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175 Cards in this Set
- Front
- Back
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increased LAP
pulmonary HTN systolic function and contractility relatively normal |
Mitral stenosis
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decreased LV afterload
increased LV preload dilatation of LV leading to eccentric hypertrophy |
chronic mitral regurge
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sudden rupture of chordae tendinae after MI
massive increase in LAP |
acute mitral regurge
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LV concentric hypertrophy
Dilatation eventually develops when hypertrophy no longer sustains CO leads to increased EDP |
Aortic stenosis
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increased LV EDV (increased preload)
LV eccentric hypertrophy |
chronic aortic regurge
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massive increase in LVEDV due to infectious endocarditis
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acute aortic regurge
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initial compensatory mechanism is LA and pulmonary hypertrophy
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mitral stenosis
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initial compensatory mechanisms are:
decreased LV afterload increased preload eccentric hypertrophy |
chronic mitral regurge
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initial compensatory mechanism is LV concentric hypertrophy
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aortic stenosis
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initial compensatory mechanism is increased LV EDV
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chronic aortic regurge
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physiology leading to dyspnea on exertion for mitral stenosis
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tachycardia and increased CO decrease diastolic filling time leading to increased LAP --> pulmonary congestion
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physiology leading to dyspnea on exertion in chronic mitral regurge
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increased LV afterload decreases SV with increases LAV which increases LAP leading to pulmonary congestion
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classic triad of symptoms seen in aortic stenosis
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angina
dyspnea on exertion syncope with physical exertion |
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physiology leading to angina and COE in aortic stenosis
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angina - increased O2 consumption from concentric hypertrophy
DOE - increased LVEDP from overstretched ventricle after dilatation sets in leads to increased LAP and pulmonary congestion |
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physiology leading to angina and DOE in chronic aortic regurge
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angina - decreased coronary perfusion due to blood being diverted away from ostia
DOE - pulmonary congestion from increased SVR (increased adrenergic tone) |
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differentiate pressure-volume curves in acute mitral/aortic regurge vs. chronic mitral/aortic regurge
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chronic - increased LV volume to dilatation from increased regurgitant flow
acute - minimal increase in LV volume because no time to dilate |
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which sort of hypertrophy increases myocardial oxygen consumption more
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concentric - therefore pressure overloading situations are more likely to develop angina (aortic stenosis)
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differentiate things that increase the intensity of murmurs heard in HCM vs. MVP
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both murmurs are increased when LV volume is decreased (increase contractility and decrease preload)
however when there is a decrease in afterload the HCM murmur is increased (increased blood flow across the stenotic area) but decreased in MVP because less regurgitant flow backwards |
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enlarged LA that is compressing the esophagus and enlarged RV seen on x-ray
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mitral stenosis
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enlarged LA and LV seen on x-ray
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mitral regurge
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how can you tell that a LA is enlarged on x-ray
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there is an added bump on the right side of the x-ray (left side of the body) - usually there are only 3 bumps now there are 4
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boot-shaped heart due to hypertrophied LV seen on x-ray
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aortic stenosis
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massive enlarged heart >1/2 the width of the thoracic cavity seen on x-ray
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aortic regurge
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differentiate the cause for ischemia in patients with aortic stenosis vs. regurge
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stenosis - concentric hypertrophy increases myocardial oxygen consumption and occludes intramural coronary arteries
regurge - blood is diverted away from coronary ostia back into the LV |
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drug of choice for chronic mitral regurge
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Hydrazoline to lower afterload so pulmonary edema doesn't occur
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this valvular disease can be confused with anxiety
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MVP due to increased adrenergic tone
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valvular disease due to active inflammatory process similar to coronary athersclerosis
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aortic stenosis
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increased in this acute phase protein seen in this valvular disease
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aortic stenosis
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most common causes of chronic aortic regurge
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essential hypertension
bicuspic aortic valve |
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exercise might have a paradoxical effect in this valvular heart disease
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chronic aortic regurge:
increase in HR - decrease time in diastole vasodilate - decrease SVR |
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drug of choice for chronic aortic regurge
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hydrazoline
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what is indicated if an austin-flint murmur is heard in chronic aortic regurge
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indicates severe regurge
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double product
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HR x systolic BP
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major determinant of coronary perfusion pressure
