physiology of blood

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  • Viscosity , the internal resistance of a liquid to flow. Blood is 3x thicker and denser than pure water. B/S of its thicker and sticky nature blood flows through blood vesssels with little difficulty.
  • Functions overlap & interact to maintainconstancy of our internal environment
  • Plasma=water 90-92%,Proteins = 6-8%,Solute= 2%
  • Osmotic pressure:Colloid: Liquid containing suspended substances that don’t settle outAlbumin: Important in regulation of water movement between tissues and bloodGlobulins: Immune system or transport moleculesFibrinogen: Responsible for formation of blood clots
  • Serum is the yellowish fluid that forms after blood is left to clot.Serum has more or less similar composition to plasma except that its fibrinogen and clotting factors (II. VI, VII) have been removed and has greater serotonin content b/s of the break down of platelets.
  • When stimulated, the stem cells are committed or differentiated and develop into erythroid (RBC line), lymphoid (WBC line) or myeloid (megakaryocytic and granulocytic line) line of blood cell formation.
  • Stem cells: All formed elements derived from single population
  • Type O is a “universal donor”, i.e. can give blood to anyone.Type AB is the “universal recipient”, i.e. can receive blood from anyone.
  • 7.13
  • Rh +  Can receive + or - Rh -  Can only receive -
  • Lymphocytes: T cells - attack foreign cells directly.B cells give rise to plasma cells, which produce antibodies
  • Lymphocytes: Immunity 2 types; b & t Cell types. IgG-infection, IgM-microbes, IgA-Resp & GI, IgE- Alergy, IgD-immune responseMonocytes: Become macrophagesLymphocytes: Make up 20 to 25% WBC’sSmall: 6-9 um in diameter, Large: 10-14 umNucleus is round or slightly indented.• B-Cells-made in bone marrow, Found in blood and produce antibodies. that attack bacteria and toxins
  • In many cases, specific antibodies are produced against platelets destroying them
  • physiology of blood

    1. 1. Presentation Out line 1. Objectives 2. Introduction 3. Blood volume and constituent 4. Plasma constituents 5. Erythrocytes and blood grouping 6. Leukocytes and immune responses 7. Platelets and Hemostasis 2
    2. 2. 1.Objectives  At the end of this session, students will able to:  List the functions of blood  Appreciate blood composition  Understand the structure and functions of RBCs, WBCsand platelets. 3
    3. 3. 2. Introduction  The Only Fluid tissue in the body.  Specialized type of connective tissue in which formed elements are suspended in non living fluid matrix called plasma. 4
    4. 4. 3. Blood volume and constituent   Physical Characteristics of Blood viscosity: sticky opaque fluid, due to the presence of RBCs(sticky and thick), Viscosity (thickness) = 4 – 5.  color : o Scarlet red-high oxygen o Dark red-poor oxygen 5
    5. 5.  PH: 7.35-7.45  Temperature: Blood temperature is slightly higher than body temperature.  Blood volume: 5–6 L for males; 4–5 L for females. Blood accounts for approximately 8% of body weight. 6
    6. 6.  The amount of blood varies with body size, changes in fluid concentration, changes in electrolyte concentration, and amount of adipose tissue.  Density ( specific gravity): Refers to the weight of blood compared to water.  Specific gravity of H20 is taken as 1(i.e.,1 ml of H2O weighing 1 gm at 4 oc). 7
    7. 7.  Male:1.052-1.063  female:1.050-1.058 ( i.e.,1 ml of whole blood weighing 1.060gm).  Osmolarity = 300 mOsm or 0.3 Osm, reflects the concentration of solutes in the plasma.  Salinity = 0.85%, Reflects the concentration of NaCl in the blood. 8
    8. 8.  Functions of blood  Blood performs a number of functions dealing with: 1. Substance distribution (Transportation ) 2. Regulation of blood levels of particular substances 3. Body protection 9
    9. 9. Cont’d…… 1.Distribution (Transports ) o Oxygen from the lungs and nutrients from the digestive tract to the tissues . o Metabolic wastes from cells to the lungs and kidneys for elimination o Hormones from endocrine glands to target organs 10
    10. 10. Cont’d…. 2.Regulations o Appropriate body temperature by absorbing and distributing heat to other parts of the body o Maintaining body PH in the body tissues using buffer system. o Maintaing adequate fluid volume in the circulatory volume. 11
    11. 11. 3. protection o Hemostasis   o Activating plasma proteins and platelets. Initiating clot formation when a vessel is broken. infection : Synthesizing and utilizing antibodies.  Activating complement proteins. Activating WBCs to defend the body against foreign invaders.
