Download - Dr Than Kyaw 13 February 2012
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Dr Than Kyaw13 February 2012
Cardiovascular System (CVS)
L-2: Hematopoiesis, Blood Groups, & Hemostasis
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HematopoiesisFormation 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
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• 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
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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
ThrombocytesErythrocytes Lymphocytes
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Hormonal control of erythropoiesis
Erythropoietin(glycoprotein
produced by kidney)
Bone marrow
Erythropoiesis
Hypoxia (decreased RBCs)Decreased O2 availabilityIncreased tissue demand for O2
Adequate supplies of iron, amino acids, and B vitamins
Stimulate
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• 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
ErythropoiesisDietary Requirements
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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)
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• Animals and human - a variety of different blood types
• In human – usually only 4 types of groups used
Blood groups in animals and man
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Blood Groups of some animals
Animal spp Blood groupsCattle 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
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• 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 antigensType AType B
• Based on presence / absence of antigens A & BType AB (presence of both antigens - A & B)Type O (absence of both antigens - A & B)
Blood groups & blood typing in man
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• 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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Blood type being tested
RBC agglutinogens Serum Reaction
Anti-A Anti-B
AB A and B + +
B B – +
A A + –
O None – –
Blood groups & blood typing in man
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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
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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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Fig. 11.13
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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 opening3. Clot formation to complete occlusion of the opening
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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
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• 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
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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.
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4 key reactions in the clot formation
1. Activation of factor IX2. Activation of factor X3. Formation of thrombin and 4. Fibrin formation
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Major components of coagulation pathwayComponent Synonym Site of synthesis
Fibrinogen Factor I Liver
Prothrombin Factor II Liver
Thrombin Plasma
Tissue factor Thromboplastin Vascular endothelium
Factor V Vascular endothelium
Factor VII Liver
Factor VIII Antihemophilic factor Vascular endothelium
Factor IX Christmas factor Liver
Factor X Stuart factor Liver
Factor XI Plasma thromboplastin antecident
Liver
Factor XII Hageman factor Liver
Factor XIII Fibrin stabilizing factor Vascular endothelium
Calcium Factor IV
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Intrincsic system
TF
Extrincsic system
Contact activation pathwayTissue factor (TF) pathway
VII
TF-VIIa complex
Endothelial damage
X Xa
IX
IXa - VIIIa –PL- Ca2+
Tenase complex
X
Surface contact
VIII
Xa - Va –PL - Ca2+
Prothrombinase complexV
Prothrombin Thrombin
FibrinFibrinogen
Positive feedback
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Endothelial contact
XII XIIa
XI XIa
IX IXa
IXa - VIIIa –PL- Ca2+
Tenase complex
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Fig. 11.9
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Fibrin (polymerized protein)
Soluble form
Fibrinogen
Thrombin + Ca2+
XIIIa XIII
Insoluble Fibrin (Stable fibrin, more elastic and less subject to lysis )
Fibrin formation
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Clot retractionShrinking of the clot
By the action of1.Platelet contractile protein2.Thrombosthenin3.Actin4.Myosin
Retraction – squeeze serum - greater blood flow
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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 plasmin
PlasminPlasminogen(Plasma protein)
t-PA (Tissue type plasminogen
activator)
Fibrin FDPs(Fibrin degradation
products)
FDPs, removed by MPS
MPS – mononuclear phagocytic system
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