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77 Cards in this Set
- Front
- Back
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Acetazolamide
-Mechanism of Action |
Inhibits carbonic anhydrase in proximal tubule
[Absorption of HCO3: HCO3- and H+ is first transformed by CA in the tubular lumen to CO2 and H20. The CO2 and H20 are reabsorbed into the tubular cell. Then an intracellular carbonic anhydrase converts the CO2 and H20 back into HCO3- and H+. The HCO3- is reabsorbed via an HCO3-/Cl- exchanger, and the H+ is exhanged for Na+ back into the lumen via an Na/H exhanger.] -Inhibits the intracellular carbonic anhydrase, which prevents both HCO3- reabsorption and Na/H+ exchange; More HCO3-, Na+, and H20 is excreted. |
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Acetazolamide
-Effects on electrolytes |
-Increases bicarbonate excretion (metabolic acidosis)
-Increases sodium excretion (hyponatremia) and water excretion -Increases K+ excretion (hypokalemia) -Increases phosphate excretion (hypophosphatemia) -Increases chloride reabsorption (hyerchloremia) |
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Therapeutic uses of acetazolamide
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-Edema
-Glaucoma -Epilepsy |
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Mannitol
-Mechanism of action |
Hypertonic solution used to acutely reduce intracranial pressure by causing fluid to move from the brain into the hypertonic blood
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Mannitol
-Therapeutic uses |
-Given IV for acute situations
-Used for anuria and oliguria because increases GFR and urine output -Used in drug intoxications -Used to reduce elevated cerebrospinal pressure -Used in glaucoma |
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Diuretic classification of:
-Hydrochlorothiazide -Chlorothiazide |
Thiazides
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Indapamide
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Thiazides
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Thiazides
-Mechanism of action |
-Blocks Na+/Cl- apical channel in distal convoluted tubule
-Not K+ sparing: Increases the amount of Na that enters collecting ducts; increases distal Na reabsorption; the increased lumenal negativity allows for the increased secretion of potassium |
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Thiazides effect on:
-Na+ -Cl- -K+ -H20 |
-Increases Na excretion (hyponatremia)
-Increases K excretion (hypokalemia) -Increases Cl excretion (hypochloremia) -Increases water excretion (increase in BUN) |
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Thiazides effect on:
-Ca2+ -HCO3- -pH -Uric acid -Magnesium |
-Increased calcium reabsorption(HYPERCALCEMIA)
-Increased bicarbonate reabsorption(hypochloremic ALKALOSIS) -alkolemia -Decreases uric acid secretion in the DCT (HYPERURICEMIA) -Decrease Mg reasborption in TAL (HYPOMAGNESIA) |
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Chlorothiazide vs. Hydrochlorothiazide vs. Chlorthaladone:
-Administration -Duration |
-Chlorthaladone: Given PO, lasts 24 hours
-Chlorothiazide: Given PO, lasts 12 hours -Hydrochlorothiazide: Given PO, IM, IV; lasts 6 hours, and produces greater Na diureses than chlorothiazide |
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Adverse reactions of thiazides
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1. Hypercalcemia
2. Hypokalemia 3. Muscle weakness and fatigue 4. Hyperglycemia; careful with diabetics 5. Hyperuricemia; careful with gout predisposition 6. Hyperlipidemia |
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Uses of thiazides
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1. #1 for chronic hypertension (also causes vasodilation)
2. Chronic edema |
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-Furosemide
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Loop diuretics
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Loop diuretics
-Mechanism of action |
-Inhibits Na/K/Cl apical cotransporter in TAL
-Non-K+ sparing -Decreases interstitial osmolaritary in medulla and causes more dilute urine |
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Loop diuretics effect on:
-Na -Cl -K -H20 |
-Greatly increases sodium excretion (hyponatremia)
-Greatly increases chloride excretion (hypochloremia) -Greatly increases K excretion (hypokalemia) -Greatly increases water excretion (dehydration and increases BUN) |
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Loop diuretics effect on:
-Ca -HCO3 -pH -uric acd -Mg |
-Decreases calcium reabsorption in DCT (HYPOCALCEMIA)
-Increased bicarbonate reabsorption (hypchloremic ALKALOSIS) -Metabolic alkalosis -Decreases uric acid secretion in DCT (HYPERURICEMIA) -Decreases Mg reabsorption in TAL (hypomagnesia) |
