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Hydralazine: mechanism
- increases cGMP to cause smooth muscle relaxation
- vasodilates arterioles more than veins, reduces afterload
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Hyrdralazine: use
- First line for HTN in pregnancy
- CHF
- Coadminister with beta blocker to prevent reflex tachycardia
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Hydralazine: toxicity
- Compensatory tachycardia
- Fluid retention, nausea, HA, angina
- Lupus-like syndrome
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Minoxidil: mechanism and use
- K channel opener, hyperpolarizes and relaxes vascular smooth muscle
- For severe HTN
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Minoxidil: toxicity
Hypertrichosis, pericardial effusion, reflex tachy, angina, salt retention
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CCBs: mechanism
BLock voltage-dependent L-type calcium channels of cardiac and smooth uscle
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CCBs: order for vascular and heart action
- Vascular: nifedipine > diltiazem > verapamil
- Heart: verapamil > diltiazem > nefedipine
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CCBs: toxicity
Catrdiac depression, AV block, edema, flushing, dizziness, constipation
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Nitroglycerin and isosorbide dinatrate: mechanism
- Release NO in SM, causing increased cGMP and relaxation.
- Dilate veins >> arteries. Decreases PRELOAD
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Nitroglycerin: toxicity
- reflex tachycardia (sympathetic activation)
- hypotension, flushing, HA
- "Monday disease" in industrial exposure (loss of tolerance over the weekend)
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Drugs for malignant hypertension
- Nitroprusside
- Fenoldopam
- Diazoxide
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Nitroprusside: MOA
- short acting
- increases cGMP by direct release of NO
- releases CN (antidote co-administered)
-
Fenoldopam: MOA
Dopamine D1 receptor agonist causes relaxation of renal vascular smooth muscle
-
Diazoxide: MOA
- K+ channel opener hyperpolarizes and relaxes vascular SM.
- Also reduces insulin release (hyperglycemia risk)
-
Beta-blockers contraindicated in angina
-
Statins: MOA
- HMG-CoA reductase inhibitors
- Inhibit formation of mevalonate
- LDL; also HDL up and TG down a little
-
Niacin: MOA
- Inhibits lipolysis in adipose tissue
- Reduces hepatic VLDL secretion
- Drops LDL and raises HDL
- Can cause hyperglycemia and hyperuricemia
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Name the bile acid resins
- cholestyramine
- colestipol
- colesevelam
-
Ezetimibe: MOA
- Cholesterol absorption blocker in small intestine brush border
- Drops LDL only
-
Fibrates: MOA and toxicity
- Upregulate LPL to increase TG clearance
- Best for TGs
- Tox: mysotis, gallstones
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Effect of beta-1 receptors on the heart
Gs - activate protein kinase A which phosphorylates L-type Ca channels and phospholamban, both of which increase intracellular Ca during contraction
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Digoxin: MOA
- Inhibition of Na/K ATPase indirectly inhibits Na/Ca exchanger
- (Less Na out means less Ca can leave the cell)
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Digoxin: use
- For CHF to increase contractility
- For a fib to decrease conduction at AV node and depress SA node
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Digoxin: toxicity
- Cholinergic: nausea, vomiting, diarrhea, funny vision
- ECG: increase PR interval, decrease QT, scooping T wave inversion, arrhythmia, hyperkalemia
- RENAL excretion
- Quinidine decreases digoxin clearance
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Class I antiarrhythmics: general
- Na channel blockers
- Slow or block conduction
- Decrease slope of phase 4 depolarization and increase threshold
- Hyperkalemia increases toxicity
-
Class IA drugs and effect
- Quinidine, procainamide, disopyramide
- Increase AP duration
- Increase effective refractory period
- Increase QT interval
- For atrial and ventricular arrhythmias
-
Quinidine: toxicity
- Cinchonism: headache, tinnitus, thrompocytopenia
- Torsades
-
Procainamide: toxicity
drug-induced SLE
-
Class IB drugs and effect
- Lidocaine, mexiletine, tocainide (phenytoin)
- Decrease AP duration
- Preferentialy affect ischemic or depolarized Purkinje and vent tissue
- Good post-MI
-
Class IC drugs and effect
- Flecainide, encainide, propafenone
- NO AP duration effect
- Prolong AV refractory period
- For v-tachs progressing to VF
- Last resort
-
Class IC: toxicity
Proarrhythmic, bad post-MI
-
Shortest acting beta-blocker
Esmolol
-
Class II antiarrhytmics (beta-blockers) general
- decrease cAMP to decrease Ca current
- Decrease slope of phase 4 to suppress abnormal pacemakers
- AV node is sensitive so PR interval increases
- For ventricular slowing
-
Beta-blockers: toxicity
- Impotence, asthma worsens, sedation
- Bradycardia, AV block, CHF
- Masks hypoglycemia
- Metoprolol: dyslipidemia
- Glucagon treats OD
-
Class III antiarrhythmics (K+ channel blockers)
- Sotalol
- ibutilide
- bretylium
- dofetilide
- amiodarone
-
K channel blockers: MOA
- Increase AP duration
- Increase effective refractory period
- Use when other antiarrhythmics fail (Increases QT interval)
-
Sotalol class and toxicity
- Class III (K channel)
- Torsades, excessive beta block
-
Ibutilide class and toxicity
- K channel blocker
- Torsades
-
Bretylium class and toxicity
- K channel blocker
- New arrhythmia, hypotension
-
Amiodarone: effects and toxicity
- Class III (K) but has effects of all classes b/c it alters membrane
- Pulmonary fibrosis, hepatotoxicty, thyroid, corneal deposits, blue/gray skin deposits, neuro effects, constipation, bradycardia/heart block/CHF
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Class IV (CCBs) antiarrhytmics: names and effect
- Verapamil, diltiazem
- Primarily affects AV node, decreasing conduction velocity
- Increases effective refractory period and PR interval
- Prevent nodal arrhythmias
-
Mg as an antiarrhytmic
Effective in torsades and digoxin toxicity
-
K as an antiarrhytmic
Depresses ectopic pacemakers in hypokalemia (digoxin toxicity)
-
Adenosine as an antiarrhythmic
- Causes K efflux causing hyperpolarization
- Diagnose/abolish SVT
- Effects are blocked by theophylline
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