CHAPTER 17: BLOOD Dr. Renata Uribe Shenzhou University November 2015 Subjects •
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Blood ComposiKon and FuncKons Plasma Formed Elements Hemostasis Transfusion Tests Developmental Aspects FuncKons of Blood •  DistribuKon –  Delivering O2 –  TransporKng metabolic wastes –  TransporKng hormones •  RegulaKon –  Maintaining body temperature –  Maintaining pH of body Kssues –  Maintaining adequte fluid volume •  ProtecKon –  PrevenKng blood loss –  PrevenKng infecKon Blood ComposiKon •  Blood is a specialized connecKve Kssue –  consisKng of living cells (formed elements), suspended in a nonliving fluid matrix (blood plasma). •  Only fluid Kssue in the body •  Slightly basic (pH 7.35–7.45) •  Higher density and viscosity than water, due to the presence of formed elements. •  45% erythrocytes (RBC´S) = Hematocrit •  Male: 5-­‐6L, Female: 4-­‐5L Blood ComposiKon Blood Components •  Only fluid Kssue in the body •  Formed elements – living cells –  Erythrocytes – RBC –  Leukocytes – WBC –  Platelets – Cell fragments •  Plasma – non-­‐living matrix –  90% water –  Disolved gases, nutrients, hormones, wastes, proteins and electrolytes (see table 17.1) –  Albumin, fibrinogen •  pH 7.35-­‐7.45 •  8% body weight Formed Elements •  Erythrocytes, leukocytes, platelets •  Most survive only a few days •  Most do not divide, but are constantly replaced Erythrocytes •
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Biconcave shape Flexible due to spectrin network Lack a nucleus and organelles Contain mostly hemoglobin (97%) Transports O2 and CO2 Anaerobic ATP producKon: –  No oxygen consumed Hemoglobin (Hb) •
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Composed of 4 protein chains Each chain contains a heme pigment Each heme contains one iron (Fe) molecule Each Hb can transport 4 molecules of O2 (oxyhemoglobin CO2 binds on protein chain –  (carbaminohemoglobin) Erythrocytes •  1 Hb molecule: 4 O2 molecules •  1 erythrocyte: 250.000.000 Hb molecules •  Oxy-­‐hemoglobin = Hemoglobin with oxygen •  De-­‐oxy-­‐hemoglobin = Hemoglobin without oxygen •  Carb-­‐amino-­‐hemoglobin = Carbon dioxide bound to amino acids of the hemoglobin molecule ProducKon of Erythrocytes •
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Hematopoiesis in red bone marrow, takes 15 days Controlled by EPO (erythropoieKn) Requirements: Iron, vitamin B12, folic acid Short life span, destroyed by macrophages Homeostasis Hypoxia •
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Hemorrhage (bleeding) Excessive erythrocyte destrucKon Insufficient hemoglobin per erythrocyte Reduced oxygen availability: lung disorder, high alKtude HomeostaKc Imbalance •  Kidney failure: EPO deficiency –  ArKficial EPO injecKon –  Testosterone enhances EPO producKon •  Dietary deficiencies Fate and DestrucKon •  Lifespan of erythrocyte 120 days •  Aging: loss of flexibility, hemoglobin degeneraKon •  Spleen is the erythrocyte graveyard –  Network of small circulatory channels in which rigid erythrocytes are trapped –  Macrophages destroy them –  Hb is degraded (RE USE) •  Iron is stored for reuse •  Bilirubin (yellow) is bound to plasma albumin Bilirubin •
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Waste product of erythrocytes Yellow color Bound to an enzyme in the liver Excreted in bile –  Liver to gallbladder to intesKne •  Jaundice –  ObstrucKon of bile –  Too much bilirubin Jaundice Anemia •  Blood has abnormally low oxygen carrying capacity –  FaKgue –  Shortness of breath –  High heart frequency –  Weakness •  Causes Anemia –  Insufficient number of RBC’s •  Hemorrhage •  Hemolysis (premature dying) •  AplasKc anemia (destrucKon or inhibiKon of bone marrow) –  Low Hb content •  Iron deficiency •  Athlete’s anemia: increased blood volume •  Pernicious anemia: intrinsic factor/vit B12 •  Abnormal Hb –  Sickle cell anemia –  Thalassemias Sickle Cell Anemia •  Autosomal recessive disorder •  RBC’s with low oxygen load sickle, clot together –  Dam small vessels –  Easily rupture •  Complains are worse when oxygen is low –  Exercise •  ProtecKve for malaria Leukocytes •  White blood cells •  Cells of the immune system •  Are able to slip out of the blood stream (diapedesis) •  Granulocytes: membrane bound granules •  Agranulocytes: lack granules Diapedesis Granulocytes •  Lobed nucleus and granulae Granulocytes Agranulocytes •  Lymphocytes and monocytes Lymphocytes •  T lymphocyte or T-­‐cell –  T is for Thymus –  Cell mediated immunity –  Many different types: T helper cells, Cytotoxic T cells, Memory T cells, Regulatory T cells, Natural Killer T cells, gamma delta T cells. •  B lymphocyte or B-­‐cell –  Humoral immunity (using anKbodies = immunoglobins) –  Many different types: Plasma cells, Memory B cells, B1 and B2 cells, Marginal-­‐zone B cells, Follicular B cells Monocytes •  When leaving the bloodstream and entering the Kssue they differenKate into macrophages –  Phagocytes –  Against viruses, intracellular bacteria –  Chronic infecKons –  AcKvaKng lymphocytes Leukopoiesis Leukopoiesis •  SKmulated by chemical messengers –  Colony SKmulaKng Factors (CSF) –  Interleukins (IL) Leukocyte Disorders •  Leukopenia: low count of leukocytes –  Radio/chemotherapy, medicaKon, cancer, leukemia, influenza, tuberculosis, malaria •  Leukemia: group of cancerous condiKons involving white blood cells –
