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MQW U4 > Pharm --Renal/Diuretic > Flashcards

Pharm --Renal/Diuretic Flashcards

1
Q

___ contracts from 1/2 of Total body fluid (TBF) to 1/3 of TBF in adults

A

ECF

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2
Q

What is solute concentation/osmolarity of ICF and ECF

A

approx. 300mOsm/L

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3
Q

ICF is __% of body weight
ECF is __% of body weight
Blood volume is __% of body weight

A

ICF = 40%
ECF = 20%
Blood volume = 7%

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4
Q

K is high ___ the cell

Na is high ___ the cell

A 
K = high inside
Na = high outside

–b/c Na/K pump sends K inside and Na out; K can leak out, Na can’t come in

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5
Q

Daily urine output is ___L which is ___% of GFR

A

1-2L

0.5-1% of GFR

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6
Q

___ is the major solute determining ECF osmolarity

A

Sodium

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7
Q

Low Na in ECF causes what compensatory change in ECF volume?

A

Decreases to maintain osmolarity

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8
Q

Can sodium be:

  • -filtered?
  • -secreted?
  • -reabsorbed?
  • -excreted?
A
  • -Duh
  • -NO!
  • -yes
  • -yes
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9
Q

What is normal GFR (mL/min)

A

125ml/min

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10
Q

Normal plasma Na concentration:

A

140mM

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11
Q

Normal plasma bicarbonate concentration:

A

24mM

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12
Q

% of Sodium reabsorbed at:

  • -Proximal tubule
  • -TAL of Loop
  • -Distal tubule
A
  • -66%
  • -25%
  • -6-8%
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13
Q

Nephrotic syndrome is excess filtration and excretion of ___

A

Albumin

–leads to decreased plasma oncotic pressure

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14
Q

Most filtered bicarbonate is reabsorbed here

A

Proximal tubule

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15
Q

This portion of the nephron has “leaky” epithelium and is unable to maintain an osmotic gradient.

A

Proximal tubule

–66% of tubular filtrate is reabsorbed

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16
Q

Loop of Henle: thin descending, thin ascending, TAL

Which is/are impermeable to water?

A

thin ascending, TAL are impermeable to water (even in presence of ADH)

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17
Q

What portion of the nephron is the physiological origin of positive free water clearance?

A

Ascending limb of Loop

–no water reabsorption –> hypoosmotic tubular fluid

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18
Q

Circulating Aldosterone hormonally regulate this mechanism at this portion of the nephron.

A

Sodium reabsorption in the late distal tubule

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19
Q

Early vs. late distal tubule:

Which portion is permeable to water?

A

Late distal tubule = permeable when induced by interaction with antidiuretic hormone (ADH) –> concentrates urine by reabsorbing water

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20
Q

What is normal filtration fraction?

A

FF = GFR/RPF = 0.2

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21
Q

What is used to measure GFR? Why?

A

Inulin clearance

–It is not reabsorbed or secreted, so filtered = excreted

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22
Q

Excretion = Filtration + Secretion - Reabsorption
How is renal handling of Potassium (K) different in low K vs. high K diets?
In what portion of the nephron does this regulation occur?

A

Low K = no secretion, more reabsorption
High K = high secretion, less reabsorption

Distal tubule and cortical collecting duct

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23
Q

How do alkalosis and acidosis affect potassium (K) secretion?

A

Alkalosis –> increased K secretion

Acidosis –> decreased K secretion

24
Q

How do diuretics (except K sparing) cause hypokalemia?

A

Block of Na reabsorption upstream (TAL for loop and early DT for thiazide) causes increased Na secretion at late DT which induces K secretion

25
Q

What is negative free water clearance?

What hormone affects it?

A

Water in tubule reabsorbed back into circulation

  • -induced by ADH
  • -generates hypertonic urine
26
Q

How does volume expansion affect Aldosterone levels?

A

Volume expansion –> low aldosterone –> less Na reabsorption –> less water reabsorption –> dilute urine

27
Q

What is the mechanism of aquaretics?

A

Decrease ability of ADH to increase water permeability in late distal tubule and collecting duct –> dilute urine

28
Q

What are 4 osmotic diuretics?

A

Mannitol
Excess glucose
Urea
Isosorbide

29
Q

How do loop diuretics affect positive and negative free water clearance?

A

–Decrease positive free water clearance (directly, by increasing osmotic clearance in TAL)

–Decrease negative free water clearance (indirectly, by reducing ADH sensitivity (ability to concentrate urine) in the medullary CD from reduced medullary gradient)

30
Q

How do thiazide diuretics affect positive and negative free water clearance?

