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133 Cards in this Set
- Front
- Back
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1. What is considered normal BP in adults?
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a. 120 / 80
b. Guidelines say check again every 2 years |
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1. What is considered prehypertension in adults?
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a. 120/80 to 139/90
b. Guidelines say check again in 1 year |
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1. What is considered stage 1 HTN?
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a. 140/90 to 160/90
b. Guidelines say confirm within 2 months |
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1. What is considered stage 2 HTN
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a. >160/100
b. Guidelines say evaluate within 1 week to 1 month |
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1. What is the short term goal of using antihypertensive drugs?
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a. Decrease elevated BP
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1. What is the long term goal of using antihypertensive drugs?
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a. Prevent renal failure , Cardiac failure, CAD, and stroke
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1. Antihypertensive drugs act where in the body?
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a. Arterioles
b. Post capillary venules c. Heart d. Kidney |
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1. How are sympathoplegic drugs used as antihypertensive drugs
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a. They lower the BP by decreasing vascular resistance, inhibiting cardiac function, and increasing venous pooling in capacitance vessels
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1. How do direct vasodilators work as antihypertensive drugs
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a. They lower the BP by relaxing vascular smooth muscle
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1. How do drugs that reduce the action of angeotensin II work as vasodilators?
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a. Decrease BP by reducing peripheral vascular resistance and , potentially, blood volume
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1. Initiqal Steps in the management of HTN
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a. Reduce body weight
b. Na+ restriction c. Alcohol restriction d. Increase Exercise |
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1. Pharmacological steps in the management of HTN
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a. Mild HTN (single drug therapy)
• Thiazides are 1st choice • Alternative choices for monotherapy include ----Ace inhibitors ----CCB, ----Combination alpha and Beta blockers (not usually first choice due to diabetes concerns), ----Central sympatholytic drugs • Presence of concomitant disease should influence choice ----Ace inhibitors are useful with diabetic patients with renal disease ----BB or CCB are useful in patients who have angina ----ACE inhibitors or diuretics are useful in pts who have CHF b. If monotherapy does not adequately control BP, drugs with different sites of action are combined to lower BP (called STEP CARE) • If a diuretic is not used at first it is often added second c. If three drugs are required these drugs are used in combination • Diuretic • Sympatholytic ore an ACE inhibitor • Direct vasodilator ----An alpha agonist may be added at this point if needed |
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1. In the treatment of HTN you want to avoid non specific BB in pts with_________
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a. Asthma
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1. In the treatment of HTN you want to avoid thiazides in pt with __________
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a. gout or diabetes
• Be cautious with BB too |
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1. In the treatment of HTN you want to avoid methyldopa in pts with___________
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a. autoimmune diseases
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1. _______are the most potent hypertensive diuretics
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a. Thiazides
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1. ________are the most potent diuretics
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a. Loop diuretics
b. Marginal hypertensive effects |
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1. Thiazides are appropriate for pts with :
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a. Mild to moderate hypertension with normal renal and cardiac function
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1. Loop diuretics are appropriate for pateients with:
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a. Renal insufficiency, cardiac failure, or cirrhosis
b. Where Na+ retention is marked c. Or in severe HTN when multiple durgs with Na+ retaining properties are used |
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1. K+ sparring diuretics are useful for:
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a. Useful to avoid hypokalemia
b. They are often given with a Thiazide to prevent hypokalemia / hyperkalemia |
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1. How do diuretics decrease BP?
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a. Decrease blood volume
b. Which decreases Cardiac output c. Which decreases BP |
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1. Diuretics do all of the following
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a. Decrease peripheral vascular resistance
b. Decrease Cardiac output c. Decrease blood volume d. No change or decrease in LVH |
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1. Which diuretics may precipitate a gout attack?
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a. All of them
b. Strong diuretics (Thiazides / loop diuretics) are more likely to do so |
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1. When would a diuretic be used in pregnancy?
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a. Only for cases of heart disease
b. Not for HTN c. Not for toxemia |
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1. How do diuretics aid in CHF?
