Term
| Acetazolamide: Chemical structure |
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Definition
a sulfonamide derivative
***any drug like this can cause Stevens Johnson syndrome** |
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Term
| Class of drug: Acetazolamide |
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Definition
| Carbonic Anhydrase inhibitor |
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Term
| Primary site of action and Mechanism of action: Acetazolamide |
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Definition
Primary site of action: proximal tubule
Mechanism of action: Inhibition of both membrane-bound and cytoplasmic carbonic anhydrase has an overall effect of inhibiting NaHCO3 reabsorption and promoting NaHCO3 diuresis |
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Term
| Toxicity, adverse reactions, and contraindications of CA inhibitors (Acetazolamide) |
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Definition
By reducing the Na-H exchange, there is an increased excretion of Na and bicarbonate without a significant excretion of Cl, resulting in mild hyperchloremia and a metabolic acidosis
Urinary alkalinization can lead to precipitation of calcium phosphate, which may lead to kidney stones
Increased K excretion due to increased lumen electronegativity in the collecting duct system
Sulfonamide allergic hypersensitivity reactions
contraindicated in hepatic cirrhosis
these drugs also inhibit CA in other tissues (eye, stomach, CNS)....CA is involved in production of aqueous humor and in the CNS its involved in CSF production...so maybe some effects there?? |
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Term
| Besides its use as a diuretic...other uses of Carbonic anhydrase inhibitors |
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Definition
treatment of Glaucoma---it inhibits CA there, decreaseing aqueous humor formation
providing relief from Mtn sickness--causes metabolic acidosis
Treatment of epilepsy
Urinary alkalinization
Creection of metabolic acidosis |
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Term
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Definition
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Term
| Pharmacokinetics: Mannitol |
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Definition
| Mannitol is administered IV and REMAINS in the extracellular compartment and does not cross the BBB...it is filtered by the glomeruli (no tubular secretion), with minimal tubular resorption |
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Term
| Mechanism of action: Mannitol |
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Definition
| Mannitol can increase the osmotic pressure of the glomerular filtrate, leading to a decreased reabsorption of water (and solutes) in nephron segments that are freely permeable to water |
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Term
| Therapeutic uses of Osmotic diuretics (4) |
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Definition
Oliguric acute renal failure: in acute renal failure, when pt experiencing oliguria...Mannitol can get at least SOME urine flow going
Reduction of intraocular and intracranial pressure --by increasing plasma osmotic pressure
urinary excretion of toxins/overdose treatment/prevention of renal toxicity--iduces urinary excretion in overdose situations and eliminate toxins
can be used alone or in combination with other diuretics to treat peripheral edemas of nephrotic, cirrhotic, and cardiac origins |
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Term
| Contraindication: osmotic diuretics (Mannitol) |
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Definition
| Osmotic diuretics extract water from peripheral intracellular stores and this increases the extracellular fluid volume...in patients with pulmonary congestion due to heart failure this effect can lead to more pulmonary edema |
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Term
| Class of drug: Furosemide |
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Definition
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Term
| Class of drug: Ethacrynic Acid |
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Definition
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Term
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Definition
| a phenoxyacetic acid derivative |
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Term
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Definition
A sulfonamide derivative
**Watch out for Stevens Johnson syndrome!!!** |
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Term
| Pharmacokinetics: Loop Diuretics |
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Definition
| These drugs are bound to plasma proteins which limits their delivery to the tubules by filtration..they are instead secreted by the proximal tubule via the organic acid secretion mechanism |
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Term
| Location of action and Mechanism of action: loop diuretics |
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Definition
The loop diuretics act in the thick ascending limb of the loop of Henle where they block the Na-K-2Cl symporter in the apical membrane
They result in enhanced excretion of not only Na, K, Cl...but also H+, Ca, Mg, ammonium, and possibly phosphate |
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Term
| Therapeutic uses of loop diuretics |
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Definition
Congestive heart failure and acute pulmonary edema
Hypertension--but thiazides preferred bc of loop diuretics short half lives
Hypercalcemia (indirectly increase calcium excretion by abolishing the driving force for paracellular reabsorption of calcium
Edema of nephrotic syndrome
Edema with liver cirrhosis
Drug overdose
Hyponatremia (paradoxical) |
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Term
| Toxicity, adverse reactions, and contraindications of Loop Diuretics |
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Definition
Profound fluid and electrolyte depletion (hypotension, hypovolemia, hyponatremia)
hypochloremic metabolic alkalosis
hypokalemia
GOUT: decreased excretion of uric acid and hyperuricemia (competition for organic acid secretory mechanism in proximal tubule, and increased reabsorption of uric acid in the proximal tubule due to diuretic-induced hypovolemia)
ototoxicity (more common with ethacrynic acid)
sulfonamide allergic hypersensitivity reactions (Furosemide, NOT Ethacrynic acid)
hyperglycemia
increased plasma levels of LDL cholesterol and triglycerides
hypomagnesia
contraindicated in patients with anuria
can increase plasma lithium and cause lithium toxicity
NSAIDS decrease their effectiveness |
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Term
| Class of Drug: Hydrochlorothiazide |
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Definition
| thiazide and thiazide-like diuretic |
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Term
| Class of Drug: Chlorothiazide |
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Definition
| Thiazide and Thiazide-like diuretic |
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Term
| Class of Drug: Chlorthalidone |
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Definition
| Thiazide and Thiazide-like diuretic |
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Term
| Class of Drug: Indapamide |
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Definition
| Thiazide and Thiazide-like Diuretic |
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Term
| Chemistry: Thiazide and Thiazide-like diuretics |
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Definition
| Like the carbonic anhydrase inhibitors, these have an unsubstituted sulfonamidegroup ...these drugs are derivatives of benzothiazide |
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Term
| Pharmocokinetics: Thiazide diuretics |
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Definition
| secreted by the organic acid secretory system in the proximal tubule, and then filtered |
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Term
| MOA: Thiazide Diuretics...does it depend on acid/base balance? |
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Definition
Thiazide diuretics inhibit the Na/Cl symporter in the early distal convoluted tubule promoting NaCl excretion and water diuresis
** this effect is INDEPENDENT of patient's acid/base balance |
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Term
| Therapeutic uses of Thiazide diuretics |
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Definition
mild/moderate edema of heart failure
treat HTN ...but this effect diminished when GFR decreased (Indapamide might still work)
Might be useful in prevention of nephrolithiasis and osteoporosis (by enhanced resorption of calcium)
used in nephrogenic diabetes insipidus
used in ascites due to liver cirrhosis |
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Term
| Toxicity/adverse reactions of Thiazide diuretics |
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Definition
Hypokalemia and metabolic alkalosis due to increased excretion of potassium and hydrogen in the late distal tubule and cortical collecting duct
Gout: decreased excretion of uric acid and hyperuricemia due to competition for the organic acid secretory mechanism in proximal tubule, and increased uric acid resorption due to diuretic -induced hypovolemia
because contain an unsubstituted sulfonamide group--Stevens-Johnson syndrome!!
