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55 Cards in this Set
- Front
- Back
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What does a Class IA drug do?
Class IB? Class IC? |
Blocks the open/activated form of Na channel (fast Na+ channels).
Blocks inactivated Na channel (H gate closed) Blocks the resting Na channel (M gate closed), open active, and inactive channels. |
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What are the Class IA drugs?
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Quinidine
Procainamide Disopyramide |
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When is Quinidine used?
What other effects does quinidine have that is contradictory? |
For atrial fibrilation. Requires initial digitation (digoxin).
It is a muscarinic receptor blocker and an alpha antagonist. |
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What are the adverse effects of quinidine?
What worsens the toxicity? |
Cinchonism (tinnitus, ocular dysfunction, CNS excitation, GI, hypotension)
Prolongation of QRS and QT interval (Torsades) Hyperkalemia Quinidine displaces Digoxin from tissue-binding sites (allowing digoxin to affect more tissue -> toxicity) |
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What are the adverse effects of procainamide?
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SLE-like syndrome
Procainamide is metabolized via N-acetyltransferase. A slow metabolizer would build up the concentration of procainamide. Procainamide is a good hapten, and as soon as it is protein bound it can cause a hypersensitivity reaction. Procainamide requires regular CBC Torsades |
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What are the class IB drugs?
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Lidocaine
Mexiletine Tocainide |
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When do you use Lidocaine?
When do you use Mexiletine or Tocainide? |
Post MI
Open-heart surgery Digoxin toxicity Mexiletine and Tocainide have the same effects as lidocaine, but can be taken orally. |
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What are the adverse effects of Lidocaine?
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CNS toxicity (seizures)
Least cardiotoxic of conventional anti-arrhythmics IV only. |
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What are the class IC drugs?
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Flecainide
Encainide Propafenone |
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When do you use class IC drugs?
When are class IC drugs contraindicated? |
As a last resort, if nothing else is working.
Never used post-MI |
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What is the function of Class II drugs?
What are the class II drugs? |
Class II drugs are beta blockers.
Propranolol (nonselective), esmolol, metoprolol, atenolol, timolol. |
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What is the mechanism of class II drugs?
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They decrease SA and AV nodal activity (bradycardia).
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What are the adverse effects of class II drugs?
How do you treat overdose? |
Impotence, asthma exacerbation, bradycardia, CNS effects (sedation)
Treat overdose with glucagon. |
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What are class III drugs?
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K+ Channel Blockers, can work on any type of AP.
They slow phase 3 down These include Amiodarone. |
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When do you use Class III blockers?
What are the adverse effects? |
Can be used for any arrhythmias.
Half life is > 80 days. Pulmonary fibrosis, "smurf skin", thyroid dysfunction, hepatic necrosis, corneal deposits, neuro defects, bradycardia |
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When is sotalol used?
What are the side effects? |
For life-threatening ventricular arrhythmias. Also has beta blocking effects.
Side effects: Torsades, excessive beta block. |
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What are the Class IV drugs?
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Ca++ channel blockers.
Verapamil, Diltiazem |
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What is the class IV drug mechanism?
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Block slow cardiac Ca channels (L-type), decreasing phase 0 and phase 4. Decreases SA and AV nodal activity
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What is the mechanism for adenosine? When is it used?
What are the adverse effects? |
Adenosine causes Gi-coupled decrease in cAMP, which leads to increased K out of cells.
Causes decreased SA and AV nodal activity. Is the DOC for paroxysmal supraventricular tachycardias and AV nodal arrhythmias. SE: bronchospasm, dyspnea, flushing, sedation. |
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What antagonizes adenosine?
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Theophylline (for use in COPD).
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What is magnesium used for?
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Effective in torsades de pointes. It competes with Ca.
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What is the drug strategy for antihypertensive medications?
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BP = CO X TPR
You want to decrease cardiac output or total peripheral resistance. TPR is inversely proportional to the 4th power of the radius. |
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What are some antihypertensive drugs that alter sympathetic activity? What are there uses?
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Clonidine and Methyldopa These are α-2 agonists. They decrease TPR and HR.
Uses: Mild-to-moderate hypertension Opiate withdrawal (clonidine) Hypertensive management in pregnancy (methyldopa) |
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What are side effects of antihypertensive drugs that alter sympathetic activity? Drug interactions?
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Methyldopa: Positive direct Coombs test = immune mediated hemolysis
Both: CNS depression, Edema (due to RAA) Diuretics (thiazides) and α-2 agonists are together in pills. Drug interactions: Tricyclic antidepressants attempt to increase NE levels. α-2 agonists lower NE. |
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What are drugs that alter sympathetic activity and result in reflex tachycardia?
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Prazosin, Doxazosin, Terazosin
These drugs are α-1 blockers, they decrease arteriolar and venous resistance. Used for hypertension, BPH. |
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How do β-blockers work to reduce hypertension?
What are the cautions with β-blocker use? |
β-blockers work by decreasing renin release.
Cautions: Asthma Vasospastic disorders Diabetes (mask hypoglycemic events) |
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When do you use hydralazine? How does it work?
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For moderate-to-severe hypertension when pregnant.
Hydralazine decreases TPR via nitric oxide (arteriolar dilation) |
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When do you use nitroprusside? How does it work? What are side effects?
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Nitroprusside is the DOC for hypertensive emergencies (IV). It increases cGMP via direct release of NO, which causes dilation of both arterioles and venules.
