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18 Cards in this Set
- Front
- Back
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Life cycle of a red blood cell |
-live for 120 days -undergo wear and tear as they squeeze through blood capillaries -plasma membrane becomes more fragile with age; cells more likely to burst (esp. as the squeeze through narrow channels to enter the spleen) -ruptured RBCs are removed from circulation and destroyed by fixed phagocytic macrophages into the spleen and liver -breakdown products recycled |
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Life cycle of a red blood cell 14 steps |
1 phagocytis 2 hemoglobin split 3 globin breakdown into amino acids 4 Fe3+ if removed from heme 5 Fe3+ detaches from transferrin and attaches to ferritin 6 Fe3+ reattaches to transferrin 7 This complex turned to red bone marrow-haemoglobin synthesis 8 erythropoiesis in red bone marrow- red blood cell production 9 non iron portion of haem converted to biliverdin and then bilirubin 10 bilirubin is released and transported to the liver 11 bilirubin is released by liver cells into bile 12 bateria convert bilirubin into urobilinogen 13 some urobilinogen absorbed back into the blood 14 most eliminated in feces |
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3 general functions of the blood |
TRANSPORTATION O2, CO2, metabolic wastes, nutrients, heat and hormones REGULATION- helps reulate ough buffer, helps regulate bod temp- coolant properties of water -vasodilation of surface vessels -regulate water content of cells by interactions with dissolved ions and proteins - PROTECTION fro disease and loss of blood |
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development of the formed elements of blood is called |
HAEMOPOIESES- before birth in the yolk sac of embryo, after brith in the liver, spleen, thymus and lymph nodes of fetes, RBM is primary site
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DEVELOPMENT OF FORMED ELEMENTS |
1PLURIPOTENT STEM CELLS- are made in the 2RBM,go on to make myeloid an lymphoid stem cells. 3MYELOID STEM CELLS begin their development of RBC, platelets, monocytes, neutraphills, eosinophils and basophils 4LYMPHOID begin in RBM, finish in lymphatic tissue as lymphocytes 5Myloid stem cells differentiate into progenitor cells. known as CFUs they eventually form RBC, platelets, granular and agranular leukocytes. 6through this development the cells are then described as precursor cells, after several divisions they develop into actual formed elements of blood.
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blood loss to an inured vessel is controlled by |
vascular spasm- platelet plug formation platelet aggregation |
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vascular spasm |
this mechanism reduces blood loss for several minutes-an hour until chemical mediated mechanisms take place. an immediate neurologic mediated reflex by the NS activated by: -damage of the small blood vessels smooth muscle --release of substances from activated thrombocytes -pain receptor |
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platelet plug formation |
if the hole in the blood vessel is small enough to be contained -platelet adhesion (platelets stick to collagen fibres) -platelet release reaction (platelets activation, projection and liberation of vesicles substances) -platelet aggregation (platelets stick together by the action of clotting factor) |
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blood clotting |
blood loss is prevented by the formation of a blood clot -the fibrin clot tightens, pulling edges of the dammaged vessel together preventing further damage. -this mechanism presents a sequence of cascade reactions in which soluble fibrinogen is converted into insoluble fibrin by thrombin.
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Extrinsic pathway |
dammaged tissues leak tissue factor (thromboplastin) into the blood stream. -in the presence of Ca+2, clotting factor X combines with V to form thrombinase. -throminase forms in seconds |
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Intrinsic pathway |
activation occurs endothelium is dammaged and platelets come in contact with collagen of blood vessel walls. -platelets are damaged releasing phospholipids -substance involves Ca2+ and clotting factor x11,X and V. -requires several minutes
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haemostatic control mechanism |
haemostatic control mechanism prevent thrombosis. -plasminogen is contained within formed clots and can be activated by blood or body tissues and converted into plasmin or vibrinolysin -fibrinolysin occurs by plasmin digesting fibrin threads and inactivating fibrinogen, prothrombin and factors XII, V11, V. small inappropriate clots get dissolved as well as the necessary clots once the damage is repaired. - normall a clot will remain contained and will not extend to other areas because fibrin absorbs thrombin into the clot and also clotting factors in the blood are not concerntrated enough to cause generalised clotting
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haemostatic control mechanism PROSTACYCLIN |
prostaglandin produced by white blood cells and endothelial cells is a powerful inhibitor of thromboxane, A2, inhibiting platelet release and adhesion |
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haemostatic control mechanism ANTICOAGULANTS |
antithromnin- blocks clotting factors Xii, X, ii heparin- combines with antithrombin to block thrombin activated protien c- enhances the activity of plasminogen activators and inactivates two major clotting factors not blocked by antithrombin |
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trace the pathway of a drop of blood as it enters the heart from the superior vena cava |
1. right atrium (deoxygenated blood) >tricuspid valve 2.Right ventricle >pulmonary valve 3. pulmonary trunk and pulmonary arteries 4. in pulmonary capillaries blood loses Co2 and gains O2 5. pulmonary veins (oxygenated blood) 6. left atrium >biscupid valve 7. left ventricle >aortic valve 8. aortic and systemic arteries 9. in systemic capillaries, blood loses O2 and gains Co2 >superia vena cave > inferior vena cava > coronory sinus 10. right atrium |
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Intrinsic conduction system phase one |
Sinostrial (SA) node spontaneously depolarizes about every .8sec. Depolarization spreads through atria by the internal pathway, causing contraction of the atria. Depolarization spreads onward to the atrioventricular (AV)node |
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Intrinsic conduction system stage two |
SA node and intermodal pathway repolarize. After delay at the AV node,the depolarization wave spreads in sequence to the bundle ofHis, the bundle branches then the Purkinji fibres , causing contraction of the ventricles. Atria relax.
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Intrinsic conduction system stage three |
the AV node, the bundle of His branches and the purkinji fibres repolarize and ventricles relax. |