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aortic pressure
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equation for coronary flow
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Q = (aortic diastolic pressure - RAP)/coronary resistance
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important determinants of coronary perfusion
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aortic pressure
time spent in diastole RAP coronary resistance |
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most important determinant of coronary artery resistance
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autoregulation
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myogenic autoregulation mechanism
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stretching of the vessel leads to opening membrane calcium channel which cause vascular smooth muscle constriction
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chemical autoregulation mechanism from increased metabolism
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increased ATP breakdown leads to increased adenosine, binds to A2 receptors which close L-type Ca channels and decreased ATP opens Katp channels leading to K efflux - all leads to vasodilation
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characteristics of NO
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produced from L-arginine
increases cGMP opening membrane K channel to depolarize and relax smooth muscle |
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what would beta blockers do to coronary flow
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inhibit B2 mediated vasodilation and lead to mild vasoconstriction due to unopposed a-1 mediated activity
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differentiate myocardial stunning vs. reperfusion injury
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stunning - acute, but brief episode of severe ischemia leading to reversible contractile dysfunction due to increased intracellular calcium
reperfusion injury - irreversible necrosis after restoration of blood flow following acute ischemic event due to increased intracellular calcium overload (much more than stunning) |
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irreversible systolic dysfunction and contraction band necrosis seen with this
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reperfusion injury
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increase intracellular calcium overload seen in reperfusion injury leads to what
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uncouple oxidate phosphorylation - decreases ATP synthesis
activates proteolytic enzymes conversion of xanthine dehydrogenase to xanthine oxidase |
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metabolism switching due to myocardial ischemia
specific receptors involved |
from fatty acid metabolism to glucose
upregulate PPAR-gamma (glucose) down-regulate PPAR-alpha (fatty acid) |
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physiologic basis for hydropic swelling seen in myocardial ischemia
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decreased ATP leads to increased [Na]
increased [H] (from increased lactic acid from anaerobic glycolysis) also leads to increased [Na] increased [Na] increases 3Na/Ca exchange reversal leading to increased [Ca] |
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what problem is seen first in myocardial ischemia
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diastolic dysfunction - which leads to pulmonary congestion
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drug of choice for diastolic dysfunction in myocardial ischemia
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Ca channel blocker
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different difference seen on EKG between subendocardial and transmural ischemia
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subendocardial - No ST elevation
transmural - ST elevation seen on EKG |
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significant Q waves seen in leads I, V2, V3, and V4
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Anterior MI
occlusion of LAD |
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significant Q waves seen in leads, II, III, and AVF
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Inferior MI
occlusion of RCA |
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significant Q waves seen in leads V5, V6, AVL
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Lateral MI
occlusion of Left Circumflex |
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uncomplicated, thick fibrous-capped atherosclerotic plaqe produced fix obstruction
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chronic stable angina
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complicated, thick-fibrous-capped atherosclerotic plaque ruptured and form a thrombus along with vasoconstriction
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unstable angina
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spasm of large epicardial coronary artery
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variant angina
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low cardiac output and increased PAWP >22 mmHg follow an MI
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LCA occlusion leads to LV infarction and cardiogenic shock ensued due to >40% of ventricle being damaged
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increased JVP and decreased PAWP following an MI
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RCA occlusion leading to RV infarction and cardiogenic shock ensued due to >40% of ventricle being damaged
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New holosystolic murmur with increased oxygenation seen in the RV following an MI
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septal infarction with septal rupture due to LAD occlusion and anterior MI
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acute mitral regurge following an MI
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posterior papillary muscle rupture from posterior descending branch of RCA occluded
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equalization of diastolic pressures across all four chambers with systemic hypotension and elevated JVP following an MI
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ventricular free wall rupture with tamponade from anteriolateral MI from occlusion of Left circumflex artery
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how endothelin-1 leads to vasoconstriction
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activates ET-A receptors in vascular smooth muscle - increases phosphlipase C - increased IP3 which increases calcium to production constriction
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different what B-agonists and digoxin seen in myocardial stunning vs. reperfusion injury
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stunning - B-agonists and digoxin overcome dysfunction
reperfusion injury - B-agonists and digoxin do nothing, irreversible dysfunction |
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where is ischemia first noted in the myocardium
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subendocardial myocardium because area futhest from epicardial arteries
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what does binding of oxidized-LDL lead to
