Presentation on theme: "Cardiovascular System (CVS)"— Presentation transcript:
1 Cardiovascular System (CVS) L-2: Hematopoiesis, Blood Groups, & HemostasisDr Than Kyaw 13 February 2012
2 Hematopoiesis Mainly formed in the red marrow of many bones. Formation of Blood ElementsErythropoiesisHematopoiesisLeukopoiesisMainly formed in the red marrow of many bones.Also can be formed in liver, spleen and lymphatic tissues.
3 HematopoiesisAll blood cells originate from pluripotent stem cells hemocytoblastsThe mother of all blood stem cellsHemocytoblasts differentiate into myeloid stem cells and lymphoid stem cellsMyeloid stem cells become myeloblasts or monoblastsGranulocytes formed from myeloblastsMonoblasts enlarge and form monocytesLymphoid stem cells become lymphoblastsLymphoblasts develop into lymphocytes
4 All blood cells originate from pluripotent stem cell hemocytoblasts Pluripotent stem cells(Hemocytoblasts)Myeloidstem cellsLymphoidstem cellsRubriblastMegakaryoblastsMyeloblastMonoblastLymphoblastGranulocytes(Neutrophils,Eosinophils,BasophilsErythrocytesThrombocytesMonocytesLymphocytes
7 Hormonal control of erythropoiesis Erythropoietin (glycoprotein produced by kidney)Hypoxia (decreased RBCs)Decreased O2 availabilityIncreased tissue demand for O2StimulateBone marrowAdequate supplies of iron, amino acids, and B vitaminsErythropoiesis
9 Erythropoiesis Dietary Requirements Erythropoiesis requires:Proteins, lipids, and carbohydratesIron, vitamin B12, and folic acidThe body stores iron in Hb (65%), the liver, spleen, and bone marrowIntracellular iron is stored in protein-iron complexes such as ferritin and hemosiderinCirculating iron is loosely bound to the transport protein transferrin
10 Blood Groups and Transfusions Large losses of blood have serious consequencesLoss of 15 to 30 % causes weaknessLoss of over 30 % causes shock, fatalTransfusions are the only way to replace blood quicklySeldom practiced in animalTransfused blood must be of the same blood groupWrong group: dead patientFirst done: William Harvey, England (about 1600)
11 Blood groups in animals and man Animals and human- a variety of different blood typesIn human – usually only 4 types of groups used
12 Blood Groups of some animals Animal sppBlood groupsCattleA, B, C, F, J, L, M, R, S, T, Z11GoatsA, B, C, M, J5SheepA, B, C, D, M, R and X7Horse8 major groups (A, C, D, K, P, Q, U, T)Over 30CatA, B, AB3DogDEA 1.1, 1.2, 4, 5, 6,7, 88HumanA, B, AB, O4DEA=Dog Erythrocyte Antigen
13 Blood groups & blood typing in man RBCs carry genetically determined proteinsCalled agglutinogens or antigens (Ag)Proteins embedded in cell membraneA foreign protein (Ag) may be attacked by the immune systemTwo types of antigensType AType BBased on presence / absence of antigens A & BType 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 BBlood typing is done based on antigen-antibody reactionWhen serum containing anti-A or anti-B agglutinins is added to blood, agglutination will occur between the agglutinin and the corresponding agglutinogensAgglutination - Positive reactions
16 Blood type being tested Blood groups & blood typing in manBlood type being testedRBC agglutinogensSerum ReactionAnti-AAnti-BABA and B+B–AONone
17 Rh Blood GroupsDepends on presence or absence of Rh antigens (agglutinogen D)Problems can occur in mixing Rh+ blood into a body with Rh– bloodCalled hemolytic disease of the newborn or Erythroblastosis fetalisDanger is only whenthe mother is Rh–the father is Rh+the child inherits the Rh+ factor
18 Rh Dangers During Pregnancy Mom’s immune system is sensitizedMakes antibodies against Rh+In a subsequent pregnancy:Mother’s blood carries antibodiesAnti-Rh antibodies cross placentaAttack the Rh+ blood in the fetusBecause 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 bleedingInvolve 3 basic reactions1. constriction of smooth m/s of blood vessels to reduce openning2. Formation platelet plug to occlude the opening3. 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 adheredThese activated platelets stimulate other platelets to those already present, thus making platelet plugMay 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 aggregationPGI2 – 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 necessaryClot – relatively solid gel plug- a fibrin mesh and entraps the plugIf the plug contains only platelets - a white thrombusIf 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 IXActivation of factor XFormation of thrombin andFibrin formation
25 Major components of coagulation pathway SynonymSite of synthesisFibrinogenFactor ILiverProthrombinFactor IIThrombinPlasmaTissue factorThromboplastinVascular endotheliumFactor VFactor VIIFactor VIIIAntihemophilic factorFactor IXChristmas factorFactor XStuart factorFactor XIPlasma thromboplastinantecidentFactor XIIHageman factorFactor XIIIFibrin stabilizing factorCalciumFactor IV
26 Extrincsic system Intrincsic system Tissue factor (TF) pathway Contact activation pathwayTFVIIIXEndothelial damageSurface contactTF-VIIa complexIXa - VIIIa –PL- Ca2+VIIITenase complexXXaXPositive feedbackXa - Va –PL - Ca2+VProthrombinase complexProthrombinThrombinFibrinogenFibrin
29 Fibrin formation Fibrinogen Fibrin (polymerized protein) Soluble form Thrombin + Ca2+XIIIaXIIIInsoluble Fibrin(Stable fibrin, more elastic and less subject to lysis )
30 Clot retractionShrinking of the clotBy the action ofPlatelet contractile proteinThrombostheninActinMyosinRetraction – squeeze serum- greater blood flow
31 MPS – mononuclear phagocytic system Removal of fibrinAfter establishment of hemostasis– damaged area repaired by new tissue growth assisted by growth factors released by platelets- Fibrin undergoes degradation (fibrinolysis) by proteolytic enzyme plasmint-PA(Tissue type plasminogen activator)Plasminogen(Plasma protein)PlasminFibrinFDPs(Fibrin degradation products)FDPs, removed by MPSMPS – mononuclear phagocytic system
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