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47 Cards in this Set
- Front
- Back
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diuretics
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-increase urine output
-treatment of HTN (before antihypertensives) -mobilization of edematous fluid in heart failure, cirrhosis, and kidney disease -prevention of renal failure |
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regions of the nephron (functional unit of the kidney)
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1) glomerulus
2) proximal convoluted tubule 3) loop of Henle 4) distal convoluted tubule |
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basic functions of the kidney
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1) cleansing of ECF and maintenance of its volume and composition
2) maintenance of acid-base balance 3) excretion of metabolic wastes and foreign substances |
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steps in ECF cleansing and maintenance
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1) filtration in glomerulus (produces hella filtrate)
2) reabsorption: >99% of stuff in filtrate is reabsorbed; this step is most affected by diuretics 3) active tubular secretion: 2 pumps in proximal convoluted tubule transport molecules from plasma to lumen (one for organic acids, one for organic bases) |
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sites of reabsorption
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-proximal convoluted tubule
-loop of Henle -distal convoluted tubule -late distal convoluted tubule and -collecting duct (Na-K exchange, regulation of urine concentration) |
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ADH acts on collecting duct to regulate water conservation
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-in absence of ADH, collecting duct is impermeable to water
-collecting duct begins in cortex and extends through medulla -tubular urine entering collecting duct is isotonic -ADH acts on collecting duct to increase its permeability to water |
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4 major diuretic categories
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-loop (furosemide)
-thiazide (hydrochlorothiazide) -osmotic (mannitol) -potassium-sparing -aldosterone antagonists (spironolactone) -nonaldosterone antagonists (triamterene) 5th group--carbonic anhydrase inhibitors |
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FUROSEMIDE (Lasix) indications, mechanism of action, and pharmacokinetics
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indications:
-HTN -edematous states -pulmonary edema mechanism of action: -acts on ascending loop of Henle to block reabsorption -pharmacokinetics: rapid onset |
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FUROSEMIDE (Lasix) adverse effects
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-hyponatremia, hypochloremia, dehydration
-hypotension -HYPOKALEMIA -ototoxicity -hyperglycemia, hyperuricemia -use in pregnancy -impact on lipids, calcium, magnesium |
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FUROSEMIDE (Lasix) drug interactions
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-digoxin
-ototoxic drugs -potassium-sparing diuretics -lithium -antihypertensives -SAIDS |
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FUROSEMIDE (Lasix) administrations
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-oral
-parenteral |
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HYDROCHLOROTHIAZIDE (HydroDIURIL)
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-most widely used
-acts on distal convoluted tubule -peaks in 4-6 hours -indications: -essential HTN -edema -diabetes insipidus |
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HYDROCHLOROTHIAZIDE (HydroDIURIL) side effects
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-HYPONATREMIA, hypochloremia, dehydration
-HYPOKALEMIA -use in pregnancy--enters breast milk -hyperglycemia -hyperuricemia -impact on lipids, calcium, metabolism |
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SPIRONOLACTONE (Aldactone)
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potassium-sparing aldosterone antagonist
-block aldosterone in distal nephron -potassium retention -increased excretion of sodium |
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SPIRONOLACTONE (Aldactone) indications
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HTN
edematous states severe heart failure primary hyperaldosteronism |
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SPIRONOLACTONE (Aldactone) side effects and drug interactions
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side effects:
-HYPERKALEMIA -benign and malignant tumors -endocrine effects drug interactions: -thiazide and loop diuretics -agents that raise potassium levels |
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TRIAMTERENE (Dyrenium) mechanism of action
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potassium-sparing nonaldosterone antagonist
-disrupts Na-K exchange in distal nephron -decreases sodium reuptake -inhibits ion transport |
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TRIAMTERENE (Dyrenium) indications
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HTN
edema |
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TRIAMTERENE (Dyrenium) side effects
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-leg cramps (cause people to switch)
-HYPERKALEMIA -N/V -dizziness -blood dyscrasias |
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MANNITOL (Osmitrol) indications
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-pulls water into lumen of nephron
-must be given parenterally (only in hospital) -indications: prophylaxis of renal failure reduction of ICP and IOP |
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MANNITOL (Osmitrol) side effects
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edema
headache n/v fluid and electrolyte imbalance |
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Urea, glycerin, and isosorbide mechanisms of action
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osmotic diuretics
