composition of blood

1. Composition of Blood Consists of formed elements (cells) suspended & carried in plasma (fluid part) Total blood volume is about 5L Plasma is straw-colored liquid consisting of H20 & dissolved solutes Includes ions, metabolites, hormones, antibodies

3. Formed Elements Are erythrocytes (RBCs) & leukocytes (WBCs) RBCs are flattened biconcave discs Shape provides increased surface area for diffusion Lack nuclei & mitochondria Each RBC contains 280 million hemoglobins

4. Leukocytes Have nucleus, mitochondria, & amoeboid ability Can squeeze through capillary walls (diapedesis) Granular leukocytes help detoxify foreign substances & release heparin Include eosinophils, basophils, & neutrophils

5. Leukocytes continued Agranular leukocytes are phagocytic & produce antibodies Include lymphocytes & monocytes

6. Platelets (thrombocytes) Are smallest of formed elements, lack nucleus Are fragments of megakaryocytes; amoeboid Constitute most of mass of blood clots Release serotonin to vasoconstrict & reduce blood flow to clot area Secrete growth factors to maintain integrity of blood vessel wall Survive 5-9 days

7. Hematopoiesis Is formation of blood cells from stem cells in marrow (myeloid tissue) & lymphoid tissue Erythropoiesis is formation of RBCs Stimulated by erythropoietin (EPO) from kidney Leukopoiesis is formation of WBCs Stimulated by variety of cytokines = autocrine regulators secreted by immune system

8. Erythropoiesis 2.5 million RBCs are produced/sec Lifespan of 120 days Old RBCs removed from blood by phagocytic cells in liver, spleen, & bone marrow Iron recycled back into hemoglobin production

9. RBC Antigens & Blood Typing Antigens present on RBC surface specify blood type Major antigen group is ABO system Type A blood has only A antigens Type B has only B antigens Type AB has both A & B antigens Type O has neither A or B antigens

10. Transfusion Reactions People with Type A blood make antibodies to Type B RBCs, but not to Type A Type B blood has antibodies to Type A RBCs but not to Type B Type AB blood doesn�t have antibodies to A or B Type O has antibodies to both Type A & B If different blood types are mixed, antibodies will cause mixture to agglutinate

11. Transfusion Reactions continued If blood types don't match, recipient�s antibodies agglutinate donor�s RBCs Type O is �universal donor� because lacks A & B antigens Recipient�s antibodies won�t agglutinate donor�s Type O RBCs Type AB is �universal recipient� because doesn�t make anti-A or anti-B antibodies Won�t agglutinate donor�s RBCs Insert fig. 13.6

12. Hemostasis Is cessation of bleeding Promoted by reactions initiated by vessel injury: Vasoconstriction restricts blood flow to area Platelet plug forms Plug & surroundings are infiltrated by web of fibrin, forming clot

13. Role of Platelets Platelets don't stick to intact endothelium because of presence of prostacyclin (PGI2--a prostaglandin) & NO Keep clots from forming & are vasodilators

14. Role of Platelets Damage to endothelium allows platelets to bind to exposed collagen von Willebrand factor increases bond by binding to both collagen & platelets Platelets stick to collagen & release ADP, serotonin, & thromboxane A2 = platelet release reaction

15. Role of Platelets continued Serotonin & thromboxane A2 stimulate vasoconstriction, reducing blood flow to wound ADP & thromboxane A2 cause other platelets to become sticky & attach & undergo platelet release reaction This continues until platelet plug is formed

16. Platelet plug becomes infiltrated by meshwork of fibrin Clot now contains platelets, fibrin & trapped RBCs Platelet plug undergoes plug contraction to form more compact plug Role of Fibrin

17. Can occur via 2 pathways: Intrinsic pathway clots damaged vessels & blood left in test tube Initiated by exposure of blood to negatively charged surface of glass or blood vessel collagen This activates factor XII (a protease) which initiates a series of clotting factors Ca2+ & phospholipids convert prothrombin to thrombin Thrombin converts fibrinogen to fibrin which polymerizes to form a mesh Damage outside blood vessels releases tissue thromboplastin that triggers a clotting shortcut (= extrinsic pathway) Conversion of Fibrinogen to Fibrin

19. Dissolution of Clots When damage is repaired, activated factor XII causes activation of kallikrein Kallikrein converts plasminogen to plasmin Plasmin digests fibrin, dissolving clot

20. Anticoagulants Clotting can be prevented by Ca+2 chelators (e.g. sodium citrate or EDTA) or heparin which activates antithrombin III (blocks thrombin) Coumarin blocks clotting by inhibiting activation of Vit K Vit K works indirectly by reducing Ca+2 availability

21. Prostaglandins (PGs) Are produced in almost every organ Belong to eicosanoid family -- all derived from arachidonic acid of plasma membrane

22. Have wide variety of functions Different PGs may exert antagonistic effects in tissues Some promote smooth muscle contraction & some relaxation Some promote clotting; some inhibit Promotes inflammatory process of immune system Plays role in ovulation Inhibits gastric secretion in digestive system Prostaglandins (PGs) continued

23. Cyclooxygenase (COX) 1 & 2 are involved in PG synthesis (Fig 11.34) Are targets of a number of inhibitory non-steroidal anti-inflammatory drugs (NSAIDs) Aspirin, indomethacin, ibuprofen inhibit both COX 1 & 2 thereby producing side effects Celebrex & Vioxx only inhibit COX 2 & thus have few side effects Prostaglandins (PGs) continued