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activates NF-kB cascade
decreases NO production increases endothelin-1 production |
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NF-kB cascade
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increases TNF-a
increases xanthine oxidase increases cell adhesion molecules- which bind T cells and monocytes |
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what does binding of T cells and monocytes via upregulation of cell adhesion molecules lead to
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T cells cause smooth muscle proliferation
Monocytes cross endothelium into subintimal space and ingest oxidized-LDL to become foam cells |
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Th1 predominates during atherosclerosis
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thin fibrous-capped plaque - unstable angina and MI
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Th2 predominates during atherosclerosis
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thick fibrous-capped plaque - chronic stable angina
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infection associated with atherosclerosis
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chlamydia pneumoniae
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activated T cells and macrophages produce what
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IL-6 which increases CRP production
good marker for presence of coronary artery disease |
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what is released by platelets activating vasoconstriction
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thromboxane A2
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differentiate STEMI and NSTEMI
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STEMI - thrombus completely obstructs artery for 30 minutes
NSTEMI - thrombus partially obstructs or fully obstructs for less than 30 minutes |
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good chemical mediator of angina
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adenosine - accumulates during ischemia
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ST segment depression
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chronic stable angina
unstable angina |
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ST segment elevation
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variant angina
STEMI |
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distinguish ST elevation in the timeline of an MI
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2 hours - ST elevated
1-2 days - decreased ST elevation 1 week - No ST elevation |
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how long does it take for significant Q waves to show up on EKG following an MI
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Few hours
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Leads V1, V2, and V3 have large R waves
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Posterior MI
occlusion of post. descending branch of RCA |
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differentiate treatment of LV and RV cardiogenic shock
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LV - diuretic
RV - isotonic fluid |
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type of hypertension that has an identifiable cause for hypertension
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secondary
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this leads to secondary hyperaldosteronism due to an increase in the RAAS system
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overactivity of RAAS from stenotic renal artery
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two ways to get renovascular hypertension
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atherosclerotic disease - older individual
fibromuscular dysplasia - young women |
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characteristics of renovascular hypertension
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1. early in the disease abnormally high plasma aldosterone, Na retention and hypokalemia
2. later the non-stenotic kidney hypertrophies and urinary Na excretion increases but the hypokalemia persists 3. bruits 4. unprovoked hypokalemia hypertension develops prior to age 30 or after age 50 |
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what should you think of in a patient who's serum creatinine concentration increases >50% within 1 month of starting treatment of ARB or ACE Inhibitors
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bilateral renal artery stenosis
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How to diagnose renovascular hypertension
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Low plasma renin activity excludes diagnosis
administration of captopril causes plasma activity to increase >150% instead or remaining normal or slightly increased |
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most common cause of secondary hypertension in the US
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chronic kidney disease
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two reasons why chronic kidney disease causes hypertension
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increased plasma volume
systemic vasoconstriction |
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when should you suspect chronic kidney disease in a patient with hypertension
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decreased renal function
following recurrent UTIs anatomically small kidneys |
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first-line agents used to treat hypertension in chronic kidney disease
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ACE inhibitors
ARBs Diuretics can be used but must be in high concentrations and some are ineffective when creatinine rises above certain levels |
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what must be monitored for in patients taking ACE inhibitors or ARBs to treat hypertension in chronic kidney disease
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hyperkalemia
because aldosterone is knocked out to excrete K |
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Conn syndrome
two most common causes |
primary hyperaldosteronism
solitary adrenal adenoma bilateral adrenal hyperplasia |
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Lab findings in primary hyperaldosteronism
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unprovoked hypokalemia (in absence of diuretics)
metabolic alkalosis low plasma renin increased serum aldosterone |
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is the volume retention severe in patients with Conn syndrome
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No, because hypervolemia stimulates the release of ANP and BNP to return Na excretion back to normal
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differentiate primary and secondary hyperaldosteronism
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primary will have an increased ratio of serum aldosterone concentration to plasma renin activity because the increased aldosterone suppresses the renin activity
secondary will have increased renin activity and aldosterone due to the ischemic kidney increasing renin release |
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patient presents with hypertension, but pressure-lowering drugs are ineffective. His serum aldosterone to plasma renin activity is greater than 20:1.
