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BIO169-Blood
Blood
| Question | Answer |
|---|---|
| what is plasma? | large # of organic and inorganic substances dissolved in H2O (organic - proteins, nutrients, metabolic waste, hormones; inorganic - mineral electrolytes) |
| what is serum? | plasma w/fibrinogen and other clotting-related proteins removed, because of clotting |
| what is albumin? | most abundant of the blood proteins; synthesized in liver |
| what is the purpose of plasma proteins? | although plasma itself is a conduit of nutrients and wastes, plasma proteins perform their functions in the plasma itself, or in the interstitial fluid |
| what is hemoglobin? | a protein with which oxygen (and to a lesser extent CO2) reversibly combine; oxygen binds to iron atoms (Fe++) in Hb |
| what is hematopoiesis? | the process of blood cell production |
| where do blood cells originate? | from multipotential stem cells (aka pluripotent hematopoietic stem cells); a stem cell may become a RBC or any type of white blood cell |
| where does hematopoiesis occur in the embryo? | in the yolk sac during the third week of embryonic development |
| where does hematopoiesis occur in the fetus? | in the liver and spleen by the fifth month of fetal development |
| where does hematopoiesis occur pre- and postpartum? | in the red bone marrow by 7 months fetal age; remains so for life |
| what do stem cells differentiate into as far as blood cell creation? | lymphoblasts, myeloblasts, and hemocytoblasts |
| what develops from lymphoblasts? | T and B lymphocytes (leukocytes) |
| what develops from myeloblasts? | monocyte/macrophage; eosinophil, basophil, neutrophil (leukocytes) |
| what develops from hemocytoblasts? | erythrocytes |
| how are RBCs specialized? | for the function of gas transport |
| what do mature RBCs mostly contain? | they are essentially bags of hemoglobin |
| describe the maturation of the RBC | early in development they have all the organelles typical of active cells, but as they mature, their organelles break down and their nuclei are extruded |
| what is special about the shape of a RBC? | is is highly adapted to its function; they are not round, but rather are biconcave disks, a shape which has a great deal of surface area per unit volume (quick diffusion) |
| what is erythropoietin? | a hormone produced by the kidneys that stimulate the production of RBCs, by stimulating the stem cell to produce many hemocytoblasts, stimulating the normoblast to differentiate into the reticulocyte, and stimulating the reticulocyte to differentiate into |
| what is the target of erythropoietin? | the bone marrow |
| what is the stimulus for erythropoietin? | a decrease in the oxygen levels of the blood; also testosterone |
| why is the kidney the ideal organ to monitor O2 levels? | because it is high priority for blood flow |
| how much blood do the kidneys receive? | about 25% of cardiac output at any given time |
| map the development of a RBC from stem cell to erythrocyte | stem cell -> many hemocytoblasts -> many erythroblasts -> many normoblasts -> each normoblast develops into one reticulocyte -> which matures into an erythrocyte |
| how does the normoblast become a reticulocyte? | 1) the reticulocyte loses its nucleus and migrates out of the bone marrow into the blood; 2) the reticulocyte still retains mRNA and rough endoplasmic reticulum; 3) the reticulocyte is the last cell in development to produce hemoglobin |
| how does the reticulocyte become an erythrocyte? | the cell loses the RER and mRNA and the mature erythrocyte can't synthesize hemoglobin |
| how many erythrocytes are formed each second? | 1 million! |
| how is the release of erythropoietin regulated? | by pO2 concentrations (i.e. blood oxygen levels) and anemia; a decrease in pO2 (hypoxia) stimulates the release of erythropoietin; an increase in pO2 inhibits the release of erythropoietin; various forms of anemia will stimulate the releaase of erythropoi |
| what are some causes of hypoxia? | high altitude, hemorrhage, and heart disease |
| how long does it take for new RBCs to appear in the bloodstream? | 5-7 days |
| what type of anemia is caused by lack of folic acid? | megaloblastic anemia |
| what type of anemia is caused by lack of vitamin B12 (intrinsic factor)? | pernicious anemia |
| what type of anemia is caused by lack of iron? | iron deficiency anemia |
| where are blood cells produced in children? | marrow of most bones produce blood cells |
| where are blood cells produced in adults? | only the bones of the chest, base of the skull, and upper portions of the limbs produce blood cells |
| what is the lifespan of an erythrocyte? | about 120 days before they are destroyed; 1% of body's erythrocytes are destroyed and replaced daily |
| why is the lifespan of an erythrocyte so short? | because they squeeze through narrow capillaries and experience wear and tear on the cell membrane |