    12. 12. Composition of Blood  2 major components  Liquid = plasma (55%)  Formed elements (45%)  Erythrocytes / red blood cells (RBCs)  Leukocytes / white blood cells (WBCs)  Platelets, fragments of megakaryocytes in marrow ( thrombocytes ).
    13. 13. Components of Whole Blood Plasma (55% of whole blood) Buffy coat: leukocyctes and platelets Formed (<1% of whole blood) element s 1 Withdraw blood and place in tube 2 Centrifuge Erythrocytes (45% of whole blood) 14
    14. 14. Cont’d…… Capillary tube Plasma 55% Buffy coat RBCs =45% Plug 15
    15. 15. 4. Plasma constituents  Blood plasma : straw colored sticky fluid, includes:   Water = 90-92%. Proteins = 6-8%. Albumin,globilin and clotting proteins  Organic nutrients – glucose, carbohydrates, amino acids  Electrolytes – sodium, potassium, calcium, chloride, bicarbonate. 16
    16. 16.  Non protein nitrogenous substances – lactic acid, urea, creatinine.  Respiratory gases – oxygen and carbon dioxide.  Plasma proteins  Albumins:  accounts 60% of Wt,Most abundant plasma protein.  Carrier to shuttle molecules through the circulation 17
    17. 17.    Important blood buffer. maintain osmotic pressure of the blood. Globulins : Accounts 36% of the plasma protein.    α and β globulins have role in transport. γ globulins are in immuno globulins( IgG, IgA). Clotting proteins : account for 4% ‾ Fibrinogen and Prothrombin. 18
    18. 18.  Serum: Plasma with clotting factors removed, yellowish color.  Determined by means of electrophoresis 19
    19. 19. Cont’d……..  Formed elements  Comprise 45% of blood  Erythrocytes, leukocytes, and platelets make up the formed elements  Only WBCs are complete cells  RBCs have no nuclei or organelles, and platelets are just cell fragments. 20
    20. 20. Cont’d…….  Most formed elements survive in the bloodstream for only a few days.  Most blood cells do not divide but are renewed by cells in bone marrow. 21
    21. 21. Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Blood 45% 55% Plasma Formed elements Platelets Red blood cells (4.8%) (95.1%) White blood cells Electrolytes (0.1%) Water (92%) Proteins Wastes (7%) Nutrients Gases Vitamins Hormones Neutrophils Eosinophils Basophils Monocytes Lymphocytes (54–62%) (1–3%) (<1%) (3–9%) (25–33%) Albumins Globulins Fibrinogen N2 O2 CO2
    22. 22. 5. Red Blood Cells ( RBCs)  Shape: flexible biconcave cell that is thinner at the center and thicker at the edges  Diameter: ~ 7.5 um - Mature, No nucleus and organelles.  Has greater surface area/volume ratio, Therefore, can bend and twist to pass through the narrow capillaries very easily. 24
    23. 23. 25
    24. 24.  The major forms of cell in the blood.  The average number of RBCs are 5 million/ mm3 blood or 5 x106 / μl of blood.  Lack of mitochondria.  Each RBC contains 280 million haemoglobin.  Half-life app.120 days. 26
    25. 25. Hematocrit (Hct) / Packed cell volume (PCV)   1. Hematocrit (Ht): is the percentage by volume of packed RBC. Procedure : Centrifuge of un –coagulated blood at a high speed (10-15 min). 2. RBC precipitate down to the bottom. 3. The plasma portion remains floating.  The cells that settle down to the bottom (mainly RBCs) form the hematocrit or packed cell volume (PCV). 27
    26. 26.  Normal value:    Males: 47% 5% Females: 42% 5% HCT increase in polycythemia and dehydration states.  Decrease in anemia 28
    27. 27. Function of RBCs : 1. Carries hemoglobin that in turn transports respiratory gases (O2 and CO2). 2. Carbonic anhydrase (CA): An enzyme located in RBC membrane.  CO2 + H2O CA H2CO3 = HCO-3 + H+  CA increases the rate of this reaction 5000 fold.  Good to transport CO2 from the tissues to the lung very fast.