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a. Thiazides and loop diuretics
• increase the excretion of NaCl and water • Which reduces plasma volume and preload • Which reduces pulmonary and peripheral edema • Which reduces cardiac size and improves the pumping efficacy b. Spirolactone • Has been shown to reduce morbidity and mortality in pts with severe CHF • They may slightly decrease the preload |
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1. Diuretics may increase the urine volume by:
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a. Increasing renal Na+ excretion (Natriuresis)
b. Exerting osmotic effects that prevent water reabsorption c. Inhibiting enzymes d. Interfering with hormone receptors |
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1. Classification of diuretic agents
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a. Carbonic anhydrase inhibitors
b. Loop diuretics c. Thiazide diuretics d. K+ sparring diuretics e. Osmotic diuretics |
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1. MOA of Thiazides
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a. Thiazide drugs inhibit NaCl reabsorption in the distal convoluted tubule
b. They also increase Ca+ reabsorption |
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1. MOA of loop diuretics
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a. Loop diuretics are the most efficacious diuretic agents available…although thay have less chronic effect on BP
b. Loop Diuretics also induce renal prostaglandin synthesis which contributes to the renal actions of these drugs |
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1. MOA of K+ sparring diuretics
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a. Increase Na+ excretion and decrease K+ secretion
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1. Effects of THIAZIDES on urinary excretion of Ca+ and K+ and Na+:
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a. Decrease excretion of Ca+
b. Increase excretion of K+ c. Increase excretion of Na+ |
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1. Effects of Loop diuretics on urinary excretion of Ca+ and K+ and Na+:
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a. Increase excretion of Ca+
b. Increase excretion of K+ c. +++ Increase excretion of Na+ (more than other diuretics) |
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1. Effects of K+ sparrign diuretics on urinary excretion of Ca+ and K+ and Na+:
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a. Decrease excretion of Ca+
b. Decrease excretion of K+ c. Increase excretion of Na+ |
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1. Effects of Osmotic diuretics on urinary excretion of Ca+ and K+ and Na+:
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a. Increase excretion of Ca+
b. Increase excretion of K+ c. +++Increase excretion of Na+ |
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1. Weak diuretics
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a. K+ sparring diuretics
b. CA inhibitors |
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1. Moderate diuretics
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a. Thiazides
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1. Strong diuretics
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a. Loop diuretics
b. Osmotic diuretics |
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1. Using Loop and Thiazide diuretics in combination
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a. Useful for tx refractory pts
b. The combination will often produce dieresis when neither agent alone does |
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1. K+ sparring diuretics in combination with loop or Thiazides
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a. Pt on Thiazides or loop diuretics usually develop hypokalemia at some point in their tx
b. A K+ sparring diuretic can be added when hypokalemia cannot be managed with low Na+ diet or with KCl supplements |
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1. Thiazides can be used to manage what disorders
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a. Diabetes insipidus ++
b. Some effect on CHF but not as much as loop diuretics c. HTN ++ d. NEPHROLITHIASIS ++ e. PULMONARY EDEMA f. RENAL IMPAIRMENT |
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1. Loop diuretics can be used to manage what disorders?
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a. CHF ++
b. HTN c. Pulmonary Edema ++ d. Renal impairment ++ |
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1. K+ sparring diuretics can be used to manage what disorders
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a. Some effect in CHF
b. Hyperaldosteronism c. HTN d. Hypokalemia ++ e. Pulmonary edema |
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1. Osmotic diuretics can be used to manage what disorders
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a. Cerebral edema
b. Glaucoma c. Renal impairment |
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1. Carbonic Anhydrase inhibitors can be used to manage what disorders
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a. Glaucoma++
b. High altitude sickness++ |
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1. Cerebral edema is best managed whith what diuretic
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a. osmotic diuretics
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1. CHF is best managed by what diuretics
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a. Loop diuretics > Thiazide = K+ sparring diuretics
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1. Diabetes insipidus is best managed by what diuretic
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a. Thiazides
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1. Glaucoma is best managed by what diuretic
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a. CA nhibitors > osmotic diuretics
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1. High altitude sickness is best managed by what diuretic
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a. CA inhibitors
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1. Hyperaldosteronism is best managed by what diuretic
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a. K sparring diuretics
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1. HTN is best managed by what diuretic
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a. Thiazides > Loop = Ksparring
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1. Hypokalemia is best managed by what diuretic
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a. K sparrign diuretics
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1. Nephrolithiasis is best managed by what diuretic
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a. Thiazides
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1. Pulmonary edema is best managed by what diuretic?
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a. Loops > Thiazides = Ksparring
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1. Renal impairment is best managed by what diuretic?
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a. Loop > Thiazide = Osmotic
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1. Which drugs are Thiazides
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a. Hydrochlorothiazide
b. Inapamide c. Metolazone |
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1. Which drugs are loop diuretics
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a. Flurosemide
b. Bumetanide c. Torsemide d. Ethacrynic acid |
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1. Which drugs are K+ sparring diuretics?
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a. Amiloride
b. Spironalactone c. Triamterene |
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1. Which drugs are Osmotic Diuretics?
