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295 Cards in this Set

  • Front
  • Back

is warfarin a prodrug?


a combination product that is only used for ischemic stroke prevention?


25 mg instant release aspirin

200 mg extended release dipyridamole

aspirin MOA?

irreversible acetylation of serine #529 residue of COX

constitutive activity, cytoprotective to GI tract, inhibits thromboxane A2 synthesis are characteristics of?


inducible with inflammation describes?


↓ gastric mucosal barrier, ↓ Prostaglandin Synthesis, ↓ Mucus/Bicarbonate Secretion, ↓ Gastric Cellular Energy, ↓ Submucosal Blood Flow, ↓ Mucosal ATP, ↓ Cell Turnover, ↓ Platelet Function (Irreversible via inhibition ofCOX-1) are all examples of?

GI tract toxicity associated with aspirin use

relationship between aspirin dose and admission for ulcer bleeding?


aspirin loading dose?

160-365 mg/day

aspirin maintenance dose?

75-160 mg/day

AHA/ACC aspirin recommendations?

men only, diabetes, intermediate risk (>10%/10 years), no bleeding risk

European Society of Cardiology aspirin recommendations?

no aspirin

primary aspirin intervention?

75-160 mg/day


oral antiplatelet


oral antiplatelet

secondary aspirin intervention?

160-365 mg stat. plain, chewed

when is secondary aspirin intervention warranted?

acute MI, ischemic stroke

GI tract bleeding is a toxicity commonly related to which antiplatelet medication?


two types of aspirin sensitivity?

immune and non-immune

aspirin risk for those 21 yo or less?

Reye's syndrome

aspirin's effect on the kidneys?


kidney issues associated with analgesics?

papillary necrosis, decreased GFR

rhinorrhea, nasal congestion, cough/wheezing, hives/rash/urticaria are all signs of?

aspirin sensitivity

asthmatics, those with nasal polyps (especially multiple), chronic urticariacs, those with angioedema, those who have had previous anaphylaxis due to any medication are all at increased risk for?

aspirin hypersensitivity

T/F: aspirin increases the incidence of CHD in high-risk adults?

false, decreases

T/F: aspirin increases the incidence of GI bleeding?


T/F: aspirin may increase the incidence of hemorrhagic strokes?


platelet therapy regimen for patients with acute coronary syndrome (unstable angina, NSTEMI, STEMI)?

aspirin + 1 or more other antiplatelets

platelet therapy regimen for patients with stents (bare metal, drug-eluting, biodegradable)?

aspirin + 1 or more other antiplatelets


1st gen antiplatelet

P2Y12 inhibitor


2nd gen antiplatelet

P2Y12 inhibitor


3rd gen antiplatelet

P2Y12 inhibitor

which antiplatelet drug is a cyclopentyltriazolopyrimidine?


P2Y12 inhibitor

which antiplatelet drug is FDA approved for treatment of BOTH ACS and prevention of acute CV events following an MI, stroke, or peripheral arterial disease?


which P2Y12 inhibitor exhibits reversible binding to its receptor target?


which P2Y12 inhibitor is mostly cleared fecally rather than renally?


which P2Y12 inhibitor exhibits significant drug interactions or genetic polymorphisms?


P2Y12 inhibitor MOA?

irreversible (except ticagrelor) inhibition of ADP activation site on platelets?

which is faster onset: clopidogrel or ticlopidine?

clopidogrel (hours)

ticlopidine (days)

which antiplatelet medication has a boxed warning regarding neutropenia/agranulocytosis, thrombocytopenia as thrombotic thrombocytopenia purpura, and aplastic anemia?


which is more potent: clopidogrel or ticlopidine?


clopidogrel dosing?

75 mg/day

300-600 mg/day loading dose

ticlopidine dosing?

250 mg BID with meals

which drug is an irreversible thienopyridine P2Y12 inhibitor?


prasugrel dosing?

loading dose (bolus): 40-60 mg

maintenance dose: 5-15 mg/day

prasugrel indication?

