Chapter 16 Blood

Chapter 16 Blood - Ch 16: Blood Ch Plasma and Cellular...

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Unformatted text preview: Ch 16: Blood Ch Plasma and Cellular Elements of Blood Hematopoiesis RBC Physiology Coagulation Blood = connective tis sue extracellular matrix: Plasma color ?? volume ?? specialized cel ls: (Formed elements) RBCs WBCs Platelets Fig 16-1 Plasma Plasma Water Plasma proteins • Albumin (60%) Osmotic Gradient • Globulins (Ab) • Fibrinogen Molecules • • • • Electrolytes Nutrients Trace Elements Dissolved gases Serum = Plasma – Clotting factors Hem(at)opoiesis = Hem(at)opoiesis Blood Cell Formation Few uncommitted, pluripotent stem cells in red bone marrow throughout life time (Fig 16­ 2) Controlled by cytokines, e.g. • Erythropoietin (hormone or cytokine?) • CSFs (Colony­stimulating factor)and ILs (interleukins): e.g. M­CSF, IL­3 (= multi CSF) Neulasta (pegfilgrastim) is a CSF • Thrombopoietin (TPO) Some Terminology: • Anemia vs. Leukemia vs. leukocytosis vs. leukopenia EPO Regulates RBC Production EPO “Hormone” synthesized by kidneys in response to hypoxemia EPO gene cloned in 1985 ⇒ Recombinant EPO now available (Epogen® , Procrit® ) Use in therapy, abuse in sport • • Bone marrow damage from chemotherapy Chronic renal failure Your book calls it a cytokine because it is made on demand, not stored. (p540). Trivia Dept.: Neulasta® (pegfilgrastim) stimulates production of WBC Running Problem: Blood Doping The Erythrocyte (RBC) The Biconcave Disk, 7 μ diameter, Carry O2 120 day lifespan No mitochondria, no nucleus • ATP from glycolysis Bag of Hb HCT = hematocrit = PCV MCV­Mean Cell Volume • ↓ in Fe-deficiency anemia in Hemoglobin (Hb) Hemoglobin [Hb] often reported in CBC • Four globulin proteins (Fig 18­8) Four (Fig 18­8) Two αTwo Two βTwo Each has the heme group Heme is a porphyrin that binds Fe Fe is considered a trace mineral • Meat, beans, spinach • Stored in liver, “recycled” • Fe deficiency Hemoglobin (Hb) Synthesis and Breakdown Breakdown Requires iron (Fe) + Vit. B12 (cobalamin) Reversible binding between Fe & O2 Hb Breakdown: • Hb → Bilirubin → bile. Hyperbilirubinemia • Too fast causes icterus (jaundice) • HbA vs. HbF Fetal Hb has two γ chains instead of two β chains RBC Disorders RBC Too high PCV: • • Polycythemia vera (PCV ~ 60-70%) (PCV Polycythemia Dehydration Anemias (O2 carrying capacity of blood too low) (O • Hemorrhagic anemia ⇒ Fe deficiency anemia Fe • Hemolytic anemia, due to genetic diseases (e.g. due Hereditary spherocytosis) or infections Hereditary • Pernicious anemia Vit. B12 Deficiency • Aplastic anemia • Renal anemia ↓ EPO EPO • Sickle Cell Anemia Sickle Cell Anemia Sickle 1st genetic illness traced to a specific mutation: DNA: CAC aa: glutamic acid HbA CTC valine (aa #6 of 146) HbS → crystallizes under low oxygen conditions Platelets = Thrombocytes Platelets Megakaryocyte (MK) is polypoid. Mechanism? MK produces ~ 4,000 platelets • Lifespan 10 days. Platelets contain gra­ nules filled with clotting proteins & cytokines Activated when blood vessel wall damaged Hemostasis Hemostasis = Opposite of hemorrhage ⇒ stops bleeding ⇒ too much bleeding Too much hemostasis ⇒ thrombi / emboli Too Too little hemostasis Too Three major steps: Three 1. Vasoconstriction 2. Platelet plug Temporarily blocks the hole 1. 3. Coagulation cascade (= clot formation seals hole until tissues repaired) until 1. 4. Platelet-derived cytokines further the process Two pathways: Extrinsic and Intrinsic After vessel repair, plasmin dissolves the clot Steps of Hemostasis Steps Vessel damage exposes collagen fibers Platelets adhere to collagen & release factors local vasoconstriction & + feedback platelet aggregation decreased blood flow platelet plug formation Fig 16-10, 11 loop Steps of Hemostasis cont. Steps 1. Two coagulation pathways converge Two onto common pathway onto 1. 2. 2. 2. 3. Intrinsic Pathway. Collagen exposure. All factors needed are present in blood. Slower. Extrinsic Pathway. Uses Tissue Factors released by injured cells and a shortcut. released Usually both pathways are triggered Usually by same tissue damaging events. by The different factors can be subject The to a variety of problems to 1. 2. Hemophilia Hypercoagulable states Common Coagulation Pathway Common Intrinsic pathway Extrinsic pathway Active factor X Prothrombin → thrombin fibrinogen → fibrin reinforces platelet plug clot Vit K needed for synthesis of several clotting factors Fig 16­12 Structure of Blood Clot Structure Plasmin, trapped in clot, will dissolve clot by fibrinolysis SEM x 4625 Clot formation limited to area of injury: Intact endothelial cells release anticoagulants (heparin, antithrombin III, protein C). Clot Busters & Anticoagulants Anticoagulants Dissolve obsolete or unwanted clots Prevent coagulation by blocking 1 or more steps in fibrin forming cascade Enhance fibrinolysis Inhibit platelet adhesion ⇒ plug plug prevention Examples: Urokinase, Examples: Streptokinase & t­PA Coumadin (warfarin) blocks Vit K EDTA chelates Ca2+ Aspirin prevents platelet plug Hemophilia Hemophilia Hemophilia A (Factor VIII Deficiency) Hemophilia A (Factor VIII Deficiency) ...
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