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primary hyperaldosteronism
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this disease has ACTH provoking aldosterone release
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glucocorticoid-remedial aldosteronism
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what two things usually control release of aldosterone
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serum [K]
ATN II |
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treatment used in glucocorticoid-remedial aldosteronism
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glucocorticoid administration - reduces ACTH secretion to decrease aldosterone secretion in the zona fasciculata
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what enzyme deactivates cortisol --> cortisone
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11B-hydroxysteroid dehydrogenase
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this hormone has the same affinity for aldosterone receptors as aldosterone
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cortisol
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what three things can cause syndrome of apparent mineralcorticoid excess (SAME)
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mutation in 11B-HSD2
black licorice chewing tobacco |
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findings in SAME
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change in 11B-HSD2 activity
hypokelemia metabolic alkalosis decreased plasma renin, ATN II, and Aldosterone |
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what is used to correct SAME
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ARBs
sprinolactone |
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what are the lab findings in a patient with SAME
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normal serum cortisol levels
increased ratio of cortisol-to-cortisone metabolites in urine is HALLMARK |
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Cushing syndrome
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glucocorticoid excess
truncal obesity, thin extremities, moon face, cervical buffalo hump |
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common cause of cushing syndrome
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chronic glucocorticoid administration
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What does excess glucocorticoid present with clinically
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1. cortisol stimulates angiotensinogen synthesis leading to increased RAAS activity
2. down regulates NOS 3. make vasopressors more affective both of these increase vasoconstriction 4. cortisol also directly stimulates aldosterone receptor |
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if you seen a patient with hypertension and diabetes mellitus that developed simultaneously you should suspect what
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Cushing syndrome
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autosomal dominant disorder that has hyperactivity of ENaC in cortical collecting tubules
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Liddle syndrome (psuedohyperaldosteronism)
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salt-sensitive hypertension with hypokalemia and metabolic alkalosis
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Liddle syndrome
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two agents that block the overactive ENaC
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amiloride
triamterene |
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why does overactive ENaC lead to hypokalemia and metabolic alkalosis
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because increased Na reabsorption without reabsorbing Cl leaves an electrical gradient in which K and H are dumped into the lumen to correct this gradient
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differentiate epinephrine or norepinephrine mediated pheochromocytoma
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epinephrine - (B1-mediated), systolic hypertension, sweating, flushing, tachycardia, anxiety, located within adrenal glands
norepinephrine - (a1-mediated), diastolic hypertension, pallor, orthostatic hypotension, usually extra-adrenal location |
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what should always be checked in patients diagnosed with pheochromocytoma
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change in [Ca] due to thyroid or parathyroid tumors
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what other endocrine tumors are associated with pheochromocytoma
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medullary carcinoma of the thyroid
parathyroid adenoma |
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what is a better diagnostic tool to look diagnosing pheochromocytoma than metanephrine and normetanephrine
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Chromogranin A
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associated with increased angiotensinogen synthesis and peripheral insulin resistance causing hyperinsulinemia
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estrogen in oral contraceptive-induced hypertension
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can cause both systolic and pulmonary HTN in non-obese patients
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obstructive sleep apnea
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associated with family history of cerebral hemorrhages, low renin, ATN II, and aldosterone
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glucocorticoid-remediable aldosteronism
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what two factors control release of renin by the JG cell
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increased cAMP
decreased [Ca] |
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What does the Macula Densa detect in the TAL
what two ways does it regular renin release |
Chloride
decreased [Cl] detection by MD leads to release of PGE2 and NO to increase renin release increased [Cl] detection by MD leads to increased ATP, increased adenosine which decreases renin release |
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differentiate A1 and A2 receptors for adenosine
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A1 found in the nephron which when bound leads to vasoconstriction of afferent arteriole
A2 is found in the heart which when bound leads to vasodilation in the coronary arteries |
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what does an increase in DAG lead to
