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Phys U4 - Blood

Physiology Unit 4 - Blood - Fofi

Fluids of the body blood and interstitial fluid
Composed of plasma, variety of cells blood
Bathes cells of the body interstitial fluid
Flow of nutrients and oxygen blood to the interstitial fluid to the cells
Flow of wastes cells to interstitial fluid to blood
Functions of blood transportation of O2, CO2, metabolic waste, nutrients, heat, hormones; regulation of pH via buffers, regulation of body temperature; protection from disease and loss of blood
Physical characteristics of blood more viscous than water, pH of 7.4 (7.35 to 7.45); 5 to 6 L in average male; 4-5 L in average female; hormonal negative feedback systems maintain constant blood volume and pressure
Components of blood 55% plasma, 45% RBCs, <1% WBCs, platelets
Components of plasma 90% water, 7% plasma proteins
Hematocrit is the percentage of blood volume occupied by RBCs; female range is average of 42%; male average is 45%
Anemia condition due to not enough RBCs
Polycythemia condition due to too many RBCs
Normal hemoglobin range females are 12-16 g/100ml of blood; males are 13.5-18
Blood plasma over 90% water, 7% plasma proteins, 2% other substances (electrolytes, hormones, gases, waste)
Plasma proteins created in liver, confined to the bloodstream; consist of albumin, globulins, and fibrinogen
Albumin plasma protein; contributes to blood osmotic pressure, used for transport
Globulin plasma protein; contributes to defense against foreign particles
Fibrinogen plasma protein; contributes to clotting
Formed elements of blood RBCs, WBCs, platelets
White blood cells (leukocytes) granular—neutrophils, eosinophils, basophils; agranular—lymphocytes, monocytes
Normal RBC count 5 million/drop
Normal WBC count 5-10,000
Platelet count 150,000-400,000
Blood cell formation occurs only in red marrow of flat bones like sternum, ribs, skull, pelvis, ends of long bones; most types need to be continually replaced because they die within weeks or days
Red blood cells contain oxygen carrying protein hemoglobin
Red blood cell shape bioconcave disk
How does RBC cell shape link its function? bioconcave disk shape gives increased surface area/volume ratio, allows for flexibility to pass through narrow passages, it has no nucleus or organelles, and no mitochondrial ATP formation
Hemoglobin globin protein consisting of 4 polypeptide chains; each chain has one heme pigment; each heme contains one iron ion that can combine with one oxygen molecule.
Hemoglobin function each can carry four oxygen molecules; acts as a buffer and balances pH of blood; transports 23% of total CO2 waste from tissue cells to lungs for release
Hemoglobin ranges females—12-16g/100mL of blood; males 13.5-18g
RBC life cycle usually only live 120 days; wear out from bending through capillaries, no repair possible due to lack of organelles; worn out cells removed by macrophages in spleen and liver
Processing of “retired” RBCs removed from circulation by macrophages in spleen/liver; globin portion broken into amino acids; recycled to make new proteins; heme portion split into iron & biliverdin which is converted into bilirubin; bilirubin secreted by liver into bile and excreted
Erythropoiesis production of RBCs; proerythroblast starts to produce hemoglobin; nucleus ejected, reticulocyte is formed, escapes from bone marrow into blood; ejects organelles, matures into RBC; factors required are erythropoietin (kidneys), vitamin B12, iron
Erythropoiesis stimulus--tissue hypoxia; kidneys detect reduced O2 capacity of blood, release erythropoietin; e.poietin catalyzes proerythroblast dev in red marrow into reticulocytes; more reticulocytes enter blood and become erythrocytes; O2 carrying capacity increases
White blood cell less numerous than RBCs; only 2% of population is circulating blood at any given time; rest remain in lymphatic fluid, skin, lungs, lymph nodes, spleen; requires colony stimulating factor
Neutrophil fastest response of all WBC to bacteria and parasites; direct actions against bacteria—release lysozymes, release defensing proteins that act like antibiotics, release strong oxidants that destroy bacteria
Basophil WBC involved in inflammatory and allergy reactions; leave capillaries and enter connective tissue as mast cells; release heparin (anticoagulant), histamine, serotonin; heighten inflammatory response, account for hypersensitivity reactions
Eosinophil WBC; leaves capillaries to enter tissue fluid; release histaminase, slows down inflammation; attack parasitic worms, phagocytize antibody-antigen complexes
Monocyte WBC; takes longer to get to site of infection, but arrives in larger numbers; become wandering macrophages once they leave capillaries; destroy microbes, clean up dead tissue following an immune response
Lymphocyte WBC B/T cells; B—destroy bacteria, their toxins, turn into plasma cells that produce antibodies; T—attack viruses, fungi, transplanted organs, cancer cells; natural—attack many dif microbes, some tumor cells; destroy foreign invaders by direct attack
Differential WBC count detection of changes in numbers of circulating WBCs; indicates infection, poisoning, leukemia, chemotherapy, parasites, or allergic reaction