| what at the erythrocytes destruction sites? | spleen and capillaries |
| how are RBCs destroyed? | in the spleen there are fixed macrophages which identify aging RBC by a change in their cell membranes which result from wear; these macrophages phagocytize RBCs and process the hemoglobin |
| how is the hemoglobin processed? | 1) split into heme and globin 2) globin is digested into amino acids (amino acids can be reused) 3) heme porphyrin component converted into bilirubin |
| what are the components of hemoglobin? | heme: complex porphyrin molecule containing iron; globin: protein chains |
| what is the evolution of bilirubin? | 1) heme porphyrin is converted into non-conjugated bilirubin; 2) non-conjugated bilirubin is transported to the liver 3) glucuronic acid is added to the non-conjugated bilirubin; 4) liver transports conjugated bilirubin via biliary system to duodenum |
| what is bilirubin? | aka bile pigment; the major breakdown product of hemoglobin |
| what is another name for bilirubin diglucuronide? | conjugated bilirubin |
| what are the 2 main categories of abnormalities of bilirubin production and extretion? | 1) increased unconjugated bilirubin in the blood; 2) increased conjugated bilirubin in the blood |
| what is the cause of increased unconjugated bilirubin in the blood? | excess destruction of erythrocytes |
| what is the cause of increased conjugated bilirubin in the blood? | blockage of the biliary system |
| what type of bilirubin would be most elevated in hemolytic anemia? | non-conjugated; this is an autoimmune disorder that increases the destruction of RBCs |
| what type of bilirubin would be most elevated in neonatal jaundice? | non-conjugated; liver function of newborns may not be fully operational; as the RBCs are broken down, the non-conjugated bilirubin accumulates |
| what type of bilirubin would be most elevated in biliary atresia? | conjugated; this is a conjenital condition where there is a lack of bile ducts in the liver; RBC destruction rate is normal, liver function is normal, formation of conjugated bilirubin is normal, but it can't be removed thru the biliary system |
| what type of bilirubin would be most elevated in biliary obstruction? | conjugated; often results from inflammatory processes in the liver in which scar tissue blocks the ducts; liver function is normal |
| what is hemostasis? | stoppage of bleeding |
| what type of responses are there in hemostasis? | immediate responses which function to decrease blood loss, followed by long-term mechanisms which keep damaged vessels occluded until they can be repaired |
| what are the 3 steps in hemostasis? | vasospasm (blood vessel spasm), platelet plug, and coagulation |
| describe vasospasm | vasospasm is an immediate response; damage to the blood vessel wall stimulates release of serotonin, which is a local reflex resulting in vasoconstriction; increased damage -> increaased vasoconstriction |
| describe how a platelet plug works | it is an immediate mechanism; the platelet contacts the roughened surface, such as a damaged blood vessel and releases chemical substances ADP & thromboxane A; platelets aggregate and can seal small holes in blood vessels |
| how do platelets contract? | they contain a high concentration of actin and myosin which are stimulated to contract in aggregated platelets |
| what are platelets? | cell fragments which function in hemostasis |
| what is the purpose of the platelet chemicals? | ADP stimulates platelet activation, then platelet aggregation (a positive feeback mechanism); thromboxane A stimulates platelet aggregation and vasoconstriction |
| what is petechiae? | thrombocytopenias are manifested by the appearance of many small, pinpoint hemorhages which are especially visible on the mucous membranes; these hemorrhages are called petechiae (tiny, broken capillary blood vessels) |
| what is thrombocytopenia? | platelet deficiency |
| what other chemicals do platelets release? | several chemicals important in the clotting process |
| what is coagulation? | a long-term mechanism; the clotting of blood in which multiple chemical factors in the blood are activated which result in the formation of a complex network of fibers and cells, called a clot |
| what is the purpose of a clot? | it occludes the lumen of the damaged vessel |
| what are the 2 mechanisms for blood clotting? | 1) extrinsic mechanism - activated by damage to tissues outside the vessels (the sub-endothelial cells are exposed to blood); 2) intrinsic mechanism - caused by disruption of laminar flow of blood, or contact with a foreign surface |
| compare the 2 types of mechanisms | 1) they are both complex chemical pathways that lead to clot formation 2) they have different initial reactions, but the later stages are the same |
