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transports gases, nutrients, waste, and hormones. regulation of body temp and pH protection against blood loss and infection |
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connective tissue made up of plasma and formed elements |
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erythrocytes, leukocytes, and platelets |
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90% water. Proteins in plasma are mostly produced by the liver. Contains respiratory gases, hormones, nutrients, and electrolytes |
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albumin, globulin, and fibrinogen |
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main factor contributing to blood viscosity. has biconcave discs for increased surface area for infusion of gases. contains hemoglobin, atp, lipis, and carbonic anhydrase. no nucleus or mitochondria. ATP is used for when RBCs bend and twist to go through capillaries |
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tetromeres. 2 alpha and 2 beta protein chains. heme. iron atom in each heme is required to transport O2. each hemoglobin can transport 4 oxygen. |
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Hemoglobin loading oxygen in the lungs |
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Hemoglobin unloading oxygen in the tissues |
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deoxyhemoglobin (dark red) |
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Hemoglobin loading carbondioxide in the tissues |
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Hemoglobin loading carbonmonoxide from combustion fumes or cigarette smoke |
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blood cell formation. hemocytoblast- stem cells in red bone marrow |
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happens in liver, yolk sac, thymus, lymph nodes, red bone marrow |
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happens in red bone marrow (skull, ribs, sternum, vertebrae, pelvis, femur/humerous) |
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-about 1% of RBCs are replaced everyday (2.5 million) -about 4 days to make a mature RBC -accumulation of hemoglobin turns cells from white to red -extrusion of nucleus makes the cell a reticulocyte, which is released into circulation. -reticulocytes take 2 days to be a mature RBC (when ribosomes are lost) |
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decrease in RBCs leads to decrease in oxygen transport, leads to hypoxia, decreased oxygen levels |
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increase in RBCs leads to increase blood viscosity leading to the heart having to work harder and increasing BP |
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Regulation of Erythropoiesis |
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Definition
adequate supplies of starting materials (iron, amino acids, B vitamins- B12 and folate) hormone control -estrogen- limits increases in erythropoiesis -testosterone- enhances erythropoiesis, which is why males hematocrit levels are higher -erythropoietin EPO |
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release by the kidneys in response to hypoxia (increased exercise, decreased cardiovascular/lung function, increased altitude, loss of RBC or iron deficiency) speeds up erythropoiesis in red bone marrow |
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fate and destruction of RBCs |
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life span- 100-120 days old RBCs become fragile and hemoglobin starts to degenerate, since there are no organelles to replace or repair damage RBCs rupture and release hemoglobin macrophages pick through blood and breakdown the damaged or old RBCs |
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fate and breakdown of hemoglobin |
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Definition
amino acids- recycled for protein synthesis iron- fe- taken up by bone marrow to be reused to make new hemoglobin non-fe-heme- transported to the liver and converted to bilirubin, released as bile, broken down in intestine and elminated in feces and urine |
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if there is too much bilirubin being released, its stored elsewhere, like the skin, causing yellow pigment. in liver disease, bilirubin seeps into the bloodstream because the liver is unable to metabolize and excrete it properly |
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blood has abnormally low oxygen carrying capasity and cannot support normal metabolism accompanied by fatigue, paleness, chills, and shortness of breath symptom not a disease |
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acute or chronic blood loss |
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RBCs rupture prematurely due to drugs, HIV, malaria |
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B12 deficiency or lack of ability to absorb B12. without B12 you cannot synthesize RBCs |
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genetic mutation causes absent or faulty globin chains |
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mutation in hemoglobin gene in beta chain of hemoglobin |
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excess of RBCs that increase blood viscosity resulting from polycythemic vera, secondary polycythemia, or blood doping |
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overproduction of RBCs by red bone marrow |
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high altitudes, or when EPO production increases. problem is some where other than red bone marrow |
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can leave capillaries via diapedesis (ooze through to tissues in between endothelial cells) move through tissues by ameboid motion toward larger concentrations of chemokine (positive chemotaxis) |
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WBC granules release chemicals at the site of damage or infection |
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granulocyte most numerous WBCs, usually first on site, polymorphonuclear very phagcytic- eating up cells or debris produce lysozymes and defensins |
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enzymes that break down gram positive cell walls |
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proteins that bind to bacteria cell walls, they squeeze in and put holes in the cell walls. water then floods in and bacteria cell bursts |
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granulocyte bilobed nucleus rnases- protect against viruses codenases- toxins to kill parasites that are too big to be phagocytosed histimases- break down histimine so immune cells stay in control of histimine during inflammation of allergic reactions |
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granulocyte rarest WBCs histimine- inflammatory chemical that acts as a vasodilator and attracts other WBCs to inflamed sites heparin- anticoagulant, prevents blood from clotting too quickly |