ACS patients contemplating PCI

for which antiplatelet drug are the following claims made: more consistent and thorough platelet inhibition, faster, 32% increase in severe or major bleeding?


how is prasugrel activated?

via a 1-step metabolism to the active compound (mostly CYP 3A4)

prasugrel best responders?

males, stented patients, diabetics, less than 65 yo, ClCr > 60 ml/min

prasugrel not beneficial or detrimental to?

strokes/transient ischemic attacks, < 65 kg, > 75 yo

antiplatelet affected most by polymorphism?


antiplatelet affected least by polymorphism?


bleeding tendency higher with clopidogrel or prasugrel?


which drug commonly interacts with clopidogrel and reduces its conversion to its active metabolite?



ticagrelor dosing?

180 mg loading dose

90 mg BID maintenance dose

typical of dosing of antiplatelets?

loading dose followed by maintenance doses

ticagrelor vs. clopidogrel: lower death rate?


how can platelet aggregation be tested in vitro?

electrical impedence, light (platelet aggregometry)

ADP binding to platelets triggers?


this drug exhibits efficacy without bleeding, is reversible within 48hours, works faster, has a greater % of inhibition, and is more consistent than clopidogrel?


dyspnea, asymptomatic ventricular pauses, no use of aspirin at greater than 100 mg/day are all concerns with?


elinogrel dosing?

10-60 mg po or iv


vorapaxar and atopaxar are both?

PAR-1 inhibitors

which drug is a synthetic analog of himbacine, the Australian magnolia?


vorapaxar dosing?

10-40 mg PO loading dose

0.5-2.5 mg/day PO maintenance dose

vorapaxar half life?

really long 159-311 hours

vorapaxar MOA?

inhibition of PAR-1 to prevent platelet activation

indicated for intermittent claudication, pain in calf, peripheral arterial disease?


cilostazol dosing?

100 mg BID

separate from meals (30 min before, 2 hours after)

cilostazol MOA?

PDE 3 inhition > increase in cAMP

can cause tachycardia

cilostazol contraindication?

chronic heart failure


GP IIb/IIIa inhibitor

parenteral antiplatelet

for ACS with PCI


GP IIb/IIIa inhibitor

parenteral antiplatelet

for ACS


GP IIb/IIIa inhibitor

parenteral antiplatelet

for ACS


GP IIb/IIIa inhibitor

for acute DVT

when are GP IIb\IIIa inhibitors given to people with ACS?

not with fibrinolytics, before diagnostic angiography, immediately after PCI

GP IIb\IIIa inhibitors most effective in those with?

high troponin, recurrent ischemia, diabetics

anticoagulants that can be used concurrently with GP IIb\IIIa inhibitors?

UFH, enoxaparin, fondaparinux, bivalrudin

absolute contraindication to use of GP IIb\IIIa inhibitors?

current bleeding


prostacyclin derivative



prostacyclin derivative


prostacyclin derivative

prostacyclin derivative effects?

vasodilation (pulmonary HTN), prevents platelet aggregation, anti-proliferative to vascular smooth muscle

prostacyclin indications?

early stage primary pulmonary HTN

early stage PVD

diarrhea, jaw pain, headaches, and flushing are all very common side effects associated with?

prostacyclin derivatives

thrombolytics WITHOUT fibrin specificity?



thrombolytics WITH fibrin specificity?

urokinase, alteplase, reteplase, lanoteplase, tenecteplase

responsible for activated plasminogen to plasmin?


optimal plasminogen to plasmin conversion time in the event of an ischemic stroke?

3 hours

optimal plasminogen to plasmin conversion time in the event of an MI?

6 hours

optimal plasminogen to plasmin conversion time in the event of a catheter occlusion?