Can induce hyperglycemia (be careful in Diabetics!!!)
INcrease plasma LOL, total cholesterol, and total triglycerides...Indapamide does NOT do this though!!
fatal hyponatrimia (extrememly rare!!)
Lithium clearance reduced--so lithium toxicity |
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Term
| Class of drug? Tiamterene |
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Definition
| K sparing diuretic (inhibitors of renal Na channels) |
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Term
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Definition
| K sparing Diuretic (inhibitors of renal Na channels) |
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Term
| Mechanism of Action and effectiveness: K Sparing diuretics (inhibitors of renal Na channels) |
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Definition
Block luminal Na channels in the principal cells of the collecting ducts...this decreases Na entering the principal cell, which decreases activity of the Na/K pump on the basolateral membrane and therefore decreases K entering the cell and thus less K leaving the cell in urine
Because the lumen of the collecting duct is more positive (more Na in it) there is also LESS H secretion by the intercalated cells of the collecting duct system
**Since the collecting duct system only reabsorbs 3% if the filtered load of Na and Cl, these agents are NOT powerful diuretics |
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Term
| Therapeutic uses: K Sparing diuretics (inhibitors of renal Na channels) |
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Definition
Because of limited diuretic capacity, these agents are mostly used in combination with other diuretics (thiazide, loop) to treat edema (CHF, hepatic cirrhosis, hyperaldosteronism) and HTN
Used to counterbalance the hypokalemia caused by thiazide and loop diuretics
Can be used to treat Liddle's syndrome (pseudohyperaldosteronism) by blocking sodium channels
Cystic fibrosis treatment |
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Term
| Toxicity/adverse reactions: K sparing diuretics (inhibitors of renal Na channels) |
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Definition
can induce life-threatening hyperkalemia, which can lead to cardiac arrhythmias and muscle weakness...are contraindicated in hyperkalemic patiens and with the use of K supplements)
Tiamterene is poorly soluble and may precipitate kidney stones |
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Term
| Contraindications: K sparing diuretics (inhibitors of renal Na channels) |
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Definition
Amiloride and Triamterene should NOT be administered with aldosterone receptor blockers (ex: spironolactone) due to rik of life-threatening hyperkalemia
Should be used with caution with blockers of the RAAS |
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Term
| Pharmacokinetics of Spironolactone |
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Definition
| Spironolactone is a synthetic steroid which is partially absorbed orally and extensively metabolized in the liver |
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Term
| Class of drug? Spironolacatone |
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Definition
| K sparing diuretic (Aldosterone receptor blockers) |
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Term
| Class of drug? Eplerenone |
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Definition
| K sparing diuretic (Aldosterone receptor blockers) |
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Term
| Class of Durg? Drospirenone |
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Definition
| K sparing diuretic (Aldosterone receptor blockers) |
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Term
| Mechanism of Action of Spironolactone, Eplerenone, and Drospirenone..what is their clinical efficacy determined by? |
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Definition
Antagonists at mineralcorticoid receptors...binding to the receptor prevents aldosterone-induced gene transcription
Clinical efficacy of these drugs is determined by the levels of endogenous aldosterone
Effects of Aldosterone in the collecting duct system: increased luminal Na conductance out of the lumen to inside of cells, increased basolateral Na/K ATPase activity, and thus increased secretion of K and H...soooo aldosterone BLOCKERS decrease Na conductance out of the lumen, decrease basolateral Na/K ATPase and decrease the secretion of K (decreasing lumen electronegativity)
Drospirinone is a progestin that is derived from Spironolactone. It retains aldosterone receptor antagonist activity, and as a result has a diuretic effect...this diuretic effect may help counterbalance the fluid retaining effect of ethinyl estradiol in Yasmin, a combination oral contraceptive |
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Term
| Therapeutic uses of K Sparing diuretics (Aldosterone receptor blockers) |
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Definition
As with amiloride and tiramterene, spironolactone and eplerenone are usually administered WITH a loop diuretic or thiazide diuretic to treat edema (CHF, hepatic cirrhosis) and hypertension...helps by reducing edema fluid and preventing hypokalemia
Spironolactone and eplerenone are effective in treating hyperaldosteronism |
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Term
| Toxicity/ adverse reactions and contraindications of K-Sparing diuretics (aldosterone blockers) |
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Definition
can induce life threatening hyperkalemia (cardiac arrhythmias , muscle weakness) and are contraindicated in hyperkalemic patients and with the use of K supplements
Are contraindicated with use of another K sparing diuretic
Have Antiandrogen effects (gynecomastiz, decreased libido, impotence in males, menstrual irregularities in women)...spironolactone is a nonselective aldosterone receptor antagonist and interacts with other steroid receptors such as progesterone and androgen receptors...Eplerenone is considered a more selective antagonist at just mineralcorticoid receptors, and unlike spironolactone it appears not to interact with androgen receptors, glucocorticoid recptors, or progesterone receptors
Use with CAUTION with drugs that block the RAAS due to increased risk of hyperkalemia |
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Term
| Class of drug? Desmopressin acetate |
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Definition
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Term
| Chemistry: Desmopressin acetate |
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Definition
| a synthetic polypeptide, similar in structure to vasopressin, avaliable in nasal, oral, and perenteral administration forms |
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Term
| MOA: Desmopressin acetate |
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Definition
increases water reabsorption by the collecting duct system in the kidney..this involves binding of desmopressin to the 7-transmembrane G-protein coupled V2 vasopressin receptor on the basolateral membrane of renal epithelial cells in the collecting duct...net result is an increase in cAMP and an increase in the insertion of water channels in the apical membrane of epithelial cells
Desmopressin has greater antidiuretic activity than vasopressin itself but LESS cardiovascular vasopressor activity compared to vasopressin |
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Term
| Therapeutic uses of Desmopressin acetate |
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Definition
| Nocturnal enuresis (bedwetting) due to central diabetes insipidus |
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Term
| Toxiticy of Desmopressin acetate |
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Definition
| water intoxication...so use with caution in patients with angina, HTN and heart failure |
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Term
| Use of Thiazides for treatment of HTN |
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Definition
| Thiazides and thiazide-like diuretics may be the most popular drugs for therapy of chronic primary HTN...often recommended for initial therapy...they differ in duration of action, which can influence side effects |
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Term
| MOA: Thiazide antihypertensives |
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Definition
