1. Chapter 11

2. White blood cells Platelets Red blood cells Artery

3. Deliver O 2 Remove metabolic wastes Maintain temperature, pH, and fluid volume Protection from blood loss- platelets Prevent infection- antibodies and WBC Transport hormones

4. Plasma- 55% Formed elements- 45% Buffy coat- <1%

5. 91% Water 9% Solutes: Proteins Albumin (60%) Globulins Fibrinogens Gas Electrolytes

6. Organic Nutrients Carbohydrates Amino Acids Lipids Vitamins Hormones Metabolic waste CO 2 Urea

7. Leukocytes – white blood cells Platelets

8. Erythrocytes (RBCs) make up 95% of the volume; 700 x more than WBCs and 17 x more than Platelets Leukocytes (WBCs) Platelets (thrombocytes)

9. Erythrocytes

10. Erythrocyte  7.5  m in dia  Anucleate- so can't reproduce; however, repro in red bone marrow  Hematopoiesis- production of RBC  Function- transport respiratory gases  Hemoglobin- quaternary structure, 2  chains and 2  chains  Lack mitochondria.  1 RBC contains 280 million hemoglobin molecules  Men- 5 million cells/mm 3  Women- 4.5 million cells/mm 3  Life span 100-120 days and then destroyed in spleen (RBC graveyard)

12. Hematopoiesis Hematopoiesis (hemopoiesis): blood cell formation –Occurs in red bone marrow of axial skeleton, girdles and proximal epiphyses of humerus and femur

13. Hematopoiesis Hemocytoblasts (hematopoietic stem cells p 307) –Give rise to all formed elements –Hormones and growth factors push the cell toward a specific pathway of blood cell development New blood cells enter blood pathway

14. Erythropoiesis Erythropoiesis: red blood cell production –A hemocytoblast is transformed into a proerythroblast –Proerythroblasts develop into early erythroblasts

15. Figure 17.5 Stem cell Hemocytoblast Proerythro- blast Early erythroblast Late erythroblast Normoblast Phase 1 Ribosome synthesis Phase 2 Hemoglobin accumulation Phase 3 Ejection of nucleus Reticulo- cyte Erythro- cyte Committed cell Developmental pathway

16. Regulation of Erythropoiesis Too few RBCs leads to tissue hypoxia (low O 2 ) Too many RBCs increases blood viscosity Balance between RBC production and destruction depends on –Hormonal controls –Adequate supplies of iron, amino acids, and B vitamins

17. Hormonal Control of Erythropoiesis Erythropoietin (EPO) –Direct stimulus for erythropoiesis –Released by the kidneys in response to hypoxia

18. Hormonal Control of Erythropoiesis Causes of hypoxia – Hemorrhage or increased RBC destruction reduces RBC numbers –Insufficient hemoglobin (e.g., iron deficiency) –Reduced availability of O 2 (e.g., high altitudes)

19. Hormonal Control of Erythropoiesis Effects of EPO (the hormone) –More rapid maturation of committed bone marrow cells –Increased circulating reticulocyte count in 1–2 days Testosterone also enhances EPO production, resulting in higher RBC counts in males

20. Formation & Destruction of RBCs

21. Anemia- when blood has low O 2 carrying capacity; insufficient RBC or iron deficiency. Factors that can cause anemia- exercise, B12 deficiency Polycythemia- excess of erythrocytes,  viscosity of blood; 8-11 million cells/mm 3 Usually caused by cancer, tissue hypoxia, dehydration; however, naturally occurs at high elevations Blood doping- in athletes  remove blood 2 days before event and then replace it; Epoetin;- banned by Olympics.

22. Sickle-cell anemia- HbS results from a change in just one of the 287 amino acids in the  chain in the globin molecule. Found in 1 out of 400 African Americans. Abnormal hemoglobin crystalizes when O2 content of blood is low, causing RBCs to become sickle-shaped. Homozygous for sickle-cell is deadly, but in malaria infested countries, the heterozygous condition is beneficial.

23. Genetics of Sickle Cell Anemia

24. Granulocytes Neutrophils- 40-70% phagocytize = pus Eosinophils- 1-4% reduce inflammation, destroy worm parasites Basophils- <1% release histamine and heparin (prevents clots) Agranulocytes Monocytes- 4-8% large, in organs = macrophage, help lymphocytes Lymphocytes- 20-45% small, B and T; Natural killers Never let monkeys eat bananas 4,000-11,000 cells/mm 3

25. Monocytes- Lymphocytes- B lymphocytes produce antibodies that are secreted into blood and lymph T lymphocytes attack cells that have antigens they recognize Natural Killer cells kill tumor or virus- infected cells but not specific

26. specific Antibodies

27. Basophil Eosinophil Neutrophil Lymphocyte Monocyte platelet

28. neutrophil RBC eosinophil monocyte lymphocyte basophil monocyte

29. ID WBC’s

30. Leukopenia Abnormally low WBC count Leukemias Cancerous conditions involving WBCs Named according to the abnormal WBC clone involved Mononucleosis highly contagious viral disease caused by Epstein-Barr virus; excessive # of agranulocytes; fatigue, sore throat, recover in a few weeks