    28. 28.  Haemoglobin : Consists of globulin and heme.  Globulin  Two alpha(α) chain polypeptide  Two beta(β) chain polypeptides  Heme: Each heme is present in one peptide chain and contains an iron {Fe++} that combines reversibly with one molecule of O2. 30
    29. 29.  Each polypeptide has one heme group, each heme with Fe2+ carries one O2 molecule, total = 4- O2 molecules Are carried with in Hb molecule.  1g Hb binds with 1.34 ml O2  15g Hb/dl x 1.34 ml O2 = 20.1 ml O2/100 ml blood. 31
    30. 30. 32
    31. 31. 33
    32. 32.  The polypeptide chain (the Globin unit) determines the physical characteristics of the Hb-molecule. Thus, there exists: a. Adult Hb (Hb A): 2α + 2β b. Fetal Hb (Hb-F): 2α + 2γ c. Sickle cell (Hb-S): glutamic acid is replaced by valine at Beta- chain so on. 34
    33. 33.  Saturation of Hb: refers to the number of O2 molecules combined with Hb.  The Hb molecule combine maximally with 4 molecules of O2 in a cascade manner(100%saturated),by Oxygenation reaction, each binding facilitates further binding of O2.  50 % saturation: means that Hb binds with 2 molecules of O2. 35
    34. 34. Hematopoiesis/ hemopoieisis  RBC and other blood cells are produced in the Bone marrow.  All cells emerge from undifferentiated (uncommitted ) stem cells in the Bone marrow.  Stem cells: All formed elements derived from single population 36
    35. 35.  Stem cells: All formed elements derived from single population  Proerythroblasts : Develop into red blood cells  Myeloblasts: Develop into basophils, neutrophils, eosinophils  Lymphoblasts: Develop into lymphocytes  Monoblasts: Develop into monocytes  Megakaryoblasts: Develop into platelets 37
    36. 36. Hematopoiesis
    37. 37. Erythropoiesis. A. Embryonic life: RBC are produced in the liver, spleen and lymph nodes. B. Infants (5 years old): Red bone marrow of all cells. C. Adults (after age 20): Membranous bones like ribs, sternum, vertebrae and pelvic bones. - But not in long bones like femur or tibia (fat). 39
    38. 38.  Stem cells differentiate to produce committed stem cells called hematocytoblasts that in turn produce : 1. Proerythroblast: where Hb synthesis begins, big nucleus. 2. Basophile erythroblast: cell divide, continues 3. Polychromatophil erythroblast: Hb synthesis increases and fills the cytoplasm, nucleus size decreases. 40
    39. 39. 4. Ortochromatic erythroblast: Nucleus decreases. 5. Reticulocytes: Contains Hb, no nucleus and the cell is expelled from the bone to circulation. 6. Erythrocytes: Mature form of RBC without nucleus, filled with Hb. 41
    40. 40. 42
    41. 41.  Physiological Mechanism 1. Low oxygen(Hypoxia ) that occurs in the kidney cells. 2. Kidney then produce a hormone called erythropoietin. 3. Erythropoietin is transported by the blood to bone marrow. 4.  Bone marrow produces and releases a increased RBC . Increased or adequate O2 then blocks the formation of more RBC.
