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6 classes of Diuretics and their sites of action
- Carbonic Anhydrase Inhibitors: proximal tubule
- Osmotic Diuretics: thin descending loop of Henle
- Loop Diuretics: thin ascending loop of Henle
- Thiazides and Congeners: early distal tubule
- Potassium-Sparing Diuretics: late distal tubule and cortical collecting duct
- Vasopressin/ADH Antagonists: medullary collecting duct
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Two Carbonic Anhydrase inhibitors (diuretics)
- Acetazolamide: PO, IV; 90% tubular secretion
- Dorzolamide: topical eye drops; binds CA in RBCs and eliminated over 5 months
- both drugs bind carbonic anhydrase, preventing bicarb breakdown in the tubule and alkalizing urine
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1 Osmotic diuretic
Mannitol: freely filtered, not reabsorbed; osmotically draws water out in TDL and PCT
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2 Loop Diuretics
- Furosemide: can give IM in emergencies, 60% bioavailable
- Ethacrynic acid: NOT a sulfonamide; 100% bioavailable
- Both inhibit Na/K/Cl symporter, inhibit macula densa detection of ions; cause alkalosis
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2 Thiazides/cogeners (diuretics)
- Hydrochlorothiazide: 70% available, T1/2 6-15hr, 100% excreted in urine
- Indapamide: 93% available, T1/2 16hr, completely metabolized
- Cause alkalosis; inhibit Na/Cl symporter (NCC) in the DCT; also weak carbonic anhydrase inhibitors (alkaline urine)
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3 Potassium-sparing Diuretics
- Triamterene: blocks epithelial sodium channel (ENaC) in late DCT and CCT
- Amiloride: same as triamterene, but lower oral availablility and longer T1/2
- Spironolactone: aldosterone receptor antagonist; canrenone active metabolite; blocks production of ENaCs and Na/K-ATPases
- All cause NaCl wasting while sparing K reabsorption; can lead to hyperkalemia, slight acidosis
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2 Vasopressin/ADH antagonists (diuretics)
- Conivaptan: IV, also hits V1a, helping diuresis
- Tolvaptan: PO, slightly longer T1/2
- Both target basolateral V2 receptor in principle cells, downregulating insertion of aquaporin channels
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Four classes of Antihypertensives
- Diuretics: reduce volume, reduce pressure
- Sympatholytics: regulate sANS signaling (α/β blockers)
- Vasodilators: lower peripheral resistance
- Inhibitors/antagonists of Renin-Angiotensin system: block end-effects of angiotensin (ups peripheral resistance, lowers diuresis, vascular/cardiac remodeling)
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4 Diuretics for hypertension
- Hydrochlorothiazide: 1st line drug, hits biporter
- Indapamide: 1st line drug, thiazide drug
- Furosemide: preferred only in malignant hypertension, concomitant chronic kidney disease (loop diuretic)
- Spironolactone: combine with thiazides to prevent hypokalemia; tx hypertension of hyperaldosteronism
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6 Sympatholytics for hypertension
- Clonidine: α2 and imidozoline receptor agonist; centrally acting (NTS, rostral ventrolateral medulla)
- Methyldopa: indirect adrenergic agonist (pre-synaptic neuron metabolizes to α2 agonist)
- Prazosin: α1 antagonist in resistance and capacitance vessels
- Propanolol: selective β-block; decrease HR, CO
- Labetalol: α/β-block; decrease TPR, venous tone
- Esmolol: similar to labetalol
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8 Vasodilators for hypertension
- Hydralazine: uncertain MOA,
- Nitroprusside:
- Minoxidil: opens arteriole smooth muscle K+ channel, hyperpolarizing membrane
- Diazoxide: K+ channel opener similar to minoxidil
- Nifedipine: dihydropyridine Ca2+ channel blocker; see anti-arrythmics
- Verapamil: class IV Ca2+ channel blocker; see anti-angina
- Diltiazem: class IV Ca2+ channel blocker; see anti-angina
- Fenoldopam: D1-dopamine receptor agonist; renal and mesenteric vessel dilator
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4 antihypertensive Renin/Angiotensin modifiers
- Aliskiren: competitive inhibitor of renin, prevents angiotensinI conversion (rate-limiting step)
- Captopril: ACE inhibitor; prevents angiotensinI -> angiotensinII conversion
- Enalapril/enalaprilat: prodrug/metabolite ACE inhibitor
- Losartan: competitive, selective angiotensinII receptor antagonist
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5 classes of Anti-Arrhythmic Drugs
- Class I: 3 subclasses (abc), all Na+ channel blockers
- Class II: β-adrenoreceptor blockers
- Class III: K+ channel blockers
