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Pharmacology Unit 4 > Unit 4 Drugs > Flashcards

Unit 4 Drugs Flashcards

1
Q

Acetazolamide (Diamox)

A
  • Class: Carbonic anhydrase inhibitors (diuretic)
  • Mechanism:
  • Inhibits luminal carbonic anhydrase at proximal tubule –> less activity of Na/H antiporter, decreased HCO3 and Na+ (and water) reabsorption
  • induces moderate increase in urine volume; increased excretion of Na+, K+ (d/t compensatory increase in downstream Na+ reabsorption coupled to increased K+ secretion), and bicarb in an alkaline urine
  • induces moderate reduction in ECF vol and ECF [K+]
  • Therapeutics: Decrease intraocular volume/pressure; prevention/treatment of mountain sickness (stimulates kidneys to excrete more bicarb in urine –> acidifies the blood –> stimulates respiratory center to increase depth and frequency of respiration –> speeds natural acclimatization process.)
  • Important Side Effects: Increased K+ excretion–> hypokalemia; metabolic acidosis (b/c decreased bicarb reabsorption)
  • Other Side Effects: Hepatic encephalopathy (b/c increased bicarb excretion –> alkalinization of urine –> less “ion trapping” of ammonium in the tubular flud –> ammonia accumulating in the ECF); bone marrow depression, skin toxicity, allergic reactions
  • Miscellaneous: Contraindicated in cirrhotic patients; FeNa = 5% (1%=normal)
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2
Q

Methazolamide (Neptazane)

A
  • Class: Carbonic anhydrase inhibitors (diuretic)
  • Mechanism: Inhibits luminal carbonic anhydrase at proximal tubule –> less activity of Na/H antiporter, decreased HCO3 and Na+ (and water) reabsorption
  • induces moderate increase in urine volume; increased excretion of Na+, K+ (d/t compensatory increase in downstream Na+ reabsorption coupled to increased K+ secretion), and bicarb in an alkaline urine
  • induces moderate reduction in ECF vol and ECF [K]
  • Therapeutics: Decrease intraocular volume/pressure; prevention/treatment of mountain sickness (stimulates kidneys to excrete more bicarb in urine –> acidifies the blood –> stimulates respiratory center to increase depth and frequency of respiration –> speeds natural acclimatization process.)
  • Important Side Effects: Increased K+ excretion–> hypokalemia; metabolic acidosis (b/c decreased bicarb reabsorption)
  • Other Side Effects: Hepatic encephalopathy (b/c increased bicarb excretion –> alkalinization of urine –> less “ion trapping” of ammonium in the tubular flud –> ammonia accumulating in the ECF); bone marrow depression, skin toxicity, allergic reactions
  • Miscellaneous: Contraindicated in cirrhotic patients; FeNa = 5% (1%=normal)
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3
Q

Dichlorphenamide (Daranide)

A
  • Class: Carbonic anhydrase inhibitors (diuretic)
  • Mechanism: Inhibits luminal carbonic anhydrase at proximal tubule –> less activity of Na/H antiporter, decreased HCO3 and Na+ (and water) reabsorption
  • induces moderate increase in urine volume; increased excretion of Na+, K+ (d/t compensatory increase in downstream Na+ reabsorption coupled to increased K+ secretion), and bicarb in an alkaline urine
  • induces moderate reduction in ECF vol and ECF [K]
  • Therapeutics: Decrease intraocular volume/pressure; prevention/treatment of mountain sickness (stimulates kidneys to excrete more bicarb in urine –> acidifies the blood –> stimulates respiratory center to increase depth and frequency of respiration –> speeds natural acclimatization process.)
  • Important Side Effects: Increased K+ excretion–> hypokalemia; metabolic acidosis (b/c decreased bicarb reabsorption)
  • Other Side Effects: Hepatic encephalopathy (b/c increased bicarb excretion –> alkalinization of urine –> less “ion trapping” of ammonium in the tubular flud –> ammonia accumulating in the ECF); bone marrow depression, skin toxicity, allergic reactions
  • Miscellaneous: Contraindicated in cirrhotic patients; FeNa = 5% (1%=normal)
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4
Q

Aminophylline

A
  • Class: Bronchodilator (Methylxanthine)
  • Mechanism: Phosphodiesterase inhibition and enhanced signalling via increased cAMP levels in proximal tubule cells –>activates protein kinase A –> increased phosphorylation of the apical membrane Na/H exchanger which inhibits its activity; decreased HCO3 and Na+ (and water) reabsorption
  • Therapeutics: Reduce inflammation and bronchospasm in moderate to severe asthma, night symptoms; NOT as diuretic
  • Important Side Effects: Larger doses give nausea, vomiting, CNS stimulation/seizures, tachycardia/arrythmias
  • Other Side Effects: –
  • Miscellaneous: FeNa = 5%; aminophylline = theophylline + ethylene diamine (solubility agent); metabolized by liver; cimetidine and quinoline increase blood levels
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5
Q

Mannitol (Osmitrol)

A
  • Class: Osmotic diuretic
  • Mechanism:
    • increases osmolarity of tubular fluid –> opposes water and sodium reabsorption at proximal tubule (in medulla)
    • (proportionately more water than Na+ is excreted)
  • Therapeutics:
    • Increased clearance of drugs
    • minimize renal failure (shock or surgery)
    • decrease intraocular/intracranial pressures
    • diagnose oliguria
  • Important Side Effects: Risk of pulmonary edema
  • Other Side Effects: –
  • Miscellaneous:
    • FeNa = 5%; must give IV
    • other osmotic diuretics include glucose, urea, isosorbide
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6
Q

Furosemide (Lasix)

A

(diuretic, antihypertensive, inotropic)

  • Class: Loop diuretic (- charge)
  • Mechanism:
    • Inhibits Cl portion of Na-K-2Cl cotransporter in luminal membrane at medullary and cortical (proximal) talH –> decreased K+, Ca++ and Na+ reabsorption
      • resultant K+ loss (d/t compensatory increase in downstream Na+ reabsorption coupled to increased K+ secretion)
    • Inotropic: decreases volume and preload, improve arterial distensibility
  • Therapeutics:
    • Crisis edema (pulmonary, CHF, cirrhosis)
    • hypercalcemia
    • drug toxicity/OD
    • severe hypertension in setting of CHF or cirrhosis
  • Important Side Effects:
    • Hypo -kalemia, -calcemia, -magnesia (–> arrhythmia)
    • contraction alkalosis (b/c volume contraction in absence of inc elim of bicarb), increased BUN and creatinine
    • ototoxicity (esp. w/aminoglycoside)
    • Inotropic:
      • be careful in pts w/ dilated cardiomyopathy since they’re already at risk for arrhythmias
      • volume contraction, electrolyte depletion; causes neurohormonal activation
  • Other Side Effects:
    • Hyper -glycemia, -lipidemia, -uricemia
    • Hyponatremia
    • gout
    • photosensitivity
    • nephrocalcinosis
    • drug interactions
    • erectile dysfunction
  • Miscellaneous:
    • FeNa = 25%
    • eventually causes increase in PT reabsorption
    • decreases positive and negative free water clearance
    • decreases cortex-medulla molarity gradient
    • avoid NSAIDs, take before salty meals, reduce salt intake
    • useful in patients with renal insufficiency (GFR < 30-40)
    • LaSix = Lasts Six hours!
    • Inotropic: contraindication in hypovolemic patients
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7
Q

Bumetanide (Bumex)

A
  • Class: Loop diuretic (- charge)
  • Mechanism:
    • Inhibits Cl portion of Na-K-2Cl cotransporter in luminal membrane at medullary and cortical (proximal) talH –> decreased K+, Ca++ and Na+ reabsorption,
    • resultant K+ loss (d/t compensatory increase in downstream Na+ reabsorption coupled to increased K+ secretion)
    • Inotropic: decreases volume and preload, improve arterial distensibility
  • Therapeutics:
    • Crisis edema (pulmonary, CHF, cirrhosis)
    • hypercalcemia
    • drug toxicity/OD
    • severe hypertension in setting of CHF or cirrhosis
  • Important Side Effects:
    • Hypo -kalemia, -calcemia, -magnesia (–> arrhythmia)
    • contraction alkalosis (b/c volume contraction in absence of inc elim of bicarb), increased BUN and creatinine
    • ototoxicity (esp. w/aminoglycoside)
    • Inotropic:
      • be careful in pts w/ dilated cardiomyopathy since they’re already at risk for arrhythmias
      • volume contraction, electrolyte depletion; causes neurohormonal activation
  • Other Side Effects:
    • Hyper -glycemia, -lipidemia, -uricemia
    • Hyponatremia
    • gout
    • photosensitivity
    • nephrocalcinosis
    • drug interactions
    • erectile dysfunction
  • Miscellaneous:
    • FeNa = 25%
    • eventually causes increase in PT reabsorption
    • decreases positive and negative free water clearance
    • decreases cortex-medulla molarity gradient
    • avoid NSAIDs, take before salty meals, reduce salt intake
    • useful in patients with renal insufficiency (GFR < 30-40)
    • Inotropic: contraindication in hypovolemic patients
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8
Q

Torsemide (Demadex)

A
  • Class: Loop diuretic (- charge)
  • Mechanism:
    • Inhibits Cl portion of Na-K-2Cl cotransporter in luminal membrane at medullary and cortical (proximal) talH –> decreased K+, Ca++ and Na+ reabsorption,
    • resultant K+ loss (d/t compensatory increase in downstream Na+ reabsorption coupled to increased K+ secretion)
    • Inotropic: decreases volume and preload, improve arterial distensibility
  • Therapeutics:
    • Crisis edema (pulmonary, CHF, cirrhosis)
    • hypercalcemia
    • drug toxicity/OD
    • severe hypertension in setting of CHF or cirrhosis
  • Important Side Effects:
    • Hypo -kalemia, -calcemia, -magnesia (–> arrhythmia)
    • contraction alkalosis (b/c volume contraction in absence of inc elim of bicarb), increased BUN and creatinine
    • ototoxicity (esp. w/aminoglycoside)
    • Inotropic:
      • be careful in pts w/ dilated cardiomyopathy since they’re already at risk for arrhythmias
      • volume contraction, electrolyte depletion; causes neurohormonal activation
  • Other Side Effects:
    • Hyper -glycemia, -lipidemia, -uricemia
    • Hyponatremia
    • gout
    • photosensitivity
    • nephrocalcinosis
    • drug interactions
    • erectile dysfunction
  • Miscellaneous:
    • FeNa = 25%
    • eventually causes increase in PT reabsorption
    • decreases positive and negative free water clearance
    • decreases cortex-medulla molarity gradient
    • avoid NSAIDs, take before salty meals, reduce salt intake
    • useful in patients with renal insufficiency (GFR < 30-40)
    • Inotropic: contraindication in hypovolemic patients
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9
Q

Ethacrynic acid (Edecrin)

A
  • Class: Loop diuretic (- charge)
  • Mechanism:
    • Inhibits Cl portion of Na-K-2Cl cotransporter in luminal membrane at medullary and cortical (proximal) talH –> decreased K+, Ca++ and Na+ reabsorption,
    • resultant K+ loss (d/t compensatory increase in downstream Na+ reabsorption coupled to increased K+ secretion)
    • Inotropic: decreases volume and preload, improve arterial distensibility
  • Therapeutics:
    • Crisis edema (pulmonary, CHF, cirrhosis)
    • hypercalcemia
    • drug toxicity/OD
    • severe hypertension in setting of CHF or cirrhosis
    • sulfa free
  • Important Side Effects:
    • Hypo -kalemia, -calcemia, -magnesia (–> arrhythmia)
    • contraction alkalosis (b/c volume contraction in absence of inc elim of bicarb), increased BUN and creatinine
    • ototoxicity (esp. w/aminoglycoside)
    • Inotropic:
      • be careful in pts w/ dilated cardiomyopathy since they’re already at risk for arrhythmias
      • volume contraction, electrolyte depletion; causes neurohormonal activation
  • Other Side Effects:
    • Hyper -glycemia, -lipidemia, -uricemia
    • Hyponatremia
    • gout
    • photosensitivity
    • nephrocalcinosis
    • drug interactions
    • erectile dysfunction
  • Miscellaneous:
    • FeNa = 25%
    • eventually causes increase in PT reabsorption
    • decreases positive and negative free water clearance
    • decreases cortex-medulla molarity gradient
    • avoid NSAIDs, take before salty meals, reduce salt intake
    • useful in patients with renal insufficiency (GFR < 30-40)
    • Inotropic: contraindication in hypovolemic patients
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10
Q

Chlorothiazide (Chlotride)

A
  • Class: Thiazide diuretic (- charge)
  • Mechanism:
    • Inhibits the Cl portion of the Na-Cl cotransporter in the luminal membrane at the early distal tubule –> decreased Na+ (and water) reabsorption, increased Ca++ reabsorption, resultant K+ loss
    • Inotropic: decreases volume and preload, improve arterial distensibility
  • Therapeutics:
    • HTN (intravascular contraction)
    • chronic edema (cardiac insufficiency)
    • idiopathic hypercalciuria (stones)
    • nephrogenic diabetes insipidus (contract ECF–> decreases GFR –> decreases vol urine voided)
  • Important Side Effects:
    • Hypokalemia, hypercalcemia
    • contraction alkalosis, increased BUN and creatinine
    • Inotropic: volume contraction, electrolyte depletion, neurohormonal activation
  • Other Side Effects:
    • Hyper -glycemia, -lipidemia, -uricemia, -calcemia
    • Hypo -magnesia, -natremia
    • gout
    • photosensitivity
    • impotence
    • drug interactions
  • Miscellaneous:
    • FeNa = 8%
    • lethal interaction w/quinidine (v. tach –> fib, may be due to hypokalemia)
    • avoid NSAIDs (decrease thiazide activity) & bile sequestrants (decrease thiazide absorption)
    • increased risk of hypokalemia w/anti-inflammatory steroids or Amphotericin B
    • decreases positive free water clearance
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11
Q

