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140 Cards in this Set
- Front
- Back
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what is the mechanism by which arterial diastolic pressure is 80 but diastolic ventricle pressure is almost 0?
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aorta and the other primary arteries are very elastic and they recoil during diastole
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what are the fluid secreting cells in the pericardial cavity and what are the cells called?
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mesothelial cells line the inside of the pericardium and the oustide of the epicardium
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what is the only biscupid valve?
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the mitral valve b/w left AV
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what are the 3 main components of intercalated discs?
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fascia adherens, desmosomes, and gap junctions (so conduction can occur in sequence)
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what is the primary fuel for cardiomyocytes?
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lipid
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in what layer of the heart do the major arteries and veins run?
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in the epicardium
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when does coronary blood flow occur?
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diastole because heart compression limits flow
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what is the difference between ischemia and infarction?
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ischemia is limited blood flow infarction is cell death (occurs from the inside out because blood flows from outside in
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what is the primary energy source for purkinje fibers?
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glycogen
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what is the tunica intima and what is its purpose?
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it is endothelium and subendothelium and it is porous to allow O2 and glucose out of lumen
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what is the tunica media?
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the muscular and elastic components (exists only in arteries!)
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what is the tunica adventitia?
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the outer connective tissue, nerves, and vasa vasorum
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what can be a result of blockage of the vasa vasorum
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necrosis of SMCs leading to aneurysm!
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what are the anticoagulant and procoagulant functions of endothelium
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anticoagulant: negative charge on the luminal surface
procoagulant: synthesis of von Willibrand factor which can activate the coagulation cascade |
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what is the function of pericytes?
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they regulate the growth of vessels, reside in basal lamina and can become SMCS or fibrocytes
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where are vasa vasorum located?
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in the tunica adventitia
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what is the normal anticoagulant mechanism of endothelial cells?
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negative charge repels platelets
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what is the main procoagulant factor of endothelial cells?
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Weibel-Palade bodies secrete von Willirand factor
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what are the important metabolic vasodilators in the heart?
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NO, ADENOSINE!, hypoxia, low pH
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what are the effects of Epi and NEpi binding to alpha and beta adrenergic receptors on vessels?
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beta: vasodilation
alpha: vasoconstriction |
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what vessel level contributes most to peripheral resistance?
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arterioles
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how does angiogenesis take place?
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proteases break down the BL, endothelial cells proliferate and then a new BL is laid down
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what are the 4 types of capillaries?
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continuous: muscle, lung (with clefts, very small pores)
continuous in CNS: no pores, no clefts, very little can get through fenestrated: kidney (high permeability, very thing endothelium with many medium holes) Sinusoidal: liver, spleen (large with large gaps and phagocytes positioned right outside) |
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how are lymph vessels different histologically from blood vessels
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they have no basal lamina, they are supported by anchoring filaments
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how does (digitalis) digoxin work?
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it blocks the Na-K pump. More sodium inside cell. drives the Na-Ca exchange, which allows for increased contractility
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what ion has the highest conductance in CMCs?
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K, very small changes in [K] change the V greatly
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what are the abbreviations for the activation and inactivation gates of Na channels?
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M: activation (march on)
H: inactivation (halt) |
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what are the two ways to increase HR at the SA node?
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increase the slope of depolarization
increase the threshold potential |
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what does greatly increasing extracellular [K] do to CMC conduction?
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the resting membrane potential is much higher, and there isn't a chem gradient to drive K. Na channels then get inactivated at these higher V
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what allows purkinje fibers to tramis their electrical potential so efficiently between each other?
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lots of gap junctions
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what is the "space constant"
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the distance required for an electric potential to decay 63% (purkinje fibers have a big space constant)
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what is the effective refractory period
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no AP no matter what
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what is the relative refractory period
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end of effective refractory period until normal excitability (if an AP is produced, the amplitude will be smaller)
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in what directions with R or L ventricular hypertorphy change the QRS axis?
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RV-hypertrophy will shift it down toward 90
LV hypertrophy will shift it up toward 0 |
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what is the convention for degrees in einthoven's triangle?
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0 degrees is facing horizontal toward the patient's left
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what is a first degree heart block?
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SLOWED conduction through AV node, every P is followed by a normal QRS but the P-R interval is LONG
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what is a second degree heart block?
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a block at the AV node where not every P is followed by a QRS
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what are the three requirements for a re-entry paroxysmal tachycardia?
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1. geometry for a conduction loop (depolarization can circle around)
2. unidirectional block (can go one way but not the other 3. slow conduction: time to effective refractory period to finish |
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what is it called when you have an extra bundle of purkinje fibers running back up through the non-conductive AV ring?