| initially induce a natiuresis, which shrinks blood volume thus reducing cardiac output...this activates mech. responsible for maintenance of fluid volume, particularly the renin-angiotensin-aldosterone system, which may then limit the degree of volume reduction and the degree of decreased BP....buuuut continued use leads to a fall in peripheral vascular resistance (and return of CO towards normal, within 6-8 weeks), which is the reason for continued antihypertensive effect...this second effect may be due to an autoregulatory phenomenon and/or to direct relaxant actions of the drugs on vascular smooth muscle |
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Term
| Considerations for dosing and populations to prescribe: Thiazide antihypertensives |
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Definition
| Most thiazides can only achieve a 10mmHg fall in diastolic BP maximally. They have a fairly FLAT dose-response curve for lowering BP, so that most of the antihypertensive effect is achieved with low to intermediate doses...those with more volume-dependent HTN (lower plasma renin) tend to respond WELL...these include many African Merican and elderly hypertensive patients...also thiazide diuretics are used widely in combination with other antihypertensive drugs |
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Term
| Resistance to Thiazide Diuretics |
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Definition
| a poor response may reflect either and overwhelming load of dietary Na or an intrinsically impaired renal capacity to excrete Na to begin with....overly vigorous diuretic therapy may activate the RAAS excessively,,,and thereby the antihypertensive effect of the diuretic may be antagonized too much by the vasoconstrictive effect of angiotensin and aldosterone-mediated exchange of K for Na (tending to retain Na and waste more K)...whe severe hypertensives are given more drugs (particularly direct vasodilators, the reduction in BP by the latter mechanism may lead to intense Na retention, mandating the use of additional diuretic |
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Term
| Side Effects of the use of thiazides for HTN |
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Definition
Hypokalemia (K wasters): can lead to muscular weakness, leg cramps, increase in ventricular ectopic activity, sudden cardiac death...this side effect can be minimized by use of SMALL doses and only moderately long-acting diuretics...by combining K sparers with the diuretic and/or adding drugs that suppress the RAAS..and my increasing dietary Na intake
Hypercholesterolemia
Glucose intolerance with hyperglycemia |
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Term
| use/indication of loop diuretics as antihypertensive agents |
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Definition
use loop diuretics in patients that require more powerful diuretics than thiazides
are primarily indicated for patients with reduced renal Na excretory function where Thiazides are ineffectual or where there is other need for more powerful diuretics, as for example with direct vasodilator therapy which can cause much Na and water retention |
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Term
| what is an example of a loop diuretic used to treat HTN and how is it dosed? |
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Definition
| Furosemide! must be given 2-3x per day to maintain the shrinkage of plasma volume needed to keep BP down |
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Term
| Use of K-Sparing diuretics as antihypertensives |
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Definition
Those recieving a thiazide or loop diuretic may be protected from K wastage by combined use of a K-Sparing agent...several are now avalialable: aldosterone antagonists and others
Have limited natriuretic and BP lowering effectiveness on their own, except for the aldosterone antagonists (Spironolactone and Eplerenone) |
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Term
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Definition
| adrenergic neuron inhibitors: peripheral neuronal inhibitors |
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Term
| MOA, length of action: Reserpine |
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Definition
| depletes storage of the peripheral neurotransmitter NE in vesicles of sympathetic nerve endings, thereby reducing the amount of NE release with each nerve impulse. This reduces BP by decreasing both CO and peripheral resistance. This depleting action on NE vesicles is IRREVERSIBLE and thus the BP lowering effect may persist for some time after stopping the drug |
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Term
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Definition
sedation and mental depression likely due to same action on CNS neurotransmitters...can precipitate migraines...also nasal congestion, postural hypotension, bradycardia, and systemic fluid retention
diarrhea and exacerbation of peptic ulcers due to unopposed parasympathetic neural effects in the GI tract |
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Term
| Class of drug: Methyldopa |
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Definition
| adrenergic neuron inhibitor/central neuron inhibitor |
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Term
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Definition
| adrenergic neuron inhibitor/central neuron inhibitor |
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Term
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Definition
a prodrug which is converted into methylnorepinephrine which then accumulates in NE storage vesicles and when released from them acts as an alpha2adrenergic agonist in the central vasomotor centers, dampening sympathetic neural outflow
**RARELY used since newer, better tolerated agents have come out...major current use is in the treatment of HTN during pregnancy bc wont harm fetus |
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Term
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Definition
peripheral fluid retention and centrally-mediated sedation and dry mouth
induces "autoimmune" disorders and may cause parkinsonian signs (possible due to accumulation of methyldopamine in the CNS dopamine neurons...this is NOT seen with the other central alpha2 drugs) |
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Term
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Definition
| accumulates in NE storage vesicles and when released from them acts as an alpha2adrenergic agonist in the central vasomotor centers, dampening sympathetic neural outflow...may also influence CNS imidazoline receptors |
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Term
| Route of administration: Clonidine |
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Definition
| oral but also in a PATCH! for many primary hypertensives, the patch provides smoother BP control with fewer side effects, although may show local skin reactions |
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Term
| what happens when you stop Clonidine quickly |
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Definition
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Term
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Definition
| Adrenergic receptor inhibitor: alpha1-receptor blocker |
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Term
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Definition
| Adrenergic receptor inhibitor: alpha1-receptor blocker |
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Term
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Definition
| Adrenergic receptor inhibitor: alpha1-receptor blocker |
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Term
| MOA: Doxazosin, prazosin, and terazosin |
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Definition
| Block arterial vascular alpha-1-receptors, competitively inhibiting binding of sympathetically-released NE, blunting the vasoconstriction normally produced by that NE and decreasing BP as well as TPR...similar effects in vv too...some say initial reduction in BP due to dilation of both resistance and capacitance vessels |
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Term
| Considerations in dosing of doxazosin, prazosin, and terazosin |
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Definition
The initial dose of any alpha-1 blocker may cause severe postural hypotension...particularly in those already taking a diuretic....can be minimized by giving a low dose of the drug initially, take first dose around bedtime or on a day where pt can lie around....stop taking their diuretic for two days before starting first dose
Prazosin must be taken at least 3x per day, whereas longer-acting doxazosin and terazosin can be given once daily |
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Term