24 hours

which thrombolytic drug exhibits antigenicity?


which thrombolytic drug activates plasmin indirectly?


which thrombolytic drug exhibits resistance to plasminogen activator inhibitor?


which thrombolytic drugs are indicated for STEMI?

streptokinase, alteplase, reteplase, tenecteplase

which thrombolytic drug is indicated for STEMI, ischemic stroke, pulmonary embolism, and central venous access device?


cheaper, more antigenic, higher lytic state describes which type of thrombolytic drugs?

fibrin non-specific

costlier, quicker and more thorough onset, less bleeding tendency describes which type of thrombolytic drugs?

fibrin specific

which antiplatelet medication has weight based dosing?


fibrinolytic enzyme derived from the venom of agkistrodon contortix?



direct fibrinolytic derived from snakes

direct fibrinolytic, not plasminogen dependent, can lyse large clots in 1-4 hours, lytic activity confined to site of drug delivery, not inactivated by PAI-1, no systemic lytic state at clinically relevant doses, potentially less bleeding?


epsilon-aminocaproic acid

thrombolytic antagonist

binds to fibrin sites of plasmin

tranexamic acid

thrombolytic antagonist

binds to fibrin sites of plasmin


thrombolytic antagonist

broad spectrum protease inhibition

drug used to treat heavy menstrual periods?

tranexamic acid

which drug was recently found to double the risk of kidney failure and cause other serious adverse events, including stroke and heart attack?


thrombolytic antagonist

atherosclerosis or coronary arteries, vasospasm, plaque rupture, platelet activation and aggregation, thrombogenesis, coronary artery occlusion (complete and partial) are all involved in the pathogenesis of?

acute MI

unexplained fatigue, sleep disturbances, shortness of breath are precursor symptoms of?

acute MI

shortness of breath, very tired, unusual fatigue, pain or discomfort centered high in thechest, weakness, shoulder blade/back pain, nausea, hot, flushed, dizziness, pain or discomfort in the left arm,shoulder, and jaw, coldsweat are symptoms of?

acute MI

differential diagnosis: chestpain or pressure may diffuse and radiate to shoulders, neck, jaw, and arms, pain lasts > 20 minutes and is often accompanied by nausea, dyspnea, or diaphoresis, ST elevations >2 mm, ECGchanges and elevated cardiac enzymes?

acute MI

differential diagnosis: chestpressure or heaviness that may radiate, usually induced by activity andrelieved by rest or nitrates, often has cardiac history and may have ECGChanges (Q-waves, ST, T changes)?

unstable angina

differential diagnosis: painis often sharp in nature, involves multiple locations, and is reproduced withpalpation or respiratory movement, heatoften provides relief, consider traumatic causes?

costochondritis pain

differential diagnosis: mayhave mid-chest pressure and often accompanied with coughing, acid taste in throat, or a choking sensation, usually postprandial and relievedwith antacids, H2 blockers, or proton pump inhibitors, be aware that nitratescan also relieve this pain and can makedifferentiation with angina difficult?

GERD, esophagitis, and esophageal spasm

differential diagnosis: sharpchest pain, dyspnea, cough, and sometimes splinting, consider pleural effusionif patient has diminished breath sounds, dullness to percussion, and decreasedtactile fremitus, chest x-ray will assist diagnosis?

pleurisy and pleural effusion

differential diagnosis: chestpain is usually sharp, retrosternal with sudden onset, it can radiate to trapezialridge, there may be a fever, pericardial friction rub, and arrhythmias such asSVT, ECG may have ST elevations or changes in multiple leads?


differential diagnosis: chesttightness or pressure may be accompanied by nervousness, tachycardia,tachypnea, nausea, diaphoresis, dizziness, and restlessness, ECG, CXR, andlaboratory findings should be negative, therefore a diagnosis can be made through ruling out more serious finding?

anxiety and panic attack

LOCATE acronym?

location, onset and duration, characteristics, associated symptoms, treatment, eliminates/aggravates

CHA2DS2-VASc, high homocysteine, high VEGF, high CRP, high TNF are all predictors of?


