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Ch 16: Blood Plasma and Cellular Elements of Blood Plasma and Cellular Elements of Blood Hematopoiesis Hematopoiesis RBC Physiology RBC Physiology Coagulation.

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Presentation on theme: "Ch 16: Blood Plasma and Cellular Elements of Blood Plasma and Cellular Elements of Blood Hematopoiesis Hematopoiesis RBC Physiology RBC Physiology Coagulation."— Presentation transcript:

1 Ch 16: Blood Plasma and Cellular Elements of Blood Plasma and Cellular Elements of Blood Hematopoiesis Hematopoiesis RBC Physiology RBC Physiology Coagulation Coagulation

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3 Fig 16-1

4 Plasma Water Water Plasma proteins Plasma proteins Albumin (60%)Albumin (60%) Osmotic Gradient Osmotic Gradient Globulins (Ab)Globulins (Ab) FibrinogenFibrinogen Molecules Molecules ElectrolytesElectrolytes NutrientsNutrients Trace ElementsTrace Elements Dissolved gasesDissolved gases Serum = Plasma – Clotting factors

5 Hem(at)opoiesis = Blood Cell Formation Few uncommitted, pluripotent stem cells in red bone marrow throughout life time (Fig 16-2) Few uncommitted, pluripotent stem cells in red bone marrow throughout life time (Fig 16-2)stem cellsstem cells Controlled by cytokines, e.g. Controlled by cytokines, e.g. Erythropoietin (hormone or cytokine?)Erythropoietin (hormone or cytokine?) CSFs (Colony-stimulating factor)and ILs (interleukins): e.g. M-CSF, IL-3 (= multi CSF)CSFs (Colony-stimulating factor)and ILs (interleukins): e.g. M-CSF, IL-3 (= multi CSF) Neulasta (pegfilgrastim) is a CSF Neulasta (pegfilgrastim) is a CSF Thrombopoietin (TPO)Thrombopoietin (TPO) Some Terminology: Some Terminology: Anemia vs. Leukemia vs. leukocytosis vs. leukopeniaAnemia vs. Leukemia vs. leukocytosis vs. leukopenia

6 EPO Regulates RBC Production “Hormone” synthesized by kidneys in response to hypoxemia “Hormone” synthesized by kidneys in response to hypoxemiakidneys EPO gene cloned in 1985  Recombinant EPO now available (Epogen , Procrit  ) EPO gene cloned in 1985  Recombinant EPO now available (Epogen , Procrit  ) Use in therapy, abuse in sport Use in therapy, abuse in sport Bone marrow damage from chemotherapyBone marrow damage from chemotherapy Chronic renal failureChronic renal failure Your book calls it a cytokine because it is made on demand, not stored. (p540). Your book calls it a cytokine because it is made on demand, not stored. (p540). Trivia Dept.: Neulasta® (pegfilgrastim) stimulates production of WBC Trivia Dept.: Neulasta® (pegfilgrastim) stimulates production of WBC Running Problem: Blood Doping

7 The Erythrocyte (RBC) Biconcave Disk, 7 μ diameter, Carry O 2 Biconcave Disk, 7 μ diameter, Carry O day lifespan 120 day lifespan No mitochondria, no nucleus No mitochondria, no nucleus ATP from glycolysisATP from glycolysis Bag of Hb Bag of Hb HCT = hematocrit = PCV HCT = hematocrit = PCV MCV-Mean Cell Volume MCV-Mean Cell Volume ↓ in Fe-deficiency anemia↓ in Fe-deficiency anemia

8 Hemoglobin (Hb) [Hb] often reported in CBC [Hb] often reported in CBC Four globulin proteins (Fig 18-8)Four globulin proteins (Fig 18-8) Two α- Two α- Two β- Two β- Each has the heme group Each has the heme group Heme is a porphyrin that binds Fe Heme is a porphyrin that binds Fe Fe is considered a trace mineral Fe is considered a trace mineral Meat, beans, spinachMeat, beans, spinach Stored in liver, “recycled”Stored in liver, “recycled” Fe deficiencyFe deficiency

