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Pharmacology Unit 4 > Diuretics: 2 Lectures (Handout pgs: 18 - 41) > Flashcards

Diuretics: 2 Lectures (Handout pgs: 18 - 41) Flashcards

1
Q

What is an aquaretic?

A

A drug which decreases the ability of ADH to increase water permeability of the late distal tubule and collecting duct

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2
Q

What are saluretics? What are the 4 classes?

A

Drugs which decrease reabsorption of solutes in 1 or more segments of the nephron; Carbonic anhydrase inhibitors, loop diuretics, thiazide diuretics, K-sparing diuretics

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3
Q

What is an osmotic diuretic?

A

Drug which enters the tubular fluid by glomerular filtration and is neither reabsorbed nor secreted along the nephron. The increased osmotic pressure within the tubule inhibits water reabsorption resulting in a more voluminous diuresis.

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4
Q

What is the main indication for diuretic use?

A

To maintain normal blood pressure

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5
Q

What are some of the many secondary indications for diuretic use?

A

Edema, hypo/hyperkalemia, hypo/hypercalcemia, Increased CSF, Increased introcular pressure

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6
Q
  1. What class of drug are aminophylline and theophylline? 2. Mechanism of action? 3. Why are these diuretics relatively ineffective?
A
  1. Phosphodiesterase inhibitors 2. Phosphodiesterase inhibitor -> increases cAMP in prox. Tubule cells -> phosphorylation of apical membrane Na/H exchanger causing inhibition of bicarbonate and Na+ absorption 3. Compensation by downstream mechanisms
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7
Q
  1. What is the mechanism of loop diuretics? 2. Why are they considered most efficacious? 3. Why does loop diuretic use result in excessive K secretion in the urine?
A
  1. Decrease reabsorption of Na, K, and Cl in thick ascending limb of Henle 2. Theey induce the largest diuresis 3. Compensatory mechanisms downstream in the late distal tubule/collecting duct couples the reabsorption of Na with the secretion of K
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8
Q
  1. Where do thiazide diuretics act? 2. Mechanism of action? 3. How are they similar to loop diuretics?
A
  1. Cortical talH/Early distal tubule 2. Decrease Na and Cl reabsorption/Inhibit proximal tubule carbonic anhydrase 3. Increased excretion of K due to compensatory Na reabsorption (they are obligately coupled)
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9
Q
  1. Where do potassium sparing diuretics work? 2. Mechanism of action? 3. What other diuretics would you combine with them? Why?
A
  1. Late distal tubule/collecting duct 2. Block the obligate functional coupling of Na reabsorption and K secretion 3.Either a loop diuretic or thiazide diuretic. K sparing diuretics will decrease the amount of Na reabsorbed in the late distal tubule/collecting duct and therefore increase the volume of diureis while maintaining blood K concentration
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10
Q

Describe the mechanism by which loop diuretics increase the time necessary to rid the body of excess fluid intake.

A

The loop diuretics increase osmolar clearance (Cosm). Therefore, less free water is excreted based on the following equation CH20 = V - Cosm and it takes more time to excrete fluid in excess of solute

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11
Q

What is the countercurrent multiplication ion concentration dependent on?

A

The magnitude of transcellular solute reabsorption in the medullary thick ascending limb of Henle

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12
Q

In a volume contracted patient, why do loop diuretics increase free water clearance?

A

A healthy kidney would attempt to concentrate the urine. In a patient on diuretics, there is a lesser countercurrent gradient, and therefore an inability to concentrate urine. This results in less negative free water clearance

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13
Q

What solutes absorbed in the cortical early distal tubule participate in the counter current concentration gradient?

A

Solutes that are reabsorbed into the cortex do not contribute to the ion concentration gradient.

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14
Q

Describe the process by which thiazide diuretics decrease free water clearance ability

A

They block solute reabsorption in the distal tubule and therefore decrease the ability to dilute the urine. Osmolar clearance increases therefore decreasing free water clearance

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15
Q

What is a risk of thiazide diuretic use in volume expanded patients?

A

Because the ability to excrete free water is decreased, it will take a longer time to decrease the excess volume. Therefore, major risk: hyponatremia

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16
Q

Describe the mechanism of the carbonic anhydrase inhibitors

A

Inhibition of luminal CA leads to the decrease of intracellular H+. Therefore, the Na/H exchanger function decreases limiting the reabsorption of Na and promoting diuresis

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17
Q

What effect do CA inhibitors have on urine pH?

A

Increased pH

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18
Q

Describe the contents of the diuresis induced by CA inhibitors

A

Increased excretion of Na, K, and HCO3- in an alkaline urine

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19
Q

What are the major complications of CA inhibitor use?

A

Hypokalemia (K loss in urine) and metabolic acidosis (bicarb loss in urine)

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20
Q

What are the current uses of CA inhibitors now that they are obsolete as diuretics?

A

Used to decrease intraocular volume and pressure

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21
Q

What can CA inhibitor-induced metabolic acidosis lead to?

A

Ammonia generated from renal metabolism is diverted from the urine to accumulation in the ECF creating the risk of hepatic encephalopathy

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22
Q

What two drugs make up aminophylline?

A

Methylxanthine theophylline and ethylene diamine

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23
Q

Describe the 3 mechanisms of osmotic diuretics

A

(1) Non reabsorbable solutes increase the osmotic pressure which opposes the isotonic reabsorption of sodium and water. (2) Increased flow of isotonic tubular fluid decreases sodium and chloride reabsorption in the LOH and distal tubule. (3) There is increased blood flow to the renal medulla which decreases the osmotic gradient decreasing urine concentrating ability.