SE: Cyanide toxicity (limits use to 24-36 hours) |
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Which hypertensive drugs act by opening K+ channels? What are their uses?
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Minoxidil and Diazoxide
Uses: Hypertensive emergencies (diazoxide) Sever hypertension (Minoxidil) Baldness (topical minoxidil) |
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What calcium channel blocker is most effective when relaxing vascular smooth muscle?
Which are most effective for cardiac muscle? |
Nifedipine > diltiazem > verapamil
Verapamil > diltiazem > nifedipine |
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What are side effects of nifedipine?
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Gingival hyperplasia
Reflex tachycardia |
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What does Aliskiren do?
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Aliskiren is a renin inhibitor, preventing the conversion of Angiotensinogen to Angiotensin I.
Thus, it inhibits vasoconstriction and aldosterone secretion. |
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What are some ACE inhibitors?
What happens to bradykinin with ACE inhibitor use? What is the limiting side effect of ACE inhibitors? |
Captopril, enalapril, lisinopril
Bradykinin degradation is prevented. Side effect: Dry cough |
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What are some Angiotensin Receptor Blocker (ARBs)?
Why would you use ARBs? |
Losartan blocks AT-1 receptors.
Use of ARBs after dry cough develops with ACE inhibitors (captopril) |
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Why does hyperkalemia develop with the use of ACE inhibitors and ARBs?
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Decreased secretion of aldosterone leads to decreased excretion of potassium.
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What conditions are containdicated for ACE inhibitors and ARBs?
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Patients with renal artery stenosis.
Pregnancy. |
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Which drugs would you prescribe in patients that have hypertension and diabetes or heart failure?
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ACE inhibitors and ARBs. These improve the blood supply to the kidney (opposing diabetic nodular glomerulosclerosis)
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Which drugs would you prescribe in patients that have hypertension and angina or post-MI?
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Beta blockers, calcium channel blockers (angina)
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Which drugs would you prescribe in patients that have hypertension and BPH?
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Alpha blockers
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Which drugs would you prescribe in patients that have hypertension and hyperlipidemia?
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Alpha blockers, calcium channel blockers, ACE inhibitors, ARBs.
Do not prescribe beta blockers or thiazides, as they increase blood lipids. |
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What drugs are used for pulmonary hypertension?
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Bosentan: endothelin (ET) receptor blocker. ER is a powerful vasoconstrictor.
Prostacyclin (PGI2) analog: epoprostenol. Given through IV pump. Sildenafil: "viagra"; inhibits PDE type V found in pulmonary arteries, leads to pulmonary artery relaxation. |
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What drugs have been proven beneficial in CHF?
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ACEIs, ARBs, carvedilol (alpha and beta blocker), and spironolactone decrease remodeling of cardiac muscle.
Inotropes (digoxin) are used to increase contractility in CHF. |
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What is the mechanism for digoxin?
What is the indirect effect of digoxin? |
Digoxin competes with K in the Na-K ATPase, which prevents Ca from being sent out of the cell. Contractility is increased (positive inotropy).
Indirect effect: Inhibition of neuronal Na-K ATPase, resulting in increased vagal and sympathetic activity. |
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What are the side effects of digoxin?
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Long half-life requires loading doses (digitalizing). Displacement by other drugs, increasing the free fraction and toxicity.
Cardiac arrhythmias Anorexia, nausea, EKG changes Visual effects (yellow halos) |
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Which drugs displace digoxin?
What is the antidote for overdose of digoxin? What makes it worse? |
Quinidine and verapamil
Use of Fab antibodies, lidocaine, phenytoin Diuretics cause hypokalemia, which makes it easier for digoxin to work on the pump. |
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What drugs do you use for Wolff-Parkinson-White syndrome?
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Do:
Block accessory pathway with IA or III drug Dont: Slow AV conduction Give digoxin, β-blocker, Ca-channel blocker, adenosine |
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What drugs can you use for CHF?
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Digoxin
Diuretics (loop and spironolactone) Metoprolol and Carvedilol (α and β blockade) Nesiritide: similar to ANP, vasodilates. |
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Where is nitroglycerin mainly metabolized? What does it require?
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In the smooth muscle cells of large veins. It requires cysteine for the metabolism.
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What are side effects of nitates?
Cautions and containdications? |
Headache, flushing, orthostatic hypotension
Reflex tachycardia, fluid retention Tachyphylaxis = acute tolerance within 24 hours Cardiovascular toxicity with sildenafil (PDE type V inhibitor), leading to a drop in BP. |
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What drugs are contraindicated in vasospastic (prinzmental) angina?
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β-blockers
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What is theophylline?
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Theophylline is a PDE inhibitor. It opposes adenosine.
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What are the side effects of HMG-CoA reductase inhibitors?
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Myalgia (muscle pain)
Myopathy Rhabdomyolysis (may lead to kidney failure) Hepatotoxicity |
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What drugs are bile acid sequestrants? What are the side effects?
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Cholestyramine
Colestipol SE: Fat malabsorption, vitamin (lipid-solube) malabsorption |
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What is the mechanism of Niacin? Side effects?
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Niacin inhibits VLDL synthesis, which results in decreased plasma VLDL, decreased plasma LDL, and increased plasma HDL.
SE: flushing, pruritis, rashes (use aspirin) Hepatotoxicity |
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What is the mechanism of Ezetimibe?
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Ezetimibe prevents intestinal absorption of cholesterol, resulting in decreased LDL.
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