Hydrochlorothiazide (Microzide)

A

(diuretic, antihypertensive)

  • Class: Thiazide diuretic (- charge)
  • Mechanism: Inhibits the Cl portion of the Na-Cl cotransporter in the luminal membrane at the early distal tubule –> decreased Na+ (and water) reabsorption, increased Ca++ reabsorption, resultant K+ loss
  • Therapeutics:
    • HTN (intravascular contraction)
      • most frequent 1st-line drug class for HTN
    • chronic edema (cardiac insufficiency)
    • idiopathic hypercalciuria (stones)
    • nephrogenic diabetes insipidus (contract ECF–> decreases GFR –> decreases vol urine voided)
  • Important Side Effects:
    • Hypokalemia (most common), hypercalcemia
    • contraction alkalosis, increased BUN and creatinine
    • Inotropic: volume contraction, electrolyte depletion, neurohormonal activation
  • Other Side Effects:
    • Hyper -glycemia, -lipidemia, -uricemia
    • Hypo -magnesia, -natremia
    • gout
    • photosensitivity
    • impotence
    • drug interactions
  • Miscellaneous:
    • FeNa = 8%
    • lethal interaction w/quinidine (v. tach –> fib, may be due to hypokalemia)
    • avoid NSAIDs (decrease thiazide activity) & bile sequestrants (decrease thiazide absorption)
    • increased risk of hypokalemia w/anti-inflammatory steroids or Amphotericin B
    • decreases positive free water clearance
    • ineffective if GFR < 30
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12
Q

Chlorthalidone (Thalitone)

A

(diuretic, antihypertensive)

  • Class: Thiazide-like diuretic
  • Mechanism: Inhibits the Cl portion of the Na-Cl cotransporter in the luminal membrane at the early distal tubule –> decreased Na+ (and water) reabsorption, increased Ca++ reabsorption, resultant K+ loss
  • Therapeutics:
    • Reduce stroke risk, CHF events
    • HTN (intravascular contraction)
      • most frequent 1st-line drug class for HTN
    • chronic edema (cardiac insufficiency)
    • idiopathic hypercalciuria (stones)
    • nephrogenic diabetes insipidus (contract ECF–> decreases GFR –> decreases vol urine voided)
  • Important Side Effects:
    • Hypokalemia (most common), hypercalcemia
    • contraction alkalosis, increased BUN and creatinine
    • Inotropic: volume contraction, electrolyte depletion, neurohormonal activation
  • Other Side Effects:
    • Hyper -glycemia, -lipidemia, -uricemia
    • Hypo -magnesia, -natremia
    • gout
    • photosensitivity
    • impotence
    • drug interactions
  • Miscellaneous:
    • FeNa = 8%
    • lethal interaction w/quinidine (v. tach –> fib, may be due to hypokalemia)
    • avoid NSAIDs (decrease thiazide activity) & bile sequestrants (decrease thiazide absorption)
    • increased risk of hypokalemia w/anti-inflammatory steroids or Amphotericin B
    • decreases positive free water clearance
    • ineffective if GFR < 30
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13
Q

Quinethazone (Hydromox)

A
  • Class: Thiazide-like diuretic
  • Mechanism: Inhibits the Cl portion of the Na-Cl cotransporter in the luminal membrane at the early distal tubule –> decreased Na+ (and water) reabsorption, increased Ca++ reabsorption, resultant K+ loss
  • Therapeutics:
    • HTN (intravascular contraction)
    • chronic edema (cardiac insufficiency)
    • idiopathic hypercalciuria (stones)
    • nephrogenic diabetes insipidus (contract ECF–> decreases GFR –> decreases vol urine voided)
  • Important Side Effects:
    • Hypokalemia, hypercalcemia
    • contraction alkalosis, increased BUN and creatinine
    • Inotropic: volume contraction, electrolyte depletion, neurohormonal activation
  • Other Side Effects:
    • Hyper -glycemia, -lipidemia, -uricemia
    • Hypo -magnesia, -natremia
    • gout
    • photosensitivity
    • impotence
    • drug interactions
  • Miscellaneous:
    • FeNa = 8%
    • lethal interaction w/quinidine (v. tach –> fib, may be due to hypokalemia)
    • avoid NSAIDs (decrease thiazide activity) & bile sequestrants (decrease thiazide absorption)
    • increased risk of hypokalemia w/anti-inflammatory steroids or Amphotericin B
    • decreases positive free water clearance
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14
Q

Metolazone (Zaroxolyn)

A

(diuretic, antihypertensive)

  • Class: Thiazide-like diuretic
  • Mechanism: Inhibits the Cl portion of the Na-Cl cotransporter in the luminal membrane at the early distal tubule –> decreased Na+ (and water) reabsorption, increased Ca++ reabsorption, resultant K+ loss
  • Therapeutics:
    • HTN (intravascular contraction)
      • most frequent 1st-line drug class for HTN
    • chronic edema (cardiac insufficiency)
    • idiopathic hypercalciuria (stones)
    • nephrogenic diabetes insipidus (contract ECF–> decreases GFR –> decreases vol urine voided)
  • Important Side Effects:
    • Hypokalemia (most common), hypercalcemia
    • contraction alkalosis, increased BUN and creatinine
    • Inotropic: volume contraction, electrolyte depletion, neurohormonal activation
  • Other Side Effects:
    • Hyper -glycemia, -lipidemia, -uricemia
    • Hypo -magnesia, -natremia
    • gout
    • photosensitivity
    • impotence
    • drug interactions
  • Miscellaneous:
    • FeNa = 8%
    • lethal interaction w/quinidine (v. tach –> fib, may be due to hypokalemia)
    • avoid NSAIDs (decrease thiazide activity) & bile sequestrants (decrease thiazide absorption)
    • increased risk of hypokalemia w/anti-inflammatory steroids or Amphotericin B
    • decreases positive free water clearance
    • *the only thiazide used in pts w/ renal insufficiency, used in combo w/ loop diuretic
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15
Q

Indapamide (Lozol)

A
  • Class: Thiazide-like diuretic
  • Mechanism: Inhibits the Cl portion of the Na-Cl cotransporter in the luminal membrane at the early distal tubule –> decreased Na+ (and water) reabsorption, increased Ca++ reabsorption, resultant K+ loss
  • Therapeutics:
    • HTN (intravascular contraction)
    • chronic edema (cardiac insufficiency)
    • idiopathic hypercalciuria (stones)
    • nephrogenic diabetes insipidus (contract ECF–> decreases GFR –> decreases vol urine voided)
  • Important Side Effects:
    • Hypokalemia, hypercalcemia
    • contraction alkalosis, increased BUN and creatinine
    • Inotropic: volume contraction, electrolyte depletion, neurohormonal activation
  • Other Side Effects:
    • Hyper -glycemia, -lipidemia, -uricemia
    • Hypo -magnesia, -natremia
    • gout
    • photosensitivity
    • impotence
    • drug interactions
  • Miscellaneous:
    • FeNa = 8%
    • lethal interaction w/quinidine (v. tach –> fib, may be due to hypokalemia)
    • avoid NSAIDs (decrease thiazide activity) & bile sequestrants (decrease thiazide absorption)
    • increased risk of hypokalemia w/anti-inflammatory steroids or Amphotericin B
    • decreases positive free water clearance
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16
Q

Amiloride (Midamor)

A

(diuretic, antihypertensive)

  • Class:
    • K+-sparing diuretic
    • Renal epithelial Na+ channel inhibitor (+ charge)
  • Mechanism: Blocks Na channel and Na/H antiporter in lumenal membrane at the late distal tubule and collecting duct –> decreased K+ secretion and distal tubule acid secretion, increased Ca++ absorption
  • Therapeutics:
    • Combination with other diuretics to prevent hypokalemia
    • edema
    • idiopathic hypercalciuria (stones) (used in combo w/ thiazides b/c too weak on own)
    • lithium-induced polyuria and toxicity
    • Liddle syndrome
    • mucocilliary clearance
  • Important Side Effects:
    • Hyperkalemia in patients with renal failure / on ACE inhibitors
    • Inotropic: volume contraction, electrolyte depletion, neurohormonal activation
  • Other Side Effects:
  • Miscellaneous:
    • Contraindicated in patients with renal failure (hyperkalemia)
    • Contraindicated in pts w/ ACEi/ARB use
    • FeNa = 2%
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17
Q

Triamterene (Dyrenium)

A
  • Class:
    • K+-sparing diuretic;
    • renal epithelial Na+ channel inhibitor (+ charge)
  • Mechanism: Blocks Na channel and Na/H antiporter in lumenal membrane at the late distal tubule and collecting duct –> decreased K+ secretion and distal tubule acid secretion, increased Ca++ absorption
  • Therapeutics:
    • Combination with other diuretics to prevent hypokalemia
    • edema
  • Important Side Effects:
    • Hyperkalemia in patients with renal failure / on ACE inhibitors
    • Inotropic: volume contraction, electrolyte depletion, neurohormonal activation
  • Other Side Effects: Megaloblastic anemia in patients with liver cirrhosis
  • Miscellaneous:
    • Contraindicated in patients with renal failure (hyperkalemia)
    • FeNa = 2%
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18
Q

Spironolactone (Aldactone)

A

(diuretic, antihypertensives, inotropic)

  • Class: K+-sparing diuretic; aldosterone receptor antagonist
  • Mechanism:
    • Competes for aldosterone receptor, inhibiting mRNA transcription and translation –> decreased Na and K channels, decreased number and activity of Na-K-ATPase pumps in the late distal tubule and collecting duct –> decreased K+ secretion, distal tubule acid secretion
    • Inotropic: Block alodesterone action; inhibits sodium reabsorption in distal tubule
  • Therapeutics:
    • Reduction in CHF mortality (30% in NYHA class III and IV)
    • combination with other diuretics to prevent hypokalemia
    • edema
    • primary and secondary aldosteronism
    • hypertension
    • anti-testosterone agent
  • Important Side Effects:
    • Hyperkalemia in patients with renal failure / on ACE inhibitors
    • male patients may have gynecomastia, erectile dysfunction, and loss of libido
    • female patients may have amenorrhea, breast soreness, and oligomenorrhea
    • Inotropic: metabolic acidosis, peptic ulcers
  • Other Side Effects:
  • Miscellaneous:
    • Contraindicated in patients with renal failure (hyperkalemia)
    • FeNa = 2%
    • requires a salt-restricted diet
    • only drug not requiring tubular lumen access
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19
Q

Eplerenone (Inspra)

A

(antihypertensives, inotropic)

  • Class: K+-sparing diuretic; aldosterone receptor antagonist
  • Mechanism: Blocks alodesterone; inhibits sodium reabsorption in distal tubule
  • Therapeutics: Reduction in CHF mortality (30% in NYHA class III and IV); combination with other diuretics to prevent hypokalemia; edema; primary and secondary aldosteronism; hypertension; anti-testosterone agent
  • Important Side Effects: Hyperkalemia; much lower incidence of gynecomastia and mennorhagia than spironolactone
  • Inotropic: metabolic acidosis, peptic ulcers
  • Other Side Effects:
  • Miscellaneous: Caution in renal failure, ACEi or ARB use, and in diabetics
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20
Q

Conivaptan (Vaprisol)

A
  • Class: Aquaretic (diuretic)
  • Mechanism: Vasopressin (ADH) receptor antagonist working at collecting duct –> increased free water excretion
  • Therapeutics: Hyponatremia (SIADH, CHF)
  • Important Side Effects:
  • Other Side Effects:
  • Miscellaneous: New drug class with unproven clinical benefit
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21
Q

Tolvaptan (Samsca)

A
  • Class: Aquaretic (diuretic)
  • Mechanism: Vasopressin (ADH) receptor antagonist working at collecting duct –> increased free water excretion
  • Therapeutics: Hyponatremia (SIADH, CHF)
  • Important Side Effects:
  • Other Side Effects:
  • Miscellaneous: New drug class with unproven clinical benefit
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22
Q

Captopril (Capoten)

A

(antihypertensives, angina, inotropic)

  • Class: short-acting ACE inhibitor (vasodilators)
    • (-pril = ACE inhibitor)
  • Mechanism: Blocks endothelial ACE from converting angiotensin I to angiotensin II (potent vasoconstrictor); as a side effect, also prevents breakdown of bradykinin (potent vasodilator)
  • Therapeutics:
    • Angina: Reduces incidence of future CAD events in patients at risk for/ with vascular disease
    • Antihypertensive and Inotropic:
      • 1st-line for CHF
      • left ventricular hypertrophy
      • post-MI (prevents left ventricular remodeling)
  • Important Side Effects: “CATCHH”; Dry cough, angioedema, hyperkalemia, hypotension, inhibits renal autoregulation
  • Other Side Effects:
  • Miscellaneous:
    • Short-acting
    • Contraindicated in:
      • pregnancy
      • renal artery stenosis
      • hyperkalemia
      • prior Angioedema (no ARB allowed, either)
    • Caution in renal failure
    • ​May reduce risk of diabetes
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23
Q