- Class IV: Ca2+ channel blockers
- Miscellaneous: different MOAs
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2 Class Ia anti-arrhythmics
- Quinidine: blocks activated Na+ channels, at high doses K+, Ca2+, and α1; a-flutter and fib, ectopic vent beats, recurrent suprav- and v-tach
- Procainamide: Blocks activated Na+ channels, some K+ channels; WPW and arrhythmias when others are poorly tolerated
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3 Class Ib anti-arrhythmics
- Lidocaine: blocks inactivated > activated Na+ channels; least cardiotoxic; acute vent arrhythmia, digitalis arrhythmias
- Mexiletine: oral lidocaine analogue for v-tach
- Phenytoin: mainly inactivated Na+ channel block; digitalis-induced arrhythmias
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1 Class Ic anti-arrhythmic
Flecainide: blocks activated Na+, some K+ channels; rhythm control of a-flutter, fib, and chronic supravent arrhythmias
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4 Class II anti-arrhythmics
- Esmolol: used in ICU for short T1/2
- Metoprolol
- Sotalol
- All are selective β1 blockers in cardiac tissue; depress contractility and slow HR; control a-flutter/fib, hypertrophic cardiomyopathy, prophylaxis of v-fib
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3 Class III anti-arrhythmics
- Amiodarone: K+ channel block, inactivated Na+ channels; most effective antiarrhythmic, used in chronic control, sustained v-tach, and hypertrophic cardiomyopathy; can lead to pulmonary fibrosis, many other toxicities
- Sotalol: nonselective β-block and K+ channel block; supravent and vent arrhythmias
- Ibutilide: blocks K+ and causes inward Na+; used only in a-flutter/fib
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3 Class IV anti-arrhythmics
- Verapamil: see anti-angina
- Diltiazem: see anti-angina
- both are activated and inactivated Ca2+ channel blockers used in acute tx of suprav-tach and acute tx, chronic control of a-flutter/fib
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3 Miscellaneous anti-arrhythmics
- Adenosine: hyperpolarization of SA and AV nodes, decreasing SA automaticity and AV conduction; 1st choice for paroxysmal supravent-tach
- Magnesium Sulfate: unknown MoA, effective prevention of recurrent torsade de pointes and digitalis induced arrhythmias
- Digoxin: see drugs for heart failure; useful in a-flutter/fib in cardiac failure where Ca2+ blockers could worsen situation
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5 classes of Heart Failure Drugs
- Inotropic Drugs: modulate contractility (inotropy) of the heart to affect preload/afterload
- Renin-Angiotensin-Aldosterone modulators: reduce afterload (angiotensin) and preload (aldosterone); cornerstone tx in all stages of heart failure
- Diuretics: prevent Na+ and H2O retention to stabilize hemodynamic decompensation
- β-Blockers: unknown MoA, possibly dangerous due to negative inotropic effect
- Vasodilators: reduce preload and afterload by reversing vasoconstriction associated with heart failure
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4 Inotropic Drugs for heart failure
- Digoxin: cardiac glycoside that blocks Na+/K+-ATPase; many actions, but primarily improves efficiency of myocyte contraction, reducing O2 demand in failure
- Dobutamine: selective β1 agonist, very + inotropy (greater than digoxin) and + dromotropy (conduction velocity)
- Dopamine: MoA dependent on dose; mid-dose gives + inotropic effects, in addition ot vasodilation from lower doses (D-1 and β1/2 agonist); especially useful in poor renal perfusion
- Milrinone: inhibitor of specific cardiac phosphodiesterase; leads to + inotropy and peripheral vasodilation
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4 Renin-Angiotensin-Aldosterone modulating drugs for heart failure
- Captopril: ACE inhibitor (hypertension)
- Enalaprilat: ACE inhibitor (hypertension)
- Losartan: AngiotensinII receptor antagonist (hypertension)
- Spironolactone: aldosterone receptor antagonist, stops ENaC insertion (diuretics); attenuate pathologic remodeling at sub-diuretic doses and synergistic with above 3
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2 Diuretics for heart failure
- Furosemide: triporter loop diuretic
- Thiazides: Na/Cl biporter DCT diuretic
- Main use for these is to prevent water and NaCl retention to reduce preload and edema
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3 β-Blockers for heart failure
- Metoprolol
- Carvedilol
- Bisoprolol
- NOT A CLASS EFFECT. They decrease HR, reduce myocardial remodeling, inhibit renin secretion, and upreg β1 receptors otherwise downregulated in failure.