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a bundle of kent
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what is the order of valves passed as blood goes through the heart?
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Tricuspid
pulmonary mitral aortic |
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in the cardiac cycle, what is diastasis?
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when the mitral valve is open but there is little flow into the ventricle (waiting to contract)
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why doesn't the aortic valve close when aortic pressure overshoots ventricular pressure?
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because the blood is moving out and has lots of kinetic energy
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what is calcium induced calcium release in CMCs?
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inflow of Ca through L-type Ca channels (DHPR) is coupled to RhR opening in SR to allow lots of Ca inflow
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how is the passive tension of cardiac muscle different than skeletal muscle?
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cardiac muscle has lots of titin and is much more rigid (much greater passive tension)
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what is the staircase phenomenon?
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increases in HR are accompanied by increases in contractility (more Ca influx)
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what is a post-extrasystolic potential?
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when you have a premature ventricular contraction, there is a longer R-R for the next contraction, and the next contraction is also way more powerful
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what medullary nuclei have autonomic input to the heart?
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dorsal motor of vagus and nuc. ambiguus via vagus (parasympathetic)
paramedian reticular nucleus input down to intermediolateral horn of thoracic spine (sympathetic) |
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what is the Neurotransmitter and receptor of parasympathetic innervation to the heart?
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Ach acts on muscarinic receptors
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what is the neurotransmitter and receptor of sympathetic innervation at the heart?
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NE acts on Beta adrenergic
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how do sympathetic and parasympathetic innervation oppose each other at the heart?
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both beta and muscarinic receptors are G-protein coupled receptors, beta receptors lead to increase in cAMP, muscarinic decreases it
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what is housed in the nodose ganglion? and where is it?
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cell bodies of sympathetic afferents
it is on the vagus, just before the vagus enters the medulla |
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do CMCs use more energy in systole or diastole?
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in DIASTOLE! because of high activity of the serca pump
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which has a great influence on ventricles, PS or Sympathetic?
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sympathetic (increases contractility a lot)
PS doesn't do much to ventricles |
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which exerts its effets on HR faster, sympathetic or parasympathetic?
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Parasympathetic
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what is the S1 heart sound?
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mitral and tricuspid valves closing
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what is the S2 heart sound
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the pulmonary and aortic valves closing
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what is the S3 heart sound?
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sudden tensing of chordae tendinae during early rapid ventricular filling
kentucky |
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what is the S4 heart sound?
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due to atrial contraction
tennessee |
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how are stenotic sounds different than regurgitation sounds?
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steonic crescendo and decrescendo
regurgitations are relatively constant (may decrescendo) |
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what are the two types of systolic murmurs?
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aortic stenosis
mitral regurgitation |
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what are the two types of diastolic murmurs?
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aortic regurgitation
mitral stenosis |
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what is the normal order of the two components of the S2 heart sound?
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the aortic
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why do the S2 heart sounds split more during inspiration?
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more blood brought into right atrium/ventricle, delays closing of P2 sound
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what would cause reversed splitting of S2 heart sounds?
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pulmonary hypertension would make the P sound so early it would be split during expiration and normal during inspiration
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what is Poiseuille's Law?
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like ohm's law
Q = deltaP/R |
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where is the only place in the body where you have resistance (two capillary beds) in SERIES
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in the kidney
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what factors PROMOTE turbulent flow?
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high velocity
high fluid density large lumen diameter low fluid viscosity after a narrowing in an artery |
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what is the windkessel effect?
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the recoil of arteries that keeps diastolic pressure relatively high
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what happens to arterial compliance with age and what effect does this have on MAP?
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decreased compliance leads to increased MAP
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how is the pulse wave velocity affected by compliance
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pulse wave velocity increases with decreasing compliance
(note, pulse wave moves faster than the actual flow) |
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what is the law of LaPlace?
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Vessel Wall Tension = intralumenal pressure x radius
(tension very low in capillaries, very high in arteries) |
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why are major arteries more susceptible to aneurysm than capillaries?
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because they have much greater tension
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what is Fick's Law?
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Diffusion = (diffusion coefficiency)x(area)x(conc. gradient) / (thickness)
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what are the major means of substance movement at capillary beds?
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diffusion (important for gas and energy exchange)
pinocytosis (important for big molecues) filtration/reabsorption (important for bulk fluid movement) |
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what is Starling's Law of Capillaries?
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fluid movt = k [(Pc + pi(i)) - (Pi + pi(c))]
k: filtraiton coefficient for the membrane Pc: capillary hydrostatic pressure pi(i): interstitial osmotic pressure (due to proteins) pi(c): capillary osmotic pressure (usually constant except in kidneys) |
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what factors can affect venous pressure?
