Cardiovascular

ErythrocytesTransport O2 and CO2; originate in bone marrow use hemoglobin that contains one Fe atom for 4 oxygen atomsProduction of RBCScellular O2 deficiency releases erythropoietin which stimulates red cell production in bone marrow 120 day lifespan Aged RBCs are removed from the blood in sinuses of spleen and are degradedErythropoietin90% produced in the glomeruli of the kidney the rest in the liver Stimulates red cell production in the bone marrowLeukocytesContains nuclei and mitochondria and move in amoeboid fashion; can squeeze through pores in capillary wall and move to site of infectionAgranularLymphocytes and monocytesGranularEosinophils Basophils NeutrophilsLymphocytesMost important cells of the immune system and act against antigens effective for fighting infectious organismsMonocytesLargest Phagocytic Kidney shaped nucleus Transform into macrophagesPlateletsBlood clotting by releasing serotonin which stimulates constriction of the blood vessel reducing the flow of blood to the injured area Also secrete growth factor, autocrine regulatorsNeutrophilsPhagocytosis of bacteria Multilobed nucleusBasophilsRelease histamine and other mediators of inflammation Hypersensitive and anaphylaxesEosinophilsTurn off allergic responses and kill parasitesMyeloid tissueRed bone marrow of Long bones; sternum, pelvis, bodies of vertebraeHematopoiesisembryo connected to yolk sac which is main site for production after 1st trimester: placenta is main site 8 weeks- livers takes over after birth, red bone marrow takes overLymphoid tissueIncludes lymph nodes, tonsils, spleen and thymusErythropoisisHappens in proerythroblasts Depends on folic acid, Vitamin B12 and ironAnemiaIron deficiency, pernicious(B12) Aplastic- destruction of bone marrow by chemicals or radiation Reynolds number is increased bc of decreased viscosity and high CO which decreases velocitythrombiblood clots in lumen of vessel; narrow the diameter which increases blood velocity increasing Reynolds number and causing turbulent blood flowshearblood travels at different velocities within a blood vessel highest at wall lowest in center breaks up RBCs and decreases viscosityhistamineincreases during inflammation in asthmatic peopleLeukopoiesisGranulocytes from myeloblasts Monoblasts form monocytes Platelets from megakaryoblastsreticulocyteconversion to erythrocyte requires Fe, folic acid anf vitamin B12T cellAttack foreign cells directlyB cellMultiply to become plasma cells, secrete antibodiesPrimary polycythmiaaka polyvera cause is based on abnormal bone marrow that produces excess RBCs, platelets, and lymphocytes which leads to thrombosisNormocyticblood loss in birth or car accident; must replace bloodMicrocytic anemiaIron deficiencyArtificial polycythemiacaused by oversecretion of erythropoietin which leads to oversecretion of RBCs NORMAL BONE MARROWPrimary polycythemia symptomshypertension headache vomiting/nausea nose bleed increased hematocrit frequent blood clotting vision problem vertigo hepato and splenomegaly risk of MI and strokeMacrocytic anemiaB12 or folic acid deficiencySickle cellInherited condition; defective hemoglobin A molecule; hemoglobin S and C which leads to hypoxemia so the deficiency of o2 to tissues makes the heart pump faster (tachycardia), weak immune system, jaundice deficiency of O2 to cells- causes pain which increases infection risk causes fatigue pain in ab cavity, joints, because of infiltration of antibodiesjaundicedamaged RBCs releases hemoglobin which is converted into bilirubin and turns skin yellow pre-hepatic: caused by damaged RBCs hepatic: caused by damaged liver post hepatic: closure of bile duct, hepatic duct or cystic ductSickle cell symptomsAnemia Jaundice Pigment gallstones Crises on back long and chest bones Ab pain Fever Fatigue Paleness Tachycardia Breathlessness Delayed growth and puberty Ulcers on lower legSickle cell treatmentSupplements of folic acid Antibiotics and vaccinesLeukemia symptomsFever and night sweats Headache Easy bleeding Bone or joint pain Swollen lymph nodes in armpit and neck A lot of infections Weakness Losing weightLeukemiaStarts in bone marrow; it makes abnormal WBC and grows rapidly; weak immune system increases infection Acute, chronic, lymphocytic- overproduction of mature WBCs myelogenous- overproduction of mature and immature WBCsLeukemia treatmentChemotherapy INFa therapy Radiation Stem cellTunica initimaSimple squamousTunica mediaSmooth muscleTunica externaConnective tissueLumenCentral blood-filled space of a vesselDifferences in A + V1- artery wall is thicker bc of elasticity 2- artery is under high pressure bc of ventricular contraction; stress volume 3- capacity of vein is higher bc walls are thinner 4- contraction of