Lisinopril (Prinivil)

A

(antihypertensives, angina, inotropic)

  • Class: long-acting ACE inhibitor (vasodilators)
    • (-pril = ACE inhibitor)
  • Mechanism: Blocks endothelial ACE from converting angiotensin I to angiotensin II (potent vasoconstrictor); as a side effect, also prevents breakdown of bradykinin (potent vasodilator)
  • Therapeutics:
    • Angina: Reduces incidence of future CAD events in patients at risk for/ with vascular disease
    • Antihypertensive and Inotropic:
      • 1st-line for CHF
      • left ventricular hypertrophy
      • post-MI (prevents left ventricular remodeling)
  • Important Side Effects: Dry cough, angioedema, hyperkalemia, hypotension, decreased renal function
  • Other Side Effects:
  • Miscellaneous:
  • Miscellaneous:
    • Long-acting
    • Contraindicated in:
      • pregnancy
      • renal artery stenosis
      • hyperkalemia
      • prior angioedema (no ARB allowed, either)
    • Caution in renal failure
    • ​May reduce risk of diabetes
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24
Q

Benazepril (Lotensin)

A

(antihypertensives)

  • Class: long-acting ACE inhibitor (vasodilators)
    • (-pril = ACE inhibitor)
  • Mechanism: Blocks endothelial ACE from converting angiotensin I to angiotensin II (potent vasoconstrictor); as a side effect, also prevents breakdown of bradykinin (potent vasodilator)
  • Therapeutics: CHF, left ventricular hypertrophy, and post-MI (prevents left ventricular remodeling)
  • Important Side Effects: Dry cough, angioedema, hyperkalemia, hypotension, decreased renal function
  • Other Side Effects:
  • Miscellaneous:
    • Long-acting
    • Contraindicated in:
      • pregnancy
      • renal artery stenosis
      • hyperkalemia
      • prior angioedema (no ARB allowed, either)
    • Caution in renal failure
    • ​May reduce risk of diabetes
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25
Q

Quinapril (Accupril)

A

(antihypertensives, angina, inotropic)

  • Class: long-acting ACE inhibitor (vasodilators)
    • (-pril = ACE inhibitor)
  • Mechanism: Blocks endothelial ACE from converting angiotensin I to angiotensin II (potent vasoconstrictor); as a side effect, also prevents breakdown of bradykinin (potent vasodilator)
  • Therapeutics:
    • Angina: Reduces incidence of future CAD events in patients at risk for/ with vascular disease
    • Antihypertensive and Inotropic:
      • 1st-line for CHF
      • left ventricular hypertrophy
      • post-MI (prevents left ventricular remodeling)
  • Important Side Effects: Dry cough, angioedema, hyperkalemia, hypotension, decreased renal function
  • Other Side Effects:
  • Miscellaneous:
    • Long-acting
    • Contraindicated in:
      • pregnancy
      • renal artery stenosis
      • hyperkalemia
      • prior angioedema (no ARB allowed, either)
    • Caution in renal failure
    • ​May reduce risk of diabetes
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26
Q

Ramipril (Altace)

A

(antihypertensives, angina, inotropic)

  • Class: long-acting ACE inhibitor (vasodilators)
    • (-pril = ACE inhibitor)
  • Mechanism: Blocks endothelial ACE from converting angiotensin I to angiotensin II (potent vasoconstrictor); as a side effect, also prevents breakdown of bradykinin (potent vasodilator)
  • Therapeutics:
    • Angina: Reduces incidence of future CAD events in patients at risk for/ with vascular disease
    • Antihypertensive and Inotropic:
      • 1st-line for CHF
      • left ventricular hypertrophy
      • post-MI (prevents left ventricular remodeling)
  • Important Side Effects: Dry cough, angioedema, hyperkalemia, hypotension, inhibits renal autoregulation
  • Other Side Effects:
  • Miscellaneous:
    • Long-acting;
    • Contraindicated in:
      • pregnancy
      • renal artery stenosis
      • hyperkalemia
      • prior Angioedema (no ARB allowed, either);
    • Caution in renal failure
    • ​May reduce risk of diabetes
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27
Q

Enalapril (Vasotec)

A

(antihypertensives, angina, inotropic)

  • Class ACE inhibitor (vasodilators)
    • (-pril = ACE inhibitor)
  • Mechanism: Blocks endothelial ACE from converting angiotensin I to angiotensin II (potent vasoconstrictor); as a side effect, also prevents breakdown of bradykinin (potent vasodilator)
  • Therapeutics:
    • Angina: Reduces incidence of future CAD events in patients at risk for/ with vascular disease
    • Antihypertensive & Inotropic:
      • 1st-line for CHF
      • left ventricular hypertrophy
      • post-MI (prevents left ventricular remodeling)
  • Important Side Effects: Dry cough, angioedema, hyperkalemia, hypotension, decreased renal function
  • Other Side Effects:
  • Miscellaneous:
    • Metabolized to enalaprilat, a more active metabolite
    • Contraindicated in:
      • pregnancy
      • renal artery stenosis
      • hyperkalemia
      • prior angioedema (no ARB allowed, either)
    • Caution in renal failure
    • May reduce risk of diabetes
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28
Q

Losartan (Cozaar)

A

(antihypertensive, inotropic)

  • Class: Angiotensin II Recepter Blocker (ARB)
    • (-sartan)
  • Mechanism:
    • Competitively inhibits binding of angiotensin II to type 1 angiotensin II receptors (AT1) in vascular endothelium
      • stimulates vascular smooth muscle contraction
      • dilates arteries and veins
      • promotes renal excretion of Na+ and water
      • inhibits cardiac and vascular remodeling
  • Therapeutics:
    • Used in place of an ACE-I when cough is an issue​
    • To decrease peripheral vascular resistance w/little change in HR or CO; same uses as ACE-I (CHF, LV hypertrophy, post MI to prevent LV remodeling)
  • Important Side Effects:
    • Angioedema
    • hyperkalemia
    • hypotension
    • decreased renal function
    • dry cough less frequent than with ACE-I
  • Other Side Effects:
  • Miscellaneous:
    • Contraindicated in:
      • pregnancy
      • renal artery stenosis
      • hyperkalemia
      • prior angioedema (no ACE-i allowed, either)
    • caution in renal failure
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29
Q

Valsartan (Diovan)

A

(antihypertensive, inotropic)

  • Class: Angiotensin II Recepter Blocker (ARB)
    • (-sartan)
  • Mechanism: Competitively inhibits binding of angiotensin II to type 1 angiotensin II receptors (AT1) in vascular endothelium
    • stimulates vascular smooth muscle contraction
    • dilates arteries and veins
    • promotes renal excretion of Na+ and water
    • inhibits cardiac and vascular remodeling
  • Therapeutics:
    • Used in place of an ACE-I when cough is an issue​
    • To decrease peripheral vascular resistance w/little change in HR or CO; same uses as ACE-I (CHF, LV hypertrophy, post MI to prevent LV remodeling)
  • Important Side Effects:
    • Angioedema
    • hyperkalemia
    • hypotension
    • decreased renal function
    • dry cough less frequent than with ACE-I
  • Other Side Effects:
  • Miscellaneous:
    • Contraindicated in:
      • pregnancy
      • renal artery stenosis
      • hyperkalemia
      • prior angioedema (no ACE-i allowed, either)
    • caution in renal failure
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30
Q

Irbesartan (Avapro)

A

(antihypertensive, inotropic)

  • Class: Angiotensin II Recepter Blocker (ARB)
    • (-sartan)
  • Mechanism: Competitively inhibits binding of angiotensin II to type 1 angiotensin II receptors (AT1) in vascular endothelium
    • stimulates vascular smooth muscle contraction
    • dilates arteries and veins
    • promotes renal excretion of Na+ and water
    • inhibits cardiac and vascular remodeling
  • Therapeutics:
    • Used in place of an ACE-I when cough is an issue​
    • To decrease peripheral vascular resistance w/little change in HR or CO; same uses as ACE-I (CHF, LV hypertrophy, post MI to prevent LV remodeling)
  • Important Side Effects:
    • Angioedema
    • hyperkalemia
    • hypotension
    • decreased renal function
    • dry cough less frequent than with ACE-I
  • Other Side Effects:
  • Miscellaneous:
    • Contraindicated in:
      • pregnancy
      • renal artery stenosis
      • hyperkalemia
      • prior angioedema (no ACE-i allowed, either)
    • caution in renal failure
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31
Q

Olmesartan (Benecar)

A

(inotropic)

  • Class: Angiotensin II Recepter Blocker (ARB)
    • ​(-sartan)
  • Mechanism: Competitively inhibits binding of angiotensin II to type 1 angiotensin II receptors (AT1) in vascular endothelium
    • stimulates vascular smooth muscle contraction
    • dilates arteries and veins
    • promotes renal excretion of Na+ and water
    • ​inhibits cardiac and vascular remodeling
  • Therapeutics: Used in place of an ACEI when cough is an issue
  • Important Side Effects: Angioedema, hyperkalemia, hypotension, decresed GFR
  • Other Side Effects:
  • Miscellaneous:
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32
Q

Telmisartan (Micardis)

A

(inotropic)

  • Class: Angiotensin Receptor Blocker (ARB)
  • Mechanism: Blocks type 1 angiotensin II receptors (stimulates vascular smooth muscle contraction, dilates arteries and veins, promotes renal excretion of Na and water, inhibits cardiac & vascular remodeling)
  • Therapeutics: Used in place of an ACEI when cough is an issue
  • Important Side Effects: Angioedema, hyperkalemia, hypotension, decresed GFR
  • Other Side Effects:
  • Miscellaneous:
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33
Q

Candisartan (Atacand)

A

(inotropic)

  • Class: Angiotensin II Recepter Blocker (ARB)
    • (-sartan)
  • Mechanism: Competitively inhibits binding of angiotensin II to type 1 angiotensin II receptors (AT1) in vascular endothelium
    • stimulates vascular smooth muscle contraction
    • dilates arteries and veins
    • promotes renal excretion of Na+ and water
    • ​inhibits cardiac and vascular remodeling
  • Therapeutics: Used in place of an ACE-I when cough is an issue
  • Important Side Effects: Angioedema, hyperkalemia, hypotension, decresed GFR
  • Other Side Effects:
  • Miscellaneous:
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34
Q

Aliskiren (Tekturna)

A

(antihyertensives)

  • Class: Renin inhibitor (“iren”–>“inhibits renin”)
  • Mechanism: inhibits renin
  • Therapeutics: Not very effective
  • Important Side Effects:
  • Other Side Effects:
  • Miscellaneous:
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35
Q

Diltiazem (Cardizem)

A

(antihypertensives, angina, anti-arrhythmic)

  • Class: Calcium channel blockers - non-dihydropyridine;
    • Class IV anti-arrhythmic
  • Mechanism:
    • Interact with L-type voltage gated plasma membrane Ca channel –> decreased calcium entry into vascular smooth muscle cell, preventing contraction
      • causes:
        • decreased contractility
        • decreased firing rate of aberrant pacemaker sites
        • and decreased conduction velocity
      • prolongs repolarization in SA node and AV node (–> decreases HR)
      • less vasodilation than the dihydropyridines
    • act on heart (in contrast to dihydropyr)
    • Anti-arrhythmic: Blockade of L-type calcium channels: slow SA & AV node activity; prolong AV refractoriness
  • Therapeutics:
    • Hypertension
    • anti-anginal (chronotropic effects –> decreased myocardial oxygen demand)
    • Anti-arrhythmic: Prevent or terminate reentrant SVTs
    • used in pts w/ chronic kidney disease
  • Important Side Effects:
    • Leg edema
    • bradycardia
    • AV nodal blockade
    • hypotension
    • dizziness
    • worsening heart failure (negative inotrope)
  • Other Side Effects:
    • Constipation (most common)
    • headache
    • flushing
    • Increased serum digoxin levels
  • Miscellaneous:
    • Contraindicated in:
      • overt decompensated systolic heart failure
      • bradycardia
      • sinus node dysfunction
      • high-degree AV block
      • WPW
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36
Q

Verapamil (Calan)

A

(antihypertensives, angina, anti-arrhythmic)

  • Class: Calcium channel blockers - non-dihydropyridine;
    • Class IV anti-arrhythmic
  • Mechanism:
    • Interact with L-type voltage gated plasma membrane Ca channel –> decreased calcium entry into vascular smooth muscle cell, preventing contraction
      • causes:
        • decreased contractility
        • decreased firing rate of aberrant pacemaker sites
        • and decreased conduction velocity
      • prolongs repolarization in SA node and AV node (–> decreases HR)
      • less vasodilation than the dihydropyridines
    • act on heart (in contrast to dihydropyr); verapamil = ventricle
    • Anti-arrhythmic: Blockade of L-type calcium channels: slow SA & AV node activity; prolong AV refractoriness
  • Therapeutics:
    • Hypertension
    • anti-anginal (chronotropic effects –> decreased myocardial oxygen demand)
    • Anti-arrhythmic: Prevent / terminate reentrant SVTs
    • used in pts w/ chronic kidney disease
  • Important Side Effects:
    • Leg edema
    • bradycardia
    • AV nodal blockade
    • hypotension
    • dizziness
    • worsening heart failure (negative inotrope)
  • Other Side Effects:
    • Constipation (most common)
    • headache
    • flushing
    • Increased serum digoxin levels
  • Miscellaneous:
    • Contraindicated in:
      • overt decompensated systolic heart failure
      • bradycardia
      • sinus node dysfunction
      • high-degree AV block
      • WPW
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37
Q