| why is the clotting pathway called a cascade? | because it consists of a complex series of reactions and the product of one reaction frequently serves as an enzyme to activate the next; it is called a cascade because it takes so many sequential steps to get to the final product |
| what is the physiological advantage in such a complex series of steps? | it shouldn't be too easy to produce a clot! |
| how many stages are involved in both the extrinsic and intrinsic mechanisms? | 3 stages |
| what happens in extrinsic stage 1? | 1) damaged tissue releases tissue thromboplastin (enzyme) 2) as blood leaks from damaged vessels in the area it contacts tissue thromboplastin 3) plasma protein,Stuart-Prower factor, activated (in presence of Ca++), 4) prothrombin activator (PCC)formed |
| what happens in extrinsic stage 2? | prothrombin activator activates plasma protein thrombin into the end product thrombin |
| what happens in extrinsic stage 3? | 1) thrombin activates plasma protein fibrinogen into fibrin monomers; 2) 2nd clotting factor (factor 13) in the presence of calcium ions, stabilizes the fibrin monomers to form fibrin polymers |
| what else is thrombin responsible for? | positive feeback on the cascade leading back to itself |
| what happens in intrinsic stage 1? | 1) plasma protein called Hageman factor is activated; 2) Hageman factor and several other clotting factors trigger prothrombin activator (PCC) |
| what happens in intrinsic stages 2 and 3? | same as extrinsic mechanism |
| how is clotting prevented? | 1) flowing blood 2) smooth endothelium 3) negative charge of endothelium 4) heparin 5) antithrombin III 6) fibrin |
| how does flowing blood prevent clotting? | moving blood is less likely to clow than blood which is still; flowing blood keeps the clotting factors from aggregating together in one place |
| how does smooth endothelium prevent clotting? | healthy endothelium is smoother than glass, which prevents adherence of clotting factors; damaged endothelium is roughened and this activates clotting factor |
| how does negative charge prevent clotting? | healthy endothelium has a slight negative charge which mildly repels clotting factors; damaged endothelium has proteins exposed which have a negative charge which attracts clotting factors |
| how does heparin prevent clotting? | heparin is an anti-coagulant found in basophils, mast cells, and is also produced by endothelial cells; it prevents clotting by stimulating activity of antithrombin III |
| how does antithrombin III prevent clotting? | antithrombin III is a plasma protein which functions to inhibit thrombin, and therefore inhibits clotting |
| how does fibrin prevent clotting? | inhibits further clothing by binding thrombin, thus preventing the cascade from continuing unchecked |
| compare venous bleeding from arterial bleeding | venous bleeding is less rapid blood loss; veins have low blood pressure |
| what is a hemotoma? | accumulation of blood in the tissue |
| how does a blood clot develop? | 1) fibrin polymers form meshwork trapping blood cells and platelets 2) soft, jelly-like clot forms 3) trapped platelets release platelet-derived growth factor (PDGF) |
| what is the purpose of PDGF? | 1) stimulate fibroblasts to repair damaged wall of blood vessel by forming connective tissue 2) stimulates enlargement of atherosclerotic plaque (stiff, scar-like plaque) by stimulating fibroblasts |
| what is retraction? | the platelets also produce actin filaments which cause the fibrin meshwork to retract, pulling the edges of the damaged vessel together, and squeezing fluid out of the clot, making it firmer |
| what is the fluid squeezed out of the clot called? | serum; it is the plasma minus the clotting factors |
| how does dissolution occur? | 1) begins as soon as clot is formed 2) plasminogen (a plasma protein) is activated to plasmin - an enzyme that digests fibrin |
| how id plasminogen activated to plasmin? | by tissue plasminogen activator (TPA), which is produced by the endothelial cells |
| how long does it take for a clot to be dissolved? | about 2 days |
| what is a thrombus? | a clot which forms in an unbroken vessel; it can occlude flow to tissues and organs upstream |
| what is an embolus? | aka embolism; a clot that breaks free and travels in the bloodstream where it can lodge in small vessels and occlude flow |
| where is a common site for embolisms? | the lungs, because of the extensive network of capillaries |
| what is the total blood volume of an average human being? | roughly 5 liters (1.3 gallons) |
| what percentage is contained in the veins, arteries, heart & lungs, and capillaries? | veins: 70%; arteries: 10%; heart and lungs: 15%; capillaries: 5% |
| because veins have the most capacity, how else do we refer to them? | as capacitance vessels or blood "reservoir" |
| what do the capillaries do? | they are gas exchange vessels |
| What is PCC? | prothrombin converting complex, aka prothrombin activator |
Created by:
debmurph
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