Cardiovascular Flashcards

1
Q

What are the main Calcium Channel blockers? What differentiate them from eachother?

What is the mechanism of action?

What are the main uses?

What are the main side effects?

How do I remember this shit?

A

Verapamil (most specific to the Ventrical/bad constipation), Diltiazem (Just different), Nifedipine, and amlodipine (Vascularture specific).

Blocks L-type calcium channels (Cardiac and smooth muscle)

HTN, variant angina, arrhythmias (Atrial), Raynaud’s (vasculature)

Cardiac depression, AV block, peripheral edema, flushing, dizziness, and constipation.

Want to keep arteries open so shove two (di**) _pine_s in them, but that is too much for the heart so **pa** says **mill them up to fit, but gives bad constipation.

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2
Q

Nitroprusside

What is its mechanism of action?

What is main use?

What is its main side effect?

How do I remember this shit?

A

short acting cGMP release by NO

Rapid vasodilator for HTN crisis

CN toxicity

A Nitro push Ide use for speedy pumping

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3
Q

Fenoldopam

What is its mechanism of action?

What is main use?

What is its main side effect?

How do I remember this shit?

A

Dopamine 1 receptor agonist** => relaxes **renal vascular smooth muscles

HTN crisis while increasing renal perfusion

Edema and edema like

Fun Old Pam swells like a balloon with all she takes, but her kidneys are fine. That is just amazing. Need her for a crisis.

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4
Q

Diazoxide

What is its mechanism of action?

What is main use?

What is its main side effect?

How do I remember this shit?

A

K channel opener => hyperpolarizes vascular smooth muscles

HTN crisis

Reduces insulin release

Makes vasculature/Beta pancreatic cells dead az ox ide only use it in a HTN emergency

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5
Q

What are the Prostanoids? What makes them note worthy?

What is its mechanism of action?

What is main use?

What is its main side effect?

How do I remember this shit?

A

Epoprost**enol (first/permanent catheter), Tre**postinil (3 things going for it; 3 routes of administration IV, inhale, Subcutaneous. Doesn’t need refrigeration. Can have site irritation)

PGI2 synthetic => powerful vasodilator/inhibits platelet aggregation.

Extreme cases of HTN (usually pulmonic)

jaw pain and arthralgias

Prostatute androids have no blood pressure, but keep my blood flowing. So I’m Postin’ an add for one (Epo), two (PGI2), or maybe even three (Tre)

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6
Q

What are the Endothelin-1 receptor antagonist (A and B)? What makes them note worthy?

What is its mechanism of action?

What is main use?

What is its main side effect?

How do I remember this shit?

A

Bosentan**(bad), Maci_tentan, and **A**_mbri**sentan** (receptor **A specific, least hepatotoxic)

All in the name => Potent vasodilator

Heart failure, etc.

Teratogenic (abortion) and hepatotoxicity

When I get drunk (hepatotoxicity) and watch naruto I see Sentan** or **Tentan** and want her **endothelin** for just **1** hour on my **dilated penis, but she won’t let me (antagonist). Just as well, it would be one fucked up baby (teratogenic)

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7
Q

What are the Phosphodiesterase 5 inhibitors?

What is its mechanism of action?

What is main use?

What is its main side effect?

How do I remember this shit?

A

Sildenafil**, Ta_dalafil, and Vardenafil_**

Prolongs vasodilator effects of NO

Dyspepsia (Bad pepsi gives me indigestion), headache, flushing, impaired blue-green color vision, and life-threatening hypotension with nitrates.

The blue and green (My dick no care what their color) _dal_es _fil_l me up with a potion in _Varden_vale and I fuck _5_ elves. Well worth the indigestion.

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8
Q

Riociguat

What is its mechanism of action?

What is main use?

What is its main side effect?

How do I remember this shit?

A

Makes NO more effective and is agonist for NO** through **Guanylate cyclase

Vasodilation (it is pretty new)

Teratogenic

Riociguat is so smooth that he must have a lot of sex, but that really is bad for the ladies.

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9
Q

Hydralazine

What is its mechanism of action?

What is main use?

What is its main side effect?

How is Ranolazine different?

How do I remember this shit?

A

increases cGMP => smooth muscle relaxation (Arterioles>veins) => reduce afterload

Severe/Pregnancy HTN and Heart failure/Blacks(the one)

Reflex tachycardia (Beta blockers usually co-administered), angina**, one of the **Lupus-like drugs

Late phase 3 and blocks potassium (arrhythmia)

Hydrate ala** limo_zine_s to keep Heart working with getting all the ladies and making them **pregnant**. That is so **HIPP it hurts my chest, but that Ranol is always late and blocks the Kick ass babes

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10
Q

Nitrates

What is its mechanism of action?

