Term
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Definition
| Carbonic Anhydrase Inhibitor -- A: PO and IV -- E: excreted in urine -- Urine Chemistry -- Increased Na+, HCO3-, water, pH, K+, Decreased Cl- -- MOA: Prevents the reabsorption of bicarb. at the proximal tubule - Na+ increases in the urine because H+ is no longer being excreted to combine w/ HCO3- -- Clinical uses: Glaucoma (carbonic anhydrase is important in the production of aqueous humor), Metabolic alkalosis, Alititude sickness -- SE: Paresthesias, Tinnitis, GI upset, Hyperchloremic metabolic acidosis, Neuropathy, Ammonia Toxicity, Sulfa drug allergy |
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Definition
| topical carbonic anhydrase inhibitor |
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Definition
| topical Carbonic Anhydrase inhibitor |
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Term
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Definition
| Loop Diuretic -- A: IV, IM, PO -- DOA: 6-8 hrs -- M: metabolized to a small degree in liver -- E: Metabolite and parent drug excreted in urine -- Urine Chemistry: Increased Na+, Cl-, K+, water, Ca, Mg, Decreased HCO3, and pH -- MOA: Block reabsorption of Na and Cl in the cortex and medullary regions of the ascending loop of henle -- Clinical Uses: Hyperkalemia, Acute hypertension states, Drugs of choice for edematous situations, Acute renal failure, Hypercalcemia, 10 times more efficacious than thiazide diuretics -- SE: Hyperglycemia, Hyperuricemia, Hypocalcemia or hypercalcemia, hypokalemia, Hypokalemic metabolic acidosis, Hyponatremia, Hypomagnesemia, Ototoxicity (reversible tinnitus), Interstitial nephritis |
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Term
| Hydrochlorothiazide (Esidrix) |
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Definition
| Thiazide Diuretic -- A: PO -- DOA: 6-12 hrs -- E: Unchanged in urine -- MOA: Increase urinary and slat output by inhibiting Na and Cl reabsorption in the distal tubule -- Clinical Uses: HTN, CHF, Nephrolithiasis due to hypercalciuria, Diabetes insipidus -- SE: ypercalcemia, Hyperglycemia, Hyperlipidemia, Hypomagnesemia, Hyperuricemia, Hypokalemia, Hyponatremia, Metabolic alkalosis, Muscle weakness, Pancreatitis, Vasodilation |
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Term
| Chlorthalidone (Hygroton) |
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Definition
| Thiazide Diuretic (compound related to thiazide) -- A: PO -- DOA: 48-72 hrs -- E: Unchanged in Urine -- MOA: Increase urinary and slat output by inhibiting Na and Cl reabsorption in the distal tubule -- Clinical Uses: HTN, CHF, Nephrolithiasis due to hypercalciuria, Diabetes insipidus -- SE: ypercalcemia, Hyperglycemia, Hyperlipidemia, Hypomagnesemia, Hyperuricemia, Hypokalemia, Hyponatremia, Metabolic alkalosis, Muscle weakness, Pancreatitis, Vasodilation |
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Term
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Definition
| Thiazide Diuretic (compound related to thiazide) |
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Term
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Definition
| Thiazide-like diuretic used in Tx of CHF -- A: PO -- M: Extensive hepatic metabolism; Rapid absorption -- E: 50% in excreted in the urine, unchanged. There is no accumulation even in the presence of renal insufficiency (an advantage over thiazides) -- MOA: inhibits Na reabsorption at cortical diluting sites, relaxation of blood vessels calcium-channel blockade in smooth muscle cells (a direct antihypertensive effect), no effects on either glucose tolerance or serum lipids -- Clinical uses: CHF, HTN, reduces LVH -- SE: Abdominal pain, diarrhea, orthostatic hypotension, less metabolic side effects than other thiazides |
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Term
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Definition
| Potassium Sparing Diuretic -- A: PO -- M: hepatic metabolism -- E: Parent drug and metabolites excreted in urine -- MOA: Retain K+ and excrete Na+ in the collecting duct but does not work on aldosterone -- Clinical Uses: Increased aldosterone states (Conn's syndrome, ectopic ACTH production, or secondary hyperaldosteronism due to CHF, nephrotic syndrome, or hepatic cirrhosis, Often combined w/ thiazides to threat HTN and prevent hypokalemia -- SE: Hyperkalemia (especially w/ ACE inhibitors, angiotensin receptor blockers, beta blockers, and NSAIDs), CNS depression causing drowsiness, Metabolic acidosis, Nephrolithasis |
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Term
| Spironolactone (Aldactone) |
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Definition
| Potassium Sparing Diuretic (aldosterone antagonist) -- A: PO -- M: metabolized to active metabolites -- E: Majority of metabolites excreted in urine; remaining excreted in feces -- Urine Chemistry: K+ is lower than Na+ -- Blocks the effects of aldosterone in the collecting duct leading to Na+ loss and K+ retention -- Clinical Uses: Increased aldosterone states (Conn's syndrome, ectopic ACTH production, or secondary hyperaldosteronism due to CHF, nephrotic syndrome, or hepatic cirrhosis, Often combined w/ thiazides to threat HTN and prevent hypokalemia -- SE: Hyperkalemia (especially w/ ACE inhibitors, angiotensin receptor blockers, beta blockers, and NSAIDs), CNS depression causing drowsiness, Metabolic acidosis, Gynecomastia |