9 Hemoglobin (Hb) Synthesis and Breakdown Requires iron (Fe) + Vit. B 12 (cobalamin) Requires iron (Fe) + Vit. B 12 (cobalamin) Reversible binding between Fe & O 2 Reversible binding between Fe & O 2 Hb Breakdown: Hb Breakdown: Hb → Bilirubin → bile.Hb → Bilirubin → bile. Hyperbilirubinemia Hyperbilirubinemia Too fast causes icterus (jaundice)Too fast causes icterus (jaundice) HbA vs. HbFHbA vs. HbF Fetal Hb has two  chains instead of two  chains Fetal Hb has two  chains instead of two  chains

10 RBC Disorders Too high PCV: Too high PCV: Polycythemia vera (PCV ~ 60-70%)Polycythemia vera (PCV ~ 60-70%) DehydrationDehydration Anemias (O 2 carrying capacity of blood too low) Anemias (O 2 carrying capacity of blood too low) Hemorrhagic anemia  Fe deficiency anemiaHemorrhagic anemia  Fe deficiency anemia Hemolytic anemia, due to genetic diseases (e.g. Hereditary spherocytosis) or infectionsHemolytic anemia, due to genetic diseases (e.g. Hereditary spherocytosis) or infections Pernicious anemiaPernicious anemia Vit. B 12 Deficiency Vit. B 12 Deficiency Aplastic anemiaAplastic anemia Renal anemiaRenal anemia ↓ EPO ↓ EPO Sickle Cell AnemiaSickle Cell Anemia

11 Sickle Cell Anemia 1 st genetic illness traced to a specific mutation: DNA: CAC CTC aa: glutamic acidvaline (aa #6 of 146) HbAHbS  crystallizes under low oxygen conditions

12 Platelets = Thrombocytes Megakaryocyte (MK) is polypoid. Mechanism? Megakaryocyte (MK) is polypoid. Mechanism? MK produces ~ 4,000 platelets MK produces ~ 4,000 platelets Lifespan 10 days.Lifespan 10 days. Platelets contain gra- nules filled with clotting proteins & cytokines Platelets contain gra- nules filled with clotting proteins & cytokines Activated when blood vessel wall damaged Activated when blood vessel wall damaged

13 Hemostasis = Opposite of hemorrhage  stops bleeding Too little hemostasis  too much bleeding Too much hemostasis  thrombi / emboli Three major steps: 1.Vasoconstriction 2.Platelet plug Temporarily blocks the hole 1. Platelet-derived cytokines further the process 3.Coagulation cascade (= clot formation seals hole until tissues repaired) 1. Two pathways: Extrinsic and Intrinsic 4.After vessel repair, plasmin dissolves the clot

14 Steps of Hemostasis Vessel damage exposes collagen fibers Platelets adhere to collagen & release factors local vasoconstriction& platelet aggregation decreased blood flow platelet plug formation + feedback loop Fig 16-10, 11

15 Steps of Hemostasis cont. 1. Two coagulation pathways converge onto common pathway 1.Intrinsic Pathway. Collagen exposure. All factors needed are present in blood. Slower. 2.Extrinsic Pathway. Uses Tissue Factors released by injured cells and a shortcut. 2. Usually both pathways are triggered by same tissue damaging events. 3. The different factors can be subject to a variety of problems 1.Hemophilia 2.Hypercoagulable states

16 Common Coagulation Pathway reinforces platelet plug fibrinogen  fibrin Prothrombin  thrombin clot Intrinsic pathway Extrinsic pathway Active factor X

17 Fig Vit K needed for synthesis of several clotting factors

18 Structure of Blood Clot SEM x 4625 Plasmin, trapped in clot, will dissolve clot by fibrinolysis Clot formation limited to area of injury: Intact endothelial cells release anticoagulants (heparin, antithrombin III, protein C).

19 Clot Busters & Anticoagulants Dissolve obsolete or unwanted clots Enhance fibrinolysis Examples: Urokinase, Streptokinase & t-PA Prevent coagulation by blocking 1 or more steps in fibrin forming cascade Inhibit platelet adhesion plug prevention Examples: Coumadin (warfarin) blocks Vit K EDTA chelates Ca 2+ Aspirin prevents platelet plug

20 Hemophilia

21 Hemophilia A (Factor VIII Deficiency)

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