    42. 42. 44
    43. 43. 45
    44. 44. Organs involved in erythropoiesis  Kidney : Erythropiotein  Liver : Store protein, vit.B12& folic acid ,Synthesize globin , Produce Erythropiotein 10%.  Bone Marrow: Site of RBCs formation  Stomach: intrinsic factor.  Small Intestine: absorption of Iron, vitamins, and amino acids. 46
    45. 45. Substances necessary for RBC maturation A. Vitamin B12: requires intrinsic factor for absorption - Important for DNA synthesis and thus for cell division.  Deficiency of Vit B12 : Megaloblastic anemia.  Characterized : macrocytic cells (big Hb in cytoplasm) Because of their big size, the cells rupture when passing through the capillary wall. 47
    46. 46.  Insufficient of intrinsic factor causes , Maturation failure for Vit. B12 is call pernicious anemia. B. Folic acid: important in DNA synthesis. c. Iron: Necessary for RBC formation. D.Trace elements : (Co, Vit. Copper etc). 48
    47. 47. Destruction of RBCs  The absence of nucleus in erythrocytes prevents them from synthesizing proteins and other important substances necessary for survival.  The cells become weak and fragile and die after about 120 days. 49
    48. 48.  The older red cells are phagotizised by macrophage cells of the reticuloendothelial system that are located in the liver, spleen, and bone marrow cells.  The macrophages release the Hb-molecule that is broken down into: a. its protein part (Globin) and b. Heme part 50
    49. 49.  Steps in the destruction of RBC: 1. RBC = Globin + Heme 2. Globin = Broken to AA‟s > used for protein synthesis 3. Heme = Fe2+ + poryphrine rings. 4. Fe 2+ = stored in the liver > used for new Hb synthesis. 5. Pyrol rings > oxidation to green pigment called Biliverdin and later reduced to bilirubin. 51
    50. 50. a. Bilirubin + serum albumin > reach liver. b. Bilirubin conjugates with glucuronic acid in liver. C. Liver releases bilirubin as bile to Small intestine. Bacteria's change bilirubin into: D.   Strrcobilinogen > stercobilin , feces (brown color). Uribilinogen > Urobilin > Urine (yellow). 52
    51. 51. Life Cycle of a Red Blood Cell
    52. 52. 54
    53. 53. Clinical correlations: Anemia A decrease in; 1- RBC number or/and 2- Hb content Below the normal for that sex and age. 1.Decreased RBC Number. - Blood loss : e.g, hemorrhage - A plastic anemia: bone marrow destruction (X-ray) - Maturation failure anemia: pernicious anemia. 55
    54. 54.  Microcytic Hypochromic Anemia: Low levels of hemoglobin in RBCs due to chronic blood loss resulting in low Fe2+ levels in newly produced RBCs. 2. Hemolytic Anemia: Different abnormalities of RBCs that make RBCs fragile and rupture easily. 56
    55. 55.  Hereditary Spherocytosis: RBC develop as small spherical cells . These spherical cells easily rupture by slight compression.    Sickle-cell Anemia: Genetic mutation causing abnormal beta chains. HgS exposed to low O2 concentrations, it precipitates into long crystals that cause the cells to become sickle-shaped. 57
    56. 56. Effects of Anemia • Due to decrease O2 supply to tissues. 1- Fatigue, muscle weakness 2- Mental effects: lack of concentration and dizziness , even Faintining 3- CVS effects: tachycardia, palpitation, heart failure if not treated 4- nausea & anorexia 5- Retarded growth in children 58
    57. 57. Polycethemia  is abnormal increase of RBC in the circulation.  Two types 1. Polycethemia Vera (8-9 million)  Tumerous or cancerous production causes highly engorged blood.  genetic mutation in the hemocytoblastic cell line that increases RBC production. Hematocrit values can reach 70% 59
    58. 58. 2. Secondary Polycethemia;   Mostly Physiologic Increase in RBC production due to hypoxic tissues. e.g. high altitudes. 60
    59. 59. Effect of polycethemia on the circulatory system 1. Increased viscosity causes sluggish blood movement. 2.thrombosis and obstruction of different blood vessels. 3.decreased blood flow to tissues and Decreased delivery of O2 to tissues. 4.Hct increases and so blood volume, blood pressure and work of the heart increases.  RX: aim to remove RBC by; phlebotomy, blood donation 61
