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Renal > Diuretics > Flashcards

Diuretics Flashcards

1
Q

loop diuretic effects on acid/base

A

thiazide and loop diuretics induce metabolic alkalosis in three ways: 1. hypovolemia -> incr Na reabs in PT via Na-H exchanger due to incr AgII (leading to more bicarb reabs), 2. hypovolemia -> hyperaldo -> three mechs -> alkalosis, 3. these diuretics cause more Na in distal tubule, where Na enters principal cell and causes negative lumen V which incr H+/K+ secr

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2
Q

thiazide diuretic effects on acid/base

A

thiazide and loop diuretics induce metabolic alkalosis in three ways: 1. hypovolemia -> incr Na reabs in PT via Na-H exchanger due to incr AgII (leading to more bicarb reabs), 2. hypovolemia -> hyperaldo -> three mechs -> alkalosis, 3. these diuretics cause more Na in distal tubule, where Na enters principal cell and causes negative lumen V which incr H+/K+ secr

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3
Q

osmotic diuretic effects on acid/base

A

osmotic diuretics induce metabolic acidosis (bicarb excreted via solvent drag?)

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4
Q

CA inhibitor effects on acid/base

A

CA inhibitors induce metabolic acidosis (more bicarb excretion)

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5
Q

K-sparing diuretics effects on acid/base

A

K-sparing diuretics induce metabolic acidosis (Na not reabsorbed, therefore lumen not negative, therefore H+ not excreted)

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6
Q

effects on acid-base by: osmotic diuretics, CAI, loop diuretics, thiazides, K sparing diuretics

A

thiazide and loop diuretics induce metabolic alkalosis in three ways: 1. hypovolemia -> incr Na reabs in PT via Na-H exchanger due to incr AgII (leading to more bicarb reabs), 2. hypovolemia -> hyperaldo -> three mechs -> alkalosis, 3. these diuretics cause more Na in distal tubule, where Na enters principal cell and causes negative lumen V which incr H+/K+ secr; CA inhibitors induce metabolic acidosis (more bicarb excretion); osmotic diuretics induce metabolic acidosis (bicarb excreted via solvent drag?); K-sparing diuretics induce metabolic acidosis (Na not reabsorbed, therefore lumen not negative, therefore H+ not excreted)

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7
Q

loop diuretic effects on K

A

loop/thiazide diuretic cause V depletion (-> aldo) and incr distal Na delivery (inhibit TAL/DCT Na reabs) -> incr K secretion -> hypokalemia; also cause alkalosis -> hypokalemia; thiazide are more kaliuretic than loop b/c they have longer DOA and thus less likely to have K conserving time periods

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8
Q

thiazide diuretic effects on K

A

loop/thiazide diuretic cause V depletion (-> aldo) and incr distal Na delivery (inhibit TAL/DCT Na reabs) -> incr K secretion -> hypokalemia; also cause alkalosis -> hypokalemia; thiazide are more kaliuretic than loop b/c they have longer DOA and thus less likely to have K conserving time periods

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9
Q

osmotic diuretic effects on K

A

osmotic diuretics cause V depletion and incr distal NaCl delivery -> hypokalemia

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10
Q

Ca inhibitor effects on K

A

acetazolamide causes V depletion (-> aldo) and incr distal Na delivery (w/ NaHCO3) and poorly resorbable anion (HCO3-) delivery -> hypokalemia

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11
Q

mannitol

A

osmotic diuresis

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12
Q

acetazolamide

A

CA inhibitors

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13
Q

furosemide

A

inhibits NKCC2 by substituting for chloride on transporter

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14
Q

how do most diuretics get into tubule?

A

most via tubular secretion rather than glomerular filtration (protein-bound)

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15
Q

mechs of “braking phenomenon”

A

neural (SNS), endocrine (RAAS), physical hypertrophy of unaffected nephron segments (chronic diuretic resistance)

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16
Q

conditions associated w/ decreased diuretic action (4)

A

bowel wall edema (no GI abs of drug); hypoalbuminemia (no proteins to bind drugs); ECV depletion (decr RPF); CKD

17
Q

CA inhibitors lost from PT, lost in urine

A

lost from PT: bicarb, Na (b/c NaH has no gradient so Na not reabs), water; however, Na reabs in distal nephron, so instead lost in urine: bicarb, K (due to distal delivery of NaHCO3)

18
Q

clinical use of CA inhibitors (4)

A

limited use as natriuretic; correction of metabolic alkalosis (be careful b/c alkalotic pts are already hypokalemic and CA inhibitor will worsen it); altitude sickness; glaucoma

19
Q

loop diuretics lost in urine

A

chlorine, K, Na, water, Ca, Mg; these diuretics also block uric acid secretion so less uric acid lost; more water than Na lost (hypotonic urine -> can use to correct hyponatremia)

20
Q

clinical use of loop diuretics (4)