Nifedipine (Procardia)

A

(antihypertensives, angina, anti-arrhythmic)

  • Class: Calcium channel blocker - 1st generation dihydropyridine; Class IV anti-arrhythmic
    • dihydropyridine CCB = -dipine
  • Mechanism:
    • Interact with L-type voltage gated plasma membrane Ca channel –> decreased calcium entry into vascular smooth muscle cell, preventing contraction
    • causes dilation of epicardial coronary arteries and arteriolar resistance arteries
    • less heart-specific activity
      • act on vascular smooth muscle (vasoselective, but less than 2nd gen)
    • anti-arrhythmic: Blockade of L-type calcium channels: slow SA & AV node activity; prolong AV refractoriness
  • Therapeutics:
    • HTN
    • Raynaud’s
    • angina (3rd choice drug b/c cause reflex tachycardia and may worsen angina by increasing myocardial O2 demand)
    • Antiarrhythmic: prevent or terminate reentrant SVTs
  • Important Side Effects:
    • Leg edema (more than 2nd generation)
    • heart failure
    • reflex tachycardia (more than 2nd gen) [lipophilic agents gain entry to brain and depress vasomotor center, causing vasodilation and rapidly dropping BP; this decreases effective stoke vol and causes more reflex sympathetic activation (Increse HR, leading to adverse CV effects) to try to maintain CO; long-acting agents are less lipophilic, and will cause less sympathetic activation and initial fall in BP]
    • Anti-arrhythmic: Hypotension, bradycardia, dizziness
  • Other Side Effects:
    • Constipation (most common)
    • headache
    • flushing
    • Increased serum digoxin levels
  • Miscellaneous:
    • Contraindicated in:
      • overt decompensated systolic heart failure
      • bradycardia
      • sinus node dysfunction
      • WPW
    • no benefit in preserving renal function
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38
Q

Amlodipine (Norvasc)

A

(antihypertensives, angina, anti-arrhythmic)

  • Class: Calcium channel blocker - 2nd generation dihydropyridine; Class IV anti-arrhythmic
    • dihydropyridine CCB = -dipine
  • Mechanism:
    • Interact with L-type voltage gated plasma membrane Ca channel –> decreased calcium entry into vascular smooth muscle cell, preventing contraction
    • causes dilation of epicardial coronary arteries and arteriolar resistance arteries
    • less heart-specific activity
      • act on vascular smooth muscle (vasoselective, and more than 1st gen)
    • anti-arrhythmic: Blockade of L-type calcium channels: slow SA & AV node activity; prolong AV refractoriness
  • Therapeutics:
    • HTN
    • Raynaud’s
    • 1st line agent for coronary vasospasm
    • angina (3rd choice drug b/c cause reflex tachycardia and may worsen angina by increasing myocardial O2 demand)
    • Antiarrhythmic: prevent or terminate reentrant SVTs
  • Important Side Effects:
    • Leg edema (less than 1st generation)
    • heart failure
    • reflex tachycardia (less than 1st gen) [lipophilic agents gain entry to brain and depress vasomotor center, causing vasodilation and rapidly dropping BP; this decreases effective stoke vol and causes more reflex sympathetic activation (Increse HR, leading to adverse CV effects) to try to maintain CO; long-acting agents are less lipophilic, and will cause less sympathetic activation and initial fall in BP]
    • Anti-arrhythmic: Hypotension, bradycardia, dizziness
  • Other Side Effects:
    • Constipation (most common)
    • headache
    • flushing
    • Increased serum digoxin levels
  • Miscellaneous:
    • Contraindicated in:
      • overt decompensated systolic heart failure
      • bradycardia
      • sinus node dysfunction
      • WPW
    • no benefit in preserving renal function
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39
Q

Felodipine (Plendil)

A

(angina)

  • Class: Calcium channel blocker - 2nd generation dihydropyridine
    • dihydropyridine CCB = -dipine
  • Mechanism:
    • Interact with L-type voltage gated plasma membrane Ca channel –> decreased calcium entry into vascular smooth muscle cell, preventing contraction
    • causes dilation of epicardial coronary arteries and arteriolar resistance arteries
    • less heart-specific activity
    • act on vascular smooth muscle
      (vasoselective, and more than 1st gen)
  • Therapeutics:
    • 1st line agent for coronary vasospasm
    • angina (3rd choice drug)
    • Raynaud’s
  • Important Side Effects:
    • Leg edema (less than 1st generation)
    • heart failure
    • reflex tachycardia (less than 1st gen)
  • Other Side Effects:
    • Constipation (most common)
    • headache
    • flushing
  • Miscellaneous:
    • Contraindicated in:
      • overt decompensated heart failure
      • bradycardia
      • sinus node dysfunction
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40
Q

Isradipine (Dynacirc)

A

(angina)

  • Class: Calcium channel blocker - 2nd generation dihydropyridine
    • dihydropyridine CCB = -dipine
  • Mechanism:
    • Interact with L-type voltage gated plasma membrane Ca channel –> decreased calcium entry into vascular smooth muscle cell, preventing contraction
    • causes dilation of epicardial coronary arteries and arteriolar resistance arteries
    • less heart-specific activity
      • act on vascular smooth muscle
        (vasoselective, and more than 1st gen)
  • Therapeutics:
    • 1st line agent for coronary vasospasm
    • angina (3rd choice drug)
    • Raynaud’s
  • Important Side Effects:
    • Leg edema (less than 1st generation)
    • heart failure,
    • reflex tachycardia (less than 1st gen)
  • Other Side Effects:
    • Constipation (most common)
    • headache
    • flushing
  • Miscellaneous:
    • Contraindicated in:
      • overt decompensated heart failure
      • bradycardia
      • sinus node dysfunction
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41
Q

Propranolol (Inderal)

A

(antihypertensives, anti-arrhythmic)

  • Class: Nonselective β-blocker, Class II anti-arrhythmic
  • Mechanism: blocks β1 and β2 receptors
    • Reduces cardiac output (primary reason for BP lowering)
    • Inhibits renin release (by blocking binding of catecholamines to B1 receptors on juxta glomerular cells)
    • Reduces norepinephrine release from neurons
    • Decreases sympathetic tone (in vessels)
    • Overall you should expect very modest BP improvement from BB’s
    • Anti-arrhythmic: Decreases SA & AV node activity (phase 4 depolarization)
  • Therapeutics:
    • HTN?
    • Control of ventricular rate in atrial fibrillation/flutter
    • long-term suppression of SVTs
    • PVCs
  • Important Side Effects:
    • Bronchospasm
    • bradycardia (negative chronotrope)
    • CHF (negative ionotrope)
    • masking of hypoglycemia symptoms
    • Heart block
    • hypotension
  • Other Side Effects:
    • Decreased exercise capacity
    • depression (crosses BBB)
    • worsening symptoms of peripheral vascular disease
    • Anti-arrhythmic: Contraindicated in WPW
    • Contraindicated in asthma
    • Contrindicated in HF
  • Miscellaneous:
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42
Q

Metoprolol (Lopressor)

A

(antihypertensive, angina, inotropic, anti-arrhythmic)

  • Class: β1-selective blocker; Class II anti-arrhythmics
  • Mechanism:
    • Antihypertensive: Moderately selective β1 blockade
      • Reduces cardiac output (primary reason for BP lowering)
      • Inhibits renin release (by blocking binding of catecholamines to B1 receptors on juxtaglomerular cells)
      • Reduces norepinephrine release from neurons
      • Decreases sympathetic tone (in vessels)
      • Overall you should expect very modest BP improvement from BB’s
    • Angina: Decrease contractility and HR (reduced myocardial O2 demand)
    • Inotropic (HF): Blocks high circulating levels of catecholamines
    • Anti-arrhythmic: Decreases SA & AV node activity (phase 4 depolarization)
  • Therapeutics:
    • hypertension?
    • Angina:
      • Prevent MIs
      • prevent sudden cardiac death
      • increase survival post-MI (if patients suddenly stop, really bad!)
    • Inotropic: Dramatically decreases mortality in CHF patients (sustained release aka metoprolol succinate)
    • Anti-arrhythmic:
      • Control of ventricular rate in atrial fibrillation/flutter
      • long-term suppression of SVTs
      • PVCs
  • Important Side Effects:
    • Less likely to have bronchospasm, hypoglycemic awareness, and depression
    • Fatigue, worsening claudication, impotence (so men don’t take)
    • Heart block, hypotension, bradycardia
    • Contraindicated in asthma
  • Other Side Effects: decreased exercise tolerance, lethargy, insomnia
    • Anti-arrhythmic: Contraindicated in WPW
  • Miscellaneous:
    • Angina:
      • Contraindicated in:
        • severe bradycardia
        • high degree AV block
        • sick sinus syndrome
        • unstable LV failure;
      • relative contraindication in:
        • asthma
        • severe depression
        • peripheral vascular disease
    • Inotropic: Should be started at very low dose and slowly ratchet up; do not stop suddenly
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43
Q

Atenolol (Tenormin)

A

(antihypertensive, angina)

  • Class: β1-selective blocker
  • Mechanism:
    • Antihypertensive: Moderately selective β1 blockade
      • Reduces cardiac output (primary reason for BP lowering)
      • Inhibits renin release (by blocking binding of catecholamines to B1 receptors on juxtaglomerular cells)
      • Reduces norepinephrine release from neurons
      • Decreases sympathetic tone (in vessels)
      • Overall you should expect very modest BP improvement from BB’s
    • Angina: Decrease contractility and HR (reduced myocardial O2 demand)
  • Therapeutics:
    • hypertension?
    • Angina:
      • Prevent MIs
      • prevent sudden cardiac death
      • increase survival post-MI (if patients suddenly stop, really bad!)
  • Important Side Effects:
    • Less likely to have bronchospasm, hypoglycemic awareness, and depression
    • Fatigue, worsening claudication, impotence (so men don’t take)
    • Contraindicated in asthma
  • Other Side Effects: Decreased exercise tolerance, lethargy, insomnia
  • Miscellaneous:
    • Angina:
      • Contraindicated in:
        • severe bradycardia
        • high degree AV block
        • sick sinus syndrome
        • unstable LV failure
      • relative contraindication in:
        • asthma
        • severe depression
        • peripheral vascular disease
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44
Q

Nadolol (Corgard)

A

(antihypertensives)

  • Class: β1-selective blocker
  • Mechanism: Moderately selective β1 blockade
    • Reduces cardiac output (primary reason for BP lowering)
    • Inhibits renin release (by blocking binding of catecholamines to B1 receptors on juxta glomerular cells)
    • Reduces norepinephrine release from neurons
    • Decreases sympathetic tone (in vessels)
    • Overall you should expect very modest BP improvement from BB’s
  • Therapeutics:
  • Important Side Effects: Less likely to have bronchospasm, hypoglycemic awareness, and depression
    • Contraindicated in asthma
  • Other Side Effects:
  • Miscellaneous: Longer-acting than other beta-blockers
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45
Q

Bisoprolol (Zebeta)

A

(antihypertensive, angina, inotropic)

  • Class: β1-selective blocker
  • Mechanism:
    • Antihypertensive: Moderately selective β1 blockade
      • Reduces cardiac output (primary reason for BP lowering)
      • Inhibits renin release (by blocking binding of catecholamines to B1 receptors on juxtaglomerular cells)
      • Reduces norepinephrine release from neurons
      • Decreases sympathetic tone (in vessels)
      • Overall you should expect very modest BP improvement from BB’s
    • Angina: Decrease contractility and HR (reduced myocardial O2 demand)
    • Inotropic: Blocks high circulating levels of catecholamines
  • Therapeutics:
    • hypertension?
    • Angina:
      • Prevent MIs
      • prevent sudden cardiac death
      • increase survival post-MI (if patients suddenly stop, really bad!)
    • Inotropic: Dramatically decreases mortality in CHF patients
  • Important Side Effects:
    • Less likely to have bronchospasm, hypoglycemic awareness, and depression
    • Fatigue, worsening claudication, impotence (so men don’t take)
    • Contraindicated in asthma
  • Other Side Effects: Decreased exercise tolerance, lethargy, insomnia
  • Miscellaneous:
    • Longer-acting than other beta-blockers
    • Angina:
      • Contraindicated in:
        • severe bradycardia
        • high degree AV block
        • sick sinus syndrome
        • unstable LV failure
      • relative contraindication in:
        • asthma
        • severe depression
        • peripheral vascular disease
    • Inotropic: Should be started at very low dose and slowly ratchet up; do not stop suddenly
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46
Q

Esmolol (Brevibloc)

A

(antihypertensives, anti-arrhythmic)

