- 44% interstitium - 17% plasma - 17% bone - 17% dens conn tiss - 5% transcellular

Exam I - Diuretics Flashcards by Kristian Melby

Drug List

Carbonic Anhydrase Inhibs

Acetazolamide

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Drug List

Osmotic Diuretics

Mannitol

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Drug List

Loop Diuretics

Furosemide

inhibit TAL Na/K/2Cl

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Drug List

Thiazides

Hydrochlorathiazide

inhib DCT Na/Cl

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Drug List

K-Sparing

Amiloride

inhib late DCT ENaC

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Drug List

ARB/K-sparing

Spironolactone
(block Aldosterone by
inhib DCT Na/K)

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Drug List

ADH antags

Tolvaptan

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Diuretic Braking

-Physiological compensation
for lost Na
-^symp, ^RAAS, ^ADH
-new steady state reached

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ECFV Body Fluid

44% interstitium
17% plasma
17% bone
17% dens conn tiss
5% transcellular

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Diuretics target what ECFV?

-plasma
-interstitial
(these compartments equilibrate)

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Edematous Indications

CHF
Pulm Edema
Nephrotic Dz
Hepatic Cirrhosis

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Hypertensive Indications

Essential
Renovasc HTN (hypoperfusion)
Renal HTN (poor excretion)
Hyperaldosteronism

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Right-sided HF

Pathophysiology/Clin

systemic edema
ascites
nocturia
hepatomegaly

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Left-sided HF

Pathophysiology/Clin

pulm edema
SOB
Wheezing

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Renal Handling Na+
Nephron Reabsorption
Percentages

67% PCT
25% TAL
4% early DCT
3% late DCT

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Renal Handling Na+
Nephron Reabsorption
Channels

PCT: glc/AA/phosph symport
PCT: H+ antiport
TAL: Na/K/2Cl symport
DCT: Na/Cl symport
DCT: Na/K antiport

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Carbonic Anhydrase

Function

drives HCO3->H2CO3-> H2O/CO2
intracellularly and in PCT
increases intracellular H+ for H+/Na+ antiport

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Carbonic Anhydrase Inhibitors

Mechanism

-CAIs secreted into PCT
-inhibs CA both
intra/extracellularly
-reduces available H+ for Na+/H+ antiport
-Na+ therefore left in PCT lumen

Carbonic Anhydrase Inhibitors

Systemic Effects

Alkalinized urine
Activates TGF
decr. Plasma HCO3 (decr. pH), Cl

Carbonic Andydrase Inhibitors

Indications

decr intraocular pressure
metabolic alkalosis
acute mountain sickness
resp alkalosis prophylaxis

Carbonic Anhydrase Inhibitors

Adverse

hyperchloremic metabolic acidosis

- renal stones

Loop Diuretics

Mechanism

secreted into PCT
Blocks TAL Na/K/2Cl symport
Abolishes corticomedullary gradient

Loop Diuretics

Adverse

abolish osmotic gradient
increase renal blood flow
increased excretion of all ions
hypokalemia (arrhythmias)
HoTN
Hyperuricemia
Ototoxicity

Loop Diuretics

Indications

-Edema of renal/pulm/cardiac/hepatic origin

Thiazides | Mechanism

- Secreted into PCT (anion transporter) - Inhibit Na/Cl contransporter in DCT - Do NOT abolish corticomedullary gradient - Ca2+ sparing

Thiazides | Adverse

- hypokalemia (combat with ACEI co-rx) - metablolic alkalosis - hypovolemia (and further hypokalemic exacerbation) - hypercalcemia/glycemia (DM)/lipidemia/uricemia - HoTN

Thiazides | Indications

- hypercalciuria - Nephrogenic diabetes insipidus - HTN, CHF

Loop/Thiazide K+ loss Cells responsible

- CD principle cells | - via apical K+ channels

Loop/Thiazide H+ loss Cells responsible

- CD intercalated cells | - via H+/K+ exchange

K-sparing ARBs | Mechanism

- do NOT need to be secreted; act on basolateral membrane - canrenone is active metabolite - complexes with and inactivates mineralocorticoid receptor in DCT - inhibits Na/K antiporter in CD

K-sparing ENaC blockers | Mechanism

- secreted into PCT by cation transporter - block luminal ENaC Na+ reabsorption in late DCT/CD - downregs complimentary K+ secretion/excretion - effects are independent from aldosterone

K-Sparing ENaC blockers | Adverse

-hyperkalemia (esp w/ renal dz)

K-Sparing ENaC blockers | indications

-adjunct to loop/thiazide tx to preserve K+

K-Sparing ARBs | adverse

- hyperkalemia (contra'd in chronic renal insufficiency) - gynecomastia :( (antiandrogenic) - menstrual irregularities

Osmotic Diuretics | Mechanism

- freely filtered at glomerulus - osmotic gradient favors water in tubules - acts on water permeable segments (PT, TDLH, CD) - incr renal blood flow

Osmotic Diuretics | Adverse

- Mg2+ wasting | - Hyperkalemia

Osmotic Diuretics | Indications

-reduce intracranial/intraocular P before/after surgery

ADH antagonists | Mechanism

-binds V2 ADH receptor on CD basolateral membrane

ADH antagonists | Adverse

-hypernatremia

ADH antagonists | Indications

-SIADH

Is EtOH diuretic?

- Yes! | - Why? Interferes with Aquaporins in CD

Diuresis not optimal? | What shoud you do?

- synergistic additive effects of co-rx loop + thiazide | - co-rx should be given with close hemodynamic monitoring

Diuresis causing hypokalemia? | What should you do?

-co-rx with K-sparing diuretic

Is caffeine diuretic?

- Yes! | - Why? it's a methylxanthine; blocks PCT Na reabsorption