and stimulate platelet aggregation PGI 2 – secreted by intact undamaged endothelial cells - acts to stop the growth of platelet plug. TXA 2 and serotonin (also secreted by adhered platelets) – vasoconstrictors stimulating smooth m/s constriction to assist with hemostasis Hemostasis and coagulation * Aspirin block the formation of TXA 2

23 Hemostasis and coagulation For more serious or large vessel damage Clot or Thrmbus formation, in addition to platelet aggregation, is necessary Clot – relatively solid gel plug - a fibrin mesh and entraps the plug If the plug contains only platelets - a white thrombus If red blood cells are present - a red thrombus. Finally, the clot must be dissolved in order for normal blood flow to resume following tissue repair. The dissolution of the clot occurs through the action of plasmin.

24 4 key reactions in the clot formation 1.Activation of factor IX 2.Activation of factor X 3.Formation of thrombin and 4.Fibrin formation

25 Major components of coagulation pathway ComponentSynonymSite of synthesis FibrinogenFactor ILiver ProthrombinFactor IILiver ThrombinPlasma Tissue factorThromboplastinVascular endothelium Factor VVascular endothelium Factor VIILiver Factor VIIIAntihemophilic factorVascular endothelium Factor IXChristmas factorLiver Factor XStuart factorLiver Factor XIPlasma thromboplastin antecident Liver Factor XIIHageman factorLiver Factor XIIIFibrin stabilizing factorVascular endothelium CalciumFactor IV

26 Intrincsic system TF Extrincsic system Contact activation pathwayTissue factor (TF) pathway VII TF-VIIa complex Endothelial damage XXa IX IXa - VIIIa –PL- Ca 2+ Tenase complex X Surface contact VIII Xa - Va –PL - Ca 2+ Prothrombinase complex V Prothrombin Thrombin FibrinFibrinogen Positive feedback

27 Endothelial contact XII XIIa XI XIa IX IXa IXa - VIIIa –PL- Ca 2+ Tenase complex

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29 Fibrin (polymerized protein) Soluble form Fibrinogen Thrombin + Ca 2+ XIIIaXIII Insoluble Fibrin (Stable fibrin, more elastic and less subject to lysis ) Fibrin formation

30 Clot retraction Shrinking of the clot By the action of 1.Platelet contractile protein 2.Thrombosthenin 3.Actin 4.Myosin Retraction – squeeze serum - greater blood flow

31 Removal of fibrin After establishment of hemostasis – damaged area repaired by new tissue growth assisted by growth factors released by platelets - Fibrin undergoes degradation (fibrinolysis) by proteolytic enzyme plasmin Plasmin Plasminogen (Plasma protein) t-PA (Tissue type plasminogen activator) FibrinFDPs (Fibrin degradation products) FDPs, removed by MPS MPS – mononuclear phagocytic system

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