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Term
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Definition
| Osmotic Diuretic -- A: IV -- M: metabolized to a minor degree in the liver to glycogen -- E: Most is excreted unchanged in the urine -- MOA: Raises solutes in the blood causing hypertonic blood, which draws fluid out of the tissues - Increased plasma volume will deliver more volume to the kidney leading to increased GFR, which leads to increased urinary output -- Clinical Uses: reduction of intraocular pressure or intracranial pressure (CNS trauma w/ swelling and edema), Maintain urinary output for renal protection (ie: rhabdomyolysis or hemolysis), Acute altitude sickness, *Good for head swelling, Bad for heart swelling* -- SE: Transiently causes increased intravascular pressure, which can exacerbate CHF or HTN, Dehydration, Hypernatremia |
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Term
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Definition
| Positive Inotropic agent used in the treatment of CHF -- A: PO -- M: Small amt metabolized in the liver -- E: Majority excreted unchanged in urine -- MOA: Inhibit the Na+/K+ ATPase, leading to an increase in IC Na+, Increase in IC Na leads to a decrease in activity for the Na/Ca exchanger, resulting in an increase in IC Ca. Increase in IC Ca means that the amt of Ca present during an AP is higher, leadeing to a more forceful contraction. Direct electrical effects on the heart include decrease in AP duration, ectopic beats, and arrhythmias -- Clinical uses: Tx of CHF, Therapeutic index in very low (high risk), Digitalis compounds must be administered slowly and in small doses -- SE: Cardiac: AV junctional rhythm, PVC, AV blockade. Non-Cardiac: Nausea, Color vision abnormality, Anorexia, Diarrhea, Disorientation, Gynecomastia, Digoxin levels in plasma double when coadministered w/ quinidine, Hypokalemia can increase the risk of toxicity by worsening arrhythmias. |
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Term
| Inamrinione (Inocor, Amrinone) |
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Definition
| Phosphodiesterase Inhibitor (bipiridine) - used in the tx of CHF -- A: IV -- M: Hepatic metabolism -- E: Parent drug and metabolites excreted in urine and feces -- MOA: Inhibition of PDE leads to an elevation of cAMP. Selective for cardiac isoform of PDE. Bypass receptor so desensitization is avoided (LTU option is prevented by toxicity) -- Clinical Uses: Tx of acute CHF -- SE: Hepatotoxicity, Nausea, Vomiting, Thrombocyopenia |
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Term
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Definition
| Sympathomimetic (Positive Inotropic Agent) used in the Tx of CHF -- A: IV -- M: metabolized in urine and plasma by COMT -- E: Metabolites excreted in urine -- MOA: Leads to an elevation of cAMP and subsequent positive inotropic effects. Low chronotropic -- Clinical Uses: Tx of acute CHF -- SE: Increased HR, BP, Angina |
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Term
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Definition
| Sympathomimetic (Inotropic agents) used for Tx of CHF -- A: IV -- M: Metabolized in liver, kidenys, and plasma by MAO and COMT -- E: metabolites excreted in urine -- MOA: Causes release of NE at the heart, which leads to beta adrenergic stimulation. Stimulates beta 1 receptors. Inhibits NE release in the periphery causing vasodilation -- Clinical Uses: Treatment of acute CHF, acute renal failure, shock, and cardiac arrest -- SE: Dyspnea, Angina, Tachycardia, Headache, Nausea, Vomiting |
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Term
| Ethacrynic Acid (Edecrin) |
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Definition
| Loop Diuretic used in the Tx of CHF -- A: IV and PO -- M: Hepatic Metabolism -- E: Parent drug and metabolite excreted in urine and feces -- MOA: Block reabsorption of Na and Cl in the cortex and medullary regions of the ascending loop of henle -- Clinical Uses: Hyperkalemia, Acute hypertension states, Drugs of choice for edematous situations, Acute renal failure, Hypercalcemia, 10 times more efficacious than thiazide diuretics -- SE: hyperglycemia, Hyperuricemia, Hypocalcemia or hypercalcemia, Hypokalemia, Hypokalemic metabolic acidosis, Hyponatremia, Hypomagnesemia, Ototoxicity, Interstitial nephritis |
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Term
| Hydrochlorothiazide (Esidrix) |
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Definition
| Thiazide Diuretic used in the Tx of CHF -- A: PO -- DOA: 6-12 hrs -- E: Unchanged in urine -- MOA: Increase urinary and salt output by inhibiting Na and Cl reabsorption in the distal tubule -- Clinical Uses: HTN, CHF, Nephrolithiasis due to hypercalciuria, Diabetes Insipidus -- SE: Hypercalcemia, Hyperglycemia, Hyperlipidemia, Hypomagnesemia, Hyeruricemia, Hypokalemia, Hyponatremia, Metabolic alkalosis, Muscle weakness (due to loss of salt), Pancreatitis (dec. insulin release), Vasodilation |
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Term
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Definition
| Thiazide diuretic used for Tx of CHF |
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Term
