transportation (respiratory gases, nutrients, wastes) regulation (hormonal and temp) protection (clotting and immunity)
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blood composition
about 5 liters arterial blood venous blood made of 45% formed elements and 55% plasma
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arterial blood
blood leaving the heart bright red, oxygenated (except for blood going to lungs)
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venous blood
entering heart dark red, deoxygenated (except for blood coming from lungs)
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blood plasma
watery portion of blood dissolved solutes (proteins and other solutes)
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formed elements in blood
RBCs, WBCs, cell fragments (platelets)
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plasma proteins
albumin, immunoglobulins, fibrinogen, clotting proteins, angiotensinogen contributes to osmotic pressure by keeping water in the blood
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normal blood pH
7.38-7.44
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normal hematocrit level
females: 36-46% males: 41-53%
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normal hemoglobin levels
females: 12-16 g/100 mL males: 13.5-17.5 g/100mL
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normal red blood cell count
4.5 to 5.9 million/mm3
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normal white blood cell count
4,500-11,000/mm3
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albumin
most abundant creates osmotic pressure to help draw water from tissues into capillaries to maintain blood volume and pressure
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alpha and beta globulins
transport lipids and fat-soluble vitamins
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gamma globulins
antibodies that function in immunity
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fibrinogen
helps in clotting after becoming fibrin serum - blood without fibrinogen
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erythrocyte
RBCs flattened, biconcave discs carry oxygen lack nuclei and mitochondria around 5 million/mm3 120-day life span iron heme is recycled from liver and spleen; carried by transferrin in blood to red bone marrow
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anemia
abnormally low hemoglobin or RBCs count
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iron-deficiency anemia
not enough hemoglobin
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pernicious anemia
a lack of intrinsic factor
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aplastic anemia
damaged blood cells
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leukocytes
WBCs have nuclei and mitochondria move in amoeboid fashion diapedesis (movement through capillary wall into CT) don't live long around 5000 to 9000/mm3
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granular leukocytes
neutrophils, eosinophils, basophils
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agranular leukocytes
monocytes and lymphocytes
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thrombocyte
platelets smallest formed element, fragments of megakaryocytic lack nuclei 5-9-day life span clot blood with other chemicals and fibrinogen release serotonin -> vasoconstriction 130,000-400,000/mm3
stimulates growth of megakaryocytes released from liver
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thrombocytosis
increase in the number of platelets in the blood which tends to cause clots to form
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antigens
found on surface of cells to help immune system recognize self cells
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antibodies
secreted by lymphocytes in response to foreign cells
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ABO system
antigens on erythrocyte cell surfaces
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transfusion reaction
if a person receives the wrong blood type, antibodies bind to erythrocytes and cause agglutination
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Type A
A antigen anti-B antibody
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Type B
B antigen Anti-A antibody
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Type AB
Both A and B antigens neither anti-A nor anti-B antibodies
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Type O
Neither A or B antigen Both ant-A and ant-B antibodies
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Rh factor
antigen D Rh-positive has the antigen Rh-negative does not have the antigen
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Rh factor issue in pregnancy
Rh- mother exposed to Rh+ fetal blood produces antibodies may cause erythroblastosis fetalis in future pregnancies as antibodies cross placenta and attack fetal RBCs Rh- mother treated with RhoGAM to inactivate ani
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hemostasis
cessation of bleeding when a blood vessel is damaged
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blood clotting
damage exposes collagen fibers to blood platelet bind to collagen Von Willebrand factor holds them there platelets recruit to form platelet plug produces vasoconstriction by serotonin and thromboxane A formation of fibrin protein web
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intact endothelium secretes:
prostacyclin and NO CD39
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Prostacyclin and NO
causes vasodilation inhibits plate
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CD39
breaks down ADP into AMP and Pi to inhibit platelet aggregation
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formation of Fibrin