vein is under ANS control and the skeletal muscle that surrounds it; valve accelerates the flowArteriesCarry oxygenated blood away from the heart; thick walled under high pressurearteriolessite of highest resistance alpha receptors constrict smooth muscle beta receptors relax skeletal muscle biggest change in resistance largest decrease in pressurelaminar blood flowvelocity of flow at vessel wall is 0 velocity of flow at center of vessel is maximal Reynolds number is below 2000turbulent blood flowstreams of blood flow radially and axially and takes more energy to drive the flow; causes heart murmurs Reynolds number is above 2000VeinsCarry blood toward the heart; merge to form larger veins; thin walled; under low pressure; contain highest proportion of blood; have alpha 1 receptors BP much lower than arteries Tunica externa is thicker Conduct blood from capillaries toward heart Skeletal muscle help pump bloodTPRResistance in capillaries due to small diameter intersectional areaVelocityDirectly proportional to blood flow Inversely proportional to cross-sectional area Higher in aorta than in all capillaries Lower in capillaries is good for exchangesCapillariesSmallest blood vessels; site of exchange of molecule; thin walled; single layer of endothelial cells surrounded by basal lamina; lipid and water soluble may cross through clefts or diffusionBlood flowFrom high to low Inversely proportional to resistance if blood vessels directly proportional to pressureResistanceDirectly proportional to viscosity of the blood and length of the vessel indirectly to sizeCapacitanceDescribes distensibility of vessels Inverse related to elastase And pressure Directly proportional to volume Greater for veins so that means higher blood volume in veins For arteries it decreases in age Bc they become stif and less distensiblePressure in circulationDecreases Highest in aorta lowest in vena cavae Largest decrease happens in arterioles Bc of their high resistanceMean pressureAorta-100 Arterioles- 50 Capillaries- 20 Vena cava- 4BPforce exerted by circulating blood on the walls of vesselsSystolic pressureHighest arterial pressure Measured after the heart contract and blood is ejected into the arterial systemDiastolic pressureLowest arterial pressure Measured when the heart is relaxed and blood is returning to the heart via veinsPulse pressureDifference between systolic and diastolic Most important is stroke volume higher in large arteries than in aorta Decreased in capacitance With age increases in pressureVenous pressureVery low High capacitance so they can hold large volumes of bloodAtrial pressureEven lower than venousPrimary HypertensionNo clear cause; factors include: diet- full of NaCl and cholesterol NaCl- increases fluid absorption, blood volume, and pressure obesity- type 2 diabetes, stress overstimulation of SNS alpha 1- vasocontriction aldosterone can increase CO and TPR Hypernatremia- causes increased sensitivity to stimulation which increases action potential opens Ca channels in post synaptic Deficiency of vasodilator like bradykinin and prostanglandins substance- no relaxationadrenal glandadrenal medulla- secretes norepinephrine and epinephrine which regulates BP and blood sugar in liver adrenal cortex- secretes aldosterone, cortisol and androgen- male sex hormonealdosteroneincreases blood pressure increases reabsorption of Na, Cl, H2O, and HCO3 back into the vessels Excretion of K and H into urineandrogenMale sex hormone in the adrenal cortex that in females increases abnormal hair growthcortisolincreases blood pressure by increasing diastolic and systolic pressures and TPR stress hormone maintains blood glucose increases appetite controls metabolismSecondary hypertensionMore Na inflow causes depolarization and opening of Ca channels which causes vasoconstriction; Caused by disorders of adrenal gland, Cushing's syndrome, hyperaldosteronism, Pheochromocytoma, kidney disease, drugs-weight loss and corticosteroids like prednisone and nonsteroidal antiinflam. drugs like aleve and mortin, BC cortisol, coarctation of aorta, preeclampsia-destruction of endothelial layer and small fetus, and thyroid and parathyroid problemssteroidssynthetic cortisol decreases inflammation but increases TPR and systolic and diastolic pressurethyroidsecretes T3 and4 controls basal metabolism rate, temp, increases O2 consumption controls development of CNS and bone in fetusdeficiency of thyroidmental retardation in fetus, direct effect on alpha 1 and beta 1, adrengic, increased sensitivityhyperthyroidismoversecretion of T3 and 4 hormones; weight loss, sweating, tachycardia, vomiting, irritation of CNS, oily skin and hair, always feel hot hypertension bc of alpha 1 palpitation bc beta 1parathyroidincreases