    60. 60. 6.Blood Groups  Erythrocytes contain genetically determined surface antigens( agglutinogens).  Blood plasma contains antibodies(agglutinins )that react with specific antigens.  Blood is named according to surface antigens that are present. 62
    61. 61. Types of blood group  In humans, there are two known blood groups that are clinically important: a. The ABO-Blood groups b. The Rh- Blood group factors 63
    62. 62. ABO Blood Group  In the ABO system, blood is classified primarily on the Basis of the A and B antigens present on the surface of red blood cell membranes (erythrocytes).  Secondly, blood is classified on the basis of the naturally occurring antibodies (agglutinins) in the serum .  A person whose red cells possess the A -antigen has antiB antibody in his serum and is classified as Blood group A. 64
    63. 63.  If B antigen is present in the Red cell membranes, Anti-A antibody is present in his serum and the person is designated as Blood group B.  If Both AB antigens are present on Red cells, then he has no antibody, so is AB blood group.  If No antigens are present on red cells, he is O Type and has both anti A and B antibody in his serum. 65
    64. 64.  ABO Blood Group  4 blood types – A, B, AB, O  Types are identified by antigens located on the RBC surface. 66
    65. 65. 67
    66. 66. ABO-blood group 68
    67. 67.  Typing and cross-matching – process by which blood type is identified and donor blood is tested for possible transfusion.  Transfusion:  Type O is a Universal Donor.  Type AB is the Universal Recipient. 69
    68. 68.  Blood group O  Universal Donor.  No antigens on their cell-membrane surfaces and therefore can not agglutinate if transfused to any blood types.  Receive only from persons with blood group “O” only because , they have anti- A & anti-B antibodies in the plasma. 70
    69. 69.  Blood group AB  Universal recipient  they have no antibodies in their blood to cause agglutination reactions.  Have antigen A and B, AB can donate blood only to a person with blood AB, not to other. 71
    70. 70.   Method of blood typing Procedures: 1. On a slide at opposite ends , drops of anti- A antibody and Anti-B antibody are added at opposite sides. 2. 2-3 drops of Blood (RBC‟s) are added on the prepared antibodies and changes for agglutination are observed after a few minutes. 72
    71. 71. A. If agglutination occurs on anti-A antibody (sera), then the blood is Blood Group A. B. If agglutination occurs on anti-B antibody , the blood is Blood Group B. C. If there is agglutination in both A and B-antibodies, then it is Blood Group AB. D. If no agglutination occurs, then it is Blood Group O. 73
    72. 72. 74
    73. 73. Agglutination Reaction 75
    74. 74. Donators and Recipients  Donators 1. 2. 3. 4.  O can donate blood to group A, B, AB, and O A “ A & AB only B “ B & AB only AB “ AB only Recipients 1. 2. 3. 4. O can receive blood from group A “ B “ AB “ O only A & O only B & O only A, B, O, & AB 76
    75. 75. RH Blood Group  Named after Rhesus monkey.  Consists of over 50 related antigens, the most clinically significant is D,C,E,c ,d and e.  The type D antigen is more antigenic and widely prevalent in the population.  Rh+, having type D antigen, 85% of the population  Rh-,lack of type D antigen , 15% of the population 77
    76. 76. • A person with Rh negative(-)blood does not have Rh antibodies naturally in the blood plasma. • If they receive blood that is Rh positive (+) , antibodies form but not a problem. • The second exposure can produce a transfusion reaction (Hemolysis and possible kidney damage). 78
    77. 77. Rh incompatibility  Father Rh + = Rh + means he has D antigen on his RBC membrane.  Mother Rh- = No Rh factor(no D antigen). Marriage: 1. Rh+ father X Rh- mother = Rh + fetus. 2. During birth through placenta , Rh+ blood (antigens) of the fetus leak (enter) to mothers blood and sensitizes her. 79
