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Cardiovascular System (CVS)

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Presentation on theme: "Cardiovascular System (CVS)"— Presentation transcript:

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

2 Hematopoiesis Mainly formed in the red marrow of many bones.
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 Rubriblast Megakaryoblasts Myeloblast Monoblast Lymphoblast Granulocytes (Neutrophils, Eosinophils, Basophils Erythrocytes Thrombocytes Monocytes Lymphocytes



7 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


9 Erythropoiesis Dietary 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

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

12 Blood Groups of some animals
Animal spp Blood groups Cattle A, B, C, F, J, L, M, R, S, T, Z 11 Goats A, B, C, M, J 5 Sheep A, B, C, D, M, R and X 7 Horse 8 major groups (A, C, D, K, P, Q, U, T) Over 30 Cat A, B, AB 3 Dog DEA 1.1, 1.2, 4, 5, 6,7, 8 8 Human A, B, AB, O 4 DEA=Dog Erythrocyte Antigen

13 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)

14 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


16 Blood type being tested
Blood groups & blood typing in man Blood type being tested RBC agglutinogens Serum Reaction Anti-A Anti-B AB A and B + B A O None

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?


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 Hemostasis and coagulation
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 * Aspirin block the formation of TXA2

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
Activation of factor IX Activation of factor X Formation of thrombin and Fibrin formation

25 Major components of coagulation pathway
Synonym Site of synthesis Fibrinogen Factor I Liver Prothrombin Factor II Thrombin Plasma Tissue factor Thromboplastin Vascular endothelium Factor V Factor VII Factor VIII Antihemophilic factor Factor IX Christmas factor Factor X Stuart factor Factor XI Plasma thromboplastin antecident Factor XII Hageman factor Factor XIII Fibrin stabilizing factor Calcium Factor IV

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

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


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

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

31 MPS – mononuclear phagocytic system
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) Plasminogen (Plasma protein) Plasmin Fibrin FDPs (Fibrin degradation products) FDPs, removed by MPS MPS – mononuclear phagocytic system


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