What is main use?

What is its main side effect?

How do I remember this shit?

A

metabolized to NO which activates cGMP => dilates systemic veins and coronary arteries => decreases diastolic wall stress. High dose => dilates systemic arteries => decreases PVR => decreases afterload => decreases systolic wall stress => lowers O2 demand.

Angina

Tolerance or desensitization, massive headaches, Flushing, orthostatic hypotension, dizziness, and reflex tachycardia

Nitrate is for old _G_rumps and their nasty _veins_

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11
Q

How does Vaughan Williams class 1 antiarrhthmics work? When do you use them? What is the effect of class 1A? 1B? 1C?

How does Vaughan Williams class 2 antiarrhthmics work? When do you use them?

How does Vaughan Williams class 3 antiarrhthmics work? When do you use them?

How does Vaughan Williams class 4 antiarrhthmics work? When do you use them?

A

Blocks Fast Na channel blockers** => increase threshold and decrease slope of phase 0. **Reentry arrhythmias.

  • Moderate** block and **Prolonged action potential duration
  • Mild block and Shortened action potential duration
  • Marked** block and **No change on action potential duration

Decreases HR and contractility**. **Decreases Mortality.

Potassium channel blockers => stability.

L-type Ca channel blockers. Atrial arrhythmias

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12
Q

Why Quinidine bad?

When do you use Procainamide? What are three major possible side effects? What could make these worse?

Why Disopyramide bad?

A

Increases mortality

Tachycardia. Torsades de pointes (K blocker), Reversible SLE/Agranulocytosis. Its metabolite N-acetylprocainamide (NAPA)

Negative inotropic

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13
Q

When do you use Amiodarone? What special about it?

What arrhythmia do you always use Magnesium?

A

Last resort for Tachycardic arrhythmia. Have to push it straight to the heart (only lasts a few seconds).

Torsades de pointes

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14
Q

What are the Statin drugs?

How do they work?

What is it for?

What are the side effects?

A

Lovastatin**, Pra_vastatin, Simvastatin, Atorvastatin, Rosuvastatin_**

HMG-CoA reductase inhibitor = inhibits Mevalonate

really good against LDL. Ok for increasing HDL and decreasing triglycerides

Hepatotoxic (Requires Liver function testing), rhabdomyolysis

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15
Q

What is the mechanism of action of niacin?

What is it good for?

What are the acute side effects? How do you treat?

What are the chronic side effects?

A

Inhibits lipolysis** and **VLDL secretion

best at increasing HDL, ok for the others

Red/flushed face (aspirin takes care of).

Hyperglycemia/uricemia

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16
Q

What are the Bile acid resins?

What is the MOA of Bile acid resins?

What is it good for?

What are the side effects?

What is unique about Ezetimibe?

A

Cholestyramine, colestipol, colesevelam

Prevents intestinal reabsorption of bile acids

ok of LDL, barely anything for HDL/triglycerides

Tastes bad, GI distress (Steatorrhea), may lead to gallstones

Rarely hepatotoxic (Ez weight loss, but be end of time for liver)

17
Q

What are the Fibrates?

What is the mechanism of action?

What is it best for?

What are the side effects?

How the hell do I remember?

A

Gemfibr**ozil, clo**fibrate**, beza_fibrate, fenofibrate_**

Upregregulates LPL => Triglyceride clearance

Best at decreasing Triglycerides, ok for others

Myositis (muscle inflammation), hepatotoxic, may cause gallstones

Fibrillates your muscles (myositiis) making you lose fat, though bad for liver/gallbladder

18
Q

Nesiritide

What is its mechanism of action?

When do you use it?

What is the main side effect?

A

Synthetic of Natriuretic Vasodilation while sparing kidney

Acute decompensated heart failure

Hypotension

19
Q

Digoxin

What is its mechanism of action?

What are its used for?

What are its side effects?

A

Directly inhibits Na/K ATPase => inhibits Na/Ca exchanger => more Ca => Positive Inotrope

Helps symptoms of heart failure and may help atrial fibrillation by stimulating vagus

GI distress, blurry yellow vision**(Digoxin Flower), increases PR interval, decreases QT interval, scooping, T-wave inversion, arrhythmias, kalemia inbalance, **bad** with **quinidine