CHADS2-VASc meaning?

congestive heart failure, hypertension (sys > 160 mmHg), age > 75 yo, diabetes, prior transient ischemic attack or stroke (2 points), vascular disease, age 65-74 years, sex category

time is tissue when it comes to?

ischemic strokes

AST acronym for responding to acute ischemic strokes?

assessment, stabilize, transport (3 to 4.5 hours for total, pre-hospital, door to needle 90 minutes max)

assessment portion of acute ischemic stroke response?

history and circumstances, 5 suddens, FAST

5 suddens of ischemic stroke?

weakness, speech impairment, visual changes, dizziness, severe headache

FAST acronym for stroke?

face drooping, arm weakness, speech difficulty, time to call 911

SCAB acronym?

stabilization, circulation, breathing, airway

the Glasgow Coma, NIHSS, Canadian Neurological Scale, and LA or Cincinnati Stroke Scales are all?

stroke severity scoring systems

door-to-needle goals?

90 minutes max

imaging, comprehensive blood work, severity scoring

common problems encountered with victims of stroke?

hyperglycemia, hyperthermia, hypertension

when should TPA fibrinolysis NOT be used in stroke patients?

if BP > 185/110

quick, objective, easy way to to assess CNS function?


O2 greater than 94%, intravascular TPA, prophylaxis of DVT with anti-thrombotics, endartectomy if TPA contraindicated, stenting in larger cerebral vessels are all treatments for?

acute ischemic stroke

typical patient characteristic when it comes to ACS?

middle aged male, elderly, diabetic, prior history or family history of CAD, CVA, PVD (angina, TIAs, intermittent claudication, erectile dysfunction)

rapid ER verification of MI?

12-lead ECG

delayed ER verification of MI?

cardiac enzyme profiles

can cardiac enzyme/protein profiles tell us whether a heart attack was STEMI or non-STEMI?


what is indicated by high troponin?

recent heart attack

how are thrombolytics used in the case of an in-hospital acute MI?

within 6 hours of onset

how are thrombolytics used in the case of an in-hospital ischemic or thrombotic stroke?

within 3 hours

alteplase is the only one that is FDA approved

what thrombolytic is used in cases of ischemic or thrombotic strokes that occur in the hospital?


what are surgical alternatives to acute MIs that occur in the hospital?

PCTL angioplasty and CABG

shortcomings with balloon angioplasty?

restenosis, embolization, rupture of blood vessel, infections, can't alleviate blockage

type of stent that is used in most coronary arteries?

balloon expandable stent

type of stent that is used in most carotid applications?

self-expanding stent

triggers a healing response that could narrow the vessel after a stent has been placed?

cracked plaque

what sort of stent is used to prevent restenosis due to cracked plaque?

drug-eluting stent

thrombosis 0-24 hours after stent implantation is known as?

acute stent thrombosis

thrombosis 24 hours to 30 days after stent implantation is known as?

subacute stent thrombosis

thrombosis 30 days to one year after stent implantation is known as?

late stent thrombosis

thrombosis one year after stent implantation is known as?

very late stent thrombosis

what are drug eluting stents made of?

cobalt chromium or stainless steel

sirolimus, paclitaxel, everolimus, and zotarolimus are all?

anti-proliferative agents that are used in drug eluting stents

stent characteristics, APT associations, angioplasty-related factors, lesion-related factors, and medical comorbidities are all factors for?

higher rates of stent thrombosis

stent used in BPH?

Spanner stent

oxygen rate for ACS?

2-4 liters per minute

potent analgesics used in treatment of ACS?

morphine, oxycodone, oxymorphone

morphine is vasodilatory

potent diuretics used in treatment of ACS?


cardiac off-loaders used in treatment of ACS?

nitroglycerin, nitroprusside

also antiplatelet activity

stool softener considerations when treating ACS?

avoid valsalva maneuver and reflexive CV changes

low dose beta blockers are used in ACS patients except those with?

cardiogenic shock, brittle COPD, poorly controlled diabetes

fibrinolytics, GP IIb/IIIa inhibitors, and antithrombins are all medications used in acute treatment of?

acute coronary syndromes

antiplatelets, beta blockers, statins, and ACE inhibitors are all medications used in?

outpatient treatment of acute coronary syndromes

cardioselective beta-blockers?