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Definition
| Thiazide-like diuretic used in Tx of CHF -- A: PO -- M: Extensive hepatic metabolism; Rapid absorption -- E: 50% in excreted in the urine, unchanged. There is no accumulation even in the presence of renal insufficiency (an advantage over thiazides) -- MOA: inhibits Na reabsorption at cortical diluting sites, relaxation of blood vessels calcium-channel blockade in smooth muscle cells (a direct antihypertensive effect), no effects on either glucose tolerance or serum lipids -- Clinical uses: CHF, HTN, reduces LVH -- SE: Abdominal pain, diarrhea, orthostatic hypotension, less metabolic side effects than other thiazides |
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Term
| Spironolactone (Aldactone) |
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Definition
| Aldosterone antagonist (potassium sparing diuretic) used in tx of CHF -- A: PO -- M: Metabolized to active metabolites -- E: Majority of metabolites excreted in urine; remaining excreted in feces -- Urine Chemistry: K is lower than Na -- MOA: Blocks the effects of aldosterone in the collecting duct leading to Na loss and K retention -- Clinical Uses: Increased aldosterone states (Conn's Syndrome, ectopic ACTH production, or secondary hyperaldosteronism due to CHF, nephrotic syndrome, or hepatic cirrhosis), often combined w/ thiazide diuretics to Tx HTN and prevent hypokalemia -- SE: Hyperkalemia (especially with ACE inhibitors, angiotensin receptor blockers, beta blockers, and NSAIDs), CNS depression causing drowsiness, Metabolic acidosis, Gynecomastia |
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Term
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Definition
| Aldosterone antagonist (potassium sparing diuretic) used in Tx of CHF |
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Term
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Definition
| B-type natriuretic peptide used in tx of CHF |
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Term
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Definition
| ACE inhibitor used in the tx of CHF and HTN -- A: PO -- M: Prodrugs converted by liver to active metabolites -- E: In urine -- MOA: Reduce peripheral resistance and, thus, afterload. Reduce aldosterone release, which decreases water and salt retention, thus, decreasing preload. Reduction in angiotensin II can lead to a decrease in sympathetic activity. Reduce long term remodeling of the heart -- Clinical Uses: Long term Tx of CHF, also used in the Tx of HTN. SE: CAPTOPRIL: Cough, Angioedema, Proteinuria, Taste Changes, hypOtension, Pregnancy problems (teratogenic), Rash, Increase renin, Lower angiotensin II |
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Term
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Definition
| ACE inhibitor used in tx of CHF and HTN -- A: IV and PO -- E Unchanged in urine -- MOA: Reduce peripheral resistance and, thus, afterload. Reduce aldosterone release, which decreases water and salt retention, thus, decreasing preload. Reduction in angiotensin II can lead to a decrease in sympathetic activity. Reduce long term remodeling of the heart -- Clinical Uses: Long term Tx of CHF, also used in the Tx of HTN. SE: CAPTOPRIL: Cough, Angioedema, Proteinuria, Taste Changes, hypOtension, Pregnancy problems (teratogenic), Rash, Increase renin, Lower angiotensin II |
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Term
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Definition
| Angiotensin II receptor inhibitor (diuretic) used in tx of CHF and HTN -- A: PO -- M: Extensive first pass hepatic metabolism by P450 system -- E: Parent drug and metabolite excreted in urine and feces -- MOA: Blocks the angiotensin I receptor so that angiotensin II cannot bind and have any effect -- Clinical Uses: HTN, CHF -- SE: Smaller incidence of side effects than ACE inhibitors, No bradykinin increase (no cough, or rash) |
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Term
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Definition
| Selective Beta-1 antagonist (beta blocker) used in the tx of CHF |
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Term
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Definition
| Non selective beta-blocker that also blocks alpha-1 receptors - Membrane stabilizer - MOA: Causes vasodilation and decreases BP w/o causing tachycardia - t1/2 = 6-8 hrs - Tx: HTN, CHF - SE: Bradycardia, Dizziness, Hypotension |
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Term
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Definition
Selective beta-1 blocker
- moderate lipid solubility - low plasma binding - t1/2 = 3-4 hrs - A: PO, IV - ISA: No - MSA: No - MOA: Tx of HTN via decreased HR, CO, contractility, renin release by kidney, and BP via CNS actions, Tx of angina via decreased HR, contractility, heart work, and oxygen consumption, Tx of hyperthyroidism by blocking thyroxin, which causes beta-1 stimulation of the heart - Tx: HTN, Angina, Hyperthyroidism |
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Term
| Sodium Nitroprusside (Nitropress) |
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Definition
