BLOOD AND CIRCULATION (Functions, components, blood clot, clotting mechanism,blood grouping, Deficiency disorder).pptx

This PPT includes the information about blood, its components, types of blood grouping, deficiency disorder, significance, blood clotting and its mechanism and more.

1. BLOOD AND CIRCULATION Rashmi M G

2. Blood Blood (connective tissue) pH alkaline (7.3-7.4). Blood volume: Males: 5-6 L Females: 4-5L Blood plasma Formed elements Cells Cell fragments Liquid extracellular matrix (1) Rashmi M G

3. Functions of blood: Transportation Regulation Protection Gases (oxygen and carbon dioxide) Nutrients Hormones Heat Wastes pH Body temperature Water content of cells Blood loss- clotting Disease – phagocytic activity Rashmi M G

4. Components of blood Blood plasma Formed elements 55% volume 45% volume Straw colored RBC- red color WBC – no color Platelets no color Blood- formed elements= blood plasma Blood- blood plasma= formed elements Components: 90-92% water 8-10% solutes (approx 7% proteins- albumin, globulin, fibrinogen) Minerals- sodium, calcium, magnesium, bicarbonates, chlorine 3 components: RBC WBC platelets HEPATOCYTES PLASMA PROTEINS ALBUMINS GLOBULIN FIBRINOGEN IMPORTANT CLOTTING FACTOR Rashmi M G

5. FORMED ELEMENTS ERYTHROCYTES LEUKOCYTES PLATELETS Red blood cells (RBC) complete cell White blood cells (WBC) Complete cell Thrombocytes Cell fragments Normal range: Male- 5.4 millions/micro litre of blood Female Female- 4.8 million/ micro litre of blood Normal range: 5000-10000 cells/ micro litre of blood Normal range: 150000-400000 / micro litre of blood Features: No nucleus and membrane bound organelles Biconcave Red colour - hemoglobin Features: Nucleus present Colorless- No hemoglobin Features: No nucleus Cytoplasm small enclosed by piece of plasma membrane Origin: hemopoietic stem cells  erythrocytes Origin: Hemopoietic stem cells  leukocytes Origin: Hemopoietic stem cells  megakaryocytes thrombocytes Rashmi M G

6. Types of Leukocytes (White blood cells) GRANULOCYTES Conspicuous chemical filled cytoplasmic granules (vesicles) present and visible after staining EOSINOPHILS BASOPHILS NEUTROPHILS Features: Nucleus- bilobed Cytoplasmic granules- red Features: Nucleus- bilobed Cytoplasmic granules- blue Features: Nucleus- multilobed , (polymorphonuclear leukocytes) Cytoplasmic granules- pink Function: Detoxification Function: Synthesis of Histamine and heparin Function: Phagocytic activity Rashmi M G

7. Types of Leukocytes (White blood cells) AGRANULOCYTES AGRANULOCYTES Conspicuous chemical filled cytoplasmic granules are may be present or absent but invisible after staining LYMPHOCYTES MONOCYTES Features: Small cells with round nucleus and little cytoplasm Features: Cells with single nucleus (Kidney shaped/ horse shoe shaped) Azurophilic granules present B-LYMPHOCYTES T- LYMPHOCYTES NO SUCH TYPES Produce antibodies which binds to antigen of foreign particle and causes destruction Directly destroy cells that have antigens of pathogen Functions: Immune response Functions: Phagocytic activity Rashmi M G

8. FUNCTIONS OF FORMED ELEMENTS ERYTHROCYTES LEUKOCYTES THROMBOCYTES Oxygen and carbon dioxide transport Defense Detoxification Anticoagulant synthesis Phagocytic activity Immune response Clotting Serotonin synthesis (2) Rashmi M G

9. BLOOD CLOTTING Coagulation. Transformation of liquid blood into solid gel “clot” Clot consists of insoluble proteins “fibrin”; formed elements are trapped. Formation of fibrin threads. Substance required for clotting are: clotting factors Calcium ions. Inactive enzymes by hepatocytes. Molecules associated with platelets/ released by damaged tissues. Main reaction: SOLUBLE FIBRINOGEN INSOLUBLE FIBRIN (3) Rashmi M G

10. 12 Clotting factors FACTOR SOURCE DESCRIPTION FACTOR I LIVER FIBRINOGEN FACTOR II LIVER PROTHROMBIN FACTOR III DAMAGED TISSUE, PLATELETS THROMBOPLASTIN FACTOR IV DIET, BONES, PLATELETS CALCIUM IONS FACTOR V LIVER, PLATELETS PROACCELEREIN FACTOR VII LIVER PROCONVERTIN FACTOR VIII LIVER ANTIHEMOPHILIC FACTOR- A FACTOR IX LIVER ANTIHEMOPHILIC FACTOR- B FACTOR X LIVER THROMBOKINASE FACTOR XI LIVER ANTIHEMOPHILIC FACTOR-C FACTOR XII LIVER ANTIHEMOPHILIC FACTOR-D FACTOR XIII LIVER, PLATELETS FIBRINASE Rashmi M G

