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Physio Ch. 16, Blood

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hrdcorhrvivor's version from 2017-04-18 06:01

Section 1

Question Answer
functions of blood1. transportation 2. regulation 3. protection
components of bloodplasma 55%: 91.5% water, 8.5% solutes (electrolytes, nutrients, proteins), serum. formed elements 45%: erythrocytes, leukocytes, platelets, buffy coat
albuminresponsible for colloid osmotic pressure, viscosity. carrier of mult substances, liver.
globulinstransport (alpha and beta), antibodies (gamma), liver and lymphocytes
fibrinogensblood clotting, liver
transferriniron transporter, liver
hematopoiesisall cells descend from pluripotent stem cell in red bone marrow.
4 elements that control production of formed elementscytokines: peptides/proteins releaased from one cell that affect growth of another, colony stimulating factors: stimulates WBC production, erythropoietin: stimulated RBC production, thrombopoietin: stimulates platelet production
erythropoiesiscontrolled by EPO, stimulated by decrease in o2 levels. 1. EPO secreted by kidney when low o2 2. bone marrow stimulated by EPO to make more RBCs 3. RBC enter blood stream
reticulocytesmature within one day of marrow release, high numbers: increase RBC production, low numbers: chemotherapy, aplastic anemia
RBCcontain hemoglobin, biconcave disc, strong flexible PM, glycolipids in PM, anucleate
hemoglobin4 polypeptide chains, 2 alpha 2 beta. heme group: pigment molecule in each chain. iron at center of each heme group binds o2
RBC life cyclelive 100-120 days, old RBC removed and destroyed by phagocytic cells in spleen and liver
recycling hemeheme degrades to bilirubin, gets converted to bile in liver
agglutinogensantigens on surface of RBC, determined genetically
agglutination reactionantibodies produced against alternate antigen without prior exposure, RBC will stick together if mixed
Rh factoranother protein found on surface of RBC, Rh positive: have Rh antigen on surface, no Rh antibodies in plasma. Rh negative: no Rh antigen on surface, no Rh antibodies in plasma
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Section 2

Question Answer
hematocritpercent of total blood volume that is packed RBC
polycythemiaabnormally high RBC counts. primary: problems in RBC production, secondary: response to other factors. leads to clotting issues. treatment: blood removal or aspirin
anemiaany condition which there is reduction in number of RBC or reduction in concentration of hemoglobin. 3 types: blood loss, decreased/ faulty cell production, blood cell destruction
microcyticsmall
normocyticnormal
macrocyticlarge
hypochromicpale
normochromicnormal
hyperchromic dark
hemorrhagic anemiadecreased RBC count due to blood loss
iron deficiency anemialow hemoglobin content due to inadequate intake of iron or cecondary result of hemorrhagic, microcytic hypochromic anemia
hemolytic anemiaabnormal or accelerated destruction of RBCs, major drawback of mechanical heart valves
sickle cell anemiacaused by single amino acid substitution, normochromic normocytic anemia
plateletsaka thrombocytes, megakaryocyte fragments into 2000 pieces, help stop blood loss, live 5-9 days
hemostasiskeeping blood within bv by repairing breaks without compromising blood flow. steps: vasocontriction, platelet plug formation, coagulation
vasocontriction processtriggered by damage to vessel, SM spasms causing contriction, release of chemicals from initial platelets
platelet plug formationbind to exposed collagen via integrins, causes more platelets to bind, release serotonin and platelet activating factor
how do platelets not spread to other uninjered sites?prostacyclin and nitric oxide
anticoagulantsclots are inhibited by blocking: platelet adhesion and coagulation cascade. heparin blocks intricsic pathway, aspirin blocks enzymes that promotes synthesis of thromboxane A2, warfarin blocks activation of vitamin k
fibrinolysisbv heals the clot is broken down by plasmin, tissue plasminogen activator converts plasminogen to plasmin
von willebrand diseasemost common bleeding disorder, missing von willebrand factor
hemophilia a and bnot as common, more severe
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