blood Ca (normal is 10) increases blood pressure constricts blood vessels oversecretion: hypercalcemia, constrict smooth muscle, hypertension, headache, vomiting, nausea,coarctation of aortacongenital problem descending aorta is narrow increased pressure in femoral artery, neck area, carotid artery intercranial symptoms: hypertension, weak pulse in femoral artery and hemorrhage treatment: removal risk of strokecushings syndromeendocrine disorder, by tumor, infection, or of adrenal cortex- increased cortisol, aldosterone, and androgen; patient has hypertension, headache, vomiting nausea, nose bleed, moon face, big belly, vision problem, vertigo, hypernatremia, hypokalemia, obesity, thick facial hair in women, suppressed female sex hormone, irregular period and ovulation, suppressed inflammation hyperglycemia, thin upper and lower limbs bc cortisol breaks down proteins in muscleshyperaldosteronicmaka Conns disease; tumor of aldosterone in adrenal cortex symptoms: hypernatremia, hypertension, hypokalemia, headache, sleep disorder, vertigo, nausea, nose bleeding, vomiting increased HCO3 (alkaline blood)pheochromocytomatumor of medulla; oversecretion of adrenaline/NA; hypertension, sweating, palpitation, heart disease, dyspneapolycystic kidney diseasecyst in the kidney no clear cause decreases filtration rate treat with kidney transplantbirth controlestrogen increases edema leads to weight gain increased NaCl absorption leads to increased blood volume and BPweight loss drugsdestroys blood vesselsSymptoms of hypertensionHeadache and dizziness Fatigue and anxiety Shortness of breath Changes in vision convulsions Nausea and vomiting Increased sweating Nose bleeds Tinnitus and pale skin Heart palpitations Increased urination Flushed face and general feeling of unwellnessDrugs to treat high blood pressureACE inhibitors, captopril, ramipril AG 2 blockers, Valsartan Diuretics like hydrochlorothiazide- renal failure; accels infiltration rate Ca channel blockers, felodipine, benidipine Beta 1 blocker- propranolol Increased aldosterone- give spironolactone but also decreases AndrogenP waveDepolarization of atriaVenulesFormed from merged capillariesLow permeability capillariesBBB highly selective only vital substances pass through Not a barrier against O2 CO2 and some anestheticsThrombocytopeniaAbnormally low concentration of plateletsPR intervalAtrial depolarization of AV node to ventricular depolarization; connects signals from atrium to ventriclesQRS complexVentricular depolarizationEctopic fociAbnormal pacemaker sites within the heart that display automaticity; post MI healed tissue may have spontaneous depolarization which send signals to other part of ventricle; shows abnormal QRSST segmentWhen ventricles completely are depolarized and ready for relaxation; important in the diagnosis of ventricular ischemia or hypoxia; is depressed or elevated also positive sign for MIT or U waveVentricular repolarizationQT intervalTime between ventricular depolarization and repolarizationVentricles and atriaPhase 0- upstroke of action potential caused by increase of Na Phase 1- initial repolarization closing of Na channels outward of K Phase 2- plateau (L-type)increase in Ca to balance K Phase 3- repolarization Ca decreases K increases Phase 4- resting K equilibrium; -85Sinoatrial nodePhase 0- upstroke of action potential increase in Ca (T-Type and L-Type) Phase 3- repolarization increase in K Phase 4- slow depolarization increase in Na; automaticity; sets HRAV nodeUpstroke of action potential is caused by inward Ca currentConduction velocityTime required for excitation to spread throughout cardiac tissue Depends on size of inward current Fastest in purkinje Slowest in AV nodeExcitatbilityCardiac cells initiate action potentials in response to inward depolarizing current Reflects the recovery of channels Changes over course of action potentialsAbsolute refractory periodNo action potential can be initiated; if there is a 2nd stimulus after phase 0 the membrane cannot accept or show a reactionEffective refractory periodConducted action potential cannot be generated; if there is a 2nd stimulus during phase 1 or 2 the membrane may accept it but doesn't show a reactionRelative refractory periodAction potential can be elicited but at a higher force; if there is a 2nd stimulus during phase 3 the membrane will accept and show a reactioneffect of aldosterone on BP1- Low BP 2- release of renin in kidneys 3- Turns into Angiotensinogen 4- Turns in to Angiotensin 1in liver 5- Turns into AG2 in blood by ACE from the lungs; 6-Vasoconstriction and increase of aldosterone from adrenal cortex in nephron and releases Na,Cl, H2O, and HCO3 into blood vessels and absorbs H and K for excretion in urine increase in BP