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Therapeutic uses of loop diuretics
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-Acute edema
-Acute pulmonary edema -Acute hypertension -Congestive heart failure -Acute hypercalcemia -Hypercalcemia and kidney stones caused by sarcoidosis and melignancies |
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Onset and duration of loop diuretics
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-Onset: 1-2 minutes
-Duration: 2-4 hrs |
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Adverse effects of furosemide
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1. Muscle weakness/fatigue
2. Hypokalemia 3. Hyperglycemia (diabetics) 4. Hyperuricemia (gout) 5. Hypocalcemia -Remember that toxicity of digoxin increases with hypokalemia |
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Adverse effects of ethacrynic acid
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1. Muscle weakness/fatigue
2. Hypokalemia (causes less than others) 3. Hyperglycemia (diabetics) 4. Hyperuricemia (gout) 5. Hypocalcemia 6. DEAFNESS -Remember that toxicity of digoxin increases with hypokalemia |
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Adverse effects of Bumetamide
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1. Muscle weakness/fatigue
2. Hypokalemia 3. Hyperglycemia (diabetics) 4. Hyperuricemia (gout) 5. Hypocalcemia -Remember that toxicity of digoxin increases with hypokalemia |
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Diuretic classification of:
-Spironolactone -Triamterene -Amiloride |
K+ sparing diuretics
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Mechanism of action of Spironolactone
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Competetive antagonist of aldosterone in the collecting ducts
-Also has an active p450 metabolite called canrenone that's an ALD antagonist |
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Mechanism of action of Triamterine
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-Inhibits sodium reabosrtion in the collecting duct; Increased tubular electropositivity prevents potassium secretion and proton secretion, as well as chloride reabsorption
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Mechanism of action of amiloride
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Blocks apical Na channel in collecting duct; Increased tubular electropositivity prevents K secretion and proton secretion, as well as chloride reabsorption
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Uses of potassium sparing diuretics
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-CHF
-Hypokalemia (esp. if using thiazide or furosemide with digoxin) -Hyperkalemia (cardiac depression) |
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Adverse effects of K+ sparing diuretics
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-Hyperkalemia
-Spironolactone only: Allopecia, gynecomastia, muscle weakness -Can't use with ACE inhibitors |
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Administration of K+ sparing diuretics
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orally
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Systolic and Diastolic pressures defining:
1. Borderline HPTN 2. Stage 1 HPTN 3. Stage 2 HPTN 4. Stage 3 HPTN 5. Stage 4 HPTN |
1. Borderline: 130-139/85-89
2. Stage 1: 140-159/90-99 3. Stage 2: 160-179/100-109 4. Stage 3: 180-209/110-119 5. Stage 4: 210+/120+ (Medical emergency) |
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Methyldopa
-Mechanism of action |
Decreases sympathetic tone in NTS and ventrolateral medulla
-Gets converted to methyl dopamine and then alpha methyl norepinephrine (inactive false transmitter) -Also inhibits dopa decarboxylase |
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Clonidine
-Mechanism of action |
alpha2 receptor agonist in NTS and medulla, decreases release of NE and sympathetic tone
(Guanabenz and Guanfacine have same MOA) |
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Methyldopa ADME
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-Given primarily orally, also IV
-Active for longer than 12 hours -Has active metabolite produced by the liver |
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Adverse effects of Methyldopa
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-Extreme impotence (95% of males)
-Sedation -Edema (Can give diuretic with K+ supplement) -Hypotension -Causes a false positive Coomb's Test (test performed before transfusion to see if have preformed Abs against RBCs) |
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Clonidine
-Administration -Uses |
-Given PO, IV, patch, or sublingually
-Used for hypertensive crisis because dry mouth so severe |
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Clonidine
-adverse effects |