A

Only affects positive free water clearance (prevent salt reabsorption –> increased tubular concentration –> increased water clearance)

–Does not affect negative free water clearance (concentrating urine)

31
Q

Relative maximal fractional excretion of Na in:

  • -PT
  • -TAL
  • -DT
  • -CD
A 
TAL = 25% --loop
DT = 8% --thiazide
PT = 5% --CA inhibitor, osmotics
CD = 2% --K+ sparing diuretics
32
Q

Carbonic anhydrase inhibitors [increase/decrease]:

  • -tubular H+
  • -tubular pH
  • -Na/H exchanger rate
  • -Intracellular carbonic acid formation
A
  • -tubular H+ = decrease
  • -tubular pH = increase –> alkaline urine
  • -Na/H exchanger rate = decrease
  • -Intracellular carbonic acid formation = decrease
33
Q

Carbonic anhydrase can induce

  • -[hyper/hypo] kalemia
  • -metabolic [acidosis/alkalosis]
A
  • -Hypokalemia

- -Metabolic acidosis – excess bicarb excretion

34
Q

Why are osmotic diuretics used in shock and surgery?

A

Prevent acute renal failure – maintain urine flow

35
Q

What is the molecular mechanism of loop diuretics?

A

–Compete w/ chloride for occupancy in 1 of 2 Cl binding sites of Na-K-2Cl cotransporter in luminal membrane of TAL

36
Q

How long does it take for loop diuretics to induce diuresis?

A 
IV = within minutes
Orally = within an hour
37
Q

How do you prevent hyponatremia caused by chronic use of loop diuretics?

A

Limit water consumption – prevent volume expansion b/c loop diuretics reduce positive free water clearance

38
Q

When loop diuretics are used together with aminoglycoside antibiotics (gentamycin), there is a markedly increasked risk for what complication?

A

Ototoxicity – hearing loss

39
Q

What are loop diuretic effects on:

  • -Calcium
  • -Magnesium
  • -Potassium
A
  • -Increase calcium excretion
  • -Increase magnesium excretion
  • -Increase potassium excretion
40
Q

What is the molecular mechanism of thiazide diuretics?

A

Inhibit Na-Cl cotransporter in luminal membrane of early DT

41
Q

A patient on [loop/thiazide] diuretic is more at risk for hyponatremia

A

Thiazide diuretic – imbalance in renal volume regulation (since it only affects + (diluting urine ability) and not - (concentrating urine ability) free water clearance)

42
Q

What is the only segment of the nephron that reabsorbs glucose?

A

Proximal tubule

43
Q

Is mannitol reabsorbed and/or secreted?

A

Neither

44
Q

Do loop diuretics increase or decrease the ability of the kidney to excrete water in excess of solutes?

A

Decrease – lowers positive free water clearance = less ability to dilute urine

45
Q

What are the 2 substituted benzothiazide drugs?

A
  • -Chlorothiazide

- -Hydrochlorithiazide

46
Q

What are the 4 thiazide-like drugs?

A
  • -Chlorthalidone
  • -Metolazone
  • -Quinethazone
  • -Indapamide
47
Q

The early distal tubule is [permeable/impermeable] to water

A

Impermeable – even in the presence of ADH

48
Q

Do thiazide diuretics affect the kidney’s ability to correct for:

  • -increase in ECF?
  • -decrease in ECF?
A

–Increased ECF – YES = reduces ability to excrete water in excess of solutes (dilute urine/ + free water clearance) after excess water consumption

–Decreased ECF – NO = doesn’t affect ability to concentrate urine

49
Q

How is calcium excretion affected by:

  • -Loop diuretics?
  • -Thiazide diuretics?
  • -Amiloride (K-sparing)?
A
  • -Loop = increased excretion
  • -Thiazide = increased paracellular reabsorption –> decreased excretion
  • -Amiloride = decreased excretion
50
Q

Assuming Na consumption is constant, loop and thiazide diuretics induce what compensatory mechanism?

A

–Compensatory increase in Na and water reabsorption in proximal tubule (upstream) –> maintain sodium balance, but not enough to maintain water –> diuresis w/o hyponatremia

51
Q

Diuretics cause contraction alkalosis through what 2 mechanisms?

A
  • -ECF volume contraction w/o increased bicarb elimination

- -ECF volume contraction induces increased PT reabsorption of bicarb (to increase water reabsorption?)

52
Q

Which class of diuretics can be used to prevent kidney stone formation?

A

Thiazide – reverese idiopathic hypercalciuria

53
Q

How do thiazide diuretics affect GFR?

A

Decreases GFR

54
Q

Thiazide drug intereractions with digitalis and quinidine increase the risk of what events?

A
  • -Digitalis – arrhytmia

- -Quinidine – torsade des pointes

55
Q

Compete with Aldostere for binding to an intracellular receptor –> decrease amount of Aldosterone-Receptor (AR) complex –> decrease proteins that maintain Na reabsorption and K secretion
Also, indirectly inhibit Na/H exchanger

This is the molecular mechanism of what drug(s)?

A

Spironolactone

56
Q

Inhibit channel mediated Na reabsorption at the late DT –> decreased intracellular Na –> decreased Na/K ATPase –> decreased intracellular K –> decreased K secretion
Also, directly inhibit Na/H exchanger

This is the molecular mechanism of what drug(s)?

A

Amiloride

Triamterene

57
Q

This diuretic is a competitive antagonist of androgen receptors which:

  • -in males, cause: gynecomastia, erectile dysfunction, loss of libido
  • -in females, cause: amenorrhea, oligomenorrhea, breast soreness

What is it?

A

Spirinolactone

MQW U4 (9 decks)

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