bisoprolol, metoprolol

noncardioselective beta-blockers?



long acting ACE inhibitor (antihypertensive)

complex clinical syndrome from any structural/functional cardiac disorder that impairs the ability of the ventricles to fill with or eject blood, other symptoms include: dyspnea, fatigue, and fluid retention?

heart failure

ventricles enlarge but fail in?

systolic failure

ventricles can't relax in?

diastolic failure

factors that contribute to diastolic, systolic, and total heart failure?

increasing age

increasing weight (BMI)

increasing A1C/hyperglycemia

increasing blood pressure

reduced ejection fraction, enlarged heart, neuroendocrine activation, increased ventricular arrhythmias, and shortened life expectancy are all manifestations of?

congestive heart failure

need to add in "deducing strokes" slide from first lecture

need to add in "deducing strokes" slide from first lecture

weakness, easy fatigue, slowed mentation, cardiac cachexia are signs and symptoms of?

low cardiac output heart failure

nocturia, cardiomegaly with tachycardia, cyanosis, and DOT (dyspnea, orthopnea, tachypnea) are signs and symptoms of?

congestive heart failure

who is at risk for HF?

previous MI survivor, poorly controlled HTN with hypertrophy, DM, abnormal ECG (esp. resting), chronic tachycardia, obesity, heart murmurs, established CAD

what are the ABD's of CHF intervention?






digoxin or digitalis

which drug has a favorable safety profile in elderly heart failure patients?


which drug is indicated for the treatment of stable chronic heart failure (NYHA class II-III) in addition to standard therapy to reduce mortality or cardiovascular hospitalizations?


nebivolol shares pharmacological properties common to which two other drugs?

metoprolol (beta-1 selectivity)

carvedilol (vasodilatory properties)

NYHA class I?

no limitation at ordinary activities

NYHA class II?

slight limitation at ordinary activities

NYHA class III?

marked limitation at ordinary activities

NYHA class IV?

always symptomatic, even at rest

what heart failure categorizations replaced the old NYHA categories?


ACC/AHA stage A?

at-risk for HF, no overt damage/symptoms

ACC/AHA stage B?

structural damage w/o symptoms

ACC/AHA stage C?

structural damage with prior/current symptoms

ACC/AHA stage D?

refractory HF with hospitalizations

which drug is approved in 71 countries but not yet in the US for treatment of HF?


objectives for CHF patients?

cure/prolong survival, make pt. asymptomatic and comfortable, increase the NYHA classification (closer to class I?), decrease the # of hospitalizations

CHF intervention lifestyle changes?

limit activity to capacity, reduce weight toward ideal, BMI reduction, control risk factors for atherosclerosis, restrict salt moderately (<3.8 grams, <1.5 grams is better), restrict water (1.5 L/day)

which type of diuretic is preferred in CHF if it is effective?


GFR for normal renal function?

120 ml/min

GFR for slightly impaired renal function?

60 ml/min

GFR for moderately impaired renal function?

30 ml/min

GFR for severely impaired renal function?

15 ml/min or less

which type of diuretic is wanted for someone with CHF and a GFR of > 30 ml/min?

thiazide diuretic

which type of diuretic is wanted for someone with CHF and a GFR or </= 30 ml/min?

loop diuretic

HCTZ (often in combos), chlorothiazide, bendroflumethazide, methyclothiazide, and polythiazide are all?

thiazide diuretics

chlorthalidone, indapamide, metolazone, quinethazone are all?

thiazide-like diuretics

which drugs are used as add on therapy to improve CHF?

spironolactone, eplerenone

moderately potent, inhibits NaCl (distal convoluted tubule), safe with respect to volume depletion and electrolyte imbalance, HF patients may not respond describes?

thiazide therapy of CHF

what are the potential thiazide toxicities?





hypokalemia (low potassium)




photosensitivity in sunlight

which thiazide toxicity differentiates it from loop diuretics?


furosemide, bumetanide, torsemide, and ethacrynic acid are all?

