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24 Cards in this Set

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Therapy for Primary (Essential) HTN

Diuretics


ACEIs/ARBs


Ca Channel Blockers

Therapy for HTN with CHF

Diuretics


ACEIs/ARBs


Beta-Blockers


Aldosterone Antagonists (Spironolactone, etc.)




DO NOT use B blockers in DECOMPENSATED CHF (CI in cardiogenic shock)

Therapy for HTN with Diabetes Mellitus

ACEIs/ARBs- protect against NEPHROPATHY.


Ca Channel Blockers


Diuretics


Beta-Blockers


Alpha-blockers

Amlodipine, Nimodipine, Nifedipine

Dihydropyridine Ca Channel Blockers -> block voltage dependent L Type Ca channels of Smooth Muscle -> reduce BV contractility.




Use:


Amlodipine, Nifedipine -> HTN, Angina (including Prinzmetal), Raynaud's


Nimodipine -> SUBARACHNOID HEMORRHAGE (prevents subsequent cerebral vasospasm).




Toxicity:


AV block, Cardiac depression, peripheral edema, Flushing, HYPERPROLACTINEMIA, constipation.

Diltiazem, Verapamil

NON-dihydropyridine Ca Channel Blockers -> block L-TYPE Ca channels in HEART.




Use: HTN, Angina, A Fib/flutter




Toxicity:


Cardiac depression, AV Block, Peripheral Edema, Flushing, HYPERPROLACTINEMIA, constipation.

Hydralazine

Increases cGMP -> causes smooth muscle relaxation (vasodilation).




Vasodilates ARTERIOLES > Veins (reduces AFTERLOAD).




Use: severe HTN, CHF.


1st line therapy for HTN in PREGNANCY (used with Methyldopa).




Administered with B BLOCKER to prevent reflex tachycardia




Toicity: Reflex tachycardia (CI in angina, CAD), fluid retention, nausea, SLE-Like syndrome.

Nitroprusside

Short acting drug that increases cGMP via DIRECT NO RELEASE




Use: HYPERTENSIVE EMERGENCY




Toxicity: CYANIDE TOXICITY -> releases Cyanide.

Fenoldopam

Dopamine D1 Receptor Agonist -> causes coronary, peripheral, renal, splanchnic vasodilation.




Use: HYPERTENSIVE EMERGENCY




Decreases BP, INCREASES NATRIURESIS





Nitroglycerin, Isosorbide Dinitrate, Isosorbide, Mononitrate

Causes Vasodilation by increasing NO in Vascular Smooth Muscle -> increases cGMP and causes smooth muscle relaxation.




Dilates VEINS >> Arteries. decreases PRELOAD.




Use: Angina, Acute Coronary Syndrome, Pulmonary Edema.




Toxicity: Reflex Tachycardia (prevent with B Blockers), hypotension, Flushing




Can cause MONDAY DISEASE (in industrial exposure) -> tolerance for vasodilation during work week, loss of tolerance over weekend. HEADACHE upon re-exposure.




Nitro/Isosorbide DInitrate -> LOW bioavailability via oral administration.




Isosorbide Mononitrate = High ORAL availability (Mouth)

Therapy for Angina

Nitrates -> affects PRELOAD (causes reflex tachycardia -> increased HR/Contractility).


B-blockers -> affects AFTERLOAD. NO reflex tachycardia -> decreased HR/Contractility.




TOGETHER, Nitrates + B blockers decrease BP, decrease HR, NO effect on contractility or ejection time. greatly decrease Myocardial O2 Consumption.




Nifedipine is similar in effect to Nitrates.


Verapamil is similar to B Blockers.




CI in Angina: Pindolol/Acetobutolol (partial B AGONISTS).





Lovastatin, Pravastatin, Simvastatin, Atorvastatin, Rosuvastatin

HMG-CoA Reductase Inhibitors -> inhibits conversion of HMG-CoA to Mevalonate.