| Side effects: Doxazosin, Prazosin, and terazosin |
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Definition
| Beyond severe first dose postural hypotension...some pts continue to experience postural dizziness...aggrevation of stress-induced urinary incontinence in elderly women...reflex tachycardia and systemic fluid retention |
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Term
| Other beneficial effects:Doxazosin, Prazosin, and terazosin |
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Definition
| may improve glucose tolerance, plasma cholesterol and trig. levels may be lowered and HDL may be raised |
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Term
| MOA: nonselective beta-blockers with NO intrinsic sympathomimetic activity (ISA) |
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Definition
| lower the arterial BP mainly by reducing cardiac output (decreasing contractility and possibly decreasing heart rate)...inhibit release of renin from renal JG cells |
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Term
| effectiveness: nonselective beta-blockers with NO intrinsic sympathomimetic activity (ISA) |
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Definition
| unfortunately, they also remove the normal physiologic level of beta2-mediated vasodilation in those peripheral vessels that contain significant numbers of beta2 receptors....the removal of such vasodilatory influence tends to offset the decrease in total peripheral vascular resistance expected from inhibition of renin release...thus limiting the overall antihypertensive effectiveness |
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Term
| effectiveness: nonselective beta blockers WITH intrinsic sympathomimetic activity |
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Definition
| lower BP without quite as much reduction in cardiac contractility (and rate) and renin levels BUT with a notable decrease in total peripheral resistance by partially stimulating vascular beta2 receptors! |
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Term
| distribution throughout body: nonselective beta blockers |
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Definition
| the more lipid soluble, the more they are taken up and metabolized on the first pass though the liver, and the more that enters the brain...Those that are less lipid soluble generally remain unmetabolized and are more likely excreted through the kidneys...also less enters the brain, thus fewer CNS side effects, patient compliance better |
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Term
| Clinical effectiveness of Beta blockers in various patient goups |
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Definition
When used alone, beta blockers are somewhat LESS effective in elderly and African American patients, because of lower plasma renin levels...also Chinese patients may be more sensitive to these drugs and require lower doses
Beta blockers esp. useful in patients with HTn assoc with tachycardia and high CO, and HTN accompanied by other cardiovascular conditions which can also be treated with beta blockers (angina, arrythmia) |
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Term
| Side effects: beta-receptor blockers |
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Definition
CARDIOVASCULAR
beta-blockers with little or no ISA can cause considerable bradycardia...those who monitor physical activity by heart rate should be made aware that maximal heart rate will be about 20%lower...conditioning can still be achieved but reduced exercise ability and easier fatigue are often noted...though less so with ISA beta-blockers
Beta blockers with littler or no ISA can also Slow A-V conduction and supress ventricular contractility too much...rebound HTN may occur with sudden withdrawl of beta-blocker therapy
PULMONARY
Bronchoconstriction may occur with nonselective agents due to inhibition of airway B2 receptors (esp a problem in those who need to inhale beta2 agonists to maintain open airways
if beta2 agonist bronchodilators are required, obviously they will be more effective in the presence of a more cardioselective beta-blocker
METABOLIC
Diabetics need to use these with great caution because they might get a more severe and longer in duration in the presence of especially nonselective beta blockers
mask tachycardia warning sign in those with hypoglycemia...sweating NOT diminished though!! Tell diabetics to pay attn to that!
insulin resistance with glucose intolerance notable in some hypertensives may be further aggravated by beta-blockers, as it is in diabetics
Hypertriglyceridemia and a fall in HDL-cholesterol
CENTRAL
Bad dreams, even hallucinations...but much less likely with lipid insoluble agents |
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Term
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Definition
| adrenergic receptor inhibitor: combined alpha-1 and beta receptor blocker |
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Term
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Definition
| The Beta-blocking action involves both beta-1 and beta-2 receptors..the alpha-blocking action involves only alpha-1 receptors....the BP falls mainly from a decrease in peripheral resistance (alpha-1 block) but with some decrease in cardiac output and renin too |
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Term
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Definition
| Orally, Labetalol is used primarily for treatment of MORE SEVERE degrees of primary HTN....intravenously, it is useful in those who have a need for rapid reduction of markedly elevated blood pressure (hypertensive emergency) |
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Term
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Definition
Some Side effects are largely related to the alpha-blockade (postural dizziness which beta blockade cannot correct)
Other side effects are largely due to the beta blockade: bradycardia, A-V block at high doses...obv, little chance of reflex tacycardia otherwise expected with regular alpha-1 blockers |
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Term
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Definition
| adrenergic receptor inhibitor: NO-releasing beta-1 receptor blocker |
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Term
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Definition
| Beta1-blocking action decreases renin release, HR and contractility...the increase in endothelial NO avaliability dilates vascular smooth muscle...thus, a decrease in BP is due to a vasodilator effect (lower TPR0 as well as a lower cardiac output |
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Term
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Definition
Good for hypertensive patients with impaired endothelial cell function
Generally considered good for mild to moderate primary HTN |
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Term
| Class of drug: Hydralazine |
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Definition
| selective arteriolar vasodilator |
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Term
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Definition
| Selective arteriolar Vasodilator |
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Term
| MOA:Hydralazine and minoxadil |
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Definition
They decrease arterial BP by decreasing TPR through directly dilating arterioles (NOT big arteries or any vv)...Hydralazine induces release of NO from the arteriolar endothelium, and Minoxadil acts via a sulfate metabolite which can open ATP-sensitivee K channels in arteriolar smooth muscle cells
**Since Hydralazine is partly inactivated by acetylation in the liver, "rapid" acetylators in the population show SMALLER drug effects than "slow" acetylators |
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Term
| Side effects: Hydralazine and minoxidil |
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Definition
ALONE, these drugs markedly dilate resistance arterioles leading to increased capillary hydrostatic pressure with increased filtration of fluid into interstitial spaces plus renal retention of Na and H2O..fall in arterial BP markedly activates sympathetic and renal compensatory mechanisms causing considerable release of catecholamines and renin resulting in stimulatoin of the heart and much more rtetention of Na and water
Side effects: tachycardia, edema, loss of antihypertensive efficacy...concimmitant use of beta blocker and diuretic ...these compensatory reactions can be inhibited and BP will fall more efficaciously
Also hydralazine can cause a LUPUS-LIKE REACTION
Minoxidial can cause considerable hair growth |