11. Clotting cascade EXTRINSIC PATHWAY INTRINSIC PATHWAY Shorter pathway Longer pathway Rapid process Slow process Activator is from cells outside the blood vessels Activators is in direct contact with blood/ within blood First reaction: Proconvertin active Proconvertin First reaction: Hageman factor active Hageman factor Rashmi M G

12. INTRINSIC PATHWAY Damaged surface of blood vessel XII Hageman factor XII Active Hageman factor XI AHF-C XII Active AHF-C IX AHF-B IX Active AHF-B VIII Active AHF-A X Thrombokinase X Active thrombokinase V Active Proaccelerin II Prothrombin II Active thrombin I Fibrinogen I Fibrin XIII Fibrinase Cross linked fibrin clot Rashmi M G

13. EXTRINIC PATHWAY Injury VII Proconvertin VII active Proconvertin X Thrombokinase X Active thrombokinase V Active Proaccelerin II Prothrombin II Active thrombin I Fibrinogen I Fibrin XIII Fibrinase Cross linked fibrin clot Thromboplastin Rashmi M G

14. Anemia- Reduced Oxygen carrying capacity of blood Iron deficiency anemia Inadequate absorption of iron or loss of iron in body Megaloblastic anemia Inadequate intake of Vit B12, red bone marrow produces abnormal RBCS Pernicious anemia Inability to produce intrinsic factor needed for absorption of Vit B12 in small intestine Hemorrhagic anemia Excessive loss of RBC through bleeding, stomach ulcers and over menstruation Hemolytic anemia Premature rupture of plasma membrane of RBCs due to invasion of RBC by malarial parasite or sickle cell (defective cells) Thalassemia Deficient synthesis of globins, hereditary hemolytic disease Aplastic anemia Destruction of red bone marrow, failure of bone marrow to produce RBC Rashmi M G

15. Blood group Type- A BLOOD GROUP RBC ANTIGEN- A ANTIBODY- B Type- B BLOOD GROUP RBC ANTIGEN- B ANTIBODY- A Type- AB BLOOD GROUP RBC ANTIGEN- A and B ANTIBODY- NO Type- O BLOOD GROUP RBC ANTIGEN- NO ANTIBODY- A and B Rashmi M G

16. Predicting blood groups Blood group- A Genotype: I A I A / I A i I A i Blood group- O Genotype: ii i Blood group- B Genotype: I B I B / I B i I B i Blood group- AB Genotype: I A I B I A I B 4 MATERNAL BLOOD GROUP ✕ 4 PATERNAL BLOOD GROUP = 16 DIFFERENT COMBINATIONS Rashmi M G

17. Parents genes AA BB AB OO AO BO AA AA AB AA,AB AO AA,AO AB,AO BB AB BB AB,BB BO AB,BO BB,BO AB AA,AB AB,BB AA,AB,BB AO,BO AA,AB,AO,BO BB,BO,AB,AO OO AO BO AO,BO OO AO,OO BO,OO AO AA,AO AB,BO AA,AB,AO,BO AO,OO AA,AO,OO AO,BO,AB,OO BO AO,AB BB,BO AB,BO,AO,BB BO,OO AB,AO,BO,OO BB,BO,OO AA, AO- BLOOD GROUP-A BB,BO- BLOOD GROUP-B OO- BLOOD GROUP-O AB- BLOOD GROUP-AB Rashmi M G

18. Rh- blood group Rh blood group-1940- Landsteiner and Wiener System based on presence/ absence of Rh- antigen/ Rh-factor on plasma membrane of RBC Rh factor- Rhesus monkey- Macacus rhesus Rh- Negative- RBC lack Rh-D antigen Rh- Positive- RBC has Rh-D antigen Parent Genotype Passes genes Rh-Negative Rh - /Rh - Rh – Allele Rh- Positive Rh + /Rh + Rh + /Rh - Rh + /Rh - Rashmi M G

19. RH- FACTOR RH- ANTIGEN Rh- d Rh- ce Rh- D Rh- CE D CE PROTEINS GENES D CE ANTIGENS Rashmi M G

20. Mother Child Rh-Positive Blood Rh-Negative Blood Fetal and mother blood Separate -Placenta During Pregnancy = Usually mother’s Rh-Negative blood is not exposed to Rh-Positive blood of Fetus There is possibility of Exposure of Maternal Blood to small Amount of Rh-Positive Blood From Fetus during Delivery of 1 st Child Mother produces Antibodies Against Rh- Antigen These antibodies cross Placenta in Subsequent Pregnancy Causes Hemolysis of Rh- Positive RBC of Fetus Anemia- Erythroblastosis Fetalis Prevention: Injecting Rh-Negative mother with Antibody prepared against Rh-Antigen (Anti-Rh Antibodies) within 72hours after birth of each Rh- Positive baby (Passive Immunization) Rashmi M G

21. References https://www.britannica.com/science/blood-biochemistry https://storymd.com/journal/joy3e6lunw-leukocytes-and-platelets/page/zvnopziy7n85-leukocytes-and-platelets https://www.msdmanuals.com/home/blood-disorders/blood-clotting-process/how-blood-clots Rashmi M G