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agranulocyte originates in red bone marrow, proliferates within lymph nodes, spleen, tonsils, and thymus few circulate in blood B cells- humoral immunity T cells- fight tumors, destructs infected host cells- cell mediated immunity |
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agranulocytes largest leukocyte leaves circulation, enters tissues, and differentiates into macrophages macrophages phagocytize viruses, bacteria, and cell debris, then present it to lymphocytes which activate and destruct. they increase in number with chronic infections like flu and colds |
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production of WBCs all leukocytes originate from hemocytoblasts stimulated by chemical messangers: interleukins (released by mature WBCs) and colony-stimulating factors (released by bone marrow and blood vessels) |
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abnormally low WBC count drug induced (chemo or HIV) |
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increased WBC count normal response to bacterial or viral infections |
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bone marrow is totally occupied with cancerous leukocytes, fails to make RBCs and platelets. immature, nonfunctional WBCs in the bloodstream death is usually caused by internal hemorrhage and overwhelming infections due to not enough platelets and not enough clotting factors treatments- irradiation, antileukemic drugs, and stem cell transplants |
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thrombocytes cytoplasm contains myosin and actin to minimize wound site plasma membrane contains glycoproteins that attach to connective tissue and activates platelets small fragments of megakaryocytes |
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platelets bind to collagen in connective tissue at the wound site platelets become activated and release coagulation factors (thromboxanes) platelets change shape, fibrinogen (from plasma) crosslinks platelets, stabilizing the wound ADP and thromboxanes also activate other platelets (positive feedback mechanism |
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endothelial cells release endothelin-paracrine cut nerve endings release factors as well smooth muscles around damaged vessels contract to close |
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1. prothrombin activator is formed -intrinsic- inside vessels (unsmooth, fat accumulation) extrinsic- external trauma 2. prothrombin is converted to thrombin 3. thrombin converts fibrinogen (soluble plasma hormone) to fibrin (insoluble) forming a mesh |
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blood cells and platelets trapped in fibrin network |
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inactivates clotting factors clotting factors and anticoagulants are always available stimulated by eliminating vitamins K or calcium |
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anticoagulant plasma protein made in the liver circulates at all times helps prevent thrombin activation |
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anticoagulant from basophils stimulates antithrombin |
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anticoagulant from endothelial cells converted from prostaglandin (derivative or lipid in the plasma membrane of endothelial cells) antagonizes the activation of platelets by inhibiting the release of clotting factors |
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myosin/actin contract, pulling fibrin network together, shrinking damaged vessel platelet-derived growth factor stimulates smooth muscle cells to divide and fibroblasts to rebuild vessel walls vascular endothelial growth factor stimulates replacement of endothelial lining |
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fibrinolysis- digest away clot begins within 2 days of clot formation plasminogen- plasma protein is converted to plasmin by tissue plasminogen activator (tPA) from endothelial cell plasmin digest fibrin |
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clot that develops in an unbroken blood vessel may block circulation, leading to tissue death |
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thrombus that breaks off and floats freely in the blood stream pulmonary embolus- blocks arteries of lung and impairs gas exchange cerebral embolus- block of blood supply to brain-> stroke |
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recessive genetic disorder linked to X (more common in men), can also spontaneously occur lack or clotting factors leads to internal bleeding internal bleeding in joints, can cause disfiguration in joints |
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glycoproteins- classify blood types sugars and proteins tell body that this cell belongs |
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Hemolytic Disease of Newborn |
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Definition
also called erythroblastosis fetalis Rh- mother becomes sensitized with exposure to Rh+ blood from fetus and causes her body to synthesize antibodies against Rh+ antibodies cross placenta and destroy RBCs of fetus problem during 2nd pregnancy because mom has full immunity |
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mom receives RhoGam, which binds to Rh on fetus RBCs, but does not destroy them mothers immune system does not see the fetus Rh+ antigens |
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diagnostic blood test erythrocytosis vs anemia |
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diagnostic blood test for anemia |
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diagnostic blood test for proportion of RBC to total sample low iron leads to low hemoglobin leads to microcyte (small) RBCs |
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diagnostic blood test leukopenia- low WBC, indicates damaged red marrow, viral infection, radiation, drugs, tumors, vitamin B12 or folate deficiency leukocytosis- high WBC, indicated bacterial infection or allergic reaction |
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diagnostic blood test high neutrophils indicates bacterial infection high basophils or eosinophils indicates allergic reaction |
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diagnostic blood test low platelet count- thrombocytopenia, chronic bleeding heredity, vitamin B12 deficiency, drugs, radiation |
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diagnostic blood test time of thromboplastin added to plasma to cause clot |
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diagnostic blood test pancreas- glucose concentration kidney- urea concentration cardiovascular disease- cholesterol concentration liver function- bilirubin concentration |
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