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a. Mannitol
b. Glycerol |
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1. Which drugs are Carbonic anhydrase inhibitors
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a. Acetazolamide
b. Dorzolamide |
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1. T/F Thiazides increase total cholesterol
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a. T
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1. Do Thiazide affect LVH?
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a. No change or decrease
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1. Adverse effects of hydrochlorothiazide
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a. Blood cell deficiency
b. Hyperlipidemia c. Hyperuricemia d. Hypokalemia e. Aggrevation of diabetes |
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1. Common drug interactions of hydrochlorothiazide
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a. Increase serum levels of lithium
b. Hypotensive effects decreased by NSAIDs and augmented by ACE inhibitors c. Potentiates the diuretic effect of loop diuretics |
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1. Clinical used of hydrochlorothiazide
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a. HTN
b. Edema • Heart failure • Kidney disease c. Nephrolithiasis • These drugs enhance Ca+ reabsorption in the distal convoluted tubule, reducing urinary Ca+ concentration d. Nephrogenic Diabetes insipidus • Thiazides can reduce poly urea and polydipsea |
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1. DOA of Hydrochlorothiazide
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a. 12 hours
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1. MOA of inapamide
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a. Thiazide
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1. Common adverse effects of inapamide
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a. Hyperlipidemia
b. Hyperuricemia c. Hypokalemia (and other electrolyte changes) d. Aggravation of diabetes |
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1. Common drug interactions of inapamide
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a. Increase serum levels of lithium
b. Hypotensive effects decreased by NSAIDs and augmented by ACE inhibitors c. Potentiates the diuretic effect of loop diuretics |
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1. Clinical use of inapamide
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a. HTN
b. Edema • Heart failure • Kidney disease c. Nephrolithiasis • These drugs enhance Ca+ reabsorption in the distal convoluted tubule, reducing urinary Ca+ concentration d. Nephrogenic Diabetes insipidus • Thiazides can reduce poly urea and polydipsea |
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1. DOA of inapamide
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a. 30 hours
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1. MOA of metolazone
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a. Thiazide
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1. Adverse effects of metolazone
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a. Blood cell deficiencies
b. Hyperlipidemia c. Hyperuricemia d. Hypokalemia (and other electrolyte changes) e. Aggravation of diabetes |
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1. Common drug interactions of metolazone
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a. Increase serum levels of lithium
b. Hypotensive effects decreased by NSAIDs and augmented by ACE inhibitors c. Potentiates the effect of loop diuretics |
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1. Clinical uses of metolazone
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a. HTN
b. Edema • Heart failure • Kidney disease c. Nephrolithiasis • These drugs enhance Ca+ reabsorption in the distal convoluted tubule, reducing urinary Ca+ concentration d. Nephrogenic Diabetes insipidus • Thiazides can reduce poly urea and polydipsea |
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1. DOA of metolazone
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a. 18 hours
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1. MOA of flurosemide
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a. Loop diuretic
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1. T/F loop diuretics increase total serum Cholesterol
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a. T
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1. Common adverse effects of flurosemide
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a. Blood cell deficiencies
b. Hyperlipidemia c. Hyperuricemia d. Hypokalemia (and other electrolyte changes) e. Aggravation of diabetes??? f. Hearing impairment g. Hypersensitivity Rxn h. Increases photosensitivity |
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1. Common drug interactions of flurosemide
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a. Increase serum levels of lithium
b. Diuretic effects decreased by NSAIDs c. When taken with an ACE inhibitors may cause excessive hypotnesion |
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1. Clinical Uses of flurosemide
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a. Edema
• Reduce edema resulting from heart failure and kidney failure b. HTN c. Hyperkalemia • These drugs increase urinary K+ secretion d. Acute renal failure • Loop diuretics can increase the rate of urine flow and enhance K+ secretion (even when the kidnes aren’t working well at all) e. Anion overdose • These drugs can prevent bromide, fluride, and iodide from being reabsorbed f. Hypercalcemia • Loop diuretics promote Ca_ dieresis |
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1. DOA of flurosemide
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a. Oral = 7 hours
a. Iv = 2 hour |
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1. MOA of Bumetanide
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a. Loop diuretic
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1. Do loop diuretics affect LVH?