A

correction of edematous disorders (CHF, pulm edema, nephrotic syndrome, renal failure); hyperkalemia; hypercalcemia; severe HTN (rarely used due to short half life)

21
Q

loop vs thiazide half life

A

thiazide longer half life (better to tx HTN, more likely to cause kaliuresis)

22
Q

loop diuretic side effects (7)

A

hypokalemia, hypocalcemia, hypercalcuria (stones), hypomagnesemia, hyperuricemia (block uric acid secretion), ototoxicity (usually reversible, worse w/ ethacrynic acid, b/c NKCC also in ear), sulfa allergy (use ethacrynic acid b/c no sulfa group)

23
Q

ethacrynic acid

A

loop diuretic used for ppl w/ sulfa allergies, has side effect of ototoxicity (so don’t use unless severe sulfa allergy)

24
Q

thiazide diuretics: onset of action timeline, natriuretic effect timeline, potency, effects on ions (Na, Cl, Ca, K, Mg)

A

onset of action 2-3 hrs, natriuretic effect < 6 hrs; less potent than loop diuretics b/c less Na reabs in DCT: loss of NaCl in urine (through NCC), increased calcium reabs (used to prevent stones and tx hypercalcuria), and loss of K and Mg in urine

25
Q

clinical use of thiazides (4)

A

1st line therapy in HTN (anti-HTN effects actually continue after braking phenomenon) along w/ low salt diet; combo w/ loop diuretic to prevent braking phenomenon in chronic edematous states (beware of hypokalemia and hypomagnesemia); prevention of stones (1st line therapy due to hypocalcuric effects); tx of hyperkalemia

26
Q

side effects of thiazides (7)

A

hypokalemia; hypomagnesiumia; hyponatremia; hyperuricemia (block uric acid secretion); incr Ca reabs; carb intolerance (impaired insulin release); sulfa allergy

27
Q

amiloride

A

blocks ENaC

28
Q

spironolactone

A

aldo receptor antagonist

29
Q

eplerenone

A

aldo receptor antagonist

30
Q

clinical uses of K sparing diuretics (4)

A

not very good natriuretics, but used w/ other diuretics to prevent hypokalemia; spironolactone doesn’t req tubular secretion and so works well at low EABV -> use to improve survival in CHF, cirrhosis, and for its anti-proteinuric effects (anti RAAS)

31
Q

side effects of K sparing diuretics (2)

A

hyperkalemia in pts prone to it (CKD, CHF -> balance w/ loop diuretic in these pts); painful gynecomastia w/ spironolactone

32
Q

osmotic diuretics (4)

A

mannitol, radiocontrast dye, glucose (in hyperglycemia), urea (after relief from obstructive uropathy or high-protein tube feedings)

33
Q

osmotic diuretics clinical uses (2)

A

lead to Na and water losses, but lose more water than Na (hypotonic fluid loss) -> can lead to hyperosmolarity of blood (use to tx incr intracranial P due to hypotonicity); exogenous osmotic agents act as volume expanders in vasculature -> don’t use in edematous states, but good for dialysis pts who are hypotensive

34
Q

how is Na loss w/ osmotic diuretics?

A

Na abs but water is not due to effective osmole (like mannitol) in tubule, thus as Na is absorbed more than water, [Na] in tubule decreases so that there is no concentration gradient remaining to drive reabsorption; so while Na and water are thus both lost in urine, there is still more water lost than sodium -> leads to hypertonicity of blood

35
Q

Na excretion (as % of filtered load) for: osmotic diuretics, CAI, loop diuretics, thiazides, K sparing diuretics

A

osmotic: 10%, CAI: 5-10%, loop: 25%, thiazide: 5-10%, K-sparing: 3-5%

36
Q

effects on Ca excretion by: osmotic diuretics, CAI, loop diuretics, thiazides, K sparing diuretics

A

osmotic diuretics incr Ca excretion (solvent drag); CAI incr Ca excretion (solvent drag) - incr calciuresis along w/ alkaline urine = stones; loop diuretics incr Ca excretion (no positive lumen to push reabs of Ca) -> can cause stones; thiazide diuretics decr Ca excretion -> tx stones; K sparing diuretics don’t affect Ca excretion

37
Q

effects on free water excretion by: osmotic diuretics, CAI, loop diuretics, thiazides, K sparing diuretics

A

osmotic diuretics and CAI incr water excretion (incr NaCl delivery to DCT allows increased dilution); loop and thiazide diuretics decr water excretion b/c can’t dilute w/ NCC and NK2Cl blocked; K sparing diuretics don’t affect dilution ability

38
Q

effects on free water reabs by: osmotic diuretics, CAI, loop diuretics, thiazides, K sparing diuretics

A

osmotic diuretics and CAI incr water reabs; loop diuretics decr water reabs (can’t concentrate b/c gradient is dissipated); thiazide and K sparing diuretics don’t affect water reabs

Renal (8 decks)

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