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UM BIOH 370 - Blood Continued
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BIOH 370 1st Edition Lecture 7Outline of Last Lecture BloodI. Functions of Bloodi. Transportationii. Regulationiii. ProtectionII. Properties of Blood- The makings of bloodIII. How Blood Cells are Made (hematopoiesis) - Hematopoiesis Throughout LifeIV. RBCs a. Hemoglobinb. CO2 Transportc. Erythropoiesis V. Causes of Anemia i. Insufficient erythrocytesii. Dietary Absorption- Iron-deficiency anemia - Pernicious anemiaiii. Genetics - Abnormal hemoglobin StructureOutline of Current Lecture Blood ContinuedI. Erythrocyte Disordersa. Polycythemia II. White Blood CellsThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.III. WBC Disordersa. Leukocytosisb. LeukopeniaIV. PlateletsV. Hemostasis 1. Vascular spasm2. Platelet plug formation3. Coagulation (blood clotting)VI. Anticoagulants Used ClinicallyVII. Clot RetractionVIII. Repair of Damaged Blood VesselsIX. FibrinolysisX. Factors Preventing Undesirable ClottingXI. Tromboembolytic ConditionsXII. Bleeding Disordersa. Thrombocytopeniab. Impaired liver function c. Hemophilias XIII. Restoring Blood VolumeCurrent LectureBlood ContinuedI. Erythrocyte Disorders:a. Polycythemia: excess of RBCs that increase blood viscosityResults from:- Polycythemia vera—bone marrow cancer- Secondary polycythemia—when less O2 is available (high altitude) or when EPO production increases- Blood doping (increases viscosity of blood)II. White Blood Cells:a. Neutrophils: 60-70%, phagocytes, send hormonal responses to call for aid/recruitment when find foreign substances in bloodb. Eosinophils: 2-4%, fight parasitic worms, allergies, anti-histamine (have histaminereceptors)=help reverse allergic reactions, get “bored” in clean (high hygiene) countries/places so increase activity which causes more asthma/allergies in those clean places.c. Basophils: 0.5-1%, allergies, histamined. Lymphocytes: 20-25%, helps fight flues/other infections, some leukemiae. Monocytes: 3-8%, helps fight flues/other infections, some leukemiaIII. WBC Disorders:a. Leukocytosis: WBC counts above 10,000/ml - Invading microbes- Strenuous exercise- Anesthesia- Surgeryb. Leukopenia: Abnormally low (below 5000/ml) WBC count—drug/medication inducedIV. 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)- Form a temporary platelet plug that helps seal breaks in blood vessels- Circulating platelets are kept inactive and mobile by NO and prostacyclin from endothelial cells of blood vessels- Get irritated easily (even in a blood draw)-when do, throw our dendrites-can cause blood clots- use heparin or EDTA to bind to calcium for anticoagulantV. Hemostasis: Fast series of reactions to stop bleeding (how blood clots)1. Vascular spasm: Vascoconstriction of damaged blood vessels. Triggers direct injury, chemicals released by endothelial cells and platelets, pain reflexes. - Arteries/veins have smooth muscles-these spasm- Veins are more likely to collapse because less smooth muscles than in arteries2. Platelet plug formation: (POSITIVE FEEDBACK CYCLE)a. Platelet adhesionb. Platelet release reactionc. Platelet aggregation3. Coagulation (blood clotting)a. Phase 1: Prothrombinase forms (through intrinsic or extrinsic pathways) –“pro”= before, “ase”= enzymeIntrinsic pathway:– Is triggered by negatively charged surfaces (activated platelets, collagen, glass)– Uses factors present within the blood (intrinsic)– Inside vesselsExtrinsic pathway:– Is triggered by exposure to tissue factor (TF) or factor III (an extrinsic factor)– Bypasses several steps of the intrinsic pathway, so is fasterb. Prothrombinase converts prothrombin to thrombinc. Thrombin converts soluble fibrinogen into insoluble fibrin, and forms a fibrin mesh-uses everything around it to make mesh(whatever it cangrab)- then pull mesh against wall and use retraction to tighten it up to form plug.VI. Anticoagulants Used Clinically:a. Warfarin: Vitamin K antagonist, blocks four clotting factors; Warfarin is reversed by Vitamin K administrationb. Heparin: increases antithrombin’s affinity for thrombin thus blocking thrombinc. Anti-thrombin: blocks XII, X and IId. Activated protein C (APC): blocks clotting factors not blocked by antithombin and enhances activity of plasminogen activatorsVII. Clot Retraction:- Actin and myosin in platelets contract within 30–60 minutes- Platelets pull on the fibrin strands, squeezing serum from the clotVIII. Repair of Damaged Blood Vessels:- Platelet-derived growth factor (PDGF) stimulates division of smooth muscle cells and fibroblasts to rebuild blood vessel wall- Vascular endothelial growth factor (VEGF) stimulates endothelial cells to multiply and restore the endothelial liningIX. Fibrinolysis:- Begins within two days- Plasminogen in clot is converted to plasmin by tissue plasminogen activator (tPA),factor XII and thrombin - Plasmin is a fibrin-digesting enzyme - Two homeostatic mechanisms prevent clots from becoming large-Swift removal and dilution of clotting factors -Inhibition of activated clotting factorsX. Factors Preventing Undesirable Clotting:- Platelet adhesion is prevented by– Smooth endothelial lining of blood vessels– Antithrombic substances nitric oxide and prostacyclin secreted by endothelial cells– Vitamin E quinine, which acts as a potent anticoagulant XI. Tromboembolytic 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• 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 fibrillationXII. Bleeding Disorders:a. Thrombocytopenia: deficient number of circulating platelets• Petechiae appear due to spontaneous, widespread hemorrhage • Due to suppression or destruction of bone marrow (e.g., malignancy, radiation)• Platelet count <50,000/mm3 is diagnostic • Treated with transfusion of concentrated plateletsb. Impaired liver function• Inability to


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