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a. No change or decrease
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1. Adverse effects of bumetanide
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a. Blood cell deficiencies
b. Hypokalemia (and other electrolyte changes) c. Hearing impairment d. Hypersensitivity Rxn |
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1. Common drug interactions of bumetanide
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a. Increase serum levels of lithium
b. Diuretic effects decreased by NSAIDs c. Administration of this drug with an ACE inhibitor may cause excessive Hypotension |
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1. DOA of bumetanide
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a. Oral = 5 hours
b. Iv = 1 hour |
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1. Clinical Uses of bumetanide
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a. Edema
• Reduce edema resulting from heart failure and kidney failure b. HTN c. Hyperkalemia • These drugs increase urinary K+ secretion d. Acute renal failure • Loop diuretics can increase the rate of urine flow and enhance K+ secretion (even when the kidnes aren’t working well at all) e. Anion overdose • These drugs can prevent bromide, fluride, and iodide from being reabsorbed f. Hypercalcemia a. Loop diuretics promote Ca_ dieresis |
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1. MOA of torsemide
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a. Loop diuretic
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1. adverse effects of torsemide
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a. Hyperlipidemia
b. Hyperuricemia c. Hypokalemia (and other electrolyte changes) d. Aggravation of diabetes e. Hypersensitivity RXN |
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1. Drug interactions of torsemide
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a. Increase serum levels of lithium
b. Diuretic effects decreased by NSAIDs c. Administration of this drug with an ACE inhibitor may cause excessive Hypotension |
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1. DOA of torsemide
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a. Oral = 7 hours
b. Iv = 7 hour |
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1. Clinical Uses of torsemide
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a. Edema
• Reduce edema resulting from heart failure and kidney failure b. HTN c. Hyperkalemia • These drugs increase urinary K+ secretion d. Acute renal failure • Loop diuretics can increase the rate of urine flow and enhance K+ secretion (even when the kidnes aren’t working well at all) e. Anion overdose • These drugs can prevent bromide, fluride, and iodide from being reabsorbed f. Hypercalcemia a. Loop diuretics promote Ca_ dieresis |
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1. MOA of ethacrynic acid
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a. Loop diuretic
b. This is the only loop diuretic that is not a sulfonamide |
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1. adverse effects of ethacrynic acid
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a. Blood cell deficiencies
b. Hypokalemia (and other electrolyte changes) c. Hearing impairment d. Rash e. Because this is not a sulfonamide…it is the only loop diuretic that does not cause a hypersensitivity rxn |
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1. drug interactions of ethacrynic acid
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a. diuretic effects decreased by NSAIDs
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1. DOA of ethacrynic acid
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a. Oral = 7 hours
b. Iv = 2 hours |
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1. Clinical Uses of ethacrynic acid
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a. Edema
• Reduce edema resulting from heart failure and kidney failure b. HTN c. Hyperkalemia • These drugs increase urinary K+ secretion d. Acute renal failure • Loop diuretics can increase the rate of urine flow and enhance K+ secretion (even when the kidnes aren’t working well at all) e. Anion overdose • These drugs can prevent bromide, fluride, and iodide from being reabsorbed f. Hypercalcemia a. Loop diuretics promote Ca_ dieresis |
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1. MOA of Amiloride
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a. K+ sparing Diuretic
b. Inhibits Na+ flux through channels expressed in the luminal membrane |
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1. Common adverse effects of Amiloride
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a. Hyperkalemia
b. Hyperchloremic metabolic acidosis c. Blood cell deficiency d. GI distress |
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1. drug interactions of amiloride
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a. Hyperkalemic effect increased by ACE inhibitors and potassium supplements
b. Administration with NSAID’s may cause renal failure |
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1. Clinical Use of amiloride
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a. Hypokalemia
• K+ sparring diuretics are useful in preventing hypokalemia in patients taking loop diuretics or Thiazide diuretics when Na+ restriction or K+ supplements are ineffective b. Heart failure • Spironolactone improves long term outcome c. Hyperaldosteronism • Can prevent the effects of mineralcorticoid excess caused by the hypersecretion or secondary aldosteronism |
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1. DOA of amiloride
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a. 24 hours
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1. MOA of Spironalactone
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a. K+ sparing Diuretic
b. (competitive antagonist for the aldosterone receptor) |
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1. adverse effects of spironalactone
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a. Hyperkalemia
b. Hyperchloremic metabolic acidosis c. Gynecomastia (spirolactone) d. Impotence (sexual dysfunction) |
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1. drug interactions of spironolactone
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a. Hyperkalemic effect increased by ACE inhibitors and potassium supplements
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1. Clinical Use of spironalactone
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a. Hypokalemia
• K+ sparring diuretics are useful in preventing hypokalemia in patients taking loop diuretics or Thiazide diuretics when Na+ restriction or K+ supplements are ineffective b. Heart failure • Spironolactone improves long term outcome c. Hyperaldosteronism • Can prevent the effects of mineralcorticoid excess caused by the hypersecretion or secondary aldosteronism |