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Term
| Clinical uses: Hydralazine and Minoxidil |
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Definition
Often previously chosen as the third drug for those NOT responding adequately to a diuretic and an adrenergic inhibitor or other "second choice" drug ...however use as such has been going away in the face of other vasodilators with fewer side effects
Minoxidil also reserved for pts with most severe hypertension, particularly when renal insufficiency is present...very good renal dilator |
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Term
| Class of drug: Amlodipine |
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Definition
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Term
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Definition
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Term
| Class of Drug: Felodipine |
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Definition
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Term
| Class of Drug: Nifedipine |
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Definition
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Term
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Definition
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Term
| chemical structure of calcium channel blockers |
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Definition
| except for diltiazem and verapamil, all CCB are dihydropyridines in structure....most are inactivated by the liver |
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Term
| MOA: Calcium Channel blockers |
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Definition
most of the dihydropyridine CCB lower BP largely by reducing calcium entry into arterial vascular smooth muscle cells through arterial L-type calcium channels...the decrease in free intracellular calcium reduces arterial vascular tone...thus TPR and BP fall
Diltiazem and especially Verapamil act largely in the heart to supresss cardiac output mainly by reducing ventricular contractility by decreasing calcium entry through ventricular L-type calcium channels
Dihydropyridines have little supressive effec upon ventricular contractility at std. therapeutic doses which readily inhibit the arterial vascualr calcium channels enough to lower BP ...some say also have intrinsic natriuretic capability |
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Term
| Clinical use and dosage considerations of CCBs |
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Definition
CCB drugs are effective antihypertensives in virtually all types of primary systemic HTN ...reduce BP particularly well in elderly and African American patients...work well in the face of high Na intake...irrespective of the degree of Na sensitivity of the patient
Nifedripine has also been approved to treat primary pulmonary HTN
The older CCBs were originally avaliable in only rapid, short-acting forms requiring 3 doses per day for a sustained 24-hr effect...now they are avaliable in slow-release formulation (for longterm use, slower longer actions have proven to be safer than rapid shorter actions |
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Term
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Definition
Differ considerably...reflecting diferent effects at different sites (reflexly increased heart rate due to peripheral vasodilation vs. directly suppressedheart rate and AV conduction
Most common side effects: slight postural dizziness, ankle edema, tachycardia (dihydropyridines)
Ankle edema may be so cosmetically bothersome as to preclude the use of these drugs
**Verapamil is MOST likely to cause real serious myocardial depression like excessive bradycardia and excessive AV nodal dysfuction
Rapid, short-acting dihydropyridine preps should be avoided for longterm use because record of too many M.I.s, likely induced by excessive rapid reflex increases in cardiac sympathetic nn activity |
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Term
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Definition
| Angiotensin Converting Enzyme (ACE) Inhibitor |
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Term
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Definition
| Angiotensin Converting Enzyme (ACE) Inhibitor |
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Term
| Class of Drug: Lisinopril |
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Definition
| Angiotensin Converting Enzyme (ACE) Inhibitor |
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Term
| Class of Drug: Fosinopril |
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Definition
| Angiotensin Converting Enzyme (ACE) Inhibitor |
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Term
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Definition
| Angiotensin Converting Enzyme (ACE) Inhibitor |
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Term
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Definition
| Angiotensin Converting Enzyme (ACE) Inhibitor |
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Term
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Definition
| Angiotensin II Receptor Blockers (ARBs) |
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Term
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Definition
| Angiotensin II Receptor Blockers (ARBs) |
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Term
| Class of Drug: Candesartan |
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Definition
| Angiotensin II Receptor Blockers (ARBs) |
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Term
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Definition
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Term
| Mode of administration and Pharmacokinetics: ACE inhibitors |
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Definition
Oral ACE inhibitors came along first...
Captopril is the prototype ACE inhibitor
Enalapril is a prodrug that is activated by deesterification to enalaprilat
Lisinopril is an active derivatice to enalaprilat
Foinopril, quinapril, and ramipril are long acting members of the class and all prodrugs activated primarily b the liver
**Many ACE inhibitors are eliminated primarily in the kidneys, so doses should be reduced in patients with renal insufficiency
Fosinopril has a balanced route of elimination which shifts toward the liver in the presence of renal impairment (SMART drug) |
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Term
| Pharmacokinetics: Losartan |
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Definition
| While the half life of Losartan is short, an ACTIVE METABOLITE persists long enough to permit 24-h BP control with 1 dose |
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Term
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Definition
ACE Inhibitors block the conversion of Angiotensin 1 into Angiotensin 2, the active form...thus A-II-mediated vasoconstriction is overcome and total arterial peripheral resistance and BP falls...also A-II mediated synthesis of aldosterone is inhibited, thereby Na and H2O retention is reduced
ACE Inhibitors also prevent ACE mediated inactivation of Bradykinin and related prostaglandin vasodilators...so MORE Bradykinin and PG vasodilators lead to MORE vasodilation and even LOWER BP by decreased peripheral vascular resistance |
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Term
| MOA: ARBs (Angiotensin Receptor Blockers) |
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Definition
| ARBs block AII from binding to its main receptor, preventing the vasoconstricting action of A-II and lowering BP |
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Term
| Clinical uses and who shouldn't get them: ARBs and ACE Inhibitors |
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Definition
ALL RAAS inhibitors should work in "normal renin" as well as "high renin" patients with primary HTN...also good for those with HTN secondary to diabetic nephropathy since these drugs can also relieve their pre-existing harmfully high glomerular capillary pressures by reducing the powerful constrictor effect of A-11 on the renal EFFERENT arterioles
Recomended by some that only SMALL doses of these drugs should be given as initial therapy in those suspected of HIGH renin primary hypertension since they might experience a precipitous FIRST DOSE hypotension when the support of BP by the high levels of A-11 are acutely removed
NOT recommended for pts with fully established bilateral renovascular HTN ...where abnormally "super" high levels of A-II maintain renal GFR beyond the stenoses by constricting the efferent arterioles..may experience MORE loss o GFR with these drugs |