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stimulates Na/H exchange leading to alkalosis which leads to VSM hypertrophy and vasoconstriction
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why is prorenin harmful
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binds to receptors in myocardium leading to cardiac remodeling, hypertrophy, and fibrosis
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what patients produce increased amounts of prorenin
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diabetics
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aliskiren
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blocks enzymatic activity of renin (angiotensinogen --> ATN I)
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drug of choice in patients with high plasma renin activity and decreased ECF
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ACE inhibitors
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drug of choice in patients with low plasma renin activity and increased plasma volume
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diuretics
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three drugs that improve large artery compliance in systolic HTN of the elderly
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nitrates
ACE inhibitors - increase bradykinin and decrease ATN II thiazide diuretics - decrease Na reabsorption |
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releases cytokines for insuline resistance in skeletal muscle
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visceral fat
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why do ACE inhibitors work in african american patients with HTN and low plasma renin
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because they have decreased levels of bradykinin and ACE inhibitor will increase their bradykinin level - vasodilato, diuretic, and natriuretic
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this drug has uricosuric properties that can be useful in patients with hyperuricemia
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Losartan - ATN II receptor blocker
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what does chronic hypokalemia lead to
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1. vasoconstriction - closing of K channels leads to depolarization and an increase in [Ca] intracellularly
2. decrease urinary Na excretion due to increase Na/H exchange 3. increases renin secretion |
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decreased plasma Ca leads to what
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increased PTH - inhibits Na/K ATPase
increased 1,25-(OH)2 vitamin D - increases Ca uptake by VSM cells |
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mutation in Adducin gene
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increases activity of Na/K ATPase leading to decreased urinary Na excretion making some Japanese more salt-sensitive
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main cause of supraventricular tachycardia
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AV nodal reentry arrhythmias
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this class of drugs shortens the QT interval by shortening phase 2
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calcium channel blockers
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why can't fast Na channels contribute to slow response action potentials
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because the resting membrane potential in slow-response is not low enough to activate fast sodium channels (slow is found at -60mV)
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how does sympathetic activity increase SA node firing rate
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increases both Na and Ca inward current - shortens phase 4
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how does parasympathetic activity decrease SA node firing rate
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decreases inward Na and increases outward delayed rectifier K current - increases phase 4
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when can a smaller than normal depolarizing stimulus initiate and propogate a new action potential
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supranormal period is after phase 3 and the beginning of phase 4
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prolongation of the QT interval can lead to what
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early afterdepolarizations (EAD)
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what can precipitate a delayed afterdepolarization (DAD)
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increase in cytoplasmic [Ca]
digoxin toxicity catecholamine excess HF |
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class of drugs that prolong the action potential and can cause EADs (torsades de pointes)
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Class IA antiarrhythmics
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most likely cause of ventricular tachycardia in patients with long QT syndrome
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EADs
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most common mechanism responsible for tachyarrhythmias
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Re-entry
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three necessary requirements for re-entry tachyarrhythmias to develop
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unidirectional block
slow conduction in one part of the cirtcuit differences in refractoriness between the two different circuits |
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what initiates a re-entrant arrhythmia
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premature impulse
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two drugs that can terminate re-entrant supraventricular tachycardia
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adenosine
verapamil |
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does adenosine help treat functional re-entrant tachycardias
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No
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what leads to the development of a functional re-entrant tachycardia
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myocardial ischemia
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what is lyme disease associated with
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decreased AV conduction
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what MI can lead to impaired AV conduction
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anterior MI due to thrombus in LAD
