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Pulmonary and systemic also coronary circuit |
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blood, which goes to the pulmonary circuit, leaves through the pulmonary artery into the lungs |
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Blood is the body's only.. |
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fluid tissue blood is connective tissue |
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liquid plasma, and formed elements |
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Formed elements of blood include |
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Erythrocytes, or RBCS (iron increases density, which seperates them from WBCS) Leukocytes or WBCS Platelets |
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the percentage of RBCs out of total blood volume |
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5-6 L for males 4-5 L for females |
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Scarlet (oxygen rich) Dark red (oxygen poor) |
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Why do veins appear blue? |
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Scattering and absorption characteristics of skin at different wavelengths of light oxygenation state of blood diameter and depth of the vessel visual perception process |
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Distribution regulation protection |
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Oxygen and nutrients metabolic wastes hormones |
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Temp PH using buffer systems Adequate fluid volume in circulatory system |
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Blood protects against blood loss by.. |
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Activating plasma proteins and platelets initiating clot formation when a vessel is broken |
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Blood protects against infection by |
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Synthesizing and utilizing antibodies activating complement proteins activating WBS |
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Blood plasma contains over 100 solutes..including |
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proteins - e.g alubumin, others non protein nitrogenous substances -urea, uric acid, creatine, ammonium salts organic nutrients - glucose, amino acids, lipids, vitamins electrolytes - sodium, potassium, calcium, chloride, bicarbonate, respiratory gases hormones |
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Plasma protein albumin! 60% |
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Carrier protein buffer prime regularity of osmolarity extreme malnutrition, loss of protein |
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nuclei, or organelles they are only little bags of hemoglobin |
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Lifespan of formed elements |
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a few days, RBS a little longer most do not divide |
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All formed elements derive from what cells |
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hemocytoblasts in red bone marrow
process called hematopoiesis |
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Biconcave discs highly flexible plasma membrane allows them to change shape as necessary when moving through capillaries |
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Composed of 4 globin structures Each a heme group Represents a quandary structure Heme group contains iron, which oxygen binds to |
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start with a hemocytoblast development consists of 3 major events: ribosome synthesis to make hemoglobin Hemoglobin accumulation cell fills up with hemoglobin till it squeezes nucleus out ejection of nucleus 3rd phase reticulocyte forms later turning into a RBC |
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How long does it take to make RBCS? |
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The production of RBCs depends on |
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adequate supplies of Iron, amino acids, and B vitamins, B12 and folic acids |
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Fate and destruction of RBCS |
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life span 100 - 120 days old RBCS become rigid and fragile HB begins to degenerate, iron is savalaged for reuse |
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Heme group is converted to |
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bilirubin > bile > stercobillin |
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Due to blood loss, infections (yellow fever, Ebola) |
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Transfusion mismatch, infection (tetanus, small pox) |
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Destruction of Red bone marrow |
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Iron deficiency anemia Pernicious anemia - intrinsic factor caused by B12 deficiency Certain glands in stomach can't absorb right |
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excess RBCS that increase blood viscosity |
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Polycethemia is caused by.. |
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Polcythemia vera - bone marrow proliferative disorder, hematocrit of up to 80% and doubling of blood volume
altitude
blood doping |
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Malaria - 600 million new cases every year 3 million deaths/year |
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less numerous than RBCS 1% can leave capillaries into extra cellular spaces |
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Granulocytes and Agranulocytes |
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what do the types of WBCS do? |
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Neutrophils -> phagocytize Eosinophil - > deal with infection Basophile - > deal with allergic reaction Lymphocytes -> produce antibodies monocytes -> become macro phages when they leave the circulatory system |
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formation of WBCs is stimulated by |