Lowers LDL >>> TG, Increases HDL




Toxicity: HEPATOTOXICITY, RHABDOMYOLYSIS (esp when used with FIBRATES/NIACIN)

Niacin (Vitamin B3)

Inhibits lipolysis in adipose, reduces Hepatic VLDL Synthesis.




RAISES HDL (the most), Lowers LDL >> TG




Toxicity:


FLUSHED FACE (prevent with ASPIRIN).


Hyperglycemia -> ACANTHOSIS NIGRICANS.


Hyperuricemia -> exacerbates GOUT.





Cholestyramine, Colestipol, Colesevelam

Bile Acid Resins -> prevent intestinal absorption of bile acids -> LIVER must use endogenous cholesterol to make more bile acids.




Lowers LDL, slightly increases HDL, Slightly INCREASES TG (CI in hypertriglyceridemia).




Toxicity:


bad taste, GI discomfort, decreased absorption of FAT SOLUBLE VITAMINS, CHOLESTEROL GALLSTONES

Ezetimibe

Blocks cholesterol Absorption at small intestinal brush border.




Lowers LDL




Toxicity:


rarely increases liver enzymes, Diarrhea.

Gemfibrozil, Clofibrate, Bezafibrate, Fenofibrate

Fibrates that Upregulate LPL -> increases TG CLEARANCE.


Activates PPAR-Gamma to increase HDL Synthesis.




GREATLY Decreases TG >>> LDL. Slightly increases HDL.




Toxicity:


Myositis (esp with statins).


Hepatotoxicity (increased Liver enzymes).


CHOLESTEROL GALLSTONES (esp with bile acid resins).

Digoxin

Cardiac Glycoside -> directly inhibits Na/K ATPase -> indirect inhibition of Na/Ca exchanger -> leads to INCREASED CALCIUM -> causes increased contractility.




Also stimulates Vagus Nerve = DECREASES HR.




Use: CHF (inc Contractility), Atrial Fibrillation (Decreased AV Node conduction + Depression of SA Node).




Toxicity:


Cholinergic -> N/V, diarrhea, BLURRY YELLOW VISION.


ECG -> Increased PR, Decreased QT, ST Scooping, T Wave Inversion, arrhythmia, AV Block.


HYPERKALEMIA (poor prognosis).




Risk factors for toxicity:


Renal Failure (decreased excretion).


Hypokalemia


use of Verapamil, Amiodarone, Quinidine (decreased digoxin clearance -> displaces digoxin from binding sites).




ANTIDOTE = slowly normalize K+, use a cardiac pacer, Anti-Digoxin Fab fragments, administer MAGNESIUM

Quinidine, Procainamide, Disopyramide

Class Ia Antiarrhythmics -> Increase AP DURATION, Increase Effective Refractory Period, Increase QT interval.  


"Abba Performed Dancing Queen"


Use: BOTH Atrial/Ventricular Arrhythmias (esp Re-entrant and Ectopic SVT/VT).  


Toxicity:
Quinidin...

Class Ia Antiarrhythmics -> Increase AP DURATION, Increase Effective Refractory Period, Increase QT interval.




"Abba Performed Dancing Queen"




Use: BOTH Atrial/Ventricular Arrhythmias (esp Re-entrant and Ectopic SVT/VT).




Toxicity:


Quinidine- CINCHONISM (tinnitis, headache).


Procainamide- SLE-LIKE SYNDROME.


Disopyramide- Heart Failure.




All can cause Thrombocytopenia, TORSADES (increased QT Interval)

Lidocaine, Mexiletine, Tocainide, Phenytoin

Class Ib Antiarrhythmics -> DECREASE AP Duration, preferentially affect ISCHEMIC or DEPOLARIZED purkinje/ventricular tissue (Class IB is BEST AFTER MI).  


"Backstreet Boys Mainly Lack Talent, Prashu"


Use: Acute Ventricular arrhythmias (esp POS...