31. Platelets Small fragments of megakaryocytes Formation is regulated by thrombopoietin Blue-staining outer region, purple granules Granules contain serotonin, Ca 2+, enzymes, ADP, and platelet-derived growth factor (PDGF)

32. Figure 17.12 Stem cellDevelopmental pathway Hemocyto- blast Megakaryoblast Promegakaryocyte MegakaryocytePlatelets

33. Hemostasis- stoppage of bleeding Tissue Damage Platelet Plug Clotting Factors Platelets: 250,000-500,000 cells/mm 3

34. Hemostasis: 4. Coagulation 1.Vessel injury 2. Vascular spasm 3. Platelet plug formation

35. Blood Clot Fibrin thread Platelet RBC

36. Disorders of Hemostasis Thromboembolytic disorders: undesirable clot formation Bleeding disorders: abnormalities that prevent normal clot formation

37. Thromboembolytic Conditions Thrombus: clot that develops and persists in an unbroken blood vessel –May block circulation, leading to tissue death Embolus: a thrombus freely floating in the blood stream –Pulmonary emboli impair the ability of the body to obtain oxygen –Cerebral emboli can cause strokes

38. Thromboembolytic Conditions Prevented by –Aspirin Antiprostaglandin that inhibits thromboxane A2 –Heparin Anticoagulant used clinically for pre- and postoperative cardiac care –Warfarin Used for those prone to atrial fibrillation

39. Thrombocytosis- too many platelets due to inflammation, infection or cancer Thrombocytopenia- too few platelets causes spontaneous bleeding due to suppression or destruction of bone marrow (e.g., malignancy, radiation) –Platelet count <50,000/mm 3 is diagnostic –Treated with transfusion of concentrated platelets

40. Impaired liver function –Inability to synthesize procoagulants –Causes include vitamin K deficiency, hepatitis, and cirrhosis –Liver disease can also prevent the liver from producing bile, impairing fat and vitamin K absorption

41. Bleeding Disorders Hemophilias include several similar hereditary bleeding disorders Symptoms include prolonged bleeding, especially into joint cavities Treated with plasma transfusions and injection of missing factors

42. Hemophiliac- a sex-linked recessive trait, primarily carried by males (x chromosome)

43. Type A Type B Type AB Type O

44. Blood type is based on the presence of 2 major antigens in RBC membranes-- A and B Blood typeAntigenAntibody A A anti-B B B anti-A A & B AB no anti body Neither A or B Oanti-A and anti-B Antigen- protein on the surface of a RBC membrane Antibody- proteins made by lymphocytes in plasma which are made in response to the presence of antigens. They attack foreign antigens, which result in clumping (agglutination)

45. Type A ABO Blood Types Produces anti-B antibodies b b b b b b b b

46. Type B ABO Blood Types Produces anti-A antibodies a a a a a a a a a a

47. Type AB ABO Blood Types Produces neither anti-A nor anti-B antibodies

48. Type O ABO Blood Types Produces both anti-A and anti-B antibodies a a a a a a a a a a b b b b b b b b

49. Rh Factor and Pregnancy RH- indicates no protein RH+ indicates protein

50. Rh Factor and Pregnancy Rh + mother w/Rh - baby– no problem Rh - mother w/Rh + baby– problem Rh - mother w/Rh - father– no problem Rh - mother w/Rh - baby-- no problem RhoGAM used @ 28 weeks

51. Type AB- universal recipients Type O- universal donor Rh factor: Rh+ 85% dominant in pop Rh- 15% recessive Blood TypeClumpingAntibody Aantigen Aanti-A serumantibody anti-b Bantigen Banti-B serumantibody anti-a ABantigen A & Banti A & B serum - Oneither A or Bno clumping w/ either anti A or B anti-a, anti-b

52. Figure 17.16 Serum Anti-A RBCs Anti-B Type AB (contains agglutinogens A and B; agglutinates with both sera) Blood being tested Type A (contains agglutinogen A; agglutinates with anti-A) Type B (contains agglutinogen B; agglutinates with anti-B) Type O (contains no agglutinogens; does not agglutinate with either serum)

53. Blood Type & RhHow Many Have ItFrequency ORh Positive1 person in 337.4% ORh Negative1 person in 156.6% ARh Positive1 person in 335.7% ARh Negative1 person in 166.3% BRh Positive1 person in 128.5% BRh Negative1 person in 671.5% ABRh Positive1 person in 293.4% ABRh Negative1 person in 167.6%

54. ABO Blood Types PhenotypeGenotype Oi i AI A I A or I A i BI B I B or I B i ABI A I B

55. Type A and Type B cross IAIA IAIA IBIB i IAiIAi IAIBIAIB IAIBIAIB IAiIAi Punnett square

56. INQUIRY 1.What is an erythrocyte, leukocyte, and thrombocyte? 2.What 2 things do red cells lack compared to white cells? 3.What dietary component is needed for the production of red blood cells? 4.The largest cells in the blood that leave the bloodstream to become macrophages are ____. 5.In an acute infection, the white cell count would show as ______. 6.Erythroblastosis fetalis, also known as hemolytic newborn disease, occurs in ____ mothers carrying ____ fetuses. 7.What antigens and antibodies found on AB red cells? 8.In a transfusion, what type blood can you give a type O person?