1. 2/1/08 Blood Chapter 17

2. 2/1/08 Cardiovascular system  Blood is a component of  Function ♦Supply O 2 to all cells & remove wastes ♦Transport hormones & other chemicals (e.g. ions) ♦Immune response  Composed of ♦The Heart ♦Blood vessels ♦BLOOD

3. 2/1/08 Characteristics of Blood  Blood = fluid connective tissue  Composed of a variety of cells and their extracellular matrix 37-54%  Formed elements ♦Red Blood Cells ♦White Blood Cells ♦Platelets 46-63%  Liquid medium =  Plasma

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6. Plasma  Contains mostly water (92%)  Electrolytes and proteins (7%)  “Free-floating stuff”  Proteins ♦Always remain in the plasma – give viscous consistency  3 main plasma proteins ♦Albumin ♦Globulins ♦Fibrinogen

7. 2/1/08 Plasma  Albumins ♦Help in maintaining osmotic pressure of blood ♦Transport thyroid hormones, fatty acids, etc.  Globulins ♦Immunoglobulins/antibodies for defense ♦Transport ions & hormones  Fibrinogen ♦Impt. in blood clotting  Blood tests: Plasma vs. Serum  Serum = plasma without fibrinogen ♦Thus the clotting factors are removed ♦but also removes Ca 2+ ions

8. 2/1/08 Formed Elements Red Blood Cells = Erythrocytes (RBCs)  Function of RBC’s ♦Transports O 2 from tissue to lungs ♦Transports CO 2 from cells/tissue to lungs  Structure ♦Saucer-shaped cell = biconcave disk  Special features ♦No nucleus ♦No mitochondrion (no mitochondria)  Lack of these organelles is advantageous to function ♦No nucleus = no cell division = less energy spent & more space for O 2 ♦Cell can assume biconcave shape – this allows for the stacking of cells

9. 2/1/08 Formed Elements: RBC’s  Importance of Shape to function (review in text)  No mitochondria ♦O 2 necessary for ATP production ♦If present, the O 2 will be consumed ♦Also gives more space in the cell Fig. 17-2

10. 2/1/08 Fig. 17-3

11. 2/1/08 Molecular content of RBC’s  Stocked with Hemoglobin (Hb) ♦Protein ♦Makes up 95% of all intracellular proteins ♦There are approx. 280 million molecules of Hb in each RBC ♦Normal range in grams per mL whole blood = g/dl ?  Hb = protein with 4 pieces (subunits)  4 polypeptide chains = Globins ♦α-globin & β-globin Fig. 17-3

12. 2/1/08 Molecular content of RBC’s  Stocked with Hemoglobin (Hb)  4 polypeptide chains = Globins ♦α-globin & β-globin  With each globin there is a heme group ♦Special chemical compound containing Fe 2+ ♦Fe 2+ of globin binds to O 2  Blood leaving lungs is rich in O 2 ♦Fe- O 2 = oxyhemoglobin – bright red in color  Blood going to lungs containing CO 2 ♦= carbaminohemoglobin – dark red in color Fig. 17-3

13. 2/1/08 Molecular content of RBC’s  RBC’s contain a special enzyme ♦Carbonic Anhydrase  Helps in CO 2 transport in the blood – (later) Fig. 17-3

14. 2/1/08 Formed Elements: White Blood Cells  White Blood Cells = Leukocytes ♦Approx. 0.1% of blood total  Come in many shapes and forms  Granular (3 types) ♦Neutrophils ♦Eosinophils ♦Basophils  Agranular (2 types) ♦Lymphocytes ♦Monocytes  Common Features ♦Prominent Nucleus ♦Large size (compared to RBC’s) ♦No Hemoglobin Fig. 17-1

15. 2/1/08 Formed Elements: White Blood Cells  Handout = specific targets of each type of WBC’s  Functions:  Clean Up & Defense ♦Detect pathogen invasions, provide protection ♦Remove dead cells and debris  “Guarding the Body” ♦“patrol the area” – travel along the edge of blood vessels  IF pathogen(s) have entered the body tissue & local defense has begun, chemicals are released  WBC’s are attracted to these chemicals & squeeze through endothelial cells to exit the blood vessel  They then find their way to the damaged tissue – this type of sensing and movement = chemotaxis

16. 2/1/08 Blood – day 2 Chapter 17

17. 2/1/08 Formed Elements: Platelets  Platelets = Thrombocytes  Packages of cytoplasm – no nucleus  Function = clotting ♦Repair of slightly damaged blood vessels ♦Stop blood loss from damaged blood vessel by forming a “platelet plug” ♦Contain numerous vessicles: release chemicals that promote clotting Fig. 17-2