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Term
| Side Effects: ACE Inhibitors and ARBs |
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Definition
Some Side effects may be related to extended therapeutic effects of some of these drugs (hyperkalemia and too much hypotension)
higher bradykinin levels with ACE inhibitors may cause a nonproductive cough
Angioedema is an uncommon but serious (potentially fatal) reaction that has been reported with various ACE inhibitors and may not occur as much with ARBs or the renin inhibitor |
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Term
| Drug interactions to avoid with ACE inhibitors and ARBs |
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Definition
any hyperkalemia may become worse with addition of a K-Sparing diuretic or K supplements
Nonsteroidal anti-inflammaroty drugs may impair the antihypertnsive effects of ACE inhibitors by blocking bradykinin-mediated vasodilation |
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Term
| Class of Drug: Nitroglycerin |
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Definition
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Term
| Class of Drug: Isosorbide Dinitrate |
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Definition
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Term
| Class of Drug: Nifedipine |
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Definition
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Term
| Class of Drug: Amlodipine |
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Definition
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Term
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Definition
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Term
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Definition
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Term
| Class of Drug: Propranolol |
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Definition
| Beta adrenergic blocker (beta1 and beta2) |
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Term
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Definition
| Beta-adrenergic blocker (beta1 and beta2) |
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Term
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Definition
| Beta-adrenergic blocker (beta1 and beta2) |
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Term
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Definition
| Beta-adrenergic Blocker (Beta-1 only) |
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Term
| Class of Drug: Metoprolol |
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Definition
| Beta-Adrenergic BLocker (beta-1 only) |
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Term
| Pharmacokinetics/ mech of dosage: Nitroglycerin, isosorbide dinitrate, Amyl nitrite |
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Definition
Nitroglycerin is avaliable in ofrms that provide a WIDE range of durations of action from minutes to hours...because of the treatment of acute anginal attacks after onset and the prevention of attacks BEFORE onset are both important aspects of therapy...the pharmacokinetics of the diff dosage forms are thought of as very clinically significant
Nitroglycerin is rapidly denitrated in the liver, first to dinitrate, which like nitroglycerin has significant therapeutic effects, and then to mononitrate, which is much less active.
Because of the high activity of the responsible enzyme in the liver, the first-pass effect for nitroglycerin is HIGH...thus, efficacy of oral nitroglycerin probably results from high levels of glyceryl dinitrate in the blood...the effects of sublingual nitroglycerin are mainly the results of the unchanged drug
After nitroglycerin...isosorbide dinitrate is the most extensively used
Amyl nitrite is a volatile and rapidly acting nitrate that was once used to treat angina by inhalation |
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Term
| MOA/Selectivity: Nitrates |
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Definition
The nitrates rapidly "become" nitric oxide in the presence of smooth muscle cells (more in the presence of some SM cells than others) and this immediately increases intracellular production of cGMP which leads immediately to SM cell relxation
venous SM is more sensitive than arterial and larger arteries more than smaller
SM relaxatino leads to extensive peripheral vascular dilation which results in reduced cardiac work through reduced preload (at low, common doses) and reduced afterload (at high, less common doses)
Indirectly, this rapidly reduces myocardial cell tension and thus oxygen demand...thus, the primary mechanism of therapeutic benefit by the nitrates in atherosclerotic angina is reductino in the cardiac oxygen demand, not necessarily an increase in coronary flow...however both may be important in relief of vasospastic angina particularly if the drug's dose is high enoug
NO can also inhibit plt aggregation |
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Term
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Definition
Can be used to treat all 3 major types of angina....is a common form for treatment of acute anginal pain after it starts is the sublingual tablet, which has a duration of action of approx. 10-30 minutes
Oral nitroglycerin has a duration of approx. 2-4 hours...for preventative treatment, sustained release forms have a longer duration
Some transdermal formulations can maintain blood levels for 18-24 hours |
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Term
| Adverse effects: Nitrates |
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Definition
The most common side effects of nitrates are extensions of their therapeutic effects...related to responses evoked by vasodilators:
Orthostatic hypotensive symptoms
throbbing HA from pulsating meningeal vasodilation
too much increase in heart rate and contractility which can compromise therapeutic goal
systemic sodium and water retention
Tolerance can develop with continuous exposure to nitrates...possibly related is rebound angina in some patients upon abruptly stopping drug after sufficient length of continuous use
Potentially fatal hypotensive interaction with Viagra and other cGMP-inactivating Phosphodiesterase-5 inhibitors used to treat erectile dysfunction in men |
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Term
| 2 major types of calcium channel blockers |
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Definition
1.) Diltiazem and Verapamil:both act largely in the heart
2.) Nifedipine and other dihydropyridines which act largely in the arterial tissue
Differ markedly in structure, but all are active orally and many have rapid, short actions unless prepared as slow-release formulations...Amlodipine is intrinsically long acting..most inactivated by the liver |
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Term
| MOA and Selectivity: CCB drugs |
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Definition
These block voltage-dependent calcium channels, especially the L-type calcium channels in cardiac muscle (verapamil and diltiazem) and in arterial vascualr smooth muscle ( dihydropyridines)...by decreasing calcium influx, they reduce the avaliability of intracellular free calcium and thereby reduce calcium functions in those specific tissues
Cardiac cells are highly dependent on transmembrane calcium influx for various normal functions (rate and contractility) Thus, verapamil and diltiazem reduce cardiac rate and contractility, the main way by which they reduce the cardiac oxygen demand in patients with angina
Nearly all types of smooth muscle cells are highly dependent on transmembrane calcium influx for normal resting tone and contractile functions...but the cells of vascular smoothe muscle appear to be the most sensitive and other dihydropyridines...moreover, aa are more sensitive than vv...thus, a reduction in after load is the main way by which dihydropyridines benefit the patient with atherosclerotic angina (reduce their cardiac demand)...but also, vasospasm in a coronary a. can be reversed by some dihydropyridines
Finally, some CCBs can inhibit plt aggregation |
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Term
| Clinical use: CCBs as antianginals |
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Definition
| All these drugs are effective as preventative treatment in all forms of angina...dihydropyridines are also used to treat acute anginal attack after its onset |
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Term
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Definition
many are direct extensions of therapeutic actions