-filtered at glomerulus -undergo limited reabsorption -promote osmotic diuresis |
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urea, glycerin, and isosorbide preparations and indications
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-urea (Ureaphil) given IV
-glycerin (Osmoglyn) and isosorbide (Ismotic) given PO -indications: reduction of ICP and IOP |
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abnormal states of hydration (volume contraction)
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-isotonic contraction: water and sodium lost in equal amounts; treated with infusion of isotonic fluids
-hypertonic contraction: more water lost than sodium; treated with infusion of hypotonic fluids -hypotonic contraction: more sodium lost than water; treated with infusion of isotonic fluids |
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causes of hypomagnesemia
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diarrhea
hemodialysis kidney disease prolonged IV feeding long-term alcoholism |
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treatment of hypomagnesemia
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*most common in patients with renal insufficiency
magnesium gluconate magnesium hydroxide magnesium sulfate |
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causes of heart failure
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inadequate tissue perfusion
volume overload chronic HTN MI valvular heart disease CAD congenital heart disease dysrhythmias aging of the myocardium |
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drugs used for heart failure
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diuretics
RAAS inhibitors beta blockers digoxin and other cardiac glycosides inotropic agents vasodilators other than ACEIs and ARBS |
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digoxin and other cardiac glycosides
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-positive inotropic
-alter cardiac electrical activity -favorably affect neurohormonal systems -second-line agents -treat symptoms but don't prolong life |
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DOPAMINE (Inotropin)
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-catecholamine
-activate beta1 adrenergic receptors and alpha1 receptors -positive chronotropic -dilates renal blood vessels |
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DOBUTAMINE
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-synthetic catecholamine
-selective activation of beta1 adrenergic receptors |
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phosphodiesterase inhibitors
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-inamrinone (inodilator)
-milrinone (Primacor) |
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hemodynamic benefits of cardiac glycosides (e.g. digoxin)
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increased cardiac output
decreased renin release decreased sympathetic tone increased urine production |
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neurohormonal benefits of cardiac glycosides
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-modulate activity of neurohormonal system
-suppress renin release in kidney -decrease sympathetic outflow from CNS -increase sensitivity of cardiac baroreceptors |
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electrical benefits of cardiac glycosides
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-increased firing rate of vagal fibers
-increases responsiveness of SA node to Ach |
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adverse effects of cardiac glycosides
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-DYSRHYTHMIAS
-anorexia -n/v -fatigue |
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DIGOXIN (Lanoxin) drug interactions
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diuretics
ACEIs ARBs sympathomimetics quinidine verapamil |
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DIGOXIN pharmacokinetics
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-eliminated primarily by renal excretion
-half life of 1.5 days -distributed widely and crosses placenta |
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DIGOXIN drugs to avoid
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antidysrhythmics
CCBs NSAIDs |
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angina pectoris
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-sudden pain beneath sternum, often radiating to left shoulder and arm
-oxygen supply to heart insufficient to meet oxygen demand -causes: excitement, large meals, cold, CAD |
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families of antianginal agents
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1) organic nitrates
2) beta blockers 3) CCBs |
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preparations and routes of administration of organic nitrates
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sublingual tabs
sustained release oral caps transdermal delivery systems translingual sprays transmucosal (buccal) tabs topical ointment IV infusion |
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drugs to prevent MI and death
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antiplatelet drugs
antilipidemics ACEIs antianginal agents |
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routine drug therapy of STEMI
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oxygen
aspirin morphine beta blockers nitroglycerin |
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reperfusion therapy
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thrombolytic therapy
PCI thrombolytic drugs (alteplase, reteplase, streptokinase, tenecteplase, urokinase) |
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complications of STEMI
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ventricular dysrhythmias
cardiogenic shock CHF cardiac rupture |
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adjuncts to reperfusion therapy
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unfractioned heparin
antiplatelet drugs (clopidogrel, glycoprotein IIb/IIIa inhibitors) magnesium ACEIs ARBs CCBs |
