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75 Cards in this Set
- Front
- Back
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Side effects of thiazide diuretics?
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HYPOkalemia
HYPERlipidemia HYPERglycemia |
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how do b-blockers lower bp?
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due to decreasing PVR by lowering of plasma renin, NOT decreasing CO
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why is b-blocker not good for asthmatics?
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may precipitate an asthma attack, b-stimulation in trachea vasodilates, b-blocker produces bronchospasm
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propanolol vs. metoprolol/atenolol
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P=non-selective, high first pass metab. in liver
M/A=b1 selective, A-renal excretion |
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bradykinin?
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powerful vasodilator
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what anti-hypertensive should not be given to pts with bilateral renal stenosis?
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ACE inhibitor, can put into renal failure
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what does ACE do?
what does ACE inhibitor do? |
angiotensin1-->angiotensinII (vasoconstrictor)
bradykinin (vasodilation)-->inactive ACE inhibitor: increases bradykinin and decreases AT-2 |
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problems with ACE inhibitor?
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develop a dry cough due to increasing bradykinin which release prostaglandins and substance B which affect vagal fibers
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common ACE inhibitors?
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enalapril, lisonopril (no hepatic metab)
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what anti-hypertensive would be beneficial for diabetics? why?
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ACE inhibitors; AT-II reduction causes vasodilation of efferent glomerular arteriole; increases renal blood flow and reduces glom cap pressure preventing diabetic nephropathy
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what is assoc with hypercoagulability?
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adenocarcinoma, prothrombin gene mutation, SLE, pregnancy
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what participates in atherosclerotic plaque formation
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monocytes, smooth muscle cells, LDL, cytokines
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what causes endothelial damage?
what happens as a result? |
flow turbulence, chem injury, infection, homocysteine
proliferation of smooth muscle cells by TXA |
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what plaques are assoc with acute thrombosis and spasm
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unstable plaques
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thrombus vs clot
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thrombus develops actively in flowing blood and has MULTIPLE layers (lines of Zahn)
clot develops passively by settling via gravity |
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what is virchows triad
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endothelial injury, blood flow alterations, hypercoagulability
causes predisposition to thrombus formation |
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atherosclerosis vs arteriosclerosus
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athero: large vessels only
arterio:affects large and small vessels |
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what do platelets release to cause medial smooth muscle prolif.
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thromboxane
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complex atherosclerotic plaques
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have signif. lipid and collagen and calcium, has a fibrous cap
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what allows monocytes to enter thru intima
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oxidized LDL
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unique feature of unstable plaques
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possibility of hemorrhage or spasm
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prostacyclin
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inihibits thrombosis and vasodilates
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what proves the formation of a thrombus prior to death
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lines of zahn
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how to distinguis embolus from thrombus
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embolus- no organization and not adherent to vascular wall
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vasospasm
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often occurs in the setting of coronary atherosclerosis; often initiating event in develop of an acute thrombus or plaque ruptures
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what are contraction bands an indication of
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marker of reperfusion injury where myocardial cells were ischemically damaged and then subsequently supplied with oxygenated blood
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characteristics of non-reperfused infarcts
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eosinophilia, myocytes arranged in parallel bundles of wavy fibers, absent of hemorrhage, scarring completed in 6-8 weeks
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what can happen during the post-infarct period
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expansion-dilation and thinning of infarct
extension-develop of additional myocardial necrosis |
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wavefront phenomenon
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time depend extension of myocardial ischemia or necrosis from subendo towards subepicardium
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determinants of myocardial oxygen consumption
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tension (aka preload and afterload), heart rate, contractility
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how can you increase oxygen delivery to cardiac muscle
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by increasing coronary blood flow, coronary artery-vein difference is very high reduces the total amt needed, but very susceptible to changes in flow
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what causes smooth muscle cells in small arterioles to dilate
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adenosine, lactate, and H+
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what happens to myocardial muscle once demand exceeds supply
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atp levels decrease
anaerobic metab ph falls causes accumulation of Ca in myoplasm (cant relax fully) and depletion in SR(cant contract); |
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Prinzmetal angina
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spasm that causes chest pain at night when resting
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unstable angina
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marker for plaque rupture and a warning for impending MI
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angina pectoris
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defined as pressure, ache or discomfort that is substernal in location that may radiate to the left arm, both arms or the neck
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stable angina
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chest pain
brought on by exertion relieved by rest or nitroglycerin |
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unstable angina
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chest pain
of increasing frequency occurring with progressively less exertion or at rest |
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hibernating myocardium