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interleukins colony stimulating factors |
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Leukemia bone marrow becomes totally occupied with cancerous leaukocytes wbcs not functional |
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infectious mononucleosis epstein barr virus- increased agranulocytes
leaishmaniasis- parasites of macrophages (eats it from the inside out) |
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fragments of megarkaryocytes |
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forming a temporary plug that helps seals breaks in blood vessels platelets stick together, and release chemicals to initiate clotting |
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Hemostasis A series of reactions designed to stop bleeding During hemostasis, three phases occur in rapid sequence |
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• Vascular spasms – immediate vasoconstriction in response to injury • Platelet plug formation • Coagulation (blood clotting) |
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Platelet Plug Formation Upon damage to blood vessel endothelium (which exposes collagen) platelets |
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• Stick to exposed collagen fibers and form a platelet plug • Release serotonin for spasm and ADP, which attracts more platelets The platelet plug is limited to the immediate area of injury by NO and PGI2 (prostacyclin) - inhibits aggregation |
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A set of reactions in which blood is transformed from a liquid to a gel Over 30 substances involved! |
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A set of reactions in which blood is transformed from a liquid to a gel Over 30 substances involved! |
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Final 3 steps of cogulation |
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The final 3 steps of this series of reactions are: • Prothrombin activator (an enzyme) is formed • Prothrombin converted into thrombin (another activated enzyme) • Thrombin catalyzes the joining of soluble fibrinogen into a fibrin mesh – the mesh traps blood cells and temporarily seals the tear in the vessel |
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Clot retraction and Repair |
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Clot retraction – stabilization of the clot by squeezing serum from the fibrin strands • Platelets contain actin and myosin Occurs within 30-60 min Repair: • Platelet-derived growth factor (PDGF) stimulates rebuilding of blood vessel wall |
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removal of unneeded clots after healing has occurred - enzyme plasmin |
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Two homeostatic mechanisms prevent clots from becoming large: |
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• Swift removal of clotting factors • Inhibition of activated clotting factors Anticoagulants, such as heparin from basophils, also inhibit thrombin activity |
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a clot that develops and persists in an unbroken blood vessel •May block circulation, resulting in tissue death • DVT |
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a thrombus freely floating in the blood stream – may cause an embolism •Pulmonary emboli can impair the ability of the body to obtain oxygen •Cerebral emboli can cause strokes |
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Hemostasis Disorders: Bleeding Disorders |
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Thrombocytopenia – condition where the number of circulating platelets is deficient Impaired liver function – reduced production of clotting factors - Vitamin K deficiency Hemophilias – hereditary bleeding disorders caused by lack of clotting factors |
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RBC membranes have glycoprotein antigens on their external surfaces |
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•Unique to the individual •Recognized as foreign (“non-self”) if transfused into another individual • Promoters of agglutination (clumping) and are referred to as agglutinogens Presence or absence of these antigens is used to classify blood groups |
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Humans have 30 varieties of naturally occurring RBC antigens The antigens of the ABO and Rh blood groups cause vigorous transfusion reactions when they are improperly transfused |
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Bad transfusion reactions |
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Donor’s RBCs are attacked by the recipient’s plasma agglutinins (antibodies) causing: • Lower O2-carrying capacity • Clumped cells that impede blood flow • Ruptured RBCs release Hb into bloodstream Circulating hemoglobin precipitates in the kidneys and causes renal failure ABO Blood Groups |
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ABO blood groups consist of |
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• Two antigens (A and B) on the surface of the RBCs • Two antibodies (agglutinins) in the plasma (anti-A and anti-B)
Agglutinogens and their corresponding antibodies cannot be mixed without serious hemolytic reactions |
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Rh Blood Groups There are many different Rh agglutinogens, called Rh factors Presence of the Rh agglutinogens on RBCs is indicated as Rh+ Anti-Rh antibodies are not spontaneously formed in Rh– individuals, so: • First transfusion is OK, but anti-Rh antibodies form • Second exposure to Rh+ blood will result in a typical transfusion reaction |
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Plasma and blood volume expanders |
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Emergency? No time to type blood? •Infuse plasma only •Infuse plasma expanders - have osmotic properties that directly increase fluid volume •Isotonic saline can also be used to replace lost blood volume |
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New techniques for blood transfusions |
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•Conversion of A, B, or AB RBC’s into O by bacterial enzymes (glycosidases) |
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