| Produces peripheral vasodilation - rapid lowering of blood pressure - Decreased cardiac preload and afterload - used in tx of CHF -- A: IV -- M: Local metabolism by tissues and erythrocytes -- E: metabolites excreted in urine, feces, and exhaled air -- MOA: Dilates arteries and veins -- Clinical Uses: Acute hypertensice emergencies, CHF -- SE: Byproduct of metabolism is cyanide, which is metabolized by the liver by rhondanase to thiocyanate (h2o soluble and excreted in urine), cyanide poisoning in pts w/ poor diets (alcoholics) where it leads to decreased sulfur availability or when administered in high doses for long period of time. Drug is broken down by UV light so IV bag must be wrapped in foil |
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Term
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Definition
| Direct-acting peripheral arteriolar vasodilator - lowering of blood pressure in hypertensive pts and decreased afterload in pts w/ CHF -- A: PO, IM, IV -- M: Extensive first-pass metabolism; hepatic acetylation (remember that certain pt populations have varying rates of acetylation), E: Metabolites excreted in urine -- MOA: Arterial smoothe muscle relaxation and vasodilation (probably through action on cAMP and Ca) -- Clinical Uses: HTN, CHF -- SE: Toxicity in slow acetylators, Tachycardia (reflex), Headache, Dizziness, Nausea, Sweating, Flushing, Nasal Congestion, Lupus like syndrome |
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Term
| Isosorbide dinitrate (Isordil) |
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Definition
| Produces vasodilation (mostly venous) - Decrease in left ventricular end-diastolic pressure and volume (preload)--> reduced myocardial oxygen consumption - Increase coronary blood flow by dilating coronary arteries and improving collateral flow to ischemic regions - used in tx of CHF |
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Term
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Definition
| Calcium Channel Blocker - systemic vasodilation resulting in decreased blood pressure - Coronary vasodilation resulting in decreased frequency and severity of attacks of angina - used in tx of CHF |
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Term
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Definition
| Prolongs action potential and refractory period - inhibits adrenergic stimulation - Slows the sinus rate, increases PR and QT intervals, and decreases peripheral vascular resistance (vasodilation) - Supression of arrhythmias - Used in tx of CHF |
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Term
| Digoxin immune fab (digibind) |
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Definition
| Digitalis antibody - an antibody produced in sheep that binds antigenically to unbound digoxin in serum - Binding and subsequent removal of digoxin, preventing toxic effects in overdose. |
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Term
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Definition
| Class IA Antiarrythmic (Na channel blocker) -- A: PO and IV -- M: Hepatic metabolism -- E: Parent drug and metabolites excreted in urine -- MOA: Inhibit fast Na channel by blocking activated Na channels. Weakly block K channels (reduces repolarization), which increases AP duration (manifests as a lengthening of QT interval) -- Clinical Uses: All type of arrhythmias, Especially useful for A flutter, A fib, and V-tach -- SE: Antimuscarinic activity can suppress vagal tone leading to an increase in AV conduction, which may cause tachycardia and arrythmias. Refractory heterogeneity: depressed conduction can further lead to torsades de pointes and eventual quinidine syncope. Chichonism, Nausea, Vomiting, Digitalis Toxicity: quinidine increases plasma digoxin levels |
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Term
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Definition
| Class IB Antiarrythmic agent -- A: IV,IM -- M: Hepatic Metabolism -- E: Parent drug and metabolites excreted in urine -- MOA: Inhibit both inactive and active Na channels, Act preferentially on depolarized arrhythmogenic tissue, Shorten AP duration -- Clinical Uses: Suppression of recurrnet ventricular tachycardia and fibrillation -- SE: CNS side effects (tramor, light-headedness, nausea of central origen, parasthesias) |
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Term
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Definition
| Class IC Antiarrythmic (Na+ channel blocker) -- A: PO, IV; well absorbed -- M: Hepatic metabolism to inactive metabolites -- E: Parent drug and metabolites excreted in urine -- MOA: Inhibits fast Na channels. Especially effective in hte His-Purkinje system (widens QRS complex), little effect on AP duration -- Clinical Uses: Ventricular arrhythmias, Superventricular arrhythmias, Paroxysmal supraventricular tachycardia, Paroxysmal atrial fib/flutter, Arrythmias associated w/ WPW syndrome -- SE: Prolongation of QRS complex, Proarrhythmic, CNS side effects |
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Term
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Definition
| Class II antiarrythmic (ß blocker) -- A: IV or PO -- MOA: Block sympathetic effects on the heart, Affect primarily the SA and AV nodes, Decrease SA node automaticity and AV node conduction -- Clinical uses: Supraventricular arrhythmia, control of ventricular rate during atrial flutter and fibrillation -- SE: Contraindicated in asthmatic pts, Sudden withdrawal can lead to rebound hypersensitivity. |