loop diuretics

which loop diuretic is the poorest choice for treatment of CHF?

ethacrynic acid

what are the peripheral effects of ADH?

vasoconstriction, fluid retention, ACTH release

what are the central effects of ADH?

learning and memory, social behaviors, autonomic functions

ADH is regulated by?

osmoreceptors and baroreceptors

in regards to ADH, which is more potent: volume or osmotic pressure?


conivaptan, tolvaptan, mozavaptan, lixivaptan, and satavaptan are all?

vasopressin receptor antagonists

what effect do the vaptans have?

decreased platelet aggregation, decreased pressure, improvement/correction of hyponatremia

what type of receptor is the vasopressin receptor?


V1a receptor activity in cardiomyocytes at low levels of vasopressin?

+ inotropy or force

V1a receptor activity in cardiomyocytes at high levels of vasopressin?

- inotropy b/c coronary vasoconstriction

V1b receptor is responsible for?

ACTH release from the pituitary

is found in the pancreatic Langerhans cells and kidneys

adenylyl cyclase with aquaporin-2 to surface as "water pore", free water retention, collecting tubules of nephrons describes which receptor?


hyponatremia level?

= 136-138 mEq/L

what is euvolemic hyponatremia?

increase in total body water with constant sodium

what is SIADH?

syndrome of inappropriate ADH secretion

causes of SIADH?

head injuries, stress, drugs

hypervolemic hyponatremia?

same sodium levels, greater total body water

causes of hypervolemic hyponatremia?

cirrhosis, heart failure


mineralocorticoid receptor antagonist

pathologic effects of aldosterone?

inhibits nitric oxide synthesis, increases inflammation and reactive fibrosis, inhibits sympathetic responses, stimulates cardiomyocyte apoptosis

increased vascular compliance, re-establishHR variability, increased fibrinolysis, resensitizationof baroreceptors, decreased platelet activation, reduced vascular inflammation, reduced vascular remodeling, reduced ventricular fibrosis, hypertrophy, and remodeling are all benefits of?

aldosterone inhibitors

which MR inhibitor's absorption is increased with food?


which MR inhibitor has a longer half-life: eplerenone or spironolactone?


problems associated with MR inhibitor class of drugs?

hyperkalemia, gynecomastia, breast pain, drug interactions (inhibition of CYP 3A4)

MR receptor antagonist dosing is based on?

observed concentration of K

MR receptor antagonist contraindications?

SCr > 2.5 mg/dL and/or GFR <30 ml/min

drug classes associated with photosensitization?

anti's, diuretics, hormones, herbs (St. John's Wort)

which drug is approved to prevent progression of TIAs to thrombotic strokes?


effects of ACE inhibitors?

decreased central and peripheral vasoconstriction, decreased aldosterone production (systemic), decreased release of ADH, decreased vascular and cardiac growth promotion or remodeling

neutropenia, angioedema, proteinuria, fetotoxic and teratogenic are severe toxicities of which drug class?

ACE inhibitors

which two drug classes improve survivability in those with CHF?

diuretics and ACE inhibitors

which ACE inhibitor CANNOT be taken with meals?


all of the ACE inhibitors are prodrugs except?

captopril and lisinopril

Dr. Smith's favorite ACE inhibitor?


which ACE inhibitor exhibits long action (once daily dosing = increased compliance, lesser reflex changes), and balanced elimination?


what two drugs make up BiDil?

isosorbide dinitrate and hydralazine

how is BiDil used in the treatment of heart failure?

as an adjunct

which ARBs are indicated on-label for heart failure?

valsartan and candesartan(?)

omapatrilat MOA?

inhibition of ACE, inhibition of neutral endopeptidase (inhibits degradation of ANP which is vasodilatory)

omapatrilat uses?


side effects of omapatrilat?


new dual inhibitor that leads to BP reduction, cardioprotection, nephroprotection and has little associated angioedema as far as we know?


which recently introduced drug is indicated for class II to IV heart failure with reduced ejection fraction?