18. 2/1/08 Formed Elements: Production  RBCs, WBCs, & Platelets are synthesized in the body  Production & recycling  Production of blood cells = Hemopoiesis  All blood cells originate from Hemocytoblast cells

19. 2/1/08 Red Blood Cell Production  Location ♦Red bone marrow (myeloid tissue) of epiphysis of vertebrae, sternum, ribs, skull, scapulae, pelvis, proximal limb bones  Process – Fig. 17.5  Hemocytoblast → becomes RBC  Process = Erythropoeisis  Requires a hormone = erythropoetin (peptide) ♦Stimulated by renal erythropoetic factor from the kidneys ♦Recall/review Fig. 16-7b

20. 2/1/08 Red Blood Cell Production Erythropoeisis  Erythropoetein (E.P.O.) = required hormone ♦Stimulated by renal erythropoetic factor from kidneys ♦Converts plasma protein to erythropoetin  Simple version  Hemocytoblast becomes proerythroblast  Loses nucleus – becomes reticulocyte ♦Hb is synthesized  Released into blood  Becomes RBC after 1-2 days

21. 2/1/08 Red Blood Cell Production Fig. 17-5

22. 2/1/08 Red Blood Cell Production Erythropoeisis  …is triggered by low O 2 levels  Requires proper supply of iron & vitamins (B 12 )  The following: ♦low O 2 / high altitudes ♦Anemia ♦Damaged lung surface  …trigger secretion of EPO

23. 2/1/08 The life of a RBC  Released into blood stream  Matures after 1-2 days  Travels all over body repeatedly  After approx. 120 days RBC becomes damaged  Therefore it is destroyed and recycled  Damaged RBC is destroyed by MACROPHAGES in the spleen, liver and bone marrow  The contents of the RBC are broken up and recycled  Some of these contents are later used as building blocks to make new RBCs

24. 2/1/08 The end of a RBC – recycle & reuse Fig. 17-4

25. 2/1/08 The end of a RBC – issues/terms  Problems with the bile duct = ♦Increase in bilirubin in blood ♦= yellow skin: Jaundice  If RBCs break in blood stream and not in macrophages ♦Hemoglobinuria  Kidney damage – you sometimes find intact RBCs in urine ♦Hematuria

26. 2/1/08 White Blood Cell Production  Also made from hemacytoblasts  Require a different hormone (set of hormones)  Colony – stimulating factors = C.S.F.  CSFs are also involved in enhancing WBC function  How do we get 5 different leukocytes??

27. 2/1/08 Fig. 17-10

28. 2/1/08 White Blood Cell Production  CSFs you need to know (most important ones):  GM-CSF = distinguishes myeloblast from monoblast  G-CSF = makes granular leukocytes  M-CSF = triggers monocyte formation  For some blood cell production hormones… ♦EPO, G-CSF, GM-CSF  …similar chemicals can by used as drug treatments to increase the levels of those cell types

29. 2/1/08 Fig. 17-10

30. 2/1/08 Platelet Production = Thromcytopoiesis  Hemocytoblast (in bone marrow)  Megakaryocyte ♦Large cells ♦Make proteins, enzymes, membrane  Shredded cytoplasm = platelets  Hormones ♦Thrombopoietin (TPO) ♦Interleucin-6 (IC-6) ♦Multi-CSF

31. 2/1/08 Back to Red Blood Cells  Another important feature of RBCs  Identification “tag” ♦Ensures that only siimilar/same type of RBCs remain in one blood stream ♦= a defense feature  ID tags = blood type  Blood type = different carbohydrates on the surface called antigens  Antigens are recognition factors

32. 2/1/08 Fig. 17-6

33. 2/1/08 Back to Red Blood Cells  Blood plasma also carries antibodies

34. 2/1/08 Back to Red Blood Cells  Antibodies match blood-type  Antibodies are there to detect if foreign blood cells are present  If B is given to A, anti-B reacts with B antigen ♦Agglutination – destroys cells ♦In the bargain it also interferes with normal blood  ABO system of blood typing OO ♦Universal donor but dilution factor is important b/c it has both antibodies

35. 2/1/08 Fig. 17-7

36. 2/1/08 Rh system  + or –  Separate from ABO, but functions similarly  Situation of concern = erythroblastosis fetalis

37. 2/1/08 Fig. 17-8

38. 2/1/08 Important Function of Platelets Fig. 17-  Wounding  Starts with breaking of skin – therefore blood vessels are torn  3 steps take place  Culminating in clot formation  Happens in 2-6 minutes

39. 2/1/08 Well known blood disorders Fig. 17-  Anemia  Leukemia  Mononucleosis

40. 2/1/08 Fig. 17-9

41. 2/1/08 Fig. 17-

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43. ro Fig. 17-2

44. 2/1/08 Fig. 17-2