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most well tolerated valvular disease
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chronic mitral regurge
symptoms present indicate the the regurge is bad |
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better indicator for chronic aortic stenosis than systolic blood pressure
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LV ESP is more accurate
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when does syncope during physical exertion develop in aortic stenosis
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when LV systolic dysfunction declines and CO falls below a level necessary to maintain perfusion
systemic vasodilation also contributes to syncope due to build-up of local metabolites in poorly perfused tissues |
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differentiate when S4 and S3 are present
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S4 - indicates ventricular hypertrophy
S3 - indicates ventricular dilatation |
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why is the diastolic blood pressure less than normal in chronic aortic regurge
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portion of CO returns to the LV from the aorta
build-up of local metabolites in poorly perfused tissues decrease SVR |
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differentiate the presence of a S3 heard in a person with chronic aortic vs. mitral regurge
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aortic - S3 indicates presence of LV dysfunction
mitral - S3 does not indicate severity or regurge |
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why is the pulse pressure in acute aortic regurge normal - not wide seen in chornic aortic regurge
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because the stroke volume does not increase like chornic therefore systolic pressure is increased
and diastolic pressure cannot drop below the very elevated LV EDP due to the massive regurge blood coming back into the LV |
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when is oxygen demand highest and lowest in the heart
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highest - during isovolemic contraction
lowest - late diastolic filling |
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a process that matches coronary resistance and blood flow to metabolic activity of the myocardium
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autoregulation
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what are the anti-atherogenic properties of NO
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inhibit lipid peroxidation
inhibit platelet activation and aggregation inhibit monocyte adhesion inhibit VSM proliferation |
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what happens during ischemic episodes when increased intracellular [Na] occur
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1. increased [Na] leads to myocardiocytes beginning to spontaneously depolarize
2. Also this upregulates Na/Ca exchange bringing in more Ca leading to decreased myocardial ATP synthesis and ultimately diastolic dysfunction by decreasing Ca uptake from SR |
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differentiate NSTEMI and unstable angina - both are due to partial obstruction of coronary artery or fully occluded coronary artery for less than 30 minutes
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NSTEMI - myocardial infarction limited to subendocardial myocardium
unstable angina - subendocardial ischemia from ruptured plaque that lead to thrombis formation and vasoconstriction |
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5 ways to get a coronary artery spasm
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1. polymphism in genes that produce endothelial NOS
2. polymorphisms in genes that decrease a2 or B2 receptors function 3. parasympathetic hypoactivity 4. overactivity of GTP rho-kinase - leads to increased sensitivity of VSM to calcium 5. cocain and amphetamine use |
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mechanism for myocardial ischemia in patients with anemia, hyperthryoidism or severe aortic stenosis
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increased myocardial oxygen demand in combination with moderate epicardial coronary artery stenosis
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differentiate effective and relative refractory period
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effect - larger than normal stimulus may cause additional depolarizations, but unable to generate a new axn potential
relative - larger than normal stimulus is capable of generation a new propogated axn potential |
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wolf-parkinson-white syndrome
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anatomical re-entrant circuits around the AV node
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ventricular tachycardia and fibrillation in the setting of myocardial ischemia is most likely do to what
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functional re-entry circuits
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what are the effects of increased aldosterone
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increased CO - aldosterone increases the number of Ca channels in ventricular myocardiocytes
elevated systemic vascular resistance - aldosterone stimulates Na uptake by VSM leading to increased [Ca] and hypertrophy via alkalosis mild increase in ECF volume - the increased Na reabsorption is limited due to release of ANP and BNP chronic hypokalemia chronic metabolis alkalosis |
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patient presents with hypertension, low renin, high ATN II, and normal aldosterone levels
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Cushing syndrome
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effects of excessive cortisol
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1. stimulates angiotensinogen synthesis by liver --> increases ATN II levels
2. increase VSM tone by making vasopressors more affective 3. activates aldosterone receptor 4. decreases plasma renin due to increased Na reabsorption 5. aldosterone levels remain normal |
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differentiate increase in VMA or metanephrine in the urine
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VMA - norepinephrine secreting pheochromocytoma
metanephrine - epinephrine secreting pheochromocytoma |
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what two things increased angiotensinogen synthesis in the liver
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estrogen oral-contraceptives
cortisol |