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Term
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Definition
| Class II antiarrythmic (Selective beta-1 blocker) - low lipid solubility - low plasma binding - t1/2 = 6-9 hrs - A: PO, IV - ISA: No - MSA: No - MOA: Block sympathetic effects on the heart, Affect primarily the SA and AV nodes, Decrease SA node automaticity and AV node conduction -- Clinical uses: Supraventricular arrhythmia, control of ventricular rate during atrial flutter and fibrillation -- Tx of HTN via decreased HR, CO, contractility, renin release by kidney, and BP via CNS actions, Tx of angina via decreased HR, contractility, heart work, and oxygen consumption, Tx of hyperthyroidism by blocking thyroxin, which causes beta-1 stimulation of the heart - Tx: HTN, Angina, Hyperthyroidism |
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Term
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Definition
| Class III antiarrhthmic (K+ channel blocker) -- A: PO; well absorbed -- E: Unchanged in urine -- MOA: Prolongs AP duration -- Possesses beta blocker and potassium channel activity -- Clinical Uses: Ventricular tachyarrhythmias (especially in post MI and CHF pts), A-fib/flutter, Paroxysmal sepraventricular tachycardia, Arrhythmias associated w/ WPW syndrome -- SE: Bradycardia, bronchospasm, fatigue, torsades de points |
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Term
| Verapamil (Calan, Isoptin) |
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Definition
| Class IV antiarrhythmic (Ca channel blocker) -- A: PO and IV -- M: Extensive first pass hepatic metabolism; metabolized by P450 enzymes to active metabolites -- E: Metabolites excreted in urine and feces -- MOA: Ca channel blocker that effects mainly the SA and AV nodes, Reduces SA node automaticity and AV node conduction -- Clinical Uses: Supraventricular arrhythmias, Ventricular Rate control in atrial flutter and fibrillation -- SE: Contraindicated w/ beta blockers, Bradycardia, Constipation, Decreased cardiac contractility, Hypotension, Lassitude, Nervousness, Peripheral edema -- *strongest cardiac effects (little effects on vessels)* |
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Term
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Definition
| Class IV antiarrythmic (Ca+ channel blocker) -- A: PO and IV -- M: Extensive first pass metabolism; metabolized by P450 enzymes to less active metabolites -- E: Excreted in urine and feces -- MOA: Ca channel blocker that effects mainly the SA and AV nodes, Reduces SA node automaticity and AV node conduction -- Clinical Uses: Supraventricular arrhythmias, Ventricular Rate control in atrial flutter and fibrillation -- SE: Bradycardia, Decreased cardiac contractility, Hypotension -- *Effects are equal between cardiac and vascular* |
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Term
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Definition
| antiarrythmic drug -- A: IV -- M: Adenosine to Inosine to AMP (inactive) -- MOA: slows conduction in the AV node and thereby interupts "Re-entry Pathways" through AV node, Ventricular slowing is not blocked by atropine but may be blocked by caffeine, Enchanced K conductance and inhibition of cAMP induced Ca influx -- Clinical Uses: Paroxysmal Supraventricular Tachycardia, WPW syndrome, only effective against arrhythmias that depend on reentry mechanism -- SE: flushing, shortness of breath, chest burning, bronchospasms, headache, hypotension, nausea, paresthesia -- Contraindications: A-V block, Sick sinus syndrome -- DOC for PSVT because of high efficacy and short duration of action |
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Term
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Definition
| Antiarrhythmic drug -- A: IV -- MOA: unknown -- Clinical uses: Digitalis induced arrhythmias, Torsades de pointes, Management of seizures and/or HTN seizures associated w/ sever toxemia of pregnancy (eclampsia) |
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Term
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Definition
| Antiarrhythmic -- Tx is aimed at normalizing K levels (hypo and hyper kalemias both lead to arrhythmias) -- inc serum K decreases (depolarizes) resting potential, thus, has a membrane stabilizing action by inc K permeability |
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Term
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Definition
| Antihypertensive (alpha 2 agonist) -- A: PO and IV -- M: Hepatic metabolism -- E: Parent drug and metabolites excreted in urine -- MOA: Believed to work in the relay area of the solitary nucleus. Act as alpha 2 receptor agonist to reduce sypathetic tone to peripheral structures (decrease peripheral resistance, HR, and plasma renin activity) -- Clinical Uses: Hypertension, CHF -- SE: Plasma volume in increased (body's attempt to reestablish homeostasis) leading to mild edema, Sedation, dizziness, and headache (diminish as tolerance develops), Mild Bradycardia, Flu-like symptoms w/ fever, Lupus like syndrome, Positive Coombs' test w/ no increase in hemolytic anemia |
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Term
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Definition