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walking (lowers venous pressure by pumping blood out)
heart failure (raises pressure) hypoproteinemia (caused by nephrosis, increases net filtration) inspiration lowers venous pressure |
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what is hyperemia?
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increased blood flow (either due to increased tissue activity (active hyperemia) or following ischemia (reactive hyperemia)
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what are the major vasodilator metabolites?
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K, adenosine, PGs, NO, and Hydrogen Peroxide
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what are the two main mechanisms of arterial pressure autoregulation?
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metabolic (decreased pressure, increased buildup of metabolites, vasodilation)
myogenic (increased pressure, increased stretch of VSM, vasoconstriction, pressure decreases back to normal) |
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what are the three strong vasoactive substances produced by endothelium?
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NO (vasodilator)
Prostacyclin (vasodilator) Endothelin (vasoCONSTRICTOR) |
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what are the actions of Serotonin?
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stimulates vasoconstriction of VSM and also vasoDILATION by increasing NO production by endothelium
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which has a bigger role in controlling blood pressure, the sympathetic or PS nervous system?
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sympathetic, PS has very little influence on BP
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how do you prevent vasoconstriction by sympathetic nerves in muscle during exercise?
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vasodilator memtabolites block NE at alpha adrenergic receptors
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what tissues respond strongly by vasoconstricting in response to sympathetic nerve activity?
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skin
resting skeletal muscle visceral organs kidneys NOT brain, heart, exercising muscle |
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what is the concept of coronary steal?
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if there is a lesion, vasodilator metabolites will be produced which dilate nearby vasculature, actually stealing more flow from the already ischemic vasculature
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what mechanisms are and aren't responsible for regulation cerebral blood flow
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local mechanisms
nervous control does not regulate cerebral blood flow |
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what adrenergic receptors are expressed in muscle and what do they do?
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alpha and beta-2.
alpha vasoconstrict in repsonse to NE from sympathetic nerve terminals beta-2 vasodilate in response to low-moderate levels of E from adrenal medulla |
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what is the exercise pressor reflex?
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reflex where sensory nerves in activate skeletal muscle stimulates increases in SNA
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what two types of capillaries vessels are present in the skin?
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normal arterioles (which respond to local and SNA)
arteriovenous anastamoses are under SNA only, important for temp control |
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what effect does serotonin have on vasculature?
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it is a vasoconstrictor
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what are two common pathologic consequences of decreased baroreceptor sensitivity?
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sudden cardiac death and arrhythmia
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what cardiac afferents are important in normal reflex function and disease function?
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normal function: vagal afferents
disease: sympathetic afferents |
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how are paraSNA and SNA different in moderate hemorrhage/orthostatic stress vs. severe?
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moderate: paraSNA decreased
SNA increased severe: paraSNA increased SNA decrased leads to vasovagal syncope |
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what is vasovagal syncope?
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in severe hemorrhage or orthostatic stress, paraSNA increases and SNA decreases paradoxically.
this could be due to heart shriveling at VERY VERY low pressures which activates vagal afferents |
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what are glomus cells?
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the sensory cells in the carotid and aortic CHEMOreceptors
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what are the components of the diver's reflex?
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apnea (stop breathing)
reflex bradycardia inc. SNA to vasculature (vasoconstriction) |
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what are the 4 classifications of cardiac shock?
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1. hypovolemic (hemmorhagic)
2. cardiogenic 3. hypermetabolic (sepsis) 4. neurogenic |
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what are the two important pharm interventions for patients with CHF?
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a vasodilator (decreases TPVR, raising both CF and VF curves)
a diuretic (lowers total blood volume and brings back to a normal state with the limited contractility it has left) |
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what is Kartagener's Syndrome?
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immobile cilia due to mutation in dynein (respiratory infections??)
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what are brush cells?
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cells with microvilli on the apical surface. have afferent innervation and are involved in the sneeze reflex
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in the lungs, what are granule cells and where are they found?
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they are cells that secrete peptide hormones and NTs, found in clusters at branch points in the conducting airways
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what are swell bodies and what is their function?
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they are venous plexuses in teh inferior and middle nasal conchae, they dilate alternately and prevent dessication of nasal mucosa
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what is Bowman's gland?
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they are serious secreting glands of the olfactory mucosa that wash away odors
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how is olfactory epithelium different than respiratory epithelium?
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olfactory is thicker, the underlying CT is thicker, has nerve buncles, and bowman's glands
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what is the one part of the nasopharynx that is stratified squamous epithelium?