Class Ib Antiarrhythmics -> DECREASE AP Duration, preferentially affect ISCHEMIC or DEPOLARIZED purkinje/ventricular tissue (Class IB is BEST AFTER MI).




"Backstreet Boys Mainly Lack Talent, Prashu"




Use: Acute Ventricular arrhythmias (esp POST-MI), Digitalis-induced Arrhythmias




Toxicity: CNS stimulation/depression, CV Depression





Flecainide, Propafenone, Encainide

Class Ic antiarrhythmics -> significantly PROLONG REFRACTORY PERIOD in AV NODE, have NO effect on AP Duration.  


"Carly is Extremely Freaking Painful"


Use: SVTs (including A Fib).  
Only LAST RESORT for Refractory VT.  


Toxicity: PROARRHYTHM...

Class Ic antiarrhythmics -> significantly PROLONG REFRACTORY PERIOD in AV NODE, have NO effect on AP Duration.




"Carly is Extremely Freaking Painful"




Use: SVTs (including A Fib).


Only LAST RESORT for Refractory VT.




Toxicity: PROARRHYTHMIC (esp POST-MI- CI).


Class IC is Contraindicated in Structural and Ischemic heart disease.

Metoprolol, Propranolol, Esmolol (short acting), Atenolol, Timolol, Carvedilol

B Blockers - Class II antiarrhythmics -> Decrease SA/AV Node ACTIVITY by Decreasing cAMP and Calcium currents (decreases slope of Phase 4, prolongs repolarization of AV node).


Can suppress abnormal pacemakers by decreasing slow of PHASE 4.




Particularly potent in affecting the AV NODE -> increases PR INTERVAL.




Use: SVT, Slowing ventricular rate during A FIB/flutter




Toxicity:


Impotence, exacerbation of COPD/Asthma, CV Fx (CHF, AV Block, Bradycardia), CNS fx (sedation).


Can MASK HYPOGLYCEMIA Fx.


Metoprolol -> DYSLIPIDEMIA.


Propranolol -> Vasospasm (exacerbates Prinzmetal's angina).




CI in COCAIN users (risk of unopposed Alpha-adrenergic receptor agonist activity.




Antidote = GLUCAGON.



Amiodarone, Ibutilide, Dofetilide, Sotolol

AIDS




Class III Antiarrhythmics -> K channel blockers -> INCREASE AP DURATION, increase effective refractory period, Increases QT Interval.




Amiodarone has Class I/II/III/IV effects and ALTERS LIPID MEMBRANE




Use: A Fib/Flutter, Ventricular tachycardia (Amiodarone, Sotalol).




Toxicity:


Sotalol -> TORSADES, excessive B BLOCKADE.


Ibutilide -> TORSADES.


Amiodarone -> PULMONARY FIBROSIS, Hepatotoxicity, HYPERTHYROIDISM (40% iodine), corneal/skin deposits, NEURO fx, CV Fx.




Class Ia/III antiarrhythmics = increased risk for TORSADES. EXCEPT AMIODARONE.


when using Amiodarone, Check: PFTs, LFTs, and TFTs.

Verapamil, Diltiazem

Ca Channel Blockers -> Class IV Antiarrhythmics -> decrease conduction velocity, Increase effective refractory period, Increase PR INTERVAL.


Causes SLOW RISE of AP and Prolonged repolarization at AV Node.




Use: NODAL Arrhythmias (SVT), and rate control in A FIB.




Toxicity: Constipation, Flushing, Edema, CV fx (CHF, AV Block, Sinus Node depression).

Adenosine

Increases K EFFLUX -> HYPERPOLARIZATION.


Causes Decreased ICa current.




VERY SHORT ACTING.




Use:


1st line use in DIAGNOSING/ABOLISHING SVT.




Toxicity: Flushing, Hypotension, Chest Pain.




Effects are BLOCKED BY THEOPHYLLINE and CAFFEINE.

Magnesium

Use: TORSADES and DIGOXIN TOXICITY