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

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

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

2 Fig 16-1 Blood = connective tissue Extracellular matrix:Specialized cells:

3 Blood Components Overview Fig 16-1/ % 50-70% 2-8% Plasma Cellular Elements Blood 1- 4% Total WBC: 4, ,000

4 Red Blood Cells O2O2 Fig 16-5

5 Hem(at)opoiesis = Blood Cell Formation Few uncommitted stem cells in red bone marrow throughout life time (Fig 16-2) Controlled by cytokines. Examples: Erythropoietin CSFs and ILs: e.g. M-CSF, IL- 3 (= multi CSF) Thrombopoietin Leukemia vs. leukocytosis vs. leukopenia

6 Compare to Fig 16-2 Controlled by ____________, specifically CSFs and ILs

7 EPO Regulates RBC Production Hormone synthesized by kidneys in response to hypoxemia kidneys EPO gene cloned in 1985 Recombinant EPO now available (Epogen, Procrit ) Use in therapy, abuse in sport

8 Erythropoiesis RBC bag of Hb for carrying O 2 lifespan ~ 120 days source of ATP for RBC? enter circulation Reticulocytes Tissue O 2 EPO release Mitotic rate Maturation speed

9 Hemoglobin (Hb) Requires iron (Fe) + Vit. B 12 (cobalamin) p.698/Ch21 Quaternary protein structure ? protein structure Reversible binding between Fe & O 2 CO: a toxic gas (not in book) Bilirubin to bile. Hyperbilirubinemia HbA vs. HbF

10 Hb Structure How many O 2 can 1Hb carry? Porphyrin ring with Fe in center

11 RBC Disorders Polycythemia vera (PCV ~ 60-70%) Anemias (O 2 carrying capacity too low) Hemorrhagic anemia Fe deficiency anemia Hemolytic anemia, due to genetic diseases (e.g. Hereditary spherocytosis) or infections Pernicious anemia Renal anemia

12 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

13 Platelets = Thrombocytes Megakaryocytes (MKs) are polyploid. Mechanism? MK produces ~ 4,000 platelets which live an average of 10 days. Platelets contain gra- nules filled with clotting proteins & cytokines Activated when blood vessel wall damaged

14 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 (temporary blockage of hole) 3. Coagulation (clot formation seals hole until tissues repaired)

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

16 Platelet Plug Formation Platelet activating factor (PAF)

17 Steps of Hemostasis cont. Two coagulation pathways converge onto common pathway Intrinsic Pathway. Collagen exposure. All necessary factors present in blood. Slower. Extrinsic Pathway. Uses TF released by injured cells and a shortcut. Usually both pathways are triggered by same tissue damaging events. Fig 16-12

18 The Coagulation Cascade Fig Cascade is complicated network! Numbering of coagulation factors according to time of discovery

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

20 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).

21 Clot Busters & Anticoagulants Dissolve inappropriate clots Enhance fibrinolysis Examples: Urokinase, Streptokinase & t-PA Prevent coagulation by blocking one or more steps in fibrin forming cascade Inhibit platelet adhesion plug prevention Examples:

22 Hemophilia

23 Hemophilia A (Factor VIII Deficiency)

24 Blood Doping

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