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the soft palate (it is kind've a foodspace)
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what is the function of the trachealis muscle?
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it pulls together the ends of the tracheal cartilage c shaped rings, making the trachea narrower during cough reflex
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what is the histological difference between bronchus and bronchioles?
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bronchus has cartilage in the walls, bronchioles do not
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what is the function of clara cells and where are they found?
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in bronchioles, they secrete clara cell protein and GAGs
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what is "ventilator pressure"
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the pressure it takes to push air into the lungs
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what is the lung volume at which the lung recoil matches the chest wall recoil?
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functional reserve capacity
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at what point does the chest wall no longer have intrinsic outward recoil?
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~70% of TLC
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what is reynold's number?
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determines whether flow will be laminar or tubulent, its turbulent when reynold's # is high. when velocity is high, density is high, radius is big
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what are the three ways CO2 is transported and what is the main one?
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dissolved
carboxyhemoglobin Bicarbonate (the main one) |
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what is the chloride shift?
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the movement of Chloride into the RBCs when HCO3- diffuses out after it has been made by carbonic anhydrase
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what is the difference between perfusion limited transport and diffusion limited transport?
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perfusion limited gases diffuse VERY quickly...
diffusion limited gases diffuse slower and would diffuse more if they had more time |
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are O2 and CO2 usually perfusion limited or diffusion limited?
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perfusion limited (unless you are on Everest or are at incredibly high Q)
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what are the two control means to match V/Q
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hyposic pulmonary vasoconstriction and airway constriction in response to low CO2
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where are O2 chemoreceptors and where are CO2 chemoreceptors?
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O2 chemoreceptors are peripheral (glomus cells in carotid bodies)
CO2 chemoreceptors are central (detect changes in pH of CSF) |
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what is the effect of pulmonary stretch receptors on ventilation?
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they fire at volumes near TLC, inhibiting inspiration and promoting expiration
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what is Odine's curse?
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lesion in the respiratory center in the medulla, you can't sleep because you have apnea upon sleeping
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what is the functional difference between the dorsal respiratory center and ventral respiratory center
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dorsal (NTS) can stim inspiration
ventral (nuc. ambiguus) can stim both inspiration and expiration |
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what happens to CO2 sensitivity during sleep?
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it decreases and PaCO2 rises 2-3
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how is central sleep apnea different than obstructive sleep apnea?
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central: no effort
obstructive: effort but no flow |
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what are the consequences of chronic obstructive sleep apnea?
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personality changes
pulmonary hypertension |
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what two factors cause O2 transport to be diffusion limited at high altitude?
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increased Q (decreased transit time)
decreased atm O2 |
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which does fluid density affect, turbulent or laminar flow?
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turbulent flow
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what parameters allow for increases in VO2max? how is this different for old people?
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increased SV
increased a-v O2 difference elderly people can't increase a-v O2 diff |
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do trained people have a lower or higher RER at rest?
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lower, they are burning more fat at rest
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what hormones are released during exercise?
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glucagon, cortisol, Epi and NEpi
note: glucagon mobilizes glucose, muscle has insulin-independent mechanisms for uptaking glucose |
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which (slow vs. fast twitch fibers) are innnervated by small/large alpha motor neurons?
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Slow twitch fibers are innervated by small alpha motor neurons
fast twitch fibers are innervated by large alpha motor neurons |
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how does endurance training change muscle morphology?
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produces mild ST fiber hypertrophy
no FT fiber changes increased mt content angiogenesis |
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how does anaerobic training change muscle morphology?
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it produces ST and FT hypertrophy, increased glycogen content
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what drives a trained person's HR down at rest?
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increased vagal drive
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how do you simply measure oxygen extraction?
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1 - SvO2
normally this is around 25%. If it is greater that is a bad sign |
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what is the definition of shock?
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widespread cellular hypoxia and vital organ dysfunction
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what are the three main categories of shock?
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hypovolemic
distributive cardiogenic |
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how does increased respiratory drive exacerbate shock?
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inc. respiratory drive, increased perfusion to diaphragm and not other organs, worsens symptoms, leads to more respiratory drive!
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what is the simple algorithm to diagnose the type of shock?
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is Q high?
yes: DISTRIBUTIVE no: is RAP high or low? high: CARDIOGENIC low: HYPOVOLEMIC |
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what are the three treatment strategies for shock?
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fluid challenge (increase BV)
inotropic challenge (increase contractility) vasopressor challenge (increase TPVR) |
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for which type of shock is dobutamine BAD?
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hypovolemic
(this is because dobutamine increases contractility but also VASODILATES) |