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myocardial tissue that does not contract but when blood flow is restored, muscle may again start to function
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how can you stress the heart (increase myocardial O2 demand)
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increasing CO thru exercise, or giving dobutamine, a b-agonist to increase HR and contractility
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what is ST segment depression indicative of
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acute, reversible subendocardial ischemia
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what meds can give to reduce the likelihood of developing ischmeia
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b-blockers which reduce maximal O2 consumption
nitrates which dilate coronary arteries and reduce preload tension |
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hypothesized factor that causes conversion from ischemia to necrosis
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Ca2+ overload; increased levels of myoplasmis Ca2+ concentration
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what does rca supply
ST elevations on ecg if infarction? |
all of right ventricle
posterior (inferior) part of septum posterior (inferior) part of L. ventricle inferior LV infarct or RV infarct II, III, avF |
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what does lad supply
ST elevations on ecg if infarction? |
anterior part of septum
anterior wall of left ventricle anterior LV infarct V1-V6 |
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what does lcx supply
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anterior and lateral walls of left ventricle
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ekg hallmark of myocardial infarction
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ST segment elevation
w/ acute onset of severe chest pain |
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when does spontan lysis of a thrombus occur
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after the majority of muscle w/in the distrib of artery has died and caused a transmural infarct
but can occur earlier causing only subendocardial infarcts |
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what are the lab markers to confirm necrosis
when can you detect them |
CPK
Cardiac troponins (I and T) become positive only after 4 -6 hours after start of infarction |
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ads disads for mechanical valves
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ads- better hemodynamics, dont calcify
disads- require anticoagulation, susceptible to mech disrupt |
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ads disads for bioprosthetic valves
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ads-no anticoagulation reqd
disads-calcification, degeneration, stenotic |
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probs with CABGs chronically
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arterialization- get thicker
atherosclerosis-form plaques |
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characteristics of SVTs
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fast
regular narrow QRS complexes no p-waves or inverted p-waves |
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treatment of choice for SVTs
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adenosine (acutely)
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Adenosine
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indirect Ca channel blocker by increasing cGMP at AV node
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chars of Afib
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No pwaves
fibrillation of baseline irregular irregular ventricular rate Narrow QRS |
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chars of Aflutter
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flutter waves are regular at 300 bpm
variable ventricular rate response narrow QRS |
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pathophys principle of afib and aflutter
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have ventricular response rates that are well above 100bpm
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drugs for rate control of aflutter and afib
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beta blockers
diltiazem/verapamil digoxin- inhibits Na/K ATPase; increases parasympathetic tone at SA and AV node |
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what do all drugs that act at the av node have in common
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all either directly or indirectly reduce Ca channel current in the node
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how do b-blockers reduce sudden death
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by reducing Ca overload from excessive catecholamine stimulation
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best treatment for sudden cardiac arrest
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defibrillator
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lipoprotein patterns
type 1-5 which are common |
type 1-hyperchylomicronemia; LPL deficiency
type 2*-a-elevated LDL b-elevated LDL and VLDL manifests early in childhood type 3- elevated IDL type 4*-elevated LDL and TGs appear in middle age type 5-accumulation of VLDL and chylomicrons |
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what values are high blood cholesterol and borderline high blood cholesterol
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high- >240
borderline- 200 to 240 |
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what are the three dietary factors that contribute significantly to plasma cholesterol
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saturated FAs
cholesterol high caloric intake |
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what would be the best treatment to give someone with primary hypercholesterolemia if lifestyle modification was unsuccessful
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lovastatin-hmg coA reductase inhibitor w/
bile acid sequestrant to lower LDL |
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how does ezetimibe work
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inhibits intestinal transport of cholesterol at the level of the enterocyte to lower LDL
does not interfere with absorption but should not be taken in pts with hepatic insufficiency |
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what are fibrates used for
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lower VLDL and raise HDL
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what is niacin used for
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lowering TGs and raising HDL
bad s/e profile |
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bile sequestering agents
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cholestyramine
binds bile acides in small intestine and prevents their reabsorption; increases rate of conversion of cholesterol to bile acids |
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nitrate toxicity
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sudden withdrawal of longstanding nitrate treatment can cause symptoms of MI
headache and tachycardia (reflex) are common among workers in production of nitrates |
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when should b-blockers not be used?
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in an enlarged heart where excessive symptathetic tone is necessary to maintain it on a compensated starling curve
if SV is low and tachycardia is needed for CO NEVER with AV conduction delay and sinus node dysfunction asthma NEVER abruptly withdraw b-blockers |
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raynaud's phenomenon
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absent pulses; a phenomenon that is a s/e of propanolol, a b-blocker
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use of ca channel blockers
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unstable and variant anginas
arrhythmias due diltiazem and verapamil's ability to slow conduction thru av node |
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what should you give for relief of chest pain
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nitrates
b-blockers ca-blockers |