sacubitril/valsartan (Entresto)

not used in severe renal/hepatic impairment


calcium sensitizer (inotropy) + potassium channel opener (vasodilation)

which has a longer half-life: digoxin or digitoxin?


effects of digitalis?

increased force of contraction

delayed conduction through AV node

decreased rate of contraction

which drug is used for heart failure with atrial tachycardias?


anorexia, N/V, diarrhea, visual changes, neurologic changes, and gynecomastia are all symptoms of?

digitalis intoxication

most common cardiotoxicities?

dysrythmia, heart block

ECG with digitalis

bradycardia due to digitalis toxicity

first degree AV block due to digitalis

second degree AV block type 1

second degree AV block type 2

third degree AV block

ventricular tachycardia


350-440 msec QT interval classification?


450-500 msec QT interval classification?

potential concern

> 500 msec QT interval classification?

very great risk


v. fib

what to do in cases of mild digitalis intoxication?

withhold doses until therapeutic/low therapeutic range is achieved, correct electrolytes/pH (low K/Mg, high Ca)

digoxin therapeutic range?

0.5 - 2.0 ng/ml

digitoxin therapeutic range?

10-25 ng/ml

what to do in cases of moderate digitalis intoxication?

same for mild + phenytoin/lidocaine for ventricular dysrhythmias

what to do in cases of severe digitalis intoxication?

DigiBind or DigiFab

# vials of DigiBind?

total digitalis in body (mg) / 0.6 mg/vial

# vials of DigiFab?

total digitalis in body (mg) / 0.5 mg/vial

empirical dosing regimen for treating digitalis toxicity?

10 vials, monitor ECG, repeat after 12-24 hours if symptomatic

ancillary medications used to treat digitalis toxicity?

low dose beta blockers

carvedilol, metoprolol, bisoprolol

patients with CHF, those who take statins, those who have familial hypercholesterolemia, and >/= 65 years of age need?

CoQ10 - ubiquinone

sources of ubiquinone?

oily fish, organ meats, whole grains

medications used for acute decompensation of CHF (acute worsening)?

inodilators (amrinone, milrinone)

inotropes (dobutamine, dopamine)

toxicities associated with inodilators?

thrombocytopenia, hepatotoxicity, GI tract disturbances

problems associated with beta-1 agonists

proarrhythmic, short-acting, tachyphylaxis, IV admin required

novel agent used in the treatment of acute decompensated CHF?

nesiritide (human, B-type natriuretic peptide)



decreased RAAS activation

toxicity associated with nesiritide?

short term, severe hypotension

long term renal toxicity with increased mortality

used to predict mortality of patients with HF?

triage BNP test & NT-pro-BNP

diagnosis when BNP < 100 pg/ml and NT-proBNP is < 300 pg/ml?

HF very improbable 2%

diagnosis when BNP 100-400 pg/ml and NT-proBNP is > 300 but < 1800 pg/ml?

ECHO needed to diagnose

diagnosis when BNP > 500 pg/ml and NT-proBNP is > 1800 pg/ml?

HF very probably 95%

false positives with BNP tests are common in?

females, african americans and hispanics, anemiacs, renal diseases

false negatives with BNP tests are common in?

those with obesity

which drugs carry a black box warning for causing or exacerbating CHF in some patients?


tioglitazone, rosiglitazone, pioglitazone

which diabetes drug is associated with hepatotoxicity?


which diabetes drug is associated with cardiovascular disease?


which diabetes drug is associated with bladder cancer?


cardiac transplantations, left ventricular assist devices, cardiomyoplasty, ventricular remodeling (the Batista technique) are all?

advancing heart failure treatment techniques

Jarvik 7, CardioWest, and AbioCor are all?

FDA-approved artificial hearts


gene replacement of SERCA2A (removes Ca from cardiomyocyte back into SR)

employs adeno-associated viral vector to get into the cardiomyocytes

1 time infusion into coronary arteries

phase II CUPID study


patient specific, expanded multicellular therapy manufactured from the patient's own bone marrow

works by increasing repair of damaged heart tissue