Pharm Block II - Diuretics Flashcards

1
Q

diuretic drugs that work on the proximal tubule

A

carbonic anhydrase inhibitors, mannitol

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2
Q

diuretic drugs that work on the loop of Henle

A

loop diuretics (ascending limb); osmotic diuretics (descending limb)

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3
Q

diuretic drugs that work on the distal convoluted tubule

A

thiazide diuretics, K+ sparing diuretics

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4
Q

Loop diuretics examples

A

Furosemide, ethacrynic acid

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5
Q

Loop diuretics MOA

A

Inhibit sodium and chloride reabsorption in ascending limb of loop of Henle; increase renal prostaglandins resulting in dilation of blood vessels and reduced peripheral vascular resistance

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6
Q

Loop diuretics indications

A

Edema associated with heart failure or hepatic/renal disease, HTN (if related to volume)

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7
Q

Loop diuretics adverse effects

A

Hypokalemia, hyperglycemia, hyperuricemia, ototoxicity

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8
Q

Thiazides examples

A

Hydrochlorothiazide, chlorthalidone, metolazone

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9
Q

Thiazides MOA

A

Inhibits tubular reabsorption (in distal tubule and ascending loop of Henle) of sodium and chloride (so water, sodium and chloride are excreted); also dilates arterioles

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10
Q

Thiazides indications

A

HTN (due to diuretic and vasodilation effects), edematous states, CHF, hypercalciuria

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11
Q

Thiazides adverse effects

A

Dizziness, headache, blurry vision, anorexia

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12
Q

Potassium sparing diuretics example

A

Spironolactone

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13
Q

Spironolactone MOA

A

Interfere with sodium/potassium exchange, competively bind to aldosterone receptors, block reabsorption of sodium/water

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14
Q

Spironolactone indications

A

Hyperaldosteronism, ascites, CHF

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15
Q

Spironolactone adverse effects

A

Hyperkalemia, nausea, gnecomastia, lethargy, mental confusion

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16
Q

volume depletion from diuretic therapy

A

where Na goes, water follows. causes reduced BP, pulmonary & systemic vascular resistance, reduced central venous pressure, and reduced L ventricular end diastolic pressure

17
Q

azotemia from diuretic therapy

A

increase in BUN and SCr due to decrease in renal perfusion & decreased GFR

18
Q

hypokalemia from diuretic therapy

A

2 mechs cause this:1. high tubular flow to the cortical collecting ducts, increase delivery of Na to the collective duct & decrease in intravasc vol as a result of salt wasting. 2. diuretics stimulate aldosterone, so low intravasc vol resulting in hyperaldosteronism & enhanced secretion of aldosterone

19
Q

hyperkalemia from diuretic therapy

A

K sparing diuretics reduce both K & H secretion in the collecting tubules

20
Q

hyperuricemia due to diuretic therapy

A

reduced urate secretion due to competition for organic acid secreting pathway. increase renal reabsorption secondary to plasma vol contraction

21
Q

hyponatremia due to diuretic therapy

A

almost all cases are due to thiazides (not loop diuretics), the ECF vol depletion stimulates ADH, causing impaired water excretion, resulting in hyponatremia

22
Q

hyperglycemia due to diuretic therapy

A

exact mech is unknown - possibly due to decreased insulin secretion, decreased tissue sensitivity to insulin or increased insulin depletion. loop diuretics have less marked effect than thiazides

23
Q

hypomagnesemia due to diuretic therapy

A

approx 70% of the filtered Mg is reabsorbed in the thick ascending limn and 10% in the distal convoluted tubule. inhibition of Na/K/Cl transporter by loop diuretics diminishes the lumen to positive potential required to reabsorb Mg

24
Q

Diuretic resistance

A

Process of eliminating excess sodium and water stops before enough fluid has been removed

25
Q

How to manage diuretic resistance

A

Switching to another diuretic class; infuse loop diuretics continuously; ultrafiltration using hemodialysis