  • Class: β1-selective blocker; Class II anti-arrhythmic
  • Mechanism:
    • Reduces cardiac output (primary reason for BP lowering)
    • Inhibits renin release (by blocking binding of catecholamines to B1 receptors on juxta glomerular cells)
    • Reduces norepinephrine release from neurons
    • Decreases sympathetic tone (in vessels)
    • Overall you should expect very modest BP improvement from BB’s
  • Anti-arrhythmic: Decreases SA & AV node activity (phase 4 depolarization)
  • Therapeutics:
    • HTN: AV nodal blockade in unstable patients
    • Anti-arrhythmic:
      • Control of ventricular rate in atrial fibrillation/flutter
      • long-term suppression of SVTs
      • PVCs
  • Important Side Effects:
    • Heart block
    • hypotension
    • bronchospasm
    • bradycardia
    • Contraindicated in asthma​
  • Other Side Effects: Contraindicated in WPW
  • Miscellaneous: Short half-life (makes it unique; used IV)
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47
Q

Labetolol (Trandate)

A

(antihypertensives)

  • Class: Combined αβ blocker
  • Mechanism: β1 blockade with vasodilatory effects
    • Reduces cardiac output (primary reason for BP lowering)
    • Inhibits renin release (by blocking binding of catecholamines to B1 receptors on juxta glomerular cells)
    • Reduces norepinephrine release from neurons
    • Decreases sympathetic tone (in vessels)
    • Overall you should expect very modest BP improvement from BB’s
  • Therapeutics: Hypertensive urgency
  • Important Side Effects: Contraindicated in asthma
  • Other Side Effects:
  • Miscellaneous:
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48
Q

Carvedilol (Coreg)

A

(antihypertensives, inotropic, anti-arrhythmic)

  • Class: Combined αβ blocker; Class II anti-arrhythmic
    • 3rd generation β-blocker
  • Mechanism:
    • Antihypertensive: β1 blockade with vasodilatory effects
      • Reduces cardiac output (primary reason for BP lowering)
      • Inhibits renin release (by blocking binding of catecholamines to B1 receptors on juxta glomerular cells)
      • Reduces norepinephrine release from neurons
      • Decreases sympathetic tone (in vessels)
      • Overall you should expect very modest BP improvement from BB’s
      • decrease afterload
    • Inotropic (HF): Blocks high circulating levels of catecholamines
    • Anti-arrhythmic: Decreases SA & AV node activity (phase 4 depolarization)
  • Therapeutics:
    • Antihypertensives: Acute coronary syndrome, CHF
    • Inotropic: *_Dramatically decreases mortality in CHF patients*_
    • Anti-arrhythmic:
      • Control of ventricular rate in atrial fibrillation/flutter
      • long-term suppression of SVTs
      • PVCs
  • Important Side Effects:
    • Heart block
    • hypotension
    • bronchospasm
    • bradycardia
    • Contraindicated in asthma
  • Other Side Effects: Contraindicated in WPW
  • Miscellaneous:
    • Inotropic: Should be started at very low dose and slowly ratchet up; do not stop suddenly
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49
Q

Terazosin (Hytrin)

A

(antihypertensives)

  • Class: α1-adrenergic receptor antagonist (α1-blocker)
    • (-zosin)
  • Mechanism: Blocks post-synaptic α1-adrenergic receptor on vascular smooth muscle
    • decrease peripheral resistance by dilating arterioles & veins
  • Therapeutics:
    • BPH
    • second-tier meds for HTN (use when other condition around, not for isolated hypertension)
      • b/c compared to thiazides, ACE-Is, & CCBs, this class os drug is more likely to cause cardiac complications
  • Important Side Effects:
    • Orthostatic hypotension
    • fluid retention
    • worsening angina
      (secondary to reflex tachycardia)
  • Other Side Effects:
  • Miscellaneous:
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50
Q

Doxazosin (Cardura)

A

(antihypertensives)

  • Class: α1-adrenergic receptor antagonist (α1-​blocker)
    • (-zosin)
  • Mechanism: Blocks post-synaptic α1-adrenergic receptor antagonist on vascular smooth muscle
    • decrease peripheral resistance by dilating arterioles & veins
  • Therapeutics:
    • BPH
    • second-tier meds (use when other condition around, not for isolated hypertension)
      • b/c compared to thiazides, ACE-Is, & CCBs, this class os drug is more likely to cause cardiac complications
  • Important Side Effects:
    • Orthostatic hypotension
    • fluid retention
    • worsening angina
      (secondary to reflex tachycardia)
  • Other Side Effects:
  • Miscellaneous:
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51
Q

Clonidine (Catapres)

A

(antihypertensives)

  • Class: Central α2-agonist
    (central-acting sympathoplegic)
  • Mechanism: Stimulation of central α2a adrenergic receptors –> reduction in sympathetic outflow from vasomotor systems in brainstem; inhibition of renin release (secondary to decreased sympathetic tone)
  • Therapeutics:
  • Important Side Effects: Rebound HTN if abruptly stopped; moderate orthostatic hypotension
  • Other Side Effects: Sedation, dry mouth, fatigue, depression
  • Miscellaneous: clonidine is the only one routinely used
52
Q

α-methyldopa (Aldomet)

A

(antihypertensives)

  • Class: Central α2-agonist
    (central-acting sympathoplegic)
  • Mechanism: Stimulation of central α2a adrenergic receptors –> reduction in sympathetic outflow from vasomotor systems in brainstem; inhibition of renin release (secondary to decreased sympathetic tone)
  • Therapeutics: Hypertension of pregnancy (only)
  • Important Side Effects: Rebound HTN if abruptly stopped; moderate orthostatic hypotension
  • Other Side Effects: Sedation, dry mouth, fatigue, depression
  • Miscellaneous:
    • Takes place of dopa, so less NE (also, methyl-NE activates α2)
53
Q

Reserpine (Serpalan)

A

(antihypertensives)

  • Class: Ganglion blocking agent (adrenergic neuron blocking agent)
  • Mechanism: blocks transport of NE, DA, & 5HT into storage granules in PNS & CNS –> less neurotransmitter available when nerves are stimulated
  • Therapeutics: Decrease cardiac output and systemic vascular resistance
  • Important Side Effects:
    • Sedation, mental depression, Parkinsonism symptoms
  • Other Side Effects:
  • Miscellaneous: not used
54
Q

Hydralazine (Apresoline)

A

(antihypertensives)

  • Class: Direct (vasodilators)
  • Mechanism: Relax smooth muscle of peripheral arterioles
  • Therapeutics: Hypertensive urgency; patients with BOTH advanced CHF and hypertension
  • Important Side Effects: Drug-induced lupus
  • Other Side Effects: reflex tachycardia
  • Miscellaneous: Serves as an antioxidant, preventing oxidation of NO
55
Q

Minoxidil (Loniten)

A

(antihypertensives)

  • Class: Direct (vasodilators)
  • Mechanism: Relax smooth muscle of peripheral arterioles
  • Therapeutics: Refractory hypertension; hair loss
  • Important Side Effects: Pericardial effusion; hirsutism
  • Other Side Effects: reflex tachycardia
  • Miscellaneous: Smooth muscle relaxation by opening cardiovascular ATP-sensitive potassium channels
56
Q

Niacin (Niaspan)

A

(hypolipidemics)

  • Class: Nicotinic acid
  • Mechanism: Reduction of liver triglyceride synthesis, leading to less hepatic VLDL (thus, LDL) production; decreases lipolysis in adipose tissue, leading to lowered FFA transport to liver (thus, less triglycerides); reduced hepatic clearance of ApoAI (raising HDL)
  • Therapeutics: Best agent to increase HDL (30-40%); as good as fibrates and statins at lowering triglycerides (35-45%); lowers LDL (20-30%); hypertriglyceridemia and low HDL
  • Important Side Effects: Flushing, pruritis of face and upper trunk, rashes, acanthosis nigricans (hyperpigmentation)
  • Other Side Effects: Hepatotoxicity, hyperuricemia, hyperglycemia; dyspepsia/reactivation of peptic ulcer disease; rarely, toxic ambylopia, tachyarrhythmias, a-fib (in elderly) and myopathy
  • Miscellaneous: Water soluble B vitamin complex at [low]; hypolipidemic at [high]; side effects limit compliance (<50% eligible patients follow on it); contraindicated in DM and gout patients; prevent flushing and pruritus with ASA
57
Q

Clofibrate (Atromid-S)

A

(hypolipidemics)

  • Class: Fibric Acid Derivatives (Fibrates)
  • Mechanism: Unknown; may interact w/peroxisome proliferator-activated receptor (esp. PPARα) to stimulate LPL synthesis (enhance TG-rich lipoprotein clearance); inhibit apoC III expression (enhance VLDL clearance); stimulation of apoAI and apoAII (increase HDL)
  • Therapeutics: Marked reduction in VLDL (thus, triglycerides); variable and small effect on LDL; small increase in HDL (10%); severe hypertriglyceridemia
  • Important Side Effects: Potentiate oral anticoagulants (displace from albumin), increase bile lithogenicity; myositis flu-like syndrome in 5%, other effects in 10% (not serious)
  • Other Side Effects:
  • Miscellaneous: Combination w/statin inadvisable due to higher myositis risk
58
Q

Gemfibrozil (Lopid)

A

(hypolipidemics)

  • Class: Fibric Acid Derivatives (Fibrates)
  • Mechanism: Unknown; may interact w/peroxisome proliferator-activated receptor (esp. PPARα) to stimulate LPL synthesis (enhance TG-rich lipoprotein clearance); inhibit apoC III expression (enhance VLDL clearance); stimulation of apoAI and apoAII (increase HDL)
  • Therapeutics: Marked reduction in VLDL (thus, triglycerides); variable and small effect on LDL; small increase in HDL (10%); severe hypertriglyceridemia
  • Important Side Effects: Potentiate oral anticoagulants (displace from albumin), increase bile lithogenicity (less than clofibrate); myositis flu-like syndrome in 5%, other effects in 10% (not serious)
  • Other Side Effects:
  • Miscellaneous: Combination w/statin inadvisable due to higher myositis risk
59
Q

Fenofibrate (Tricor)

A

(hypolipidemics)

  • Class: Fibric Acid Derivatives (Fibrates)
  • Mechanism: Unknown; may interact w/peroxisome proliferator-activated receptor (esp. PPARα) to stimulate LPL synthesis (enhance TG-rich lipoprotein clearance); inhibit apoC III expression (enhance VLDL clearance); stimulation of apoAI and apoAII (increase HDL)
  • Therapeutics: Marked reduction in VLDL (thus, triglycerides); variable and small effect on LDL; small increase in HDL (10%); severe hypertriglyceridemia
  • Important Side Effects: Potentiate oral anticoagulants (displace from albumin), increase bile lithogenicity (less than clofibrate); myositis flu-like syndrome in 5%, other effects in 10% (not serious)
  • Other Side Effects:
  • Miscellaneous: Combination w/statin inadvisable due to higher myositis risk
60
Q

Colestipol (Colestid)

A

(hypolipidemics)

  • Class: Bile acid sequestrants
  • Mechanism: Very positively charged resins binds negative charged bile acids, inhibiting reabsorption and increasing cholesterol loss; leads to increase in LDL receptors in liver (to make more cholesterol), decreasing LDL in blood
  • Therapeutics: Decrease LDL (25%), but slight increase (5%) in TG and HDL
  • Important Side Effects: Very safe (only hypolipidemic indicated for children) because not systematically absorbed; impairs fat soluble vitamin absorption, binds other drugs (e.g., cardiac glycosides, coumarins)
  • Other Side Effects: Bloating, dyspepsia, constipation, gritty/unpleasant taste
  • Miscellaneous: Standard treatment in combo w/statin; contraindicated in hypertriglyceridemia
61
Q

Cholestyramine (Questran)

A

(hypolipidemics)

  • Class: Bile acid sequestrants
  • Mechanism: Very positively charged resins binds negative charged bile acids, inhibiting reabsorption and increasing cholesterol loss; leads to increase in LDL receptors in liver (to make more cholesterol), decreasing LDL in blood
  • Therapeutics: Decrease LDL (25%), but slight increase (5%) in TG and HDL
  • Important Side Effects: Very safe (only hypolipidemic indicated for children) because not systematically absorbed; impairs fat soluble vitamin absorption, binds other drugs (e.g., cardiac glycosides, coumarins)
  • Other Side Effects: Bloating, dyspepsia, constipation, gritty/unpleasant taste
  • Miscellaneous: Standard treatment in combo w/statin; contraindicated in hypertriglyceridemia
62
Q

Colesevelam (Welchol)

A

(hypolipidemics)

  • Class: Bile acid sequestrants
  • Mechanism: Very positively charged resins binds negative charged bile acids, inhibiting reabsorption and increasing cholesterol loss; leads to increase in LDL receptors in liver (to make more cholesterol), decreasing LDL in blood
  • Therapeutics: Decrease LDL (25%), but slight increase (5%) in TG and HDL
  • Important Side Effects: Very safe (only hypolipidemic indicated for children) because not systematically absorbed; impairs fat soluble vitamin absorption, binds other drugs (e.g., cardiac glycosides, coumarins)
  • Other Side Effects: Bloating, dyspepsia, constipation, gritty/unpleasant taste
  • Miscellaneous: Standard treatment in combo w/statin; contraindicated in hypertriglyceridemia
63
Q

Lovastatin (Mevacor)

A

(hypolipidemics)

