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physio- exam 3 > renal part 4 > Flashcards

renal part 4 Flashcards

1
Q

how do Osmotic diuretics work?

A

retain water by increasing osmotic pressure

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2
Q

where in the nephron do osmotic diuretics work?

A

Proximal Tubule

&

descending Loop of Henle

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3
Q

how do carbonic anhydrase inhibitors work?

A

reduce Na+ reabsorption

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4
Q

the __________ is the major site of action for carbonic anhydrase inhibitors

A

proximal tubule

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5
Q

how do loop diuretics work?

A

inhibit Na+ reabsorption via the Na+ K+ 2Cl- symporter

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6
Q

where do loop diuretics primarily work on?

A

act in Thick Ascending Loop

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7
Q

________ diuretics block Na+Cl- symporter

A

thiazide diuretics

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8
Q

what part of the nephron do thiazide diuretics work on?

A

the early distal tubule

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9
Q

K+ sparing diuretics work by doing what?

A

inhibit sodium reabsorption AND potassium secretion

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10
Q

what part of the nephron do K+ sparing diuretics effect?

A

actin in:

late Distal Tubule

Cortical Collecting Duct

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11
Q

what are the 2 classes of potassium-sparing diuretics?

A
  1. aldosterone antagonists

2. ENaC blockers

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12
Q

what are Aquaretics?

A

ADH receptor antagonists

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13
Q

_______ diuretics act where tubule is freely permeable to water

A

osmotic

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14
Q

osmotic diuretics work by impairing __________ reabsorption

A

Na+

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15
Q

what % of filtered Na+ is excreted when taking an osmotic diuretic?

A

10% of filtered Na+ is excreted

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16
Q

_________ is also not reabsorbed when taking an osmotic diuretic, due to the lack of solvent drag

A

Calcium

Ca2+

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17
Q

what are 2 examples of osmotic diuretics?

A

1) mannitol

2) glucose

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18
Q

what is the effect of inhibiting Carbonic anhydrase in the proximal tubule?

A

reduces the H+ available for the Na+/H+ antiporter

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19
Q

why are Carbonic anhydrase inhibitors most effective in the proximal tubule?

A

its where about 1/3 of Na+ reabsorption occurs

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20
Q

why are Carbonic anhydrase inhibitors not particularly effective?

A

downstream segments will increase Na+ reabsorption when tubular Na+ increases

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21
Q

____________ diuretics Inhibit Na+K+2Cl- symporters in the thick ascending limb

A

loop diuretics

22
Q

what is the effect of inhibiting Na+K+2Cl- symporters in the thick ascending limb?

A
  • inhibits Na+ reabsorption

- urine leaving loop is not dilute

23
Q

why does the loop diuretic’s ability to stop dilution of urine make it so effective?

A

no osmotic gradient established in the medulla interstitium so water not reabsorbed along collecting duct

24
Q

Loop diuretics can increase Na+ excretion to as much as _____% of filtered load

A

25%

25
Q

_______ diuretics block Na+Cl- transporter in the distal tubule

A

thiazide

26
Q

what percentage of Na+ is excreted when a thiazide diuretic is taken?

A

5-20% of the filtered Na+ is excreted

27
Q

how do aldosterone antagonists work?

A

block aldosterone’s ability to increase Na+ transporters in principal cells of the collecting duct & distal tubule

28
Q

aldosterone antagonists must get inside _____ cells to block aldosterone receptors

A

tubular

29
Q

How do ENaC blockers work?

A

block Na+ reabsorption across the apical membrane of the collecting duct & distal tubule

30
Q

________ (a ENaC blocker) is secreted into the proximal tubule

A

amiloride

31
Q

why does the continued use of diuretics lessen their effectiveness?

A

diuretics decrease ECV, which means compensatory mechanisms get activated

32
Q

diuretics will cause the decreased release of ______________

A

natriuretic peptides

33
Q

what occurs in the juxtaglomerular apparatus when a diuretic is taken?

A
  • secretes renin
  • causes increased angiotensin 2 & aldosterone
  • end result: decreased Na+ excretion
34
Q

why do many diuretics also increase the excretion of K+?

A

due to:
- increased rate of flow of tubular fluid which stimulates K+ secretion

  • Reduced ECV which stimulates aldosterone production
35
Q

________ balance is affected by all diuretics

A

Acid-base

36
Q

metabolic acidosis is caused by what class of diuretics?

A

CA inhibitors

and

K+ sparing diuretics

37
Q

metabolic alkalosis is caused by which classes of diuretics?

A

Loop and thiazide diuretics

38
Q

why would K+ sparing diuretics cause metabolic acidosis ?

A

because H+ secretion in distal tubule and cortical collecting duct is inhibited

39
Q

Except for the K+ sparing diuretics, all other diuretics alter _______ excretion

A

calcium (Ca2+)

40
Q

which 2 diuretics act in the proximal tubule and reduce reabsorption of calcium in this segment (so excretion is increased)?

A

Osmotic and CA inhibitors

41
Q

Loop diuretics increase calcium excretion by what mechanism?

A

by affecting the transepithelial voltage

its normally the driving force for paracellular transport of calcium

42
Q

_________ diuretics stimulate calcium reabsorption in the distal tubule and thus reduce excretion

A

thiazide

43
Q

the distal tubule reabsorbs ____% of filtered calcium via active transport

A

9%

44
Q

Patients with chronic renal failure are almost always diagnosed with ________

A

anemia

45
Q

why does chronic renal failure cause anemia?

A

due inadequate secretion of erythropoietin (EPO) and loss of erythrocytes.

46
Q

EPO produced by ________________ in renal cortex

A

interstitial fibroblasts

47
Q

when is EPO production stimulated?

A

when PO2 is low

48
Q

what does EPO stimulate?

A

EPO stimulates differentiation of erythrocyte progenitor cells in the bone marrow

49
Q

EPO production is controlled at the ____________ level

A

transcriptional

50
Q

T/F: hypoxia-inducible factors 1 and 2 (HIF-1 and HIF-2) are produced when there is a drop in PO2

A

FALSE

they are continually produced

51
Q

why do HIF-1 and HIF-2 not continually act as transcription factors?

A

they are targeted for degradation when O2 normal

physio- exam 3 (9 decks)

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