Diuretics Flashcards

1
Q

Carbonic anhydrase inhibitor

A

Acetazolamide

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2
Q

NaK 2Cl symport inhibitor

A

Furosemide

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3
Q

Na Cl symport inhibitors

A

Hydrochlorthiazide

Chlorothiazide

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4
Q

2 groups of K sparing diuretics

A

Epithelial Na channel inhibitors

Aldosterone antagonists

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5
Q

Epithelial Na channel inhibitors

A

Amiloride

Triamterene

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6
Q

Aldosterone antagonists

A

Spironolactone

Eplerenone

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7
Q

Osmotic diuretics

A

Mannitol

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8
Q

Vasopressin receptor antagonists

A

Demeclocycline

Tolvaptan

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9
Q

Endogenous OAT substrates (4

A

Urate
Bile acids
Oxalate
Prostaglandins

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10
Q

Exogenous OAT substrates (6)

A
Hydrochlorothiazide
Furosemide
Acetazolamide
Probenecid
Pencillin
Aspirin
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11
Q

OCT endogenous substrates (3)

A

Creatinine
Epinephrine
Histamine

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12
Q

OCT exogenous substrates (5)

A
Amiloride
Triamterene
Cimetidine
Atropine
Quinine
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13
Q

Site of action is in proximal tubule, where it competitively inhibits carbonic anhydrase

A

Acetazolamide

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14
Q

Carbonic anhydrase is responsible for ___ reabsorption and __ secretion

A

NaHCO3, acid (H+)

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15
Q
Control vs. \_\_\_\_
Vol: 1 vs 3 (ml/min)
pH: 6 vs 8
Na+: 72 vs. 302
K+: 22 vs. 260
Cl-: 85 vs. 95
HCO3-: 1 vs. 120
A

Acetazolamide (CA inhibitor)

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16
Q

Acetazolamide effect on renal hemodynamics

A

Increases NaCl delivery to macula densa, reducing RBF (afferent arterioles constricted) and GFR

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17
Q

Uses=
Open-angle glaucoma
Altitude sickness
Epilepsy

A

Acetazolamide

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18
Q

ADEs=
Renal stone formation (urinary alkalinization)
Potassium wasting
Worsens hepatic encephalopathy (diversion of ammonia into systemic circulation)

A

Acetazolamide

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19
Q

Site of action is in thick ascending limb of the loop of Henle, inhibits Na+-K+-2Cl- symporters

A

Furosemide (also abolishes trans-epithelial potential difference that drives paracellular transport of Ca and Mg)

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20
Q
Control vs. \_\_\_\_
Vol: 1 vs 8 (ml/min)
pH: 6 vs 6
Na+: 72 vs. 1615
K+: 22 vs. 115
Cl-: 85 vs. 990
HCO3-: 1 vs. 1
A

Furosemide

21
Q

Urinary effects:
Increase in Ca and Mg excretion
Decreased uric acid excretion (chronic effect, exacerbates gout)
Reduces ability of kidney to dilute urine when over-hydrated and concentrate urine during dehydration

A

Furosemide

22
Q

Furosemide renal hemodynamic effects:

A
  1. Increases RBF and redistributes it to cortex (prostaglandin-mediated)
  2. Stimulates release of renin (blocks TGF by inhibiting salt transport into the macula densa)
23
Q

Acutely increases systemic venous capacitance and decreases left ventricular filling pressure
May be beneficial to patients with pulmonary edema

A

Furosemide (prostaglandin mediated)

24
Q

PK= highly protein bound
Delivered to apical membrane by OAT
Short half-life
“Post-diuretic” sodium retention

