Chapter 15: Diuretics & Other Drugs That Act on the Kidney Flashcards

1
Q

Carbonic anhydrase inhibitors

The effects of this diuretic agent are predictable from in which segment of the nephron?

A

Proximal convoluted tubule

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2
Q

Loop diuretics

The effects of this diuretic agent are predictable from in which segment of the nephron?

A

Thick ascending limb of LoH

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3
Q

Thiazides

The effects of this diuretic agent are predictable from in which segment of the nephron?

A

Distal convoluted tubule

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4
Q

K+ sparing diuretics

The effects of this diuretic agent are predictable from in which segment of the nephron?

A

Cortical collecting tubule

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5
Q

The kidney filters plasma water and solutes at the glomerulus at a very high rate (_____ L/day) and must recover a significant percent- age of most of these substances before excretion in the urine.

A

180 L/day

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6
Q

A shift in body electrolyte and pH balance involving elevated serum chloride, diminished bicarbonate concentration, and a decrease in pH in the blood. Typical result of bicarbonate diuresis

A

Hyperchloremic metabolic acidosis

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7
Q

A shift in body electrolyte balance and pH involving a decrease in serum potassium and an increase in blood pH. Typical result of loop and thiazide diuretic actions

A

Hypokalemic metabolic alkalosis

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8
Q

Loss of urine-concentrating ability in the kidney caused by lack of responsiveness to antidiuretic hormone (ADH is normal or high)

A

Nephrogenic diabetes insipidus

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9
Q

Loss of urine-concentrating ability in the kidney caused by lack of antidiuretic hormone (ADH is low or absent)

A

Pituitary diabetes insipidus

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10
Q

This segment carries out isosmotic reabsorption of amino acids, glucose, and numerous ions.

It is the major site for sodium chloride and sodium bicarbonate reabsorption.

It is responsible for 60–70% of the total reabsorption of sodium.

A

Proximal convoluted tubule

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11
Q

What is the mechanism of action of carbonic anhydrase inhibitors?

A

The mechanism of action is inhibition of carbonic anhydrase in the brush border and cytoplasm

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12
Q

What are the causes of high anion gap metabolic acidosis (HAGMA)?

A

MUDPILES:

  1. Methanol
  2. Uremia
  3. DKA
  4. Paraldehyde
  5. Isoniazid, Iron
  6. Lactic Acid
  7. Ethanol, Ethylene glycol
  8. Salicylates
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13
Q

What are the causes of normal anion gap metabolic acidosis (NAGMA)?

A

HARDUP:

  1. Hyperalimentation
  2. Acetazolamide
  3. RTA
  4. Diarrhea
  5. Ureteral diversion
  6. Pancreatic fistula
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14
Q

This segment pumps sodium, potassium, and chloride out of the lumen into the interstitium of the kidney.

It is also a major site of calcium and magnesium reabsorption.

A

Thick ascending limb of LoH

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15
Q

Reabsorption of sodium, potassium, and chloride are all accomplished by a _____, which is the target of the loop diuretics.

This cotransporter provides part of the concentration gradient for the countercurrent concentrating mechanism in the kidney and is responsible for the reabsorption of 20–30% of the sodium filtered at the glomerulus.

A

Na+/K+/2Cl– carrier (NKCC2)

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16
Q

This loop diuretic is a moderately effective uricosuric drug if blood volume is maintained.

A

Ethacrynic acid

17
Q

This is an important toxic effect of the loop agents.

A

Ototoxicity

18
Q

The site of significant dilution of urine

A

Loop of Henle

19
Q

Toxicities of Loop diuretics:

A
Hemoconcentration
Hypokalemic metabolic alkalosis
Hypovolemia and cardiovascular complications
Ototoxicity
Sulfa allergy
20
Q

The DCT actively pumps sodium and chloride out of the lumen of the nephron via the _____.

A

Na+/Cl– carrier (NCC)

21
Q

What is the mechanism of action of thiazide diuretics?

A

Inhibit Na+/Cl- transporter in distal convoluted tubule.

Cause moderate diuresis and reduced excretion of calcium.

22
Q

Side effects of thiazide diuretics:

A

HyperGlycemia
HyperLipidemia
HyperUricemia
HyperCalcemia

23
Q

Uses of thiazide diuretics:

A
  1. Hypertension
  2. Mild heart failure
  3. Chronic renal calcium stone formation can sometimes be controlled with thiazides because they reduce urine calcium concentration.
  4. Nephrogenic diabetes insipidus.
24
Q

Cortical collecting ducts

A
  1. Last tubular site of sodium reabsorption
  2. Under the influence of aldosterone
  3. Primary site of acidification of the urine
  4. Last site of potassium excretion
  5. Sites of action of the potassium-sparing diuretics
25
Q

A potasium-sparing diuretic that causes gynecomastia

A

Spironolactone

26
Q

Side effects of spironolactone and eplerenone:

A
  1. Hyperkalemia
  2. Impotence
  3. Benign prostatic hyperplasia
  4. Hyperchloremic metabolic acidosis
  5. Gynecomastia (spironolactone only)
27
Q

This is a potassium sparing diuretic (Na blocker), inhibiting ENaC epithelial sodium channels in cortical collecting duct, reduces Na reabsorption and K
excretion

A
  1. Amiloride

2. Triamterine

28
Q

Because they are freely filtered at the glomerulus but poorly reabsorbed from the tubule, they remain in the lumen and “hold” water by virtue of their osmotic effect.

A

Osmotic diuretics

29
Q

What is the major location for the action of osmotic diuretics?

A

Proximal convoluted tubule

30
Q

Indications of osmotic diuretics (e.g. mannitol)

A
  1. Rhabdomyolysis
  2. Hemolysis
  3. Increased intracranial pressure
  4. Acute glaucoma
31
Q

Site of action of ADH agonists and antagonists

A

Medullary Collecting Duct

32
Q

Diuretics causing acidosis

A
  1. Carbonic anhydrase inhibitors

2. K+-sparing diuretics

33
Q

Diuretics causing alkalosis

A
  1. Loop diuretics

2. Thiazides

34
Q

A drug that increases the formation of dilute urine and is used to treat SIADH is

A

ADH Antagonists

demeclocycline and conivaptan or tolvaptan