Diuretic Summary

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					Diuretic Agents Summary/ Emphasis (Phcl 5103; Spring 2008); the exam questions will
focus on

Knowledge Objectives:

1.     Understand the etiology of edema. (slide 2, page 1 of course packet)

2.       Be able to recognize the most likely drug interactions/ concerns that might affect your
treatment of dentistry patients taking diuretics. (slide 1, page 2 of course packet). Remember that
diuretics can cause issues due to causing hypovolemia and hypokalemia, and that NSAIDs have
the potential to counteract the antihypertensive effect of diuretics.

3.     Understand how diuretics and endogenous subtances (autacoids and hormones with
important renal actions) interact with the molecular targets shown on slide 2, page 5 of course
packet). *Note that, although not listed on this slide, receptors are targets for some diuretics (e.g.
the dopamine DA1 receptor, the mineralocorticoid receptor, the adenosine A1 receptor,
prostaglandin receptors, the vasopressin V2 receptor).

4.     Understand the mechanism and nephron site of action of each class of the diuretics.

5.     Know the influence of prototype diuretics on the excretion of various electrolytes. (see

6.     Understand how diuretics can cause hypokalemia (slide 1, p 13) or hyperkalemia (see K+
sparing diuretics).

7.     Understand the mechanisms of action of endogenous autacoids/ hormones that exert
prominent effects on renal function (including dopamine, adenosine, prostaglandins,
angiotensin, aldosterone, atrial and brain natriuretic peptides, antidiuretic hormone

Drug list for exam (Names used in questions will be restricted to the agents in bold print):
osmotic diuretic                    - mannitol
carbonic anhydrase inhibitor        - acetazolamide
loop diuretics                      - furosemide, bumetanide, torsemide, ethacrynic acid
thiazides & thiazide-like agents    - hydrochlorothiazide, chlorothalidone, indapamide
Potassium sparing diuretics         - spironolactone, eplerenone, triamterine, amiloride

Class and/or Mechanism, prototype, primary site of action: and (excretory effect)

1.   Carbonic anhydrase inhibitors
 Inhibition of carbonic anhydrase (both types IV and II);
Acetazolamide ;
Primary site is the proximal tubule, collecting duct system is a secondary site of action;
(mild ↑ in excretion of H20, NaCl, relatively marked ↑ K+ , marked ↑ -HCO3 ; no change in
Ca++ excretion, Mg++ excretion is variable

2.    Osmotic diuretic
      Reduce passive water reabsorption by washing out corticomedullary osmotic gradient and
by decreasing water movement out of the tubule via osmotic effect; also, the increased water in
the tubule causes a small increase in sodium excretion by reducing the gradient for sodium

     Nephron segments which are freely permeable to water (PT, descending limb of loop of
     Henle, collecting tubule (if ADH is present)
     (primarily ↑ in excretion of H20, small increase in Na+ excretion)

3.   Loop diuretics
     Inhibit Na+/K+/2Cl- cotransporter
     Thick ascending limb of loop of Henle
     (↑↑↑ in excretion of H20 and NaCl, ↑ excretion of K+ , Ca++ and Mg++)

4.   Thiazides
     Inhibit Na+/Cl- cotransporter
     Early distal tubule
     (↑ in excretion of H20, NaCl, K+ , and Mg++ ; Ca++ excretion is decreased)

5.   Potassium-sparing diuretics
     Blockade of Na+ channels - Amiloride and Triamterene
     collecting tubules/duct
     Competitive antagonism of aldosterone action - Spironolactone
     (much smaller ↑ in excretion of H20 and NaCl [these are weak diuretics when used alone];
     excretion of K+ and H+ is decreased)

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