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Acute forms in children, chronic forms in the elderly One clone Red bone marrow replaced by dividing cancer cells Anemia, thrombopenia •  Mononucleosis InfecKosa –  Epstein-­‐Barr virus, excessive agranulocytes –  Tired, achy, sore throat, low-­‐grade fever. Platelets (Thrombocytes) Thrombocytes •
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EssenKal for blood clomng Fragments of extraordinarily large cells: megakaryocytes FormaKon regulated by thrombopoieKn Short lifespan Athlete’s Anemia •  DiluKonal Pseudoanemia Hemostasis •  Complex process which causes bleeding to stop –  Vascular spasm –  Platelet plug formaKon –  CoagulaKon •  Heme (red) = blood •  Stasis = standing sKll Hemostasis •  1. Vascular Spasm –  Direct injury, platelets releasing chemicals, and reflexes from pain receptors leads to vasoconstric=on •  2. Platelet plug forma=on –  Platelets sKck to exposed collagen fibers (rough spot) –  Platelets release ADP, serotonin and thromboxane •  3. Coagula=on –  Fibrin threads form around aggregated platelets •  Prothrombin ac=vator released from platelets acKvate prothrombin (already in blood) •  Thrombin combines with fibrinogen to develop fibrin Hemostasis Hemostasis: Vascular Spasm •  Blood vessel is damaged •  Chemicals released by endothelial cells of the vessel, platelets and reflexes from pain receptors •  VasoconstricKon (vessel narrowing by contracKon of smooth muscle) –  ReducKon of blood loss and Kme for blood clomng Hemostasis: Platelet plug formaKon •  Endothelial cell releases nitric oxide and prostacyclin •  AggregaKon of platelets temporarily seals the break in the vessel wall •  Platelets adhere to exposed collagen fibers in damaged endothelium •  Platelets release: –  ADP: aggregaKng agent –  Serotonin and Thromboxane A2: enhance vascular spasm and aggregaKon. •  PosiKve feedback mechanism Hemostasis: CoagulaKon •  Platelet plug is reinforced by fibrin threads •  Process is regulated by clomng factors numbered I-­‐XIII •  AcKvaKon turns a clomng factor into an enzyme •  It’s a cascade Clot RetracKon and Repair •  Platelets contain acKn and myosin –  draw ruptured ends of the vessel together •  Platelets contain PDGF (platelet derived growth factor) –  sKmulates smooth muscle cells and fibroblasts to divide and rebuild vessel wall •  VEGF (vascular endothelial growth factor) –  sKmulates restoring the endothelium of the vessel. Fibrinolysis •  Removal of the blood clot by plasmin (fibrin digesKng enzyme) •  Plasminogen à Plasmin –  Endothelial cells secrete Kssue Plasminogen AcKvator HemostaKc Disorders •  Thromboembolic CondiKons –  Thrombus: blood clot that develops and persists in an unbroken vessel –  Embolus: thrombus that breaks away and floats through the circulaKon –  Embolism: vessel obstrucKon (cardiac, cerebral, pulmonary) –  Risk factors: atherosclerosis and inflammaKon of the vessel wall, slow blood flow (long flights) –  Aspirin inhibits thromboxane A2 and prevents platelet aggregaKon Thromboembolism Bleeding Disorders •  Thrombocytopenia –  An abnormally low concentraKon of platelets/
thrombocytes –  Spontaneous bleeding from small vessels all over the body –  Due to bone marrow disorder, cancer, radiaKon, medicaKon –  Petechiae: Bleeding Disorders •  Impaired liver funcKon –  Vitamin K deficiency, hepaKKs, liver cirrhosis –  The liver produces clomng factors •  Hemophilia –  Type A (factor VIII), B (factor IX) and C (factor XI) –  A and B are X-­‐chromosomal inherited: mostly in males –  From childhood –  Minor Kssue trauma can cause life threatening bleeding –  Dependent on blood transfusions/ clomng factor injecKons Human Blood Groups •  Many different anKgens –  AB0 –  Rhesus –  Kell –  Duffy –  Kidd –  Lutheran –  … •  In general: if you do not have the anKgen, you have (or can develop) the anKbody against it. Human Blood Groups RBC plasma membranes have glycoproteins on their surface –  Called anKgens or aggluKnogens •  ABO blood groups are most common to result in an immune reacKon –  Type A – Has A aggluKnogens –  Type B – Has B aggluKnogens –  Type AB has A and B aggluKnogens –  Type O – has none •  Every person has aggluKnins (anKbodies) in the blood that funcKon to react to aggluKnogens not present on their RBC´s –  Type A – has B aggluKnins (anKbodies) –  Type B – has A aggluKnins (anKbodies) –  Type AB – has no aggluKnins –  Type O – has A and B aggluKnins (anKbodies) Human Blood Groups •  AB is the universal recipient (no anKbodies) •  0 is the universal donor (no anKgens) Blood Type Matching Transfusion ReacKons •  If donated red blood cells bear anKgens the recipient has/
develops anKbodies against –  The oxygen carrying capacity of transfused blood cells is disrupted –  Clumping of red blood cells can obstruct small vessels, hindering blood flow to certain Kssues •  Symptoms include fever, chills, hypotension (low blood pressure) •  The kidneys are the most important target of damage The End Thank You!