  • Class: HMG-CoA reductase Inhibitors (-statins)
  • Mechanism: Inhibits HMG-CoA reductase formation of mevalonate; leads to activation of SREBP, a membrane-bound transcription factor that increases LDL-R synthesis and lessens degradation; reduction in cholesterol decreases VLDL synthesis, lowering TG
  • Therapeutics: Reduce LDL (20-55%) and TG (25%), while increasing HDL (5-10%); treatment of dyslipidemia (reduces fatal & nonfatal CHD, strokes; total mortality reduction is 20%)
  • Important Side Effects: Very few; hepatic dysfunction in 1% (serious hepatotoxicity rare); myopathy/rhabdomyolysis (reduced if factors inhibiting statin catabolism lacking)
  • Other Side Effects:
  • Miscellaneous: Lactone prodrug (modified in liver to hydroxy acid form); must be taken in evening; Advicor = niacin + lovastatin
64
Q

Simvastatin (Zocor)

A

(hypolipidemics)

  • Class: HMG-CoA reductase Inhibitors (-statins)
  • Mechanism: Inhibits HMG-CoA reductase formation of mevalonate; leads to activation of SREBP, a membrane-bound transcription factor that increases LDL-R synthesis and lessens degradation; reduction in cholesterol decreases VLDL synthesis, lowering TG
  • Therapeutics: Reduce LDL (20-55%) and TG (25%), while increasing HDL (5-10%); treatment of dyslipidemia (reduces fatal & nonfatal CHD, strokes; total mortality reduction is 20%)
  • Important Side Effects: Very few; hepatic dysfunction in 1% (serious hepatotoxicity rare); myopathy/rhabdomyolysis (reduced if factors inhibiting statin catabolism lacking)
  • Other Side Effects:
  • Miscellaneous: Lactone prodrug (modified in liver to hydroxy acid form); must be taken in evening; Vytorin = ezetemibe + simvastatin
65
Q

Pravastatin (Pravachol)

A

(hypolipidemics)

  • Class: HMG-CoA reductase Inhibitors (-statins)
  • Mechanism: Inhibits HMG-CoA reductase formation of mevalonate; leads to activation of SREBP, a membrane-bound transcription factor that increases LDL-R synthesis and lessens degradation; reduction in cholesterol decreases VLDL synthesis, lowering TG
  • Therapeutics: Reduce LDL (20-55%) and TG (25%), while increasing HDL (5-10%); treatment of dyslipidemia (reduces fatal & nonfatal CHD, strokes; total mortality reduction is 20%)
  • Important Side Effects: Very few; hepatic dysfunction in 1% (serious hepatotoxicity rare); myopathy/rhabdomyolysis (reduced if factors inhibiting statin catabolism lacking)
  • Other Side Effects:
  • Miscellaneous: Must be taken in evening
66
Q

Fluvastatin (Lescol)

A

(hypolipidemics)

  • Class: HMG-CoA reductase Inhibitors (-statins)
  • Mechanism: Inhibits HMG-CoA reductase formation of mevalonate; leads to activation of SREBP, a membrane-bound transcription factor that increases LDL-R synthesis and lessens degradation; reduction in cholesterol decreases VLDL synthesis, lowering TG
  • Therapeutics: Reduce LDL (20-55%) and TG (25%), while increasing HDL (5-10%); treatment of dyslipidemia (reduces fatal & nonfatal CHD, strokes; total mortality reduction is 20%)
  • Important Side Effects: Very few; hepatic dysfunction in 1% (serious hepatotoxicity rare); myopathy/rhabdomyolysis (reduced if factors inhibiting statin catabolism lacking)
  • Other Side Effects:
  • Miscellaneous: Must be taken in evening
67
Q

Atorvastatin (Lipitor)

A

(hypolipidemics)

  • Class: HMG-CoA reductase Inhibitors (-statins)
  • Mechanism: Inhibits HMG-CoA reductase formation of mevalonate; leads to activation of SREBP, a membrane-bound transcription factor that increases LDL-R synthesis and lessens degradation; reduction in cholesterol decreases VLDL synthesis, lowering TG
  • Therapeutics: Reduce LDL (20-55%) and TG (25%), while increasing HDL (5-10%); treatment of dyslipidemia (reduces fatal & nonfatal CHD, strokes; total mortality reduction is 20%)
  • Important Side Effects: Very few; hepatic dysfunction in 1% (serious hepatotoxicity rare); myopathy/rhabdomyolysis (reduced if factors inhibiting statin catabolism lacking)
  • Other Side Effects:
  • Miscellaneous: Due to longer half-life, can be taken anytime per day
68
Q

Rosuvastatin (Crestor)

A

(hypolipidemics)

  • Class: HMG-CoA reductase Inhibitors (-statins)
  • Mechanism: Inhibits HMG-CoA reductase formation of mevalonate; leads to activation of SREBP, a membrane-bound transcription factor that increases LDL-R synthesis and lessens degradation; reduction in cholesterol decreases VLDL synthesis, lowering TG
  • Therapeutics: Reduce LDL (20-55%) and TG (25%), while increasing HDL (5-10%); treatment of dyslipidemia (reduces fatal & nonfatal CHD, strokes; total mortality reduction is 20%)
  • Important Side Effects: Very few; hepatic dysfunction in 1% (serious hepatotoxicity rare); myopathy/rhabdomyolysis (reduced if factors inhibiting statin catabolism lacking)
  • Other Side Effects:
  • Miscellaneous: Due to longer half-life, can be taken anytime per day
69
Q

Pitavastatin (Livalo)

A

(hypolipidemics)

  • Class: HMG-CoA reductase Inhibitors (-statins)
  • Mechanism: Inhibits HMG-CoA reductase formation of mevalonate; leads to activation of SREBP, a membrane-bound transcription factor that increases LDL-R synthesis and lessens degradation; reduction in cholesterol decreases VLDL synthesis, lowering TG
  • Therapeutics: Reduce LDL (20-55%) and TG (25%), while increasing HDL (5-10%); treatment of dyslipidemia (reduces fatal & nonfatal CHD, strokes; total mortality reduction is 20%)
  • Important Side Effects: Very few; hepatic dysfunction in 1% (serious hepatotoxicity rare); myopathy/rhabdomyolysis (reduced if factors inhibiting statin catabolism lacking)
  • Other Side Effects:
  • Miscellaneous: Due to longer half-life, can be taken anytime per day
70
Q

Ezetimbe (Zetia)

A

(hypolipidemics)

  • Class: Inhibits enterocyte absorption of cholesterol in intestine
  • Mechanism: Decreases LDL-C alone (15-20%) or in combination w/statin (60%)
  • Therapeutics: Inhibits cholesterol absorption by enterocytes in jejunum (70% in mice), leading to less cholesterol in chylomicrons; reduction in chylomicron remnant cholesterol delivery to liver; may also decrease atherogenesis directly (remnants very atherogenic)
  • Important Side Effects: None (rare allergies)
  • Other Side Effects:
  • Miscellaneous: Long-term decrease in endpoints not seen yet (questionable effectiveness)
71
Q

Alirocumab

A

(hypolipidemics)

  • Class: PCSK9 inhibitors
  • Mechanism: Inhibits an endopeptidase (PCSK9) responsible for LDL-R degradation, resulting in higher numbers of LDL-Rs on hepatocytes
  • Therapeutics: 2nd line therapy for hypercholesterolemia not controlled by diet and statins
  • Important Side Effects: Injection site reactions; flu-like symptoms; nose and throat irritation; muscle pain; diarrhea
  • Other Side Effects:
  • Miscellaneous:
72
Q

Evolucumab

A

(hypolipidemics)

  • Class: PCSK9 inhibitors
  • Mechanism: Inhibits an endopeptidase (PCSK9) responsible for LDL-R degradation, resulting in higher numbers of LDL-Rs on hepatocytes
  • Therapeutics: 2nd line therapy for hypercholesterolemia not controlled by diet and statins
  • Important Side Effects: Injection site reactions; flu-like symptoms; nose and throat irritation; muscle pain; diarrhea
  • Other Side Effects:
  • Miscellaneous:
73
Q

Aspirin

A

(angina)

  • Class: NSAID - Antiplatelet agent
  • Mechanism: Irreversible inhibition of COX (thus no TxA2 synthesis), so blocks platelet aggregation
  • Therapeutics: Reduction in adverse events (MI, CVA, death); for those w/stable angina, unstable angina, acute MI, prophylaxis
  • Important Side Effects:
  • Other Side Effects:
  • Miscellaneous: Low-doses; if you’re allergic, you’ll get asthma
74
Q

Ticlopidine (Ticlid)

A

(angina)

  • Class: Thienopyridine antiplatelet agent
  • Mechanism: Inhibits platelet aggregation by ADP; reduces blood viscosity by decreasing plasma fibrinogen and increasing RBC deformability
  • Therapeutics: Aspirin alternative
  • Important Side Effects: Neutropenia and, rarely, TTP
  • Other Side Effects:
  • Miscellaneous: Not really used anymore
75
Q

Clopidogrel (Plavix)

A

(angina)

  • Class: Thienopyridine antiplatelet agent
  • Mechanism: Selectively and irreversibly inhibits ADP binding to P2Y12 (blocks ADP-dependent activation of glycoprotein IIb/IIIa complex)
  • Therapeutics: Great antithrombotic; standard of care w/ stent
  • Important Side Effects: Bleeding
  • Other Side Effects:
  • Miscellaneous: No surgical or dental procedures if patient taking this
76
Q

Prasugrel (Effient)

A

(angina)

  • Class: Thienopyridine antiplatelet agent
  • Mechanism: Irreversibly binds P2Y12 receptor (G protein-coupled chemoreceptor for ADP)
  • Therapeutics: Reduce thrombotic events in those w/percutaneous coronary intervention (e.g., stent)
  • Important Side Effects: Massive bleeding risk
  • Other Side Effects:
  • Miscellaneous: Drug is limited to patients under 75 in age, greater than 60 Kg in weight, and no history of stroke or TIA.
77
Q

Ticagrelor (Brilinta)

A

(angina)

  • Class: Adenosine-like antiplatelet agent
  • Mechanism: Reversibly blocks ADP receptors
  • Therapeutics: Great antithrombic
  • Important Side Effects: Bleeding
  • Other Side Effects:
  • Miscellaneous: Requires bid dosing
78
Q

Dipyradimole (Persantine)

A

(angina)

  • Class: Pyrimido-pyrimidine antiplatelet agent
  • Mechanism: Increases platelet intracellular cAMP (inhibits phosphodiesterase 5, activates adenylate cyclase, inhibits uptake of adenosine from vascular endothelium and RBCs)
  • Therapeutics: Decrease peripheral vascular disease (as an adjunct); stress test of heart
  • Important Side Effects: Vasodilation of coronary arteries can enhance exercise-induced ischemia (because it elevates extracellular adenosine levels)
  • Other Side Effects:
  • Miscellaneous:
79
Q

Cilostazol (Pletal)

A

(angina)

  • Class: Quinoline antiplatelet agent
  • Mechanism: Inhibits cellular phosphodiesterase & so raises intracellular cAMP
  • Therapeutics: Treatment for claudication with peripheral vascular disease
  • Important Side Effects: Vasodilation
  • Other Side Effects:
  • Miscellaneous: Contraindicated in heart failure
80
Q

Fosinopril (Monopril)

A

(angina, inotropic)

  • Class: long-acting ACE inhibitor (vasodilators)
  • Mechanism: Blocks endothelial ACE from converting angiotensin I to angiotensin II (potent vasoconstrictor); as a side effect, also prevents breakdown of bradykinin (potent vasodilator)
  • Therapeutics:
    • Angina & Inotropic: 1st-line for CHF; post-MI (prevents left ventricular remodeling);
      Reduces incidence of future CAD events in patients at risk for/ with vascular disease
  • Important Side Effects: Dry cough, angioedema, hyperkalemia, hypotension, inhibits renal autoregulation
  • Other Side Effects:
  • Miscellaneous:
    • Long-acting;
    • Contraindicated in pregnancy, renal artery stenosis, hyperkalemia, and prior Angioedema (no ARB allowed, either);
    • Caution in renal failure;
81
Q

Isosorbide dinitrate (Isordil)

A

(angina)

  • Class: Vasodilator
  • Mechanism: Endothelium independent vasodilator; endothelial effects (inhibits platelet aggregation, inhibits leukocyte-endothelial interactions (anti-inflammatory))
  • Therapeutics: For acute episodes; long-acting formulations are for those already on other drugs and still can’t control angina
  • Important Side Effects: Tolerance w/chronic use (need nitrate free periods of 8-12 hours), headaches, hypotension, activation of Bezold-Jarisch reflex (causes bradycardia)
  • Other Side Effects: Decrease preload
  • Miscellaneous: Contraindicated in hypertrophic cardiomyopathy, severe aortic stenosis, significant hypotension, use of phosphodiesterase inhibitors
82
Q

Isosorbide mononitrate (Imdur)

A

(angina)

  • Class: Vasodilator
  • Mechanism: Endothelium independent vasodilator; endothelial effects (inhibits platelet aggregation, inhibits leukocyte-endothelial interactions (anti-inflammatory))
  • Therapeutics: For acute episodes; long-acting formulations are for those already on other drugs and still can’t control angina
  • Important Side Effects: Tolerance w/chronic use (need nitrate free periods of 8-12 hours), headaches, hypotension, activation of Bezold-Jarisch reflex (causes bradycardia)
  • Other Side Effects: Decrease preload
  • Miscellaneous: Contraindicated in hypertrophic cardiomyopathy, severe aortic stenosis, significant hypotension, use of phosphodiesterase inhibitors
83
Q