| Antihypertensive (alpha 2 agonist) -- A: PO and transdermal patch (good for noncompliant pts; provides steady state blood levels, also fewer side effects) -- M: 50% hepatic metabolism -- E: Majority excreted unchanged in urine -- MOA: Believed to work in the relay area of the solitary nucleus. Act as alpha 2 receptor agonist to reduce sypathetic tone to peripheral structures (decrease peripheral resistance, HR, and plasma renin activity) -- Clinical Uses: HTN, As effective as methyldopa but requires smaller doses, CHF -- SE: High dose will cause interaction w/ alpha 1 receptors leading to vasoconstriction and increased BP. Drowsiness, dizziness, and headache (subside w/ tolerance). Plasma volume in increased (body's attempt to reestablish homeostaisis) leading to mild edema. Mild bradycardia, Xerostomia, Constipation. Patch can cause itching, irritation, and redness. |
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Term
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Definition
| Antihypertensive (Peripheral acting sympatholytic) -- A: PO -- E: Unchanged in urine -- MOA: Non-depolarizing ganglionic blocker. Competitive inhibhitor of Ach at nicotinic receptors on postganglionic autonomic neurons. Blocks sympathetic ganglia causing vasodilation and decreased HR -- Clinical Uses: HTN (numerous SE's preclude its common use) -- SE: CNS side effects (convulsions, mental changes, tremors, confusion), Hypotension |
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Term
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Definition
| Antihypertensive (Adrenergic blocker) -- A: PO -- M: Hepatic metabolism -- E: Parent drug and metabolites excreted in urine -- MOA: Replaces NE bound to ATP in vesicles. Results in decreased NE released w/ nerve stimulation. Leads to reduced arteriolar vasoconstriction -- Clinical Uses: Moderate to severe HTN -- SE: Angina, Edema (peripheral and pulmonary), Fatigue, Severe diarrhea |
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Term
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Definition
| Antihypertensive (Selective alpha 1 antagonist) -- A: PO -- M: Hepative metabolism to active metabolites -- E: parent drug and metabolites excreted in bile and feces -- MOA: alpha adrenergic blockade leads to decreased systemic vascular resistance, results in decreased BP -- Clinical Uses: HTN, BPH, Cause less reflex tachycardia than non-selective alpha blockers -- SE: First dose orthostatic hypotension (can lead to syncope) requires careful dosing (usually before bed), dizziness, drowsiness, headache, peripheral edema, palpitations |
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Term
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Definition
| Antihypertensive (Selective alpha 1 antagonist) -- A: PO -- M: Hepative metabolism to active metabolites -- E: parent drug and metabolites excreted in bile and feces -- MOA: alpha adrenergic blockade leads to decreased systemic vascular resistance, results in decreased BP -- Clinical Uses: HTN, BPH, Cause less reflex tachycardia than non-selective alpha blockers -- SE: First dose orthostatic hypotension (can lead to syncope) requires careful dosing (usually before bed), dizziness, drowsiness, headache, peripheral edema, palpitations |
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Term
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Definition
| Antihypertensive (Selective alpha 1 antagonist) -- A: PO -- M: Hepative metabolism to active metabolites -- E: parent drug and metabolites excreted in bile and feces -- MOA: alpha adrenergic blockade leads to decreased systemic vascular resistance, results in decreased BP -- Clinical Uses: HTN, BPH, Cause less reflex tachycardia than non-selective alpha blockers -- SE: First dose orthostatic hypotension (can lead to syncope) requires careful dosing (usually before bed), dizziness, drowsiness, headache, peripheral edema, palpitations |
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Term
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Definition
| Non selective beta-blocker - moderate lipid solubility - t1/2 = 3-4 hrs - A: PO - ISA: yes (high) MOA: Has intrinsic sympathomimetic activity - Tx: HTN, Angina.....the risk of bradycardia may be lower, also don't affect plasma lipids as much as other beta blockers |
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Term
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Definition
| Non-selective beta blocker w/ selective alpha-1 blocking -- A: PO, IV -- M: Hepatic metabolism -- E: Parent drug and metabolites excreted in urine and feces -- MOA: Nonselective beta-blocker (predominant activity) w/ selective alpha 1 blocker activity. Decreases HR, decreases plasma renin activity, and increases plasma volume (beta-blockade). Decreases PVR (alpha blockade). Alpha blocker activity counteracts vasoconstriction that leads to cold toes and fingers that is associated w/ beta-blockers -- Clinical Uses: HTN -- SE: Postural hypotension, Dizziness, nausea, fatigue |
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Term
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Definition
