Cardiovascular pharmacology V Flashcards

(28 cards)

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?

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?

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?

25
what is the main effect of loop diuretics?
venodilation - decrease right atrial pressure and pulmonary capillary wedge pressure within minutes
26
what is the mechanism of action for loop diuretics?
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
what are the clinical applications of loop diuretics?
1. pulmonary edema 2. CHF 3. acute renal failure 4. hyperkalemia - saline and loop diuretics
28
what are the major adverse effects of loop diuretics?
1. HYPOKALEMIA 2. hyponatremia 3. hypocalcemia 4. hypomagnesia 5. ototoxicity 6. hyperuricemia