Digoxin (Lanoxin)

A

(inotropic, anti-arrhythmic)

  • Class: Cardiac glycoside, anti-arrhythmic
  • Mechanism: Inhibits Na/K/ATPase (increases contractility d/t more Ca); increases vagal activity to heart (reduces SA firing rate, slows conduction through AV node)
  • Therapeutics: Improves LV function, decreases neurohormonal activation, increases vagal tone, normalizes arterial baroreceptors; decreases hospitalizations in CHF (no mortality benefit);
  • anti-arrhythmic: Atrial fibrillation/flutter, chronic SVT, HF
  • Important Side Effects: Very narrow therapeutic-toxic window (mostly arrhythmias)
  • anti-arrhythmic: Nausea, cognitive dysfunction, blurred or yellow vision
  • Other Side Effects: May cause DAD arrhythmias
  • Miscellaneous: Eliminated in kidneys, so dose according to renal function
84
Q

Dobutamine (Dobutrex)

A

(inotropic)

  • Class: β1 receptor agonist
  • Mechanism: Positive inotrope and chronotrope
  • Therapeutics: Acutely decompensated patients (about half will die after 6 months)
  • Important Side Effects: Quick acting, but can develop tachyphylaxis after 48 hours
  • Other Side Effects:
  • Miscellaneous: No NE release; given IV
85
Q

Milrinone (Primacor)

A

(inotropic)

  • Class: Phosphodiesterase IIIa inhibitor
  • Mechanism: Inhibits cAMP breakdown
  • Therapeutics: Acute setting of heart failure; short-term only
  • Important Side Effects: Increased hypotensive and atrial arrhythmia events acutely. 2 month mortality nearly 50% higher than placebo
  • Other Side Effects:
  • Miscellaneous: Given IV, depends on renal clearance, no tolerance after 72 hours
86
Q

Albuterol

A

(asthma)

  • Class: Bronchodilator - short-acting β2 agonist)
  • Mechanism: Relax bronchial smooth muscle, inhibit mediator release (mast cells, basophils), increase mucociliary clearance, suppression of microvascular permeability
  • Therapeutics: Prevent or reduce exercise-induced bronhospasms; mild asthma & acute exacerbations
  • Important Side Effects: Musculoskeletal tremor, Tachycardia, hyperglycemia, hypokalemia, hypomagnesemia
  • Other Side Effects: Tolerance with chronic use, Prolonged QTc, lactic acidosis, paradoxical bronchospasm
  • Miscellaneous: 5 minutes to take action, 4-6 hours duration; nebulizer delivers more, but greater side effects. Note: Levalbuterol is R-isomer of albuterol.
87
Q

Terbutaline

A

(asthma)

  • Class: Bronchodilator - short-acting β2 agonist)
  • Mechanism: Relax bronchial smooth muscle, inhibit mediator release (mast cells, basophils), increase mucociliary clearance, suppression of microvascular permeability
  • Therapeutics: Prevent or reduce exercise-induced bronhospasms; mild asthma & acute exacerbations
  • Important Side Effects: Musculoskeletal tremor, Tachycardia, hyperglycemia, hypokalemia, hypomagnesemia
  • Other Side Effects: Tolerance with chronic use, Prolonged QTc, lactic acidosis, paradoxical bronchospasm
  • Miscellaneous: 5 minutes to take action, 4-6 hours duration; nebulizer delivers more, but greater side effects. Note: Levalbuterol is R-isomer of albuterol.
88
Q

Metoproterenol

A

(asthma)

  • Class: Bronchodilator - short-acting β2 agonist)
  • Mechanism: Relax bronchial smooth muscle, inhibit mediator release (mast cells, basophils), increase mucociliary clearance, suppression of microvascular permeability
  • Therapeutics: Prevent or reduce exercise-induced bronhospasms; mild asthma & acute exacerbations
  • Important Side Effects: Musculoskeletal tremor, Tachycardia, hyperglycemia, hypokalemia, hypomagnesemia
  • Other Side Effects: Tolerance with chronic use, Prolonged QTc, lactic acidosis, paradoxical bronchospasm
  • Miscellaneous: 5 minutes to take action, 4-6 hours duration; nebulizer delivers more, but greater side effects. Note: Levalbuterol is R-isomer of albuterol.
89
Q

Pirbutal

A

(asthma)

  • Class: Bronchodilator - short-acting β2 agonist)
  • Mechanism: Relax bronchial smooth muscle, inhibit mediator release (mast cells, basophils), increase mucociliary clearance, suppression of microvascular permeability
  • Therapeutics: Prevent or reduce exercise-induced bronhospasms; mild asthma & acute exacerbations
  • Important Side Effects: Musculoskeletal tremor, Tachycardia, hyperglycemia, hypokalemia, hypomagnesemia
  • Other Side Effects: Tolerance with chronic use, Prolonged QTc, lactic acidosis, paradoxical bronchospasm
  • Miscellaneous: 5 minutes to take action, 4-6 hours duration; nebulizer delivers more, but greater side effects. Note: Levalbuterol is R-isomer of albuterol.
90
Q

Salmeterol (Serevent)

A

(asthma)

  • Class: Bronchodilator - long-acting β2 agonist
  • Mechanism: Relax bronchial smooth muscle, inhibit mediator release (mast cells, basophils), increase mucociliary clearance, suppression of microvascular permeability
  • Therapeutics: used for long-term control of asthma symptoms (always in comination with inhaled steroids)
  • Important Side Effects: Musculoskeletal tremor, Tachycardia, hyperglycemia, hypokalemia, hypomagnesemia
  • Other Side Effects: Tolerance with chronic use, Prolonged QTc, lactic acidosis, paradoxical bronchospasm
  • Miscellaneous: 10-15 minutes to take action, 6-12 hours (max) of duration; nebulizer delivers more, but greater side effects; oral is least effective (requires more dose –> side effects); can be used night symptoms, but not ideal
91
Q

Formoterol

A

(asthma)

  • Class: Bronchodilator - long-acting β2 agonist
  • Mechanism: Relax bronchial smooth muscle, inhibit mediator release (mast cells, basophils), increase mucociliary clearance, suppression of microvascular permeability
  • Therapeutics: used for long-term control of asthma symptoms (always in comination with inhaled steroids)
  • Important Side Effects: Musculoskeletal tremor, Tachycardia, hyperglycemia, hypokalemia, hypomagnesemia
  • Other Side Effects: Tolerance with chronic use, Prolonged QTc, lactic acidosis, paradoxical bronchospasm
  • Miscellaneous: 10-15 minutes to take action, 6-12 hours (max) of duration; nebulizer delivers more, but greater side effects; oral is least effective (requires more dose –> side effects); can be used night symptoms, but not ideal
92
Q

Indacaterol

A

(asthma)

  • Class: Bronchodilator - long-acting β2 agonist
  • Mechanism: Relax bronchial smooth muscle, inhibit mediator release (mast cells, basophils), increase mucociliary clearance, suppression of microvascular permeability
  • Therapeutics: used for long-term control of asthma symptoms (always in comination with inhaled steroids)
  • Important Side Effects: Musculoskeletal tremor, Tachycardia, hyperglycemia, hypokalemia, hypomagnesemia
  • Other Side Effects: Tolerance with chronic use, Prolonged QTc, lactic acidosis, paradoxical bronchospasm
  • Miscellaneous: 10-15 minutes to take action, 6-12 hours (max) of duration; nebulizer delivers more, but greater side effects; oral is least effective (requires more dose –> side effects); can be used night symptoms, but not ideal
93
Q

Theophylline (Theolair)

A

(asthma)

  • Class: Bronchodilator (Methylxanthine)
  • Mechanism: Phosphodiesterase inhibition and enhanced signalling via increased cAMP and cGMP; relax bronchial smooth muscle
  • Therapeutics: Reduce inflammation and bronchospasm in moderate to severe asthma, night symptoms
  • Important Side Effects: CNS stimulation or seizures, tachycardia/arrythmias, anorexia, nausea
  • Other Side Effects:
  • Miscellaneous: Low therapeutic index! Metabolized by liver; cimetidine and quinoline increase blood levels
94
Q

Theobromine

A

(asthma)

  • Class: Bronchodilator (Methylxanthine)
  • Mechanism: Phosphodiesterase inhibition and enhanced signalling via increased cAMP and cGMP; relax bronchial smooth muscle
  • Therapeutics: Reduce inflammation and bronchospasm in moderate to severe asthma, night symptoms
  • Important Side Effects: CNS stimulation or seizures, tachycardia/arrythmias, anorexia, nausea
  • Other Side Effects:
  • Miscellaneous: Low therapeutic index! Metabolized by liver; cimetidine and quinoline increase blood levels
95
Q

Caffeine

A

(asthma)

  • Class: Bronchodilator (Methylxanthine)
  • Mechanism: Phosphodiesterase inhibition and enhanced signalling via increased cAMP and cGMP; relax bronchial smooth muscle
  • Therapeutics: Reduce inflammation and bronchospasm in moderate to severe asthma, night symptoms
  • Important Side Effects: CNS stimulation or seizures, tachycardia/arrythmias, anorexia, nausea
  • Other Side Effects:
  • Miscellaneous: Low therapeutic index! Metabolized by liver; cimetidine and quinoline increase blood levels
96
Q

Roflumilast

A

(asthma)

  • Class: Methylxanthine
  • Mechanism: Selective PDE4 inhibitor; more of an anti-inflammatory agent than bronchodilator
  • Therapeutics: COPD
  • Important Side Effects: CNS stimulation or seizures, tachycardia/arrythmias, anorexia, nausea
  • Other Side Effects:
  • Miscellaneous:
97
Q

Ipratropium (Atrovent)

A

(asthma)

  • Class: Quarternary amine antimuscarinic
  • Mechanism: Blocks vagal pathways and decreases vagal tone to bronchial smooth muscle; also blocks the reflex bronchoconstriction caused by inhaled irritants
  • Therapeutics: First-line agent for chronic COPD; status asthmaticus (w/ nebulized β2-agonists); no role in chronic stable asthma
  • Important Side Effects: Typical antimuscarinic effects; acute angle glaucoma; paradoxical bronchospasm
  • Other Side Effects:
  • Miscellaneous: Note: tiotropium has anti-inflammatory properties and decreases mucus secretion.
98
Q

Tiotropium

A

(asthma)

  • Class: Quarternary amine antimuscarinic
  • Mechanism: Blocks vagal pathways and decreases vagal tone to bronchial smooth muscle; also blocks the reflex bronchoconstriction caused by inhaled irritants
  • Therapeutics: First-line agent for chronic COPD; status asthmaticus (w/ nebulized β2-agonists); no role in chronic stable asthma
  • Important Side Effects: Typical antimuscarinic effects; acute angle glaucoma; paradoxical bronchospasm
  • Other Side Effects:
  • Miscellaneous: Note: tiotropium has anti-inflammatory properties and decreases mucus secretion.
99
Q

Atropine

A

(asthma)

  • Class: Quarternary amine antimuscarinic
  • Mechanism: Blocks vagal pathways and decreases vagal tone to bronchial smooth muscle; also blocks the reflex bronchoconstriction caused by inhaled irritants
  • Therapeutics: First-line agent for chronic COPD; status asthmaticus (w/ nebulized β2-agonists); no role in chronic stable asthma
  • Important Side Effects: Typical antimuscarinic effects; acute angle glaucoma; paradoxical bronchospasm
  • Other Side Effects:
  • Miscellaneous: Note: tiotropium has anti-inflammatory properties and decreases mucus secretion.
100
Q

Aclidinium Bromide

A

(asthma)

  • Class: Quarternary amine antimuscarinic
  • Mechanism: Blocks vagal pathways and decreases vagal tone to bronchial smooth muscle; also blocks the reflex bronchoconstriction caused by inhaled irritants
  • Therapeutics: Functionally similar to tiotropium
  • Important Side Effects: Less systemic & CNS side effects than other antimuscarinics due to extremely short circulation half-life.
  • Other Side Effects:
  • Miscellaneous:
101
Q

Budesonide

A

(asthma)

  • Class: Corticosteroid - anti-inflammatory agent
  • Mechanism: Anti-inflammatory effects: inhibition of growth factor secretion, inhibition of arachidonic acid metabolites and platelet activation factor, inhibition of leukocyte accumulation, decreased vascular permeability, inhibition of neuropeptide-mediated responses, inhibition of mucous glycoprotein secretion
  • Therapeutics: Cornerstone treatment of persistent asthma; beneficial comination with beta-2 agonist; limited role in COPD
  • Important Side Effects: Inhaled has thrush, hoarseness, dry cough, mild adrenal suppression (higher doses); oral has mood-swings, increased appetite, and suppression of adrenocorticotropic hormone secretion (Cushing’s Syndrome)
  • Other Side Effects:
  • Miscellaneous:
102
Q

Fluticasone propionate

A

(asthma)