24
Q

What is the most widely administered osmotic diuretic?

A

Mannitol

25
Q

What is the FE of Na for CAI?

A

< 5%

26
Q

What are four loop diuretics and what do they act upon?

A

Furosemide, bumetanide, torsemide, ethacrynic acid; inhibit the Na-K-Cl cotransporter in the talH

27
Q

How is mannitol administered?

A

IV

28
Q

What changes in ECF solute concentration can result from loop diuretic induced ECF volume contraction?

A

Hyperbicarbonatemia-alkalosis, Hyperuricemia, Increased BUN, Increased serum creatinine

29
Q

What are the therapeutic indications of mannitol?

A

Drug OD (drugs eliminated via urine), shock (treat acute renal failure), Increased intraocular/intracranial pressure

30
Q

What is the mechanism causing hypokalemia in a patient on loop diuretics and thiazide diuretics?

A

Excess sodium is delivered to the distal tubule which induces potassium secretion and elimination

31
Q

What is a risk factor of mannitol use?

A

Pulmonary edema

32
Q

What solutes are increased in the diuresis of a patient on loop diuretics?

A

Na, K, Cl, Mg, Ca

33
Q

A loss in body weight is seen on administration of loop diuretics but then the body weight plateaus. Why is this?

A

Compensatory Na reabsorption in the proximal tubule counters the Na excretion induced by the loop diuretics

34
Q

How is hyponatremia caused by loop diuretics? How is it corrected?

A

The kidney has an inability to excrete water in excess of solute; Hyponatremia may be corrected with water restriction

35
Q

What are the indications for loop diuretic use?

A

Crises involving pulmonary edema, edema from HF, cirrhosis; Hypercalcemia; Drug toxicity

36
Q

What serious side-effect can be caused by loop diuretics especially in the presence of aminoglycoside antibiotics?

A

Ototoxicity

37
Q

What are the diuretics that belong to the thiazide and thiazide-like classes, respectively?

A

Chlorothiazide, hydrochlorothiazide; chlorthilidone, metolazone, quinethazone, indapamide

38
Q

What are the possible side-effects of thiazide and thiazide-like diuretics?

A

Hypokalemia-diabetes, hyponatremia, contraction alkalosis, hyperuricemia, increased BUN, increased serum creatinine, hypercalcemia

39
Q

Describe the mechanism of thiazide and thiazide-like diuretics

A

The diuretics block the Na-Cl cotransporter decreasing transcellular Na and Cl reabsorption in the early distal tubule

40
Q

What ability of the kidney do the thiazide diuretics limit? What does this put the patient at risk for?

A

The ability to dilute the urine; Hyponatremia

41
Q

What type of mechanism is induced by the kidney to compensate for loss of Na due to thiazide diuretics?

A

Increased sodium reabsorption in the proximal tubule

42
Q

What is the primary use of thiazide diuretics? Secondary uses?

A

HTN; Chronic edema due to cardiac insufficiency, Idiopathic hypercalciuria, nephrogenic diabetes insipidus

43
Q

What are the potassium sparing diuretics?

A

Spironolactone; Amiloride and Triamterene

44
Q

What is the mechanism of spironolactone?

A

Sprionolactone competes with aldosterone for the aldosterone receptor. This downregulates proteins necessary for Na reabsorption and K secretion in the LDT and CD

45
Q

What is a major risk of K sparing diuretic use?

A

Risk of hyperkalemia

46
Q

What is required to make spironolactone induce diuresis?

A

Presence of aldosterone in the blood

47
Q

What is the mechanism of action of amiloride and triamterene?

A

Amiloride and triamterene both block Na channel and Na/H exchanger in the luminal membrane of the LDT and CD

48
Q

What is the main clinical application of the potassium sparing diuretics?

A

They are used in combination with thiazide or loop diuretics to minimize potassium depletion while controlling hypertension

49
Q

What are secondary clinical applications of K sparing diuretics?

A

Control edema caused by CHF, cirrhosis, and nephrotic syndrome; Primary/Secondary aldosteronism; Idiopathic hypercalciuria; Li-induced polyuria

50
Q

What side effects are associated with spironolactone use?

A

Androgen receptor antagonism resulting in gender-specific effects (male - gynecomastia, etc; female - amenorrhea etc)

51
Q

What are the 5 factors determining the quantity of of diuretic present at its site of action?

A

Plasma concentration, RBF, Glomerular Filtration, Tubular secretion, Tubular Fluid Concentration

52
Q

By what transporter are thiazide/loop diuretics secreted into the tubular fluid across the luminal membrane? Amiloride and triamterene?

A

Passively thru the organic anion transporter; Actively thru the organic cation/H+ transporter

53
Q

Why are higher doses of diuretic needed to give to a patient with kidney failure?

A

Organic anion metabolites build up in the circulation because they cannot adequately be secreted by the kidney. Therefore, there is a greater competitition for the OA transport. Higher doses of diuretics can outcompete the higher levels of metabolites

54
Q

Why are higher doses of diuretic needed in a patient with nephrotic syndrome?

A

In nephrotic syndrome, excess protein is in the tubular filtrate. This protein absorbs the diuretic limiting its action. Therefore, higher doses are needed.

55
Q

Order the diuretics from greatest to least FENa

A

Loop, Thiazide, CAI, K-sparing

Pharmacology Unit 4 (9 decks)

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