Cardiovascular pharmacology V Flashcards

1
Q

where is potassium primarily reabsorbed?

A

proximal convoluted tubule

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2
Q

what is reabsorbed at the proximal convoluted tubule?

A
  1. bicarb
  2. sodium (and water)
  3. potassium
  4. glucose
  5. amino acids
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3
Q

what is reabsorbed at the thin descending limb?

A

water

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4
Q

what is the main transporter of the thick ascending limb?

A

Na/K/2Cl

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5
Q

what is the main transporter of the distal convoluted tubule?

A

Na-Cl

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6
Q

reabsorption of what molecules takes place in the collecting duct?

A
  1. sodium
  2. water

at the effect of aldosterone

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7
Q

where does aldosterone exert its effects?

A

collecting duct (sodium and water reabsorption)

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8
Q

where does ADH exert its effects?

A

collecting duct - blocking water reabsorption

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9
Q

what is the result of increased tubular solute concentration?

A

secretion of potassium at the collecting duct (loss of potassium - can cause arrhythmias)

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10
Q

what are the three main mechanisms of action of the carbonic anhydrase inhibitors?

A
  1. decrease reabsorption of bicarb in PCT (main)
  2. increase in U-HCO3 excretion
  3. loss of bicarb / increase ammonium secretion
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11
Q

what is the result of decreasing reabsorption of bicarb in the PCT?

A
  1. increase solute delivery to macula densa
  2. TGF - tubular glomerular feedback
  3. increase afferent arteriole resistance
  4. decrease in renal blood flow and GFR
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12
Q

what is the result of increasing U-HCO3 excretion?

A
  1. increased NaCl excretion
  2. diuresis, increased potassium excretion
  3. increased urine pH and metabolic acidosis
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13
Q

what is the result of losing bicarb and increaseing ammonium secretion?

A
  1. increased urine pH

2. metabolic acidosis

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14
Q

what class of drug is acetazolamide?

A

carbonic anhydrase inhibitor

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15
Q

what are the clinical applications of acetazolamide?

A
  1. glaucoma
  2. acute mountain sickness
  3. induce urinary alkalinization
  4. edema
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16
Q

what are the contraindications of acetazolamide use?

A

cirrhosis

17
Q

what is the mechanism of action of osmotic diuretics?

A
  1. freely filtered but poorly reabsorbed
  2. increase tubular fluid osmotic pressure - decrease tubular fluid reabsorption
  3. stimulation of potassium secretion (risk of hypokalemia)
18
Q

what is the main site of action for osmotic diuretics?

A

thin limbs of the loop of Henle

19
Q

what is the main osmotic diuretic agent?

A

mannitol

20
Q

what are the clinical applications of osmotic diuretics?

A
  1. prophylaxis of acute renal failure
  2. cerebral edema
  3. dialysis disequilibrium syndrome
  4. acute attacks of glaucoma
21
Q

how do osmotic diuretics prevent acute renal failure?

A
  1. expand ECV
  2. maintain GFR
  3. increase tubular fluid flow
  4. prevent tubule obstruction from shed cell constituents or crystals
  5. reduce renal edema
22
Q

what are the adverse effects of osmotic diuretics?

A

extracellular volume expansion

23
Q

loop diuretics act on what transporter? where?

A
  1. Na-K-2Cl pump

2. thick ascending limb

24
Q

furosemide is what type of diuretic?

A

loop

25
Q

what is the main effect of loop diuretics?

A

venodilation - decrease right atrial pressure and pulmonary capillary wedge pressure within minutes

26
Q

what is the mechanism of action for loop diuretics?

A
  1. increase fractional calcium excretion by 30% by decreasing lumen-positive transepithelial potential that promotes paracellular calcium reabsorption
  2. increase fractional magnesium excretion more than 60% by decreasing voltage-dependent paracellular transport
  3. an alternative way to decrease plasma calcium
27
Q

what are the clinical applications of loop diuretics?

A
  1. pulmonary edema
  2. CHF
  3. acute renal failure
  4. hyperkalemia - saline and loop diuretics
28
Q

what are the major adverse effects of loop diuretics?

A
  1. HYPOKALEMIA
  2. hyponatremia
  3. hypocalcemia
  4. hypomagnesia
  5. ototoxicity
  6. hyperuricemia