Very short acting dihydropyridines cause reflex increases in cardiac activities that might be especially excessive and dangerous |
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Term
| MOA and selectivity: Beta Blocking Drugs used for antianginal effects |
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Definition
| at cellular level...all are competative antagonists of the beta-adrenergic receptor...largely act on the Beta receptors in the SA node and ventricles of the heart...actions include several beneficial effects (decreased heart rate, cardiac contractility, and arterial blood pressure...reducing oxygen demand) |
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Term
| Clinical Use: Beta-Blocking Drugs |
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Definition
Primarily used as preventative treatment of angina...especially in exercise-induced angina in the stable atherosclerotic patient
Also useful in treating "silent" angina
Also used in combo with the nitrates to prevent the reflex effects evoked by the nitrates |
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Term
| Adverse effects: Beta-Blocking Drugs |
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Definition
Many adverse effects are extensions of the peripheral beta receptor blockade--sinus bradycardia, AV blockade
Beta blockers shouldn't be discontinued abruptly as their sudden withdrawl may precipitate a rebound angina (or even a MI)
High heart rate as a warning of severe hypoglycemia to an insulin overdose may be masked
CNS adverse effects include sedation, fatigue, and sleep alterations. Atenolol and nadolol have less marked CNS action because they do not enter the CNS as readily as other beta-blockers (less lipid soluble) |
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Term
| Classification: Ranolazine |
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Definition
| New oral agent tentatively classified as a fatty acid oxidation inhibitor |
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Term
| Two proposed MOA of Ranolazine |
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Definition
1.) Shifting the source of fuel used by the myocardium from fatty acid to glucose, which demands less oxygen to produce an equivalent amt of energy for contraction...thus, increased efficiency of oxygen utilization by the heart...least likely mech
2.) more likely: selective inhibition of increased "late" inward-directed sodium current caused by myocardial ischemia |
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Term
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Definition
| Used often in combo with other antianginal agents or alone for patients still suffering from symptoms of chronic stable angina despite taking other agents |
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Term
| Adverse effects: Ranolazine |
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Definition
| high concentrations can prolong the cardiac QT interval, thus it is contraindicated with paitents with preexisting cardiac QT prolongation or those taking QT-prolonging drugs |
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Term
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Definition
| Cholesterol Absorption inhibitor |
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Term
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Definition
Selectively inhibits absorption of dietart and biliary cholesterol across the brush border of the small intestineal epithelial cells..theoretically does so by inhibiting a specific protein-mediated transport system on or withing the brush border membrane of the intestinal walls
less cholesterol delivered by chylomicrons and chylomicron remnants to the liver=reduced delivery of intestinal cholesterol to the liver=increased cholesterol biosynthesis and increased LDL receptors on the hepatic membranes |
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Term
| Therapeutic uses: Ezetimibe |
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Definition
| used alone or in combo with other drugs (often statins) in treatment of mostly high LOL-type hyperlipoproteinemias |
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Term
| Pharmacokinetics of Ezetimibe |
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Definition
| long duration of action...rapid uptake by intestinal wall cells..converted to an active glucuronide metabolite in the small intestinal walls and in the liver where recycled back into the intestinal lumen via biliary system--> this enterohepatic recirculation presents MORE active metabolite to these intestinal cells for inhibiting more cholesterol absorption |
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Term
| Adverse reactions/Interactions of Ezetimibe |
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Definition
diarrhea and abdominal pain (in intestine)
slightly greater risk of liver enzymes in serum |
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Term
| Cholestyramine Class of Drug |
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Definition
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Term
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Definition
in the intestine, resins exchange chloride for bile acids...unlike free bile acids, the bile-acid-resin complex is not functional and cannot be resorbed...as a result MORE cholesterol must be converted to bile acid and secreted by the liver into the intestine=liver starts to synthesize more cholesterol and increases hepatic LDL receptors
**INITIALY, VLDL synthesis and release into the plasma may be increased for a variable length of time in some patients |
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Term
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Definition
| resins are used along with diet and other drugs for treatment of mostly high LDL type hyperlipoproteinemias...have little->no benefit in treatment of the other types...may aggravate some other types by raising plasma VLDL |
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Term
| Pharmacokinetics: Cholestyramine |
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Definition
| ORAL administration, obviously...are NOT metabolized but excreted directly into the feces |
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Term
| Adverse reacitons: cholestyramine |
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Definition
| because not absorbed they do NOT cause systemic toxicity....G.I. adverse reactions are common...bloating, mild nausea, constipation, fecal impartation, and epigastric distress...not very palatable |
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Term
| Drug and Nutrient interactions: Cholestyramine |
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Definition
Bile acid binding resins can sequester and inhibit absorption of many other drugs--thiazide diuretics, abx, barbituates, and ezetimbe and certain statins...interference with fat soluble vitamin and iron absorption
at very high doses, cause wt loss by malabsorption of various other nutrients |
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Term
| Class of Drug: Lovastatin |
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Definition
| HMG-CoA Reductase inhibitor--commonly called "statins"-the PROTOTYPE drug for this class!!! |
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Term
| MOA: Lovastatin (and other statins!) |
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Definition
the LIVER is the main site of action where the statins inhibit HMG CoA reductase which catalyzes the conversion of HMG-CoA to mevolonate, and early rate limiting step in the biosynthesis of cholesterol...By inhibiting its synthesis and output in the liver, the statins reduce overall systemic availability of circulating endogenous cholesterol....accordingly the statins indirectly induce the liver and other peripheral tissues to increase the number of LDL receptors on their cell membranes...
may also increase HDL levels slightly more than ezetimibe and resins (mech. unclear) |
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Term
| Therapeutic uses: Lovastatin |
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Definition
| MOST EFFECTIVE DRUGS AT LOWERING LDL CHOLESTEROL!!!!!! they are primarily indicated alone or as an adjunct to diet or other drugs for the reduction of elevated LDL cholesterol...other antiatherosclerotic benefits include anti-inflammatory action |
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Term
| Pharmacokinetics of Lovastatin (and other statins) |
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Definition
Oral administration...extensive FIRST PASS hepatic metabolism for most statins, which can be inhibited by a variety of other drugs and lots of GRAPEFRUIT JUICE!!!