A

Furosemide

25
Uses= 1. Hyponatremia + IV hypertonic saline 2. Hypercalcemia + IV isotonic saline 3. Edema of nephrotic syndrome 4. Congestive heart failure 5. Acute pulmonary edema
Furosemide
26
ADEs= boxed warning for electrolyte and fluid loss Hyponatremia, hypokalemia, hypocalcemia (cause in osteoporosis) Hyperuricemia
Furosemide
27
ADEs= ototoxicity (tinnitus, vertigo, deafness) Hyperglycemia (caution in co-admin with sulfonylureas) NSAIDs reduce diuretic effect
Furosemide
28
Site of action is in distal convoluted tubule, where it inhibits Na+-Cl- symporter ALSO weak inhibitor of carbonic anhydrase in PCT
Hydrochlorothiazide (chlorothiazide)
29
``` Moderate efficacy (5% of filtered load) Shallow dose-response Efficacy substantially reduced when GFR is low (<30-40 mL/min) ```
Hydrochlorothiazide
30
``` Control vs. ____ Vol: 1 vs 3 (ml/min) pH: 6 vs 7.4 Na+: 72 vs. 650 K+: 22 vs. 110 Cl-: 85 vs. 650 HCO3-: 1 vs. 25 ```
Hydrochlorothiazide
31
DECREASES excretion of Ca Decreases kidney's ability to dilute urine during water diuresis (concentration ability is OK) No effect on renal hemodynamics
Hydrochlorothiazide
32
Protein bound and delivered by OAT | Longer half-lives
Hydrochlorothiazide
33
Uses= 1. Hypertension 2. Mild edema 3. Nephrogenic diabetes insipidus (paradoxical effect) 4. Calcium nephrolithiasis and osteoporosis
Hydrochlorothiazide
34
``` ADEs= Hyponatremia, hypokalemia Hyperuricemia Hyperglycemia & hyperlipidemia Erectile dysfunction ```
Hydrochlorothiazide
35
DDIs of HCT (2)
1. NSAIDs reduce diuretic efficacy | 2. Quinidine- hypokalemia increases risk of torsades de pointes (arrhythmia)
36
Site of action is the late DCT and collecting duct, where they block epithelial Na+ channels on the apical membrane of principal cells
Triamterene and amiloride (ENaC inhibitors)
37
Site of action is the late DCT and collecting duct, where they block CYTOSOLIC mineralocorticoid receptors in principal cells, reducing expression of some proteins
Spironolactone and eplerenone (Aldosterone antagonists)
38
Abolish the trans-epithelial potential that drives tubular secretion of K+ and H+
ENaC inhibitors and aldosterone antagonists (ROMK channels and Type A intercalated cell H+-ATPase)
39
``` Control vs. ____ Vol: 1 vs 2 (ml/min) pH: 6 vs 7.2 Na+: 72 vs. 375 K+: 22 vs. 15 Cl-: 85 vs. 345 HCO3-: 1 vs. 15 ```
Triamterene (SOME ACTION ON CARBONIC ANHYDRASE)
40
Potassium-sparing diuretics' effect on renal hemodynamics
None
41
Uses: Prevent K+-wasting Liddle syndrome Cystic fibrosis
ENaC inhibitors (triamterene and amiloride, K-sparing diuretics)
42
``` Uses: Prevent K+-wasting Primary hyperaldosteronism Hepatic cirrhosis CHF ```
Aldosterone antagonists (spironolactone, eplerenone)
43
ADEs= boxed warning for hyperkalemia (use cautiously with ACE inhibitors and NSAIDs)
Potassium sparing diuretics (triamterene, amiloride, spironolactone, eplerenone)
44
ADEs= gynecomastia, impotence, hirsutism, decreased libido
Aldosterone antagonists (spironolactone > eplerenone)
45
Site of action is entire tubule | Reduces renal medullary tonicity, which reduces the passive reabsorption of NaCl in the ascending limb
Mannitol (osmotic diuretic, increases the osmolarity of the tubular fluid)
46
Expands ECF volume | Increases excretion of ALL electrolytes
Mannitol (osmotic diuretic)
47
Increases RBF GFR is unchanged Inhibits release of renin
Mannitol
48
Given IV for dialysis disequilibrium syndrome, reducing CSF and intra-ocular pressure, and minimizing acute tubular necrosis
Mannitol
49
Contraindicated in heart failure (edema) and active cranial bleeding
Mannitol