- CARBIME: mnemonic
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3 Vasodilators for heart failure
- Nitrates: very large reduction in preload/afterload
- Hydralazine: direct vasodilator, unknown MoA
- Nesiritide: ANF analogue (recomb brain natriuretic peptide); arteriolar and venous vasodilator
- Arteriolar dilators preferred in 1* low CO
- Venous dilators preferred in 1* pulmonary congestion
- Losartan, Milrinone, and Captopril also considered vasodilators
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5 classes of Anti-Hyperlipidemic drugs
- HMG-CoA inhibitors: prevents mevalonic acid formation (rate-limiting step)
- Bile Acid Binding Resins: increase excretion of bile acids by up to 10x
- VLDL Secretion Inhibitors: prevent lipolysis in adipose tissue
- Fibric Acid Derivatives: activate nuclear transcription receptor PPAR-α, increasing LPL synth and VLDL hydrolysis
- Intestinal Sterol Absorption Inhibitors: selectively inhibits absorption of sterols at small intestine brush border
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1 HMG-CoA Inhibitor for hyperlipidemia
- Lovastatin: 20-55% drop of LDL, 10-35% drop of triglycerides, 5-10% increase in HDL
- includes any drug with '-statin'
- Good for high cholesterol or LDL, atherosclerosis, prevention of coronary artery disease and stroke
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1 Bile-Acid Binding Resin for hyperlipidemia
- Cholestyramine: 10-35% reduction of LDL; little effect on HDL, VLDL, or triglycerides
- all resins basically just bind and remove cholesterol from the GI tract
- Good for all isolated increases of LDL
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1 VLDL Secretion Inhibitor for hyperlipidemia
- Niacin: 15-25% drop of LDL, 15-40% drop of VLDL, 30-50% drop of triglycerides, and 15-30% bump of HDL
- Strongly inhibits adipose lipolysis and reduces catabolism of apo-A1 from HDL
- Good high VLDL, LDL, and low HDL
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1 Fibric Acid Derivative for hyperlipidemia
- Gemfibrozil: 30-60% drop of triglycerides, 20-30% drop of VLDL, 5-10% bump of HDL, and variable effect on LDL
- Drug of choice for Hyperlipoproteinemia Type III
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1 Intestinal Sterol Absorption Inhibitor for hyperlipidemia
- Ezetimibe: 15-20% drop of LDL, 5-8% drop of triglycerides, 16% drop of Apo-B, little effect on HDL
- Used for hyperlipidemias in conjunction with statins
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3 classes of Anti-Anginal Drugs
- Nitrates and Nitrites: marked relaxation of large veins and large arteries to lesser extent, decreasing preload and afterload respectively
- Ca2+ Channel Blockers: cause vasodilation (decrease afterload), decrease conduction, automaticity, and contractility, and increase refractoriness
- β-Adrenoreceptor Blockers: reduction in heart rate, contractility, and blood pressure lead to decreased O2 demand and increase subendocardial perfusion
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3 Nitrates/Nitrites for angina
- Amyl Nitrite: 3-5min duration
- Nitroglycerin: many RoA with variant onset and duration
- Isosorbide Mononitrate: oral RoA, 15-40min onset with 6-10hr duration
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2 Subclasses of Ca2+ Channel Blockers for angina
- Dihydropyridines: selectively block vessel Ca2+ channels (no direct cardiac action)
- Others: block Ca2+ channels in heart and vessels (nonselective)
- Also good for Raynaud's phenomenon
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2 Dihydropyridines for angina
- Nifedipine: high vascular selectivity
- Nicardipine: very high vascular selectivity
- Both Ca2+ channel blockers; decrease afterload; also dilate cerebral vessels, inhibiting delayed reactive vasospasm from subarachnoid hemorrhage
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3 "other" Ca2+ channel blockers for angina
- Verapamil: low vascular selectivity
- Diltiazem: low vascular selectivity; improves diastolic compliance
- Bepridil: no selectivity
- All have cardiac effects in addition to vascular effects
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3 β-Blockers for angina
- Propanolol: nonselective β-blockade
- Metoprolol: selective β1-blockade
- Atenolol: selective β1-blockade
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