    78. 78. 3. Mother „s blood produces anti-Rh antibodies (anti-D antibodies ) against the Rh+ blood. 4. During the 2nd pregnancy and there after, the Anti-Rh+ antibodies (agglutinins) enter into the fetus and agglutinate or hemolyze the RBC’s the fetus. 80
    79. 79.  This type of hemolytic disease is called Erythroblastosis fetalis.  If the baby is born alive from the incidence, then there is a higher risk of being Anemic and jaundiced. 81
    80. 80.  Prevention • Shortly after each birth of an Rh+ baby, the mother is given an injection of anti-Rh antibodies (or Rhogam).  These passively acquired antibodies destroy any foetal cells that got into her circulation before they can elicit an active immune response in her. 82
    81. 81. Bio 130 Human Biology
    82. 82. Erythroblastosis Fetalis 19-84
    83. 83. 7. White Blood Cells( Leukocytes ) and immune response 85
    84. 84. Properties  The only formed element that are complete cells.  Normal number: 4000-10,000 / mm3 of blood  Mobility: Are highly mobile and reach tissue fluids.  When infection occurs, WBC increase in number e.g., Neutrophils.  Life span : Many (not all) live only a few days, may be b/s of their engagement with pathogens.  Grouped into two main categories. 86
    85. 85.  Granulocytes : contain specialized membrane-bound cytoplasmic granules.  Contain cytoplasmic granules that stain specifically (acidic, basic, or both) with Wright‟s stain  Are larger and usually shorter-lived than RBCs.  Have lobed nuclei, Are all phagocytic cells.  include neutrophils, eosinophils and basophiles. 87
    86. 86.  Agranulocyte : Lack obvious granules; Lymphocytes and Monocytes. 88
    87. 87. Granulocytes 1.Neutrophils: Make up 60 to 70% of WBC‟s.  Diameter of 10-15 μm, Phagocytic  First to arrive at infections.  Nucleus 2-5 lobes (increase with cell age)  Increase: stress, burns and bacterial infections.  Decrease: Radiation exposure, B12 deficiency. 89
    88. 88. 2.Eosinophils : Account for 1-4% of WBCs  10 –12 um in diameter, Nucleus 2–3 lobed  Increase: allergic reactions, parasitic infections and autoimmune disease. 1. Kill parasitic worms 2. Destroy antigen-antibody complexes. 3. Inactivate some inflammatory chemical of allergy (histamine). 90
    89. 89. 3. Basophils: Account for 0.5% -1% of WBCs.  Liberate heparin and histamines during allergic reactions.  Intensify inflammatory response  Increase: Allergic reactions, leukemia, cancers, hypothyroidism.  Decrease: Pregnancy, ovulation, stress, hyperthyroidism 91
    90. 90. Agranulocyte 1.  Lymphocytes: Make up 20 to 25% WBC‟s Small: 6-9 um in diameter, Large: 10-14 um, Nucleus is round or slightly indented.  B cells produce antibodies.  T cells attack viruses, cancer cells, and transplanted tissues  Natural killer cells attack infectious microbes and tumor cells. 92
    91. 91.  2. Monocytes  Account for 4-8% of WBCs and the largest WBCs.  They leave the circulation enter tissue and differentiate into macrophages.  Activate lymphocytes to mount an immune response.  Phagocytize bacteria, dead cells, and other debris. 93
    92. 92. 94
    93. 93. mobility through the tissues 1. Diapedesis: WBC Squeeze out through the capillary pore (e.g. Neutrophils, Monocytes ). 2. Amoeboid motion: Produce pseudopodia and reach the microbes in the tissues 3. Chemotaxis: WBC are attracted by chemicals or toxins produced by the microbe or inflamed tissues 4.Phagocytosis: engulfing and destroying e.g., Neutrophils, macrophages . 95
    94. 94. 96
    95. 95. Clinical correlation  Leukemia (increased WBC No):  cancerous production of WBC.  These occurs: a. in the bone marrow b. in the lymph.  Their increased production takes the space of platelets & RBC causing anemia + impaired blood clotting 97
    96. 96.  Leucopenia: Decreased production of WBC - Bone marrow stops producing them - Drug poison, X-rays 98
    97. 97. Practical hematology/leukocyte differential  Lists the different percentages of leukocytes  ↑Neutrophils : Bacterial Infection  ↑ Lymphocytes: Viral Infection  ↑ Monocytes: Chronic Infection  ↑ Basophils: Allergic Rxns  ↑Eosinophils: parasitic infections 99