  • Class: Corticosteroid - anti-inflammatory agent
  • Mechanism: Anti-inflammatory effects: inhibition of growth factor secretion, inhibition of arachidonic acid metabolites and platelet activation factor, inhibition of leukocyte accumulation, decreased vascular permeability, inhibition of neuropeptide-mediated responses, inhibition of mucous glycoprotein secretion
  • Therapeutics: Cornerstone treatment of persistent asthma; beneficial comination with beta-2 agonist; limited role in COPD
  • Important Side Effects: Inhaled has thrush, hoarseness, dry cough, mild adrenal suppression (higher doses); oral has mood-swings, increased appetite, and suppression of adrenocorticotropic hormone secretion (Cushing’s Syndrome)
  • Other Side Effects:
  • Miscellaneous:
103
Q

Beclomethasone

A

(asthma)

  • Class: Corticosteroid - anti-inflammatory agent
  • Mechanism: Anti-inflammatory effects: inhibition of growth factor secretion, inhibition of arachidonic acid metabolites and platelet activation factor, inhibition of leukocyte accumulation, decreased vascular permeability, inhibition of neuropeptide-mediated responses, inhibition of mucous glycoprotein secretion
  • Therapeutics: Cornerstone treatment of persistent asthma; beneficial comination with beta-2 agonist; limited role in COPD
  • Important Side Effects: Inhaled has thrush, hoarseness, dry cough, mild adrenal suppression (higher doses); oral has mood-swings, increased appetite, and suppression of adrenocorticotropic hormone secretion (Cushing’s Syndrome)
  • Other Side Effects:
  • Miscellaneous:
104
Q

Ciclesonide

A

(asthma)

  • Class: Corticosteroid - anti-inflammatory agent
  • Mechanism: Same as other corticosteroids, but is a prodrug and only activated by airway esterase.
  • Therapeutics: Cornerstone treatment of persistent asthma; beneficial comination with beta-2 agonist; limited role in COPD
  • Important Side Effects: Less side effects than other corticosteroids (on site activation required)
  • Other Side Effects:
  • Miscellaneous:
105
Q

Sodium cromoglycate

A

(asthma)

  • Class: Anti-inflammatory agent
  • Mechanism: Prevent mast cell degranulation and mediator release from mast cells
  • Therapeutics: Prophylaxis for inhibiting both early and late phase reactions; best results in mild and allergic asthma
  • Important Side Effects: Minimal local side effect (cough & throat irritation)
  • Other Side Effects:
  • Miscellaneous:
106
Q

Nedocromil sodium

A

(asthma)

  • Class: Anti-inflammatory agent
  • Mechanism: Prevent mast cell degranulation and mediator release from mast cells
  • Therapeutics: Prophylaxis for inhibiting both early and late phase reactions; best results in mild and allergic asthma
  • Important Side Effects: Minimal local side effect (cough & throat irritation)
  • Other Side Effects:
  • Miscellaneous:
107
Q

Montelukast (Singulair)

A

(asthma)

  • Class: Leukotriene inhibitor
  • Mechanism: Leukotriene receptor antagonist
  • Therapeutics: Add-on therapy in mild persistent asthma; aspirin-induced asthma; prophylaxis for exercise-induced bronchospasm
  • Important Side Effects: Well tolerated
  • Other Side Effects:
  • Miscellaneous: Must monitor liver function test.
108
Q

Pranlukast (Azlaire)

A

(asthma)

  • Class: Leukotriene inhibitor
  • Mechanism: Leukotriene receptor antagonist
  • Therapeutics: Add-on therapy in mild persistent asthma; aspirin-induced asthma; prophylaxis for exercise-induced bronchospasm
  • Important Side Effects: Well tolerated
  • Other Side Effects:
  • Miscellaneous: Must monitor liver function test.
109
Q

Zafirlukast (Accolate)

A

(asthma)

  • Class: Leukotriene inhibitor
  • Mechanism: Leukotriene receptor antagonist
  • Therapeutics: Add-on therapy in mild persistent asthma; aspirin-induced asthma; prophylaxis for exercise-induced bronchospasm
  • Important Side Effects: Well tolerated
  • Other Side Effects:
  • Miscellaneous: Must monitor liver function test.
110
Q

Zileuton (Zyflo)

A

(asthma)

  • Class: Leukotriene inhibitor
  • Mechanism: Inhibits 5-lipoxygenase and blocks leukotriene synthesis
  • Therapeutics: Add-on therapy in mild persistent asthma; aspirin-induced asthma; prophylaxis for exercise-induced bronchospasm
  • Important Side Effects: Liver toxicity
  • Other Side Effects:
  • Miscellaneous:
111
Q

Omalizumab

A

(asthma)

  • Class: Anti-IgE mAB
  • Mechanism: Blocks IgE function.
  • Therapeutics: Poorly controlled severe asthma
  • Important Side Effects:
  • Other Side Effects:
  • Miscellaneous: Administered by subQ injection every 3 weeks
112
Q

Quinidine

A

(anti-arrhythmics)

  • Class: Class IA anti-arrhythmics
  • Mechanism: Block inward potassium rectifying channel (slow rate) at normal concentrations; blocks sodium channels (fast rate) at high concentrations
  • Therapeutics: Atrial fibrillation/flutter, paroxsymal supraventricular tachycardia, ventricular tachycardia
  • Important Side Effects: QT prolongation; TdP arrhythmias; heart block; hypotension; lupus-like syndrome
  • Other Side Effects: GI symptoms; cinchonism, hepatitis, & thrombocytopenia w/ quinidine; anticholinergic effects w/ disopyramise
  • Miscellaneous:
113
Q

Procainamide

A

(anti-arrhythmics)

  • Class: Class IA anti-arrhythmics
  • Mechanism: Block inward potassium rectifying channel (slow rate) at normal concentrations; blocks sodium channels (fast rate) at high concentrations
  • Therapeutics: Atrial fibrillation/flutter, paroxsymal supraventricular tachycardia, ventricular tachycardia
  • Important Side Effects: QT prolongation; TdP arrhythmias; heart block; hypotension; lupus-like syndrome
  • Other Side Effects: GI symptoms; cinchonism, hepatitis, & thrombocytopenia w/ quinidine; anticholinergic effects w/ disopyramise
  • Miscellaneous:
114
Q

Disopyramide

A

(anti-arrhythmics)

  • Class: Class IA anti-arrhythmics
  • Mechanism: Block inward potassium rectifying channel (slow rate) at normal concentrations; blocks sodium channels (fast rate) at high concentrations
  • Therapeutics: Atrial fibrillation/flutter, paroxsymal supraventricular tachycardia, ventricular tachycardia
  • Important Side Effects: QT prolongation; TdP arrhythmias; heart block; hypotension; lupus-like syndrome
  • Other Side Effects: GI symptoms; cinchonism, hepatitis, & thrombocytopenia w/ quinidine; anticholinergic effects w/ disopyramise
  • Miscellaneous:
115
Q

Lidocaine

A

(anti-arrhythmics)

  • Class: Class IB anti-arrhythmics
  • Mechanism: Block sodium channels in inactivated state mostly; no action on atrial tissue
  • Therapeutics: Digitalis toxicity
  • Important Side Effects: Tremor; nausea; seizures; local anesthetic action
  • Other Side Effects: GI toxicity w/ mexiletine
  • Miscellaneous:
116
Q

Mexiletine

A

(anti-arrhythmics)

  • Class: Class IB anti-arrhythmics
  • Mechanism: Block sodium channels in inactivated state mostly; no action on atrial tissue
  • Therapeutics: Digitalis toxicity
  • Important Side Effects: Tremor; nausea; seizures; local anesthetic action
  • Other Side Effects: GI toxicity w/ mexiletine
  • Miscellaneous:
117
Q

Flecainide

A

(anti-arrhythmics)

  • Class: Class IC anti-arrhythmics
  • Mechanism: Sodium channel blockers (most potent in class I), acting as negative ionotrope
  • Therapeutics: Atrial fibrillation/flutter, paroxsymal supraventricular tachycardia, ventricular tachycardia
  • Important Side Effects: Worsened heart failure, proarrhythmia in ischemic tissue, increased mortality
  • Other Side Effects: Blurred vision w/ flecainide; sinus bradycardia & brochospasm w/ propafenone
  • Miscellaneous:
118
Q

Propafenone

A

(anti-arrhythmics)

  • Class: Class IC anti-arrhythmics
  • Mechanism: Sodium channel blockers (most potent in class I), acting as negative ionotrope
  • Therapeutics: Atrial fibrillation/flutter, paroxsymal supraventricular tachycardia, ventricular tachycardia
  • Important Side Effects: Worsened heart failure, proarrhythmia in ischemic tissue, increased mortality
  • Other Side Effects: Blurred vision w/ flecainide; sinus bradycardia & brochospasm w/ propafenone
  • Miscellaneous:
119
Q

Moricizine

A

(anti-arrhythmics)

  • Class: Class IC anti-arrhythmics
  • Mechanism: Sodium channel blockers (most potent in class I), acting as negative ionotrope
  • Therapeutics: Atrial fibrillation/flutter, paroxsymal supraventricular tachycardia, ventricular tachycardia
  • Important Side Effects: Worsened heart failure, proarrhythmia in ischemic tissue, increased mortality
120
Q

Acebutolol

A

(anti-arrhythmics)

  • Class: Class II anti-arrhythmics - beta blockers (selective)
  • Mechanism: Blocks beta-adrenergic receptors; decrease SA, AV node activity (phase 4 depolarization)
  • Therapeutics: Control of ventricular rate in atrial fibrillation/flutter; long-term suppression of SVTs; PVCs
  • Important Side Effects: Heart block; hypotension, brochospasm; bradycardia
  • Other Side Effects: Contraindicated in WPW
  • Miscellaneous: Decreases mortality in CHF.
121
Q

Sotalol

A

(anti-arrhythmics)

  • Class: Class III anti-arrhythmics
  • Mechanism: K channel blockade = prolongs refractoriness
  • Therapeutics: Atrial fibrillation/flutter, paroxsymal supraventricular tachycardia, ventricular tachycardia
  • Important Side Effects: Torsades de Pointes; QT prolongation, bradycardia; pulmonary fibrosis, peripheral neuropathy, hepatic dysfunction, hypotension, brochospasm
  • Other Side Effects: Photosensitivity (blue-gray skin; numerous drug interactions; N & V w/ dronedarone
  • Miscellaneous:
122
Q

Amiodarone

A

(anti-arrhythmics)

  • Class: Class III anti-arrhythmics
  • Mechanism: K channel blockade = prolongs refractoriness
  • Therapeutics: Atrial fibrillation/flutter, paroxsymal supraventricular tachycardia, ventricular tachycardia
  • Important Side Effects: Torsades de Pointes; QT prolongation, bradycardia; pulmonary fibrosis, peripheral neuropathy, hepatic dysfunction, hypotension, brochospasm
  • Other Side Effects: Photosensitivity (blue-gray skin; numerous drug interactions; N & V w/ dronedarone
  • Miscellaneous:
123
Q

Dofetilide

A

(anti-arrhythmics)

  • Class: Class III anti-arrhythmics
  • Mechanism: K channel blockade = prolongs refractoriness
  • Therapeutics: Atrial fibrillation/flutter, paroxsymal supraventricular tachycardia, ventricular tachycardia
  • Important Side Effects: Torsades de Pointes; QT prolongation, bradycardia; pulmonary fibrosis, peripheral neuropathy, hepatic dysfunction, hypotension, brochospasm
  • Other Side Effects: Photosensitivity (blue-gray skin; numerous drug interactions; N & V w/ dronedarone
  • Miscellaneous:
124
Q

Ibutelide

A

(anti-arrhythmics)

  • Class: Class III anti-arrhythmics
  • Mechanism: K channel blockade = prolongs refractoriness
  • Therapeutics: Atrial fibrillation/flutter, paroxsymal supraventricular tachycardia, ventricular tachycardia
  • Important Side Effects: Torsades de Pointes; QT prolongation, bradycardia; pulmonary fibrosis, peripheral neuropathy, hepatic dysfunction, hypotension, brochospasm
  • Other Side Effects: Photosensitivity (blue-gray skin; numerous drug interactions; N & V w/ dronedarone
  • Miscellaneous:
125
Q

Dronedarone

A

(anti-arrhythmics)

  • Class: Class III anti-arrhythmics
  • Mechanism: K channel blockade = prolongs refractoriness
  • Therapeutics: Atrial fibrillation/flutter, paroxsymal supraventricular tachycardia, ventricular tachycardia
  • Important Side Effects: Torsades de Pointes; QT prolongation, bradycardia; pulmonary fibrosis, peripheral neuropathy, hepatic dysfunction, hypotension, brochospasm
  • Other Side Effects: Photosensitivity (blue-gray skin; numerous drug interactions; N & V w/ dronedarone
  • Miscellaneous:
126
Q

Adenosine

A
  • Class: Anti-arrhythmic
  • Mechanism: Adenosine receptors in atrium, sinus node, AV node; activates K current, shortening AP, hyperpolarizing tissue, and slowing down automaticity and AV conduction
  • Therapeutics: AF, paroxsymal supraventricular tachycardia
  • Important Side Effects: Sedation, dyspnea, hypotension
  • Other Side Effects:
  • Miscellaneous:
127
Q

Magnesium sulfate

A
  • Class: Anti-arrhythmic
  • Mechanism:
  • Therapeutics: Prevents recurrent TdP and some digitalis-induced arrhythmias
  • Important Side Effects:
  • Other Side Effects:
  • Miscellaneous: Alternative to amiodarone for shock-refractory cardiac arrest.

Pharmacology Unit 4 (1 decks)

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