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1. DOA of spironalactone
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a. 60 hours
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1. MOA of trimterene
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a. K+ sparing Diuretic
b. Inhibits Na+ flux through channels expressed in the luminal membrane |
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1. Adverse effects of triamterene
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a. Hyperkalemia
b. Hyperchloremic metabolic acidosis c. Kidney stones (Triamterene) d. Impotence (sexual dysfunction) |
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1. drug interactions of triamterene
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a. Hyperkalemic effect increased by ACE inhibitors and potassium supplements
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1. Clinical Use of triamterenee
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a. Hypokalemia
• K+ sparring diuretics are useful in preventing hypokalemia in patients taking loop diuretics or Thiazide diuretics when Na+ restriction or K+ supplements are ineffective b. Heart failure • Spironolactone improves long term outcome c. Hyperaldosteronism • Can prevent the effects of mineralcorticoid excess caused by the hypersecretion or secondary aldosteronism |
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1. DOA of triamterene
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a. 14 hours
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1. MOA of manitol
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a. Osmotic diuretic
• Osmotic diuretics draw water into plasma from the interstitial and cellular sites |
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1. ROA of manitol
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a. IV only
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1. Clinical use of manitol
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a. Increase urine volume
• Mannitol is useful in treating acute remal failure • The maitol is filtered but nor reabsorbed, water follows • It can maintain urine volume and prevent anuria b. Reduction of intracranial (mannitol) and intraocular pressure (glycerol and mannitol) • Reduces total body water greater than total cation content • This results in a reducetion of the intracellular volume |
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1. Common adverse effects of mannitol
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a. Heart failure
b. Nausea and vomiting c. Pulmonary congestion d. Edema |
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1. Common drug interactions of mannitol
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a. Potentiates effects of other diuretics
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1. DOA of mannitol
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a. 7 hours (IV)
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1. MOA of Glycerol
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a. Osmotic diuretics
• Osmotic diuretics draw water into plasma from the interstitial and cellular sites |
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1. Clinical use of Glycerol
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a. Reduction of intraocular pressure (glycerol and mannitol)
• Reduces total body water greater than total cation content • This results in a reducetion of the intracellular volume |
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1. Common adverse effects of glycerol
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a. Heart failure
b. Nausea and vomiting c. Pulmonary congestion d. Edema |
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1. Common drug interactions of glycerol
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a. Potentiates effects of other diuretics
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1. DOA of glycerol
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a. 1 hour (oral)
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1. MOA of Acetazolamide
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a. CA inhibitor
• CA inhibitors work by blocking the Na+/HCO3 reabsorption Na / HCO3 diuresis and the reduction in total HCO3 stores • CA inhibitors cause a significant loss of HCO3 that may result in hyperchloremic metabolic acidosis • These diuretics produce a mild, short term dieresis |
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1. Clinical Uses of Acetazolamide
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a. Glaucoma
• Inhibition of CA decreases the rate of aqueous humor formation decreased intraocular pressure b. Acute Mountain sickness • Decreases the formation and the pH of CSF • Can counteract respiratory alkylosis |
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1. DOA of Acetazolamide
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a. 10 hours (oral)
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1. Common adverse effects of Acetazolamide
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a. Blood cell deficiency
b. Drowsiness c. Hepatic insufficiency • Usually contraindicated with live disease d. Hyperglycemia e. Hypokalemia f. Metabolic acidosis g. Parasthesia h. Uremia |
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1. Common drug interactions of Acetazolamide
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a. Serum levels of weak bases (such as amphetamine, epinephrine, and quinidine) are increased by CA inhibitors.
a. Serum levels of CA inhibitors are increased by salicylates |
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1. MOA of Dorzolamide
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a. Carbonic anhydrase inhibitors
• CA inhibitors work by blocking the Na+/HCO3 reabsorption Na / HCO3 diuresis and the reduction in total HCO3 stores • CA inhibitors cause a significant loss of HCO3 that may result in hyperchloremic metabolic acidosis • These diuretics produce a mild, short term dieresis |
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1. Clinical Uses of Dorzolamide
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a. Glaucoma
• Inhibition of CA decreases the rate of aqueous humor formation decreased intraocular pressure b. Acute Mountain sickness • Decreases the formation and the pH of CSF • Can counteract respiratory alkylosis |
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1. DOA of Dorzolamide
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a. 8 hours (Topical)
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1. Adverse effects of Dorzolamide
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a. Bitter taste
b. Blurred vision c. Ocular discomfort a. Allergic reactions |