| Antihypertensive (vasodilator) -- A: PO, IM, IV -- M: Extensive first pass hepatic metabolism; hepatic acetylation (remember that certain patient populations have varying rates of acetylation) -- E: Metabolites excreted in urine -- MOA: Arterial smooth muscle relaxation and vasodilation (probably through action of cAMP and Ca) -- Clinical Uses: HTN, CHF -- SE: Toxicity in slow acetylators, tachycardia, headache, dizziness, nausea, sweating, flushing, nasal congestion, lupus like syndrome |
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Term
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Definition
| Antihypertensive (vasodilator) -- A: PO and topical -- M: hepatic metabolism -- E: Metabolites excreted in urine -- MOA: Inhibits PDE leading to increased levels of cAMP, which through Ca modulation leads to arterial smooth muscle relaxation and vasodilation -- Clinical Uses: HTN, Alopecia -- SE: Tachycardia, massive fluid retention, hypertrichosis, ECH changes, pericarditis |
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Term
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Definition
| Antihypertensive (direct acting vasodilator) -- A: PO or IV -- M: Partial hepatic metabolism -- E: Parent drug and metabolites excreted in urine -- MOA: Decreases PVR via direct vasodilatory effect on smooth muscle in peripheral arterioles. -- Clinical Uses: Acute hypertensive emergencies, Hypoglycemia (secondary to hyperinsulinemia via inhibition of insulin release) -- SE: reflex tachycardia |
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Term
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Definition
| Antihypertensive (direct acting vasodilator) -- A: IV -- M: Hepatic -- MOA: Specific agonist on Dopamine 1 receptors (D 1), postsynaptic D1 receptor stimulation relazes arterial smooth muscleDecreases PVR via direct vasodilatory effect on smooth muscle in peripheral arterioles. -- Clinical Uses: Acute hypertensive emergencies, Hypoglycemia (secondary to hyperinsulinemia via inhibition of insulin release) -- SE: reflex tachycardia, headache, flushing |
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Term
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Definition
| Antihypertensive (Calcium channel blocker, and angiotensin antagonist) -- A: PO -- M: Extensive first-pass metabolism; metabolized by P450 enzymes to inactive metabolites -- E: In urine and feces -- MOA: Block voltage sensitive calcium channels located primarily in the cardiac muscle and in vascular smooth muscle causing decrease in IC Ca. Also block cyclic nucleotide PDE, which increases cGMP and decreases Ca influx. Results in dilation of peripheral arterioles and venules -- Clinical Uses: HTN, Angina -- SE: Peripheral edema, hypotension, palpitations due to reflex tachycardia, Dizziness, headaches, constipation, nausea, abdominal cramps -- *strongest vasodiltor (little cardiac effects)* |
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Term
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Definition
| Antihypertensive (Calcium channel blocker, and angiotensin antagonist) -- A: PO -- M: Extensive first-pass metabolism; metabolized by P450 enzymes to inactive metabolites -- E: In urine and feces -- MOA: Block voltage sensitive calcium channels located primarily in the cardiac muscle and in vascular smooth muscle causing decrease in IC Ca. Also block cyclic nucleotide PDE, which increases cGMP and decreases Ca influx. Results in dilation of peripheral arterioles and venules -- Clinical Uses: HTN, Angina -- SE: Peripheral edema, hypotension, palpitations due to reflex tachycardia, Dizziness, headaches, constipation, nausea, abdominal cramps -- *strongest vasodiltor (little cardiac effects)* |
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Term
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Definition
| Antihypertensive (Calcium channel blocker, and angiotensin antagonist) -- A: PO -- M: Extensive first-pass metabolism; metabolized by P450 enzymes to inactive metabolites -- E: In urine and feces -- MOA: Block voltage sensitive calcium channels located primarily in the cardiac muscle and in vascular smooth muscle causing decrease in IC Ca. Also block cyclic nucleotide PDE, which increases cGMP and decreases Ca influx. Results in dilation of peripheral arterioles and venules -- Clinical Uses: HTN, Angina -- SE: Peripheral edema, hypotension, palpitations due to reflex tachycardia, Dizziness, headaches, constipation, nausea, abdominal cramps -- *strongest vasodiltor (little cardiac effects)* |
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Definition
| Phosphodiesterase 5 inhibitor (antianginal) -- A: PO -- M: hepatic cytochrome P450 CYP3A4 -- MOA: PDE5 inhibitor, cGMP inhibitor -- Clinical Uses: Impotence, angina, pulmonary HTN -- SE: headache, flushing, dyspepsia, nasal congestion, urinary tract infection, transient color tinge to vision, photophobia, blurred vision -- Contraindications: Pregnant or lactating women, infants, children, anyone taking nitrates or nitrites |
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Term
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Definition
| Phosphodiesterase 5 inhibitor -- faster onset than other 2 -- less visual side effects than Sildenafil |
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Definition
| Phosphodiesterase 5 inhibitor -- Duration of action up to 24-36 hrs -- less visual side effects than sildenafil |
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Term
| Cholestryamine (Questran) |
