Blood. 5 Lin women. Erythrocytes (red blood cells) Platelets. Average volume. 5.5 Consists of 3 cell types in plasma

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1 Structure & Function Lect # 6 Blood Fluid Prof Kumlesh K. Dev Department of Physiology

2 Blood Represents about 8% of total body weight Average volume 5 Lin women 55Linmen 5.5 Consists of 3 cell types in plasma Erythrocytes (red blood cells) Leukocytes (white blood cells) Platelets

3 Composition of blood I: Plasma Water (90% of plasma) Electrolytes (membrane excitability and osmotic properties) Nutrients, wastes, gases, hormones Plasma proteins (6-8% of plasma) Albumins (most abundant) Contribute to colloid osmotic pressure Transport molecules, l bile salts and drugs Globulins (3 subclasses - ɑβγ) ɑβ - Transport molecules ɑ - Inactive precursors protein γ - Immunoglobulins (antibodies) Fibrinogen (clotting factor) Converted to fibrin All produced by liver - except for γ-globulins (produced by lymphocytes) Serum is fluid left when blood clots

4 Composition of Blood II: Cells

5 Composition of Blood II: Cells

6 Haemopoiesis (production of blood cells & blood lineages)

7 Layout of Lecture

8 White Blood Cells (Leukocytes) See previous lecture p (Lect 4 General Connective Tissue)

9 Layout of Lecture

10 Red Blood Cells (Erythrocytes) Anatomy No nucleus, organelles or ribosomes Biconcave discs Large surface area Very thin Very flexible shape Efficient diffusion O 2 /CO 2 carriage

Haemoglobin Structure/Function Hb red-pigmented protein key factor to carry O 2 an erythrocyte has ~ 280 million Hb molecules each Hb molecule has four iron ions which bind four O2 molecules each RBC

11 Haemoglobin Structure/Function Hb red-pigmented protein key factor to carry O 2 an erythrocyte has ~ 280 million Hb molecules each Hb molecule has four iron ions which bind four O2 molecules each RBC can carry 1 Billion O2 molecules! O2 binding is weak to ensure rapid exchange O2 binds to Hb when RBCs in lungs O2 leaves Hb when RBCs in tissues Hb also bind CO2 (from tissue to lungs) This buffers the ph of the blood CO has higher affinity for Hb than O2 (CO poisoning) NO in lungs binds to Hb, which induces dilatation of local arterioles.

12 Key erythrocyte enzymes Glycolytic enzymes generates energy to fuel active transport involved in maintaining ionic concentrations in cell rely on glycolysis for ATP formation Carbonic anhydrase for CO2 transport converts metabolically yproduced CO2 into bicarbonate ion (HCO3-) primary form in which CO2 is transported in blood Think about how mutations in these enzymes will alter RBC function

13 Erythropoesis: Synthesis of new RBCs make about 1 Trillion RBC/day reticulocytes make up about 1% of total RBC

14 Erythropoetin from kidney stimulates erythropoesis Increased EPO production at altitude Synthetic EPO used clinically: Epogen, Procrit

15 - Erythrocytes form in red bone marrow - they survive 120 days - old erythrocytes removed by macrophages in spleen and bone marrow - iron recycled back into y hemoglobin production Erythrocyte life span

16 Anaemia Causes - below-normal O2-carrying capacity of blood causes of anemia 1. reduced Hb in RBCs - Iron deficiency 2. Reduced RBC Number - Reduced cell production - Increased cell loss - Haemolysis (membrane changes)

17 Anaemia Type of Anemia Nutritional Pernicious Aplastic Renal Hemorrhagic Hemolytic Cause Iron deficiency (can t make sufficient haemoglobin) can t absorb Vit B12 in GIT (deficient intrinsic factor) bone marrow not produce enough RBCs (Cancer chemotherapy, radiation) impaired EPO synthesis due to Kidney disease loosing a lot of blood rupture of RBCs - Malaria (parasite) invades RBCs and causes rupture - Sickle cell disease (genetic mutation in b-chain of Hb)