Normal WBC counts N 60-70%; L 20-25%; M 3-8%; E 2-4%; B <1%
Platelet/thrombocyte disc-shaped cell fragment with no nucleus; normal count is 150,000-400,000/drop blood; form in marrow; short life span; aged ones removed by fixed macrophages in spleen; release ADP and other chemicals needed for platelet plug formation
Platelet formation formed in marrow; myeloid stem cells eventually become megakaryocytes whose cell fragments form platelets
Hemostasis stoppage of bleeding in a quick and localized fashion when blood vessels are damaged; prevents hemorrhage; methods—vascular spasm, platelet plug formation, blood clotting
Vascular spasm damage to blood vessel stimulates pain receptors; reflex contraction of smooth muscle of small blood vessels; can reduce blood loss for several hours until other mechanisms take over; only for small blood vessel/arteriole
Platelet plug formation platelet adhesion, platelet release action, platelet aggregation
Platelet adhesion platelets stick to exposed collagen underlying damaged endothelial cells in vessel wall
Platelet release action activated platelets extend projections to make contact to other platelets; release thromboxane A2, serotonin, ADP—activating other platelets; thromboxane A2 & serotonin vasoconstrict and ADP causes stickiness activating other platelets
Platelet aggregation activated platelets stick together and activate new platelets to form a mass called platelet plug; plug is reinforced by fibrin threads formed during clotting process
Blood clotting/coagulation substances required are Ca++, enzymes made by liver cells (clotting factors), substances released by platelets/damaged tissues; cascade of reactions in which clotting factor activates next in fixed sequence resulting in formation of fibrin threads
Coagulation reactions in which blood is transformed from liquid to gel; follows extrinsic and intrinsic pathways; final three steps—prothrombin activator formed, prothrombin converted to thrombin, thrombin catalyzes polymerization of fibrinogen into fibrin mesh.
Pathways to prothrombin activator initiated by intrinsic/extrinsic pathway; triggered by tissue damaging events; involves series of procoagulants, each pathway cascades toward factor X; activation of factor X—it then complexes w/ Ca ions, PF3, and Factor V to form prothrombin activator
Intrinsic pathway several min; Damaged endothelium activates FXII; Platelet contacts damaged endo, release Platelet FactorIII (PF3); FXII & PF3 + Ca2+ & Clotting factors 8 & 9--creates FX activator complex--activates FX--complexes with Ca2+, PF3 & FV, forms prothrombinase
Extrinsic pathway takes seconds; damaged tissue leaks tissue factor thromboplastin into blood; activates FVII, which combines w/ Ca2 & clotting FVII to make FVII tissue factor complex, which activates FX, which complexes w/ Ca2, PF3, FV to make prothrominase
Common pathway prothrominase+Ca2 catalyze prothrombin to thrombin; thrombin+Ca2 catalyze fibrinogen into fibrin; fibrin strands form basis of clot; fibrin causes plasma to be gel trap; fibrin+Ca2 activate FXIII that crosslinks fibrin mesh, strengthens/stabilizes clot
Clot dissolution heparin acts as anticoagulant; plasminogen becomes plasmin, fibrinolytic enzyme that dissolves small clots at site of completed repair; clot formation remains localized
Thrombosis clot formed in unbroken blood vessel; attached to rough inner lining of BV; slow flowing blood allows clot factors to build up and cause coagulation; may dissolve and travel
Embolus free floating clot in blood; may cause strokes, myocardial infarctions; low dose aspirin can help prevent this
Blood group/type determined by presence/absence of surface antigens; glycoproteins, glycolipids; antigens A, B, and Rh(D); antibodies in plasma; cross reactions occur when antigens meet antibodies
Blood type A surface antigen for A, anti-B antibodies
Blood type B surface antigen for B, anti-A antibodies
Blood type AB surface antigen for A and B; no antibodies
Blood type O no surface antigen; antibodies for both anti-A and anti-B
RH blood groups Pple w/ Rh isoantigens on RBC surface--Rh+; Normal plasma has no anti-Rh antibodies; Antibodies develop only in Rh- blood type & only w/ exposure to antigen; Transfusion reaction upon 2nd exposure to antigen results in hemolysis of the RBCs
Rh and moms Rh negative mom & Rh+ fetus will mix blood @ birth; Mom's body creates Rh antibodies unless she gets RhoGam shot after first delivery, miscarriage or abortion; In 2nd child, Hemolytic Disease of the Newborn may develop causing hemolysis of the fetal RBCs
Universal Donors and Recipients AB blood “universal recipients” since no antibodies in plasma, only true if cross match the blood for other antigens; type O blood “universal donors” since have no antigens on cells; theoretically can be given to anyone
iron-deficiency anemia lack of absorption or loss of iron
pernicious anemia lack of intrinsic factor for B12 absorption
hemorrhagic anemia loss of RBCs due to bleeding (ulcer)
hemolytic anemia defects in cell membranes cause rupture
thalassemia anemia hereditary deficiency of hemoglobin
aplastic anemia destruction of bone marrow (radiation/toxins)
Created by: michellerogers



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