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Definition
| Bile acid sequestrant -- A: PO -- E: Drug/bile acid complex is excreted in feces -- MOA: Anion exchange resin that binds bile acids in the intestine and prevents reabsorption. Reduction in bile acid reabsorption results in an increase in production of bile acids from cholesterol in the liver. This increased demand for cholesterol by the liver increases the expression of LDL receptors by the liver. LDL is cleared from the plasma more quickly due to the increased population of receptors -- Clinical Uses: Greatest effect is seen at lowest doses of the drug. Decreases LDL 10-30%. Increases HDL 2-4% . Increases VLDL-TG levels by 5-30%. No effect on Lp(a) -- SE: Abdominal pain, bloating, constipation, pancreatitis, interference w/ absorption of fat soluble vitamins (A,E,D,K). Binds to HMG-CoA reductase inhibitors |
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Term
| Nicotinic Acid (Niacin, Nicobid) |
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Definition
| Antihyperlipidemic -- A: PO; rapidly absorbed -- M: Extensive first pass hepaatic metabolism -- E: Metabolites and parent drug excreted in urine -- MOA: Decreases the production of VLDL, Increases circulating levels of HDL, Decreases Lp(a) -- Clinical Uses: Decreases LDL 10-25%, Decreases VLDL-TG 50%, Increases HDL 30-40% -- SE: Acanthosis nigricans, aggravation of asthma, atrail arrhythmias, cutaneous flushing, gastritis/ulcer disease, glucose intolerance, hepatitis, hyperurecemia, Increased risk of hepatotoxicity at dose required for sustained release formula: adjust dose when switching from sustained release form to normal form. |
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Definition
| Antihyperlipidemic (HMG-CoA reductase Inhibitor) -- A: PO; well absorbed -- M: Extensive first pass hepatic metabolism -- E: Parent drug and metabolites excreted in urine and feces -- MOA: Inhibits HMG-CoA reductase, the enzyme required for cholesterol synthesis. Increased production of LDL receptors in the liver, Increased uptake of LDL from the plasma, Decreases VLDL secretion -- Clinical Uses: Decreases LDL 20-50%, Decreases TG 10-20%, Increases HDL 5-10%, no effect on Lp(a) -- SE: Elevated liver transaminases (3 times normal), Headaches, Myopathy (uncommon and dose dependant), Cataracts (unproven) |
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Definition
| Antihyperlipidemic (Fibric Acid Derivatives) -- A: PO; well absorbed -- M: Hepatic metabolism -- E: Parent drug and metabolites excreted in urine -- MOA: Unknown but may increase the activity of LP lipase, thereby increasing the catabolism of VLDL. May inhibit lipolysis of stored fat and decrease hepatic extraction of free fatty acids. Stimulate the production of Apo A-1, the major protein component of HDL -- Clinical Uses: Decreases VLDL 50-55%, Decreases LDL < 10%, Increases HDL 20%, May decrease platelet reactivity and aggregability and concentration of fibrinogen -- SE: Alopecia, decreased libido, drowsiness, GI distress, Lithogenicity of bile, Myositis, neutropenia, weight gain, LTU can lead to increased gall bladder toxicity, increased appendectomies, and potential risk for human carcinogenesis |
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Definition
| Antihyperlipidemia (Inhibitor of cholesterol absorption) |
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Definition
| Partial fatty-acid oxidation (PFox) inhibitor -- A: PO -- M: Hepatic by CYP3A and to lesser extent CYP2D6, and is a substrate of P-glycoprotein -- E: 75% excreted in urine, 25% excreted in feces -- MOA: partial fatty acid oxidation (PFox) inhibitor, inhibits late inward sodium current, decreases left ventricular wall stiffness, improves coronary circulation -- Clincial Uses: Chronic Stable Angina in pts who don't respond to other anti-anginal meds -- SE: Dizziness, headache, constipation, nausea, vomiting -- Contraindications: Hypokalemia, QT prolongation, renal failure, torsade de pointes, ventricular arrhythmias, ventricular tachycardia |
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Term
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Definition
| Endothelin-receptor antagonist -- only indicated in severe pulmonary HTN -- Specific and competitive antagonist for both type A and B endothelin-1 receptors -- associated w/ high frequency of elevated hepatic enzymes, potential teratogen, multiple drug interactions, admin PO, M: CYP2C9 and CYP3A4 |
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Term
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Definition
| Class III antiarrythmic (prolong repolarization, K channel blocker) -- A: IV and PO; slow GI absorption; long period to reach steady state -- M: Hepatic metabolism to active metabolite -- E: Excreted by lacrimal glands, skin, and biliary tract -- MOA: Prolongs AP duration by blocking K channels. Does not effect conduction velocity. Blocks Na channels. Some beta blocker activity. Coronary and peripheral vasodilator -- Clinical Uses: Ventricular tachyarrhythmias (especially post MI and CHF pts). Atrial Fib/Flutter. Paroxysmal supraventricular tachycardia. Arrhythmias associated w/ WPW syndrome. -- SE: Pulmonary fibrosisi, hypothyroidism or hyperthyroidism, paresthesias/tremor, Torsades de pointes |
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