-Severe xerostomia (can give pilocarpine Ach agonist to stimulate saliva)
-Edema -Impotence -Hypotension |
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Guanethidine and Guanadril
-MOA |
Displace NE from synaptic vesicle, which causes NE to enter cytoplasm and be degraded by MAO
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Guanethidine and Guanadril
-Administration -Uses |
-Given IV
-Used in ER as last resort for hypertensive crisis |
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Guanethidine and Guanadril
-Adverse effects |
-Very potent; cause hypotension
[-Cause orthostatic hypotension, dizziness, weakness, and syncope -stuffy nose -Bradycardia -Edema and impotence -Severe diarrhea -No CNS effects] |
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Prazosin, Terazosin, Doxazosin
-MOA |
Selective alpha1 blockers
-Cause vasodilation |
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Prazosin, Terazosin, Doxazosin
-ADME |
-Given orally
-Very potent -Long duration; last greater than 12 hours |
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Prazosin, Terazosin, Doxazosin
-Uses |
-Benign prostatic hypertrophy (can cause hypotension in normotensives)
-HPTN (Also decrease LDL and raise HDL) |
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Prazosin, Terazosin, Doxazosin
-Adverse reactions |
-#1=syncope, esp. first 2-3 doses
-Headaches -Impotence, hypotension, edema -Only slight reflex tachycardia (because has no effect on alpha2 receptors) |
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Propanolol
-ADME |
-Greater than 90% is bound to plasma proteins (drug interactions)
-metabolized by P450 -Given both oral and IV |
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Propanolol
-MOA |
-non-selective Beta blocker
-Decreases bp by working both centrally to reduce sympathetic tone and peripherally to decrease HR and contractility |
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Propanolol Adverse effects
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-#1=insomnia
-Exacerbates ashthma (B2) -Causes hyperglycemia (B2) -Exacerbates peripheral vascular disease and cold extremities (some arterioles in extremities are dilated by B2; if block B2, leave alpha receptors unopposed) -Fatigue more easily with exercise (b/c of decrease in HR) |
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Atenolol
-Mechanism of actions -ADME |
-Selective B1 blocker
-Decreases HR and contractility, which decreases blood pressure -Low plasma binding (less drug interactions than propanolol) -taken 1x day |
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Atenolol
-Adverse effects |
-Causes fatigue with exercise
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Hydralazine
-MOA |
-Produces NO
-Mostly dilates arteries and reduces bp |
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Hydralazine
-ADME |
-Given PO or IV
-short duration (few hours) -Acetylated by the liver to an inactive metabolite; some people are slow acetylators |
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Hydralazine
-Adverse effects |
-Slow acetylators: hydralazine will last longer
-#1=Lupus like syndrome: rash, arthralgia, Rheumology workup positive but no kidney damage -Causes sympathetic reflexes: Tachycardia and increased renin release -Tolerated better if use with Beta blocker |
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Minoxidol
-MOA -Uses -Adverse effects |
-Generates NO and causes vasodilation
-Mostly effects hair follicles and increases their blood flow -Used to increase hair (Rogaine) -Given IV to decrease blood pressure, but causes hypertrichosis (increased body hair) |
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Diazoxide
-MOA |
-MOA unknown; produces NO
-Causes mostly arterial dilation to lower bp |
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Diazoxide
-Administration -Uses |
-Used in ER as IV to lower bp
-Also used orally for hypoglycemia syndrome/hyperinsulinemia -Rapid onset; rapidly reaches peak levels; lasts 3-8 hrs. |
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Diazoxide
-Adverse effects |
-Sedation
-Reflex tachycardia -Causeses hyperglycemia; inhibits insulin release; has thiazide-like structure |
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Nitroprusside
-MOA |
-Generates NO
-dilates both arteries and veins; decreases bp |
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Nitroprusside
-ADME -Uses |
-Given only as IV infusion
-Half life less than 1 hour -Metabolized by RBCs |
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Nitroprusside
-Adverse effects |
-Reflex tachycardia
-Need to have liver function: Metabolism by RBCs releases cyanide; the cyanide is detoxified by the enzyme rodanase in the liver by converting cyanide and thiosulfate to the inactive thiocyanide; need to measure how much thiocyanide is being produced to prevent toxicity |