most statins are excreted in the feces by secretion in the bile
PRAVASTATIN is active as ingested, but Lovastatin, Simvastatin and most others are PRODRUGS which require ACTIVATION before they can inhibit synthesis of cholesterol in the liver |
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Term
| Adverse reactions of the statins |
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Definition
usually well tolerated, mild and transient side effects if any....maight see some liver dysfunction: increase in serum transaminase, but rare (reg. liver checkups recommended)
Might see MYOPATHY and an increase in plasma CK levels |
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Term
| Contraindications to the use of statins |
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Definition
| active liver disease...pregnancy and lactation |
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Term
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Definition
| Niacin inhibits intracellular lipolysis in fat cells presumably by inhibiting the intracellular lipase activity in adipocytes...this reduces the major source of fatty acids for hepatic trig biosynthesis...thus it reduces plasma VLDL by indirectly inhibiting VLDL synthesis in the liver...it ALSO increases VLDL CATABOLISM by enhancing the activity of the extracellular lipoprotein lipase...this lowers VLDL even more! Finally, niacin lowers levels of lipoprotein A (an unusual, small, highly atherogenic form of LDL), and considerably increases HDL by mech. not fully understood |
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Term
| Therapeutic uses of Niacin |
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Definition
| Suggested for treatment of nearly all primary hyperlipidemias...decreases plasma VLDL and LDL levels in patients plus increases their HDL...used for pts with isolated HDL deficiency too! Also might be the least expensive of all lipid lowering drugs |
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Term
| Pharmacokinetics of Niacin |
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Definition
Oral admin
Metabolized to nicotinamide, the vitamin, which has NO lipid lowering activity...duration relatively SHORT, except for sustained release preps |
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Term
| adverse reactions of niacin |
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Definition
flushing and itching of the skin is the most common adverse reaction...may be mediated by prostaglandin release and therefore may be diminished by taking 300mg of aspirin approx 30 min b$ taking niacin
sometimes hypotension in those already on antihypertensive drugs
moderately increased liver enzymes
mild hyperglycemia and glucose intolerance especially in diabetics
GI disturbances and peptic ulcers, except when combined with a bile acid binding resin
renal effects, including elevated plasma uric acid |
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Term
| Class of drug: Gemfibrozil |
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Definition
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Term
| Class of drug: Fenofibrate |
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Definition
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Term
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Definition
increased clearance of VLDL via increased lipoprotein lipase activity which for all fibrates involves increased activity of peroxisome proliferator-activated receptor alpha (PPAR-alpha)....also a second PPAR-alpha-related mechanism may be increased enzymes for oxidation of free fatty acids in liver and thus less free fatty acids available for VLDL production and secretion
May be more effective than all other drugs at decreasing VLDL and therefore triglycerides |
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Term
| Therapeutic uses: Fribrates |
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Definition
recommended for the treatment of primary hyperlipidemias with high VLDL
also used for hypertriglyceridemia secondary to some defect in apolipoprotein E |
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Term
| Adverse reactions/interactions: Fibrates |
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Definition
| gallstone formation (rare), GI upset and nausea, risk of myopathy especially when combined with statins |
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Term
| MOA: Omega-3-acid ethyl esters |
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Definition
Inhibit hepatic synthesis of triglycerides from endogenous free fatty acids (eFFA) by multiple mechanisms:
1: increased beta-oxidation of eFFA
2: decreased delivery of eFFA to the liver
3: decreased synthesis of eFFA
4: decreased activity of triglyceride-synthesizing enzymes |
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Term
| MOA: Omega-3-acid ethyl esters |
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Definition
Inhibit hepatic synthesis of triglycerides from endogenous free fatty acids (eFFA) by multiple mechanisms:
1: increased beta-oxidation of eFFA
2: decreased delivery of eFFA to the liver
3: decreased synthesis of eFFA
4: decreased activity of triglyceride-synthesizing enzymes |
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Term
| Therapeutic Uses: Omega-3-acid ethyl esters |
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Definition
used as an adjunct to diet to reduce very high plasma trig levels...thus decreases VLDL like fib rates (LDL not decreased)
used in combination with statins to treat patients with both high LDL and VLDL (less risk of myopathy than combinations like fibrates with statins to treat the same patients)
Have an anti-inflammatory action |
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Term
| Adverse effects of Omega-3-acid ethyl esters |
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Definition
| symptoms of the flu and or infections, mild GI distress, taste perversion, and fishy belching, may inhibit plt aggregation and cause bleeding (esp if taken with anticoagulants) |
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Term
| Diuretics secreted by organic acid secretion in the Proximal tubule |
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Definition
| CA inhibitor, loop diuretics, thiazides |
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Term
| Diuretics that are sulfonamide derivatives and thus can induce SJS |
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Definition
| CA inhibitors, furosemide (but NOT ethacrynic acid), thiazides |
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Term
| Diuretics secreted by organic base secretion in the proximal tubule |
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Definition
| triamterene and amiloride |
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Term
| NSAIDS decrease the effectiveness of what 3 drugs |
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Definition
| NSAIDS decrease effectiveness of loop diuretics, ACE inhibitors, ARBs |
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Term
| drugs which work well with pts with low plasma renin--volume dependent HTN (usually blacks and elderly) |
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Definition
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Term
| Drugs that work well in the face of high Na intake |
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Definition
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Term
| Drugs that work LESS well in blacks and elderly |
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Definition
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Term
| drugs in which Chinese are more susceptible |
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Definition
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Term
| Drugs which mask high heart rate as a warning sign of hypoglycemia |
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Definition
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Term
| drugs which increase cholesterol and trigs |
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Definition
| loop diuretics and thiazides (except Indapamide) |
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Term
| drugs which can induce GOUT |
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Definition
| thiazides and loop diuretics |
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Term
| drugs that can induce hyperglycemia |
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Definition
| thiazides, loop diuretics, niacin, and beta blockers |
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Term
| drugs metabolized into an active metabolite |
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Definition
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Term
| what diuretic can be used to treat osteoporosis |
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Definition
| thiazides (enhance resorption of Ca) |
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Term
| ankle edema is a common side effect of what type of drugs? |
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Definition
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Term
| drugs which IMPROVE glucose tolerance, plasma cholesterol, and triglycerides |
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Definition
| doxazosin, prazosin, and terazosin |
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Term
| drugs that can cause formation of kidney stones |
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Definition
| CA inhibitors (b/c cause urinary alkalinization!) |
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Term
| What diuretic can paradoxically treat hponatremia? |
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Definition
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Term
| What diuretic is used for the treatment of central diabetes insipidus? |
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Definition
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