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Dr Than Kyaw 13 February 2012

Cardiovascular System (CVS) L-2: Hematopoiesis , Blood Groups, & Hemostasis. Dr Than Kyaw 13 February 2012. Hematopoiesis Formation of Blood Elements. Erythropoiesis. Hematopoiesis. Leukopoiesis. Mainly formed in the red marrow of many bones.

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Dr Than Kyaw 13 February 2012

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  1. Cardiovascular System (CVS) L-2: Hematopoiesis, Blood Groups, & Hemostasis Dr Than Kyaw13 February 2012

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

  3. Hematopoiesis • 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

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

  5. Hormonal control of erythropoiesis Erythropoietin (glycoprotein produced by kidney) • Hypoxia (decreased RBCs) • Decreased O2 availability • Increased tissue demand for O2 Stimulate Bone marrow Adequate supplies of iron, amino acids, and B vitamins Erythropoiesis

  6. ErythropoiesisDietary Requirements • Erythropoiesis requires: • Proteins, lipids, and carbohydrates • Iron, vitamin B12, 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

  7. 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 Blood Groups and Transfusions • Transfused blood must be of the same blood group • Wrong group: dead patient • First done: William Harvey, England (about 1600)

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

  9. Blood Groups of some animals DEA=Dog Erythrocyte Antigen

  10. Blood groups & blood typing in man • 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)

  11. Blood groups & blood typing in man • Two types of antibodies - Agglutinins (Ab) Anti A and Anti B • Blood typing is done based on antigen-antibody reaction • 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

  12. Blood groups & blood typing in man

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

  14. 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. Rh Dangers During Pregnancy What will happen to the Rh+ baby?

  15. 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

  16. 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 Hemostasis and coagulation *  granules and dense granules: containing many of the coagulation factors, proteins, calcium, serotonin, ADP, ATP; all assist or potentiate the coagulation process

  17. Platelets aggregation – regulated by 2 eicosanoids • - Thromboxane A2 (TXA2) and • - Prostacyclin (PGI2) • TXA2 – secreted by adhered platelets and stimulate platelet aggregation • PGI2 – secreted by intact undamaged endothelial cells • - acts to stop the growth of platelet plug. • TXA2 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 TXA2

  18. 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. Hemostasis and coagulation

  19. Activation of factor IX • Activation of factor X • Formation of thrombin and • Fibrin formation 4 key reactions in the clot formation

  20. Major components of coagulation pathway

  21. Extrincsic system Intrincsic system Tissue factor (TF) pathway Contact activation pathway TF VII IX Endothelial damage Surface contact TF-VIIa complex VIII IXa - VIIIa –PL- Ca2+ Tenase complex X Xa X Positive feedback Xa - Va –PL - Ca2+ V Prothrombinase complex Prothrombin Thrombin Fibrinogen Fibrin

  22. Endothelial contact XIIa XII XIa XI IXa IX IXa - VIIIa –PL- Ca2+ Tenase complex

  23. Fibrin formation Fibrinogen Fibrin (polymerized protein) Soluble form Thrombin + Ca2+ XIIIa XIII Insoluble Fibrin (Stable fibrin, more elastic and less subject to lysis )

  24. Clot retraction Shrinking of the clot • By the action of • Platelet contractile protein • Thrombosthenin • Actin • Myosin • Retraction – squeeze serum • - greater blood flow

  25. 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 t-PA (Tissue type plasminogen activator) Plasmin Plasminogen (Plasma protein) Fibrin FDPs (Fibrin degradation products) FDPs, removed by MPS MPS – mononuclear phagocytic system

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