    98. 98. 8. Platelets and Hemostasis 100
    99. 99. Platelets/Thrombocytes  Small, non nucleated (anucleated), round/oval cells/cell fragments.  Their size ranges 1-4 m in diameter.  The cytoplasm stain pale blue and contain many pink granules.  They are produced in the bone marrow by fragmentation of megakaryocytes, which are large and multinucleated cells. 101
    100. 100. • Their primary function is preventing blood loss from hemorrhage by forming a platelet plug • Normal value – 150,000 to 300,000/mm3.  Platelets have a life span of approximately 10 days.  Senescent platelets are removed by the spleen. 102
    101. 101.  Attracted to hemorrhage.  Plugs leaks.  Promotes constriction of blood vessel.  Triggers inflammation.  Initiates clotting. 103
    102. 102. Hemostasis • • Hemostasis refers to the stoppage/arresting of bleeding. Actions that limit or prevent blood loss include: • Blood vessel spasm • Platelet plug formation • Blood coagulation 104
    103. 103. 105
    104. 104.   Blood coagulation Triggered by cellular damage and blood contact with foreign surfaces. • • A blood clot forms Causes the formation of clot via a series of reactions which activates the next in a cascade • Occurs extrinsically or intrinsically. 107
    105. 105.  Extrinsic clotting mechanism • Triggered when blood contacts damaged blood vessel walls or tissues. • Chemical outside of blood vessel triggers blood coagulation. • Triggered by tissue thromboplastin (factor III) (not found in blood).
    106. 106. • A number of events occur that includes factor VII, factor X, factor V, factor IV, and factor II (prothrombin).  Intrinsic clotting mechanism  Triggered when blood contacts a foreign surface • Chemical inside blood triggers blood coagulation • Triggered by Hageman factor XII (found inside blood) • Factor XII activates factor XI which activates IX which joins with factor VIII to activate factor X.
    107. 107. Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Extrinsic Clotting Mechanism Intrinsic Clotting Mechanism Blood contacts foreign surface Tissue damage Releases Activates Tissue thromboplastin (Factor lll) Activates (Ca+2) Hageman Factor Xll Activates Factor Vll Factor Xl Activates (Ca+2) Activates Factor X Factor lX Activates Factor V (Ca+2) Factor Vlll platelet phospholipids Factor X Activates (Ca+2) Activates Factor V (Ca+2) Prothrombin activator Converts Thrombin (Factor lla) Prothrombin (Factor ll) Converts Fibrinogen (Factor l) Fibrin Factor Xlll Stabilizes Fibrin clot 110
    108. 108. 111
    109. 109. Fate of Blood Clots • After a blood clot forms it retracts and pulls the edges of a broken blood vessel together while squeezing the fluid serum from the clot.  Platelet-derived growth factor stimulates smooth muscle cells and fibroblasts to repair damaged blood vessel walls.  Plasmin digests the blood clots. 112
    110. 110. Clinical correlations 1. Hemophilia A: Deficiency of Factor VIII accounts for 85% cases. Almost exclusively in males.  Females are usually carriers, caused by a gene mutation on the “X” chromosome. Occurs in about 1/10,000 male births  Other Hemophilias account for another 15% ,Hemophilia B (Factor IX),Hemophilia C (Factor XI) and Hemophilia D (Factor XII) 113
    111. 111. 2.Thrombocytopenia: Abnormally low levels of platelets. Usually below 50,000/ μl of blood. 3.Thrombus: Abnormal clot that develops in a blood vessel. 4.Embolus: Free thrombic clots carried in the blood that usually get caught in arterioles in the brain, kidney, and lungs. 114
    112. 112. Practical hematology/Tests for Bleeding 1. Bleeding time : The time interval that takes between start of bleeding (oozing) until arrest of blood. Normal duration : 36 min 2. Clotting time: The duration of time it takes for the blood to clot (normal duration is 3-8 min). 3.Prothrombin time: Deals with the duration of formation of Prothrombin after addition of oxalate and Ca2+ ions to the blood.
    113. 113.  Reading assignment on immunity 116

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