18 Sickle cell anaemia Normal RBC Sickled RBC Defective Haemoglobin molecules join together to make the RBCs stiff and unnaturally shaped Crescent or sickle shaped

19 Polycythemia too many circulating RBCs elevated haematocrit increased blood viscosity 2 types Primary tumor of bone marrow; uncontrolled erythropoiesis Secondary Erythropoietin-induced in response to prolonged reduced oxygen high altitudes, chronic lung disease, cardiac failure

20 Haematocrit (Red Blood Cell Fraction) under various circumstances

21 Layout of Lecture

Platelets (thrombocytes) smallest elements in blood lack nucleus fragments of megakaryocytes make most of mass of blood clots release serotonin (vasoconstrict, reduce blood flow to clot) secrete

22 Platelets (thrombocytes) smallest elements in blood lack nucleus fragments of megakaryocytes make most of mass of blood clots release serotonin (vasoconstrict, reduce blood flow to clot) secrete growth factors (maintain integrity of blood vessel wall) survive 5-9d days (removed dby tissue macrophages) Thrombopoietin Hormone produced by liver increases number of megakaryocytes y and therefore increases platelet production

23 Haemostasis process of keeping blood within a damaged blood vessel opposite of haemostasis is haemorrhage Involves 2 major steps 1. Formation of a platelet plug 2. Blood coagulation (clotting) transformation of blood from liquid into a solid gel

1. Formation of the Platelet Plug platelets aggregate on contact with exposed collagen in damaged wall of vessel intact endothelium releases NO and prostacyclin

24 1. Formation of the Platelet Plug platelets aggregate on contact with exposed collagen in damaged wall of vessel intact endothelium releases NO and prostacyclin to inhibit platelet adhesion platelets release ADP causes surface of nearby circulating platelets to become sticky adhere to first layer of aggregated platelets

2. Blood Clotting reinforces platelet plug converts blood in vicinity into a non-flowing gel clotting factors present in blood plasma in inactive precursor

25 2. Blood Clotting reinforces platelet plug converts blood in vicinity into a non-flowing gel clotting factors present in blood plasma in inactive precursor form vessel damage exposes collagen initiates cascade activation of clotting factors convert fibrinogen to fibrin Red blood cells trapped in a mesh of fibrin

26 2 blood clotting cascades Extrinsic: i Short & faster Intrinsic: Requires more upstream factors Blood clotting cascade Series of steps involving 12 clotting factors Need Ca2+ at many points Final common pathway Activation of Factor X Prothrombin to Thrombin Fibrinogen to Fibrin

27 Dangers and Limitation of clotting Clot dissolution Plasminogen converted to Plasmin Plasmin dissolves clots Phagocytic WBCs remove clot Clot prevention Tissue Plasminogen Activator t (tpa) Converts plasminogen in plasmin prevents inappropriate clot formation tpa used clinically as a clot buster Thrombomodulin Binds thrombin No fibrinogen conversion Activates Protein C anticoagulant G&S Fig

28 Abnormal Blood Clotting Thrombus intravasculaar clot attached to a vessel wall Emboli freely floating clots Factors causing thromboembolism roughened vessel surfaces due to atherosclerosis imbalance in clotting-anticlotting systems slow-moving blood release of tissue thromboplastin into blood from damaged tissue Hemophilia Excessive bleeding due to deficiency of clotting factors Haemophillia A: Clotting Factor XIII deficiency Haemophillia B: Clotting Factor IX deficiency

Thibodeau: Anatomy and Physiology, 5/e. Chapter 17: Blood

Thibodeau: Anatomy and Physiology, 5/e Chapter 17: Blood This chapter begins a new unit. In this unit, the first four chapters deal with transportation one of the body's vital functions. It is important