fibrinogen is converted to fibrin intrinsic: activated by exposure to collagen and factor VII extrinsic: inhibited by tissue thromboplastin (factor III) Ca2+ and phospholipids convert prothrombin to activate thrombin fibrinogen -> fibrin vitamin K needed by liver to make several of clotting factors
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dissolution of clots
plasmin digests fibrin clotting can be prevented with certain drugs
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anti-clotting drugs
calcium chelator heparin: blocks thrombin coumadin: inhibits vitamin K
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right atrium
receives deoxygenated blood from the body
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left atrium
receives oxygenated blood from the lungs
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right ventricle
pumps deoxygenated blood to the lungs
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left ventricle
pumps oxygenated blood to the body
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fibrous skeleton
separates atria from ventricles atria works as one unit, ventricles works as separate units forms annuli fibrosi rings, which holds the heart valves
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pulmonary
between heart and lungs blood pumps to lungs via pulmonary arteries blood returns to heart via pulmonary arteries
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systemic
between heart and body tissues blood pumps to body tissue via aorta blood returns to heart via superior and inferior venae ca
located between the ventricles and arteries leaving the heart
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pulmonary semilunar valve
between right ventricle and pulmonary trunk
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aortic semilunar valves
between left ventricle and aorta
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heart sounds
Lub: closing of AV valves, at ventricular systole Dub: closing of semilunar valves, at ventricular diastole
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cardiac cycle
repeating pattern of contraction and relaxation of the heart systole: contraction diastole: rel
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end-diastolic volume
total volume of blood in the ventricles at the end of diastole
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end-systolic volume
amount of blood left in the left ventricle after systole 1/3 of end-diastolic volume
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pressure changes during cardiac cycle
ventricles begin contraction, pressure rises, AV valves close (lub); isovolumetric contraction pressure builds, SL valves open and blood is ejected into arteries pressure in ventricles falls; SL valves close (dub); isovolumetric relaxation Pvent < Patria -> AV valve opens atria contracts, sending blood to ventricles
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extrinsic pathway
VII activated by tissue factor VII complex produced
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common pathway
VII and VIII complexes activate X V complex created V complex converts prothrombin to thrombin thrombin converts fibrinogen to fibrin
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intrinsic pathway
XII activated by collagen, glass, and others XI activated by active XII IX activated by active XI VIII complex created
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dicrotic notch
slight inflection in pressure during isovolumetric relaxation
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automaticity
automatic nature of the heartbeat
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sinoatrial node
pacemaker located in right atrium
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AV node and Purkinje fibers
secondary pacemakers of ectopic pacemakers slower rate
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pacemaker potential
slow spontaneous depolarization between heartbeats -40 mV: Ca2+ VGC open -> AP and contraction repolarization: K+ VGCs open
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pacemaker potential modulators
epinephrine and norepinephrine increase cAMP and keep channels open (HCN channels) ACh slows heart rate
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myocardial action potentials
RMP: -85 mV depolarization by AP from SA node Na+ VGCs open and potential plateaus at -15 mV more K+ channels open repolarization prevents summation and tetanus
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intercalated discs
spread APs in heart
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SA node
stimulates atrial contraction
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AV node
base of right atrium stimulate ventricles
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bundle of His
stimulate ventricles
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interventricular septum
divides the bundle of His into right and left branches
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Purkinje fibers
stimulate ventricular contraction
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conduction of impulses in heart
AP in SA node are quick AV node is slow bundle of His speeds things up
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repolarization in heart
Ca2+ goes back into SR by Na+-Ca2+ exchanger myocardium relaxes
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Excitation-Contraction Coupling
Ca2+ released AP conducted along sarcolemma and T tubules Ca2+ VGCs open Ca2+ diffuses into cells Ca2+ release channels open in SR Ca2+ binds to troponin and stimulates contraction
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refractory periods in heart
atria and ventricles cannot sustain a contraction APs are long, so refractory periods are also long