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the microscopic structures and functions of Blood.ppt
- 2. White blood cells Platelets Red blood cells Artery
- 3. • Deliver O2 • Remove metabolic wastes • Maintain temperature, pH, and fluid volume • Protection from blood loss- platelets • Prevent infection- antibodies and WBC • Transport hormones
- 5. 90% Water 8% Solutes: • Proteins – Albumin (60 %) – Alpha and Beta Globulins – Gamma Globulins – fibrinogens • Gas • Electrolytes
- 6. • Organic Nutrients • Carbohydrates • Amino Acids • Lipids • Vitamins • Hormones • Metabolic waste • CO2 • Urea
- 8. • Erythrocytes (red blood cells) • Leukocytes (white blood cells) • Platelets (thrombocytes)
- 9. Erythrocytes
- 10. Erythrocyte7.5m in dia Anucleate Hematopoiesis- production of RBC Function- transport respiratory gases Hemoglobin- quaternary structure, 2 chains and 2 chains Lack mitochondria. Why? 1 RBC contains 280 million hemoglobin molecules Men- 5 million cells/mm3 Women- 4.5 million cells/mm3 Life span 100-120 days and then destroyed in spleen (RBC graveyard)
- 11. Hemoglobin
- 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) – 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 sinusoids
- 14. Erythropoiesis • Erythropoiesis: red blood cell production – A hemocytoblast is transformed into a proerythroblast – Proerythroblasts develop into early erythroblasts
- 15. Erythropoiesis – Phases in development 1. Ribosome synthesis 2. Hemoglobin accumulation 3. Ejection of the nucleus and formation of reticulocytes – Reticulocytes then become mature erythrocytes
- 16. 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
- 17. Regulation of Erythropoiesis • Too few RBCs leads to tissue hypoxia • 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
- 18. Hormonal Control of Erythropoiesis • Erythropoietin (EPO) –Direct stimulus for erythropoiesis –Released by the kidneys in response to hypoxia
- 20. Hormonal Control of Erythropoiesis • Causes of hypoxia – Hemorrhage or increased RBC destruction reduces RBC numbers –Insufficient hemoglobin (e.g., iron deficiency) –Reduced availability of O2 (e.g., high altitudes)
- 21. Hormonal Control of Erythropoiesis • Effects of EPO – 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
- 23. Formation & Destruction of RBCs
- 24. Anemia- when blood has low O2 carrying capacity; insufficient RBC or iron deficiency. Factors that can cause anemia- exercise, B12 deficiency RBC Diseases
- 25. 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. • Homozygous for sickle-cell is deadly, but in malaria infested countries, the heterozygous condition is beneficial. RBC Diseases
- 27. Sickle cell is prevalent in parts of all of the following areas: • Africa • Mediterranean countries (such as Greece, Turkey, and Italy) • The Arabian peninsula • India • Spanish-speaking regions (South America, Central America, and parts of the Caribbean) Sickle Cell Anemia
- 28. Distribution of the sickle cell gene
- 30. Genetics of Sickle Cell Anemia Genetics of Sickle Cell Anemia
- 31. HbA HbS HbA HbS HbAHbS HbAHbS HbAHbS HbAHbS 1 parent has sickle cell 1 doesn’t A = Normal S = sickle cell
- 32. HbS HbS HbA HbA HbAHbA HbAHbS HbAHbS HbSHbS both parents are carriers for sickle cell A = Normal S = sickle cell
- 33. Polycythemia- excess of erythrocytes, viscosity of blood; 8-11 million cells/mm3 Usually caused by cancer; however, naturally occurs at high elevations Blood doping- in athletesremove blood 2 days before event and then replace it- banned by Olympics. RBC Diseases
- 34. Granulocytes Neutrophils- 40-70% Eosinophils- 1-4% Basophils- <1% Agranulocytes Monocytes- 4-8% Lymphocytes- 20-45% Never let monkeys eat bananas 4,000-11,000 cells/mm 3
- 36. Leukocyte Squeezing Through Capillary Wall
- 37. Leukopenia • Abnormally low WBC count—drug induced 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
- 38. Platelets • Small fragments of megakaryocytes • Formation is regulated by thrombopoietin • Blue-staining outer region, purple granules • Granules contain serotonin, Ca2+, enzymes, ADP, and platelet-derived growth factor (PDGF)
- 39. Figure 17.12 Stem cell Developmental pathway Hemocyto- blast Megakaryoblast Promegakaryocyte Megakaryocyte Platelets
- 40. Hemostasis- stoppage of bleeding Tissue Damage Platelet Plug Clotting Factors Platelets: 250,000-500,000 cells/mm3
- 41. Hemostasis: 4. Coagulation 1. Vessel injury 2. Vascular spasm 3. Platelet plug formation
- 42. Hemostasis (+ feedback) Prothrombin Thrombin Fibrinogen Fibrin Clotting Factors thromboplastin Traps RBC & platelets Platelets release thromboplastin
- 44. Disorders of Hemostasis • Thromboembolytic disorders: undesirable clot formation • Bleeding disorders: abnormalities that prevent normal clot formation
- 45. 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
- 46. 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
- 47. 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/mm3 is diagnostic – Treated with transfusion of concentrated platelets
- 48. • 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
- 49. • Hemophilias include several similar hereditary bleeding disorders • Symptoms include prolonged bleeding, especially into joint cavities • Treated with plasma transfusions and injection of missing factors
- 50. Hemophiliac- a sex-linked recessive trait, primarily carried by males (x chromosome)
- 51. Type A Type B Type AB Type O
- 52. Blood type is based on the presence of 2 major antigens in RBC membranes-- A and B Blood type Antigen Antibody A A anti-B B B anti-A A & B AB no anti body Neither A or B O anti-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)
- 56. Type AB
- 57. Rh Factor and Pregnancy RH- indicates no protein RH+ indicates protein RH+ indicates protein
- 58. 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
- 59. Type AB- universal recipients Type O- universal donor Rh factor: Rh+ 85% dominant in pop Rh- 15% recessive Blood Type Clumping Antibody A antigen A anti-A serum antibody anti-b B antigen B anti-B serum antibody anti-a AB antigen A & B anti A & B serum - O neither A or B no clumping w/ either anti A or B anti-a, anti-b
- 60. 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)
- 61. Blood Type & Rh How Many Have It Frequency O Rh Positive 1 person in 3 37.4% O Rh Negative 1 person in 15 6.6% A Rh Positive 1 person in 3 35.7% A Rh Negative 1 person in 16 6.3% B Rh Positive 1 person in 12 8.5% B Rh Negative 1 person in 67 1.5% AB Rh Positive 1 person in 29 3.4% AB Rh Negative 1 person in 167 .6%
- 62. ABO Blood Types Phenotype Genotype O i i A I A I A or I A i B I B I B or I B i AB I A I B
- 63. Type A and Type B cross IA IA IB i IAi IAIB IAIB IAi Punnett square
- 64. 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?