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Nitroglycerin
-MOA -ADME -Uses |
-Generates NO; causes dilation of arteries and esp. veins
-Given sublingually for angina or as a patch -Given as IV infusion for hypertension -High frist pass effect -Lasts less than 1 hour |
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Nitroglycerin
-Adverse effects |
Hypotension
-Reflex tachycardia (add B blockers or Ca blockers to blunt) -Unavoidable tolerance after use for several hours: Need to withold drug for 10 hours to remove tolerance -Extensive cross tolerance between nitrates |
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Primary treatments for Essential Hypertension
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-Diet
-Diuretics (hydrochlorothiazide) -B blockers (Atenolol) -Clonidine -CCBs (nifedapine) -ACEIs (enalopril and lisinopril) -ARBs *Standard of care to give diabetics with HPTN an ACE-I because preserves kidney function |
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Secondary and Tertiary treatments for essential HPTN
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-Secondary: Hydralazine
-Tertiary: Reserpine and Guanethdine |
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Verapimil
-MOA -admnistration -adverse effects -uses |
-non-DHP CCB
-Mostly causes cardiac depression; also vasodilates -Given PO and IV -Causes constipation -Used for hypertension and as an antiarrhythmic |
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Diltiazam
-MOA -administration -adverse effects -uses |
-non-DHP CCB
-Vasodilates and causes cardiac depression -Given PO and IV -Causes constipation and edema -Used for hypertension and as an anti-arrhythmic |
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Nifedipine
-MOA -administration -adverse effects -uses |
-DHP CCB
-Vasodilates -Given orally -Causes edema -Used to treat hypertension |
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Classes of ACE-I
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-Class I: Captopril only member, active as is and has some active metabolites
-Class II: majority in this class; are prodrugs requiring deesterification via hepatic metabolism (ex. enalopril) -Class III: Lisinopril is only member; active as is and excreted unchanged by the kidney |
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General adverse effects of ACE-Is
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-Elevated bradykinin levels cause dry cough and skin rash
-Hyperkalemia, esp. in patients on K+ sparing diuretics -Acute renal failure-decreases golomerular filtration -Can't use if have bilateral renal stenosis because lowers bp too much to get blood into kidneys -Teratogin due to importance of AT2 receptors; don't give to patients in 2nd or 3rd trimester -Neutropenia -Will not work if have a high sodium diet because Na+ inhibits renin release; need to decrease salt intake to maintain sensitivity |
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Captopril
-Kinetics -Adeverse effects |
-Short acting, 4-6 hours (Give 2-3x/day)
-Causes bad cough reflex and metallic taste |
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Enalopril
-Kinetics -Adverse effects |
-intermediate acting, 6-12 hours
-No metallic taste and less bradykinin side effects |
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Lisinopril
-Kinetics -Adverse effects |
-Long lasting, greater than 12 hours, given 1x day
-Onset in less than 1 hour -Decrease cardiac hypertrophy and remodelling; fewer side effects; very popular |
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Losartan and Valsartan
-MOA -Administration -Kinetics -Adverse effects |
-Aldosterone receptor blockers; use if cough and rash from ACE-Is unbearable
-Given orally -t1/2=2-6 hours -Cause headache and hypotension |
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Treatment of systolic hypertension
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-Need to decrease cardiac output: Give a diuretic plus a Beta blocker of CCB
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Chlorthalidone
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Thiazide
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-Metolazone
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Thiazide
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-Ethacrynic acid
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loop diuretic
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-Bumetamide
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loop diuretic
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-Torsemide
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loop diuretic
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