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Renal Week 1 > Diuretics II > Flashcards

Diuretics II Flashcards

1
Q

What are some K-sparing diuretics? Structure?

A

Triametrene [Dyrenium] & Amiloride [Midamor]

organic bases and are not structurally related to aldosterone.

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2
Q

How do K sparing diuretics work?

A

They block ENaC sodium channels to inhibit Na reabsorption in DCT and CD

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3
Q

What are the effects of K sparing diuretics?

A
  • Increase Urinary excretion of Na+ (weak effect).

* inhibit the secretion of K+ and H+ (K-sparring)

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4
Q

Clinical uses of K sparing diuretics?

A

•Diuretics. Combined with HCTZ [Dyazide] to increase their effectiveness and decrease K+ excretion.

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5
Q

Side effects of K sparing diuretics?

A
  • Hyperkalemia,
  • Megaloblastic anemia in patients with cirrhosis

Triamterene rarely forms kidney stones

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6
Q

Responses to diuretics (thiazides in particular) are seen at lower doses, which produce a small but optimal natriuretic effect; higher doses should be avoided because of increase risk of side effects.

A

Responses to diuretics (thiazides in particular) are seen at lower doses, which produce a small but optimal natriuretic effect; higher doses should be avoided because of increase risk of side effects.

The antihypertensive effect of thiazides plateaus at 25mg of HCTZ.

A single morning dose of HCTZ will provide sustained effect, while reducing K+ wastage during the nighttime.

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7
Q

T or F. Most popular drugs for treatment of mild or moderate hypertension.

A

T.

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8
Q

What diuretics may be effective in patients with impaired renal function?

A

Metolazone and indapamide

However, most of these compounds are usually ineffective when GFR lower than 30 mL/min and/or serum
creatinine above 2.5 mg/dL.

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9
Q

T or F. Patients with “volume dependent” hypertension (notably African Americans and elderly, with low renin levels) show better responses.

A

T.

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10
Q

A poor response to thiazides may reflect what?

A

Either an overwhelming

load of dietary sodium or impaired renal capacity to excrete sodium

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11
Q

When are loop diuretics used?

A

More efficient diuretics than the thiazides. Used in patients
with severe hypertension unresponsive to thiazides,
especially with renal insufficiency, cardiac failure or cirrhosis.

Due to their high efficacy, these diuretics (furosemide in
particular) is administered I.V. in acute pulmonary edema.

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12
Q

Why do loop diuretics require more monitoring than thiazides?

A

They cause excessive natriuresis leading to more side effects than
thiazides. Therefore, they require more frequent monitoring.

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13
Q

What is a common cause of diuretic resistance?

A

Co-administration of NSAID (such as aspirin, Motrin.) with loop diuretics

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14
Q

When are K+ sparing diuretics particularly useful?

A

Useful in patients at risk of K+ depletion and in patients with hyperuricemia.

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15
Q

Spironolactone is the diuretic of choice in what disease?

A

cirrhosis and can
be titrated up to 400 mg/day in very rare cases.

If GFR is

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16
Q

Other uses of spirolactone?

A

Equipotent to Thiazides as antihypertensives, useful to
enhance the natriuretic effects of other diuretics.

Available combination formulations include:
Spironolactone+Hydrochlorothiazide; Triameterene
+Hydrochlorothiazide = [Dyazide] a very popular
antihypertensive diuretic.

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17
Q

Contraindications for spirolactone?

A

They are contraindicated in significant renal insufficiency

GFR

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18
Q

When is ADH released?

A
  • Elevation in plasma osmolarity > 280 mOsm/Kg.
  • Depletion of extracellular volume
  • Other: pain, nausea hypoxia
19
Q

What does ADH bindings to the VI receptor cause?

A

Binding of vasopressin to V1R activates Gq-PLC-IP3 pathway and mobilizes Ca2+ causing vasoconstriction of vascular smooth muscle

20
Q

Where are ADH V2 receptors located?

A

in principal cells in renal collecting ducts (CD)

21
Q

What does ADH bindings to the V2 receptor cause?

A

activates Gs-cAMP, PKA.

  • PKA increases rate of insertion of water channel containing vesicles (WCV’s) into the apical membrane of CD.
  • PKA phosphorylates the water forming channel aquaporin- 2, which are then inserted as tetramers into the apical membrane.
  • Aquaporin channels increase the permeability of CD to water.

• PKA also phosphorylates the urea transporter (termed
VRUT or UT1), and increases the permeability of CD to urea.

• This in concert with the TALH and the multiplier
concentrates urine, up to 4 times the osmolarity of plasma.

22
Q

What is the difference between central and nephrogenic DI?

A

Impaired water conservation caused by:

  • Inadequate AVP secretion (Central DI)
  • insufficient kidney AVP response (nephrogenic DI).
23
Q

What are some causes of central DI?

A
  • Head injury, surgery or trauma in the pituitary or hypothalamus, tumors, CNS ischemia etc.
  • Autosomal dominant (chrom 20) cause a gradual loss of AVP.
24
Q

What are some causes of nephrogenic DI?

A
  • Acquired: obstructive renal disease, Drugs: Lithium, clozapine.
  • Genetic: X-linked caused by gene encoding V2R that result in frame shift, truncated receptor or single amino acid mutations.
25
Q

What are the symptoms of Central and Nephrogenic DI?

A
  • Excrete large volumes or dilute urine.

* Drink a lot of water (polydipsia)

26
Q

How is Central DI distinguished from nephrogenic DI?

A

by the administration of a V2R agonist (such as desmopressin), which will increase urine osmolarity in patients with central
DI but not nephrogenic DI.

27
Q

How is Demopressin given for the treatment for central DI? Does it have V1 action?

A

Administered nasally (10 μg/whiff), IV, or oral tablet.

minimal V1 action

28
Q

What else is Demopressin used to treat?

A
  • Also used in bleeding disorders, given IV. or nasally to increase circulating levels of factor VIII and von Willebrand factor via extrarenal V2 receptors
  • Used also in nocturnal enurisis (bed wetting in children).
29
Q

How is nephrogenic DI treated?

A

• Maintain adequate water intake.

  • Thiazide Diuretics: might reduce polyuria by ~50%.
  • Cause mild depletion of extracellular water and sodium.

• Compensatory renal mechanisms increase the
reabsorptive capacities of the proximal convoluted
tubule, reducing the volume of (filtrate, i.e. water)
delivered to the distal tubule.

30
Q

What are some V1 receptor agonists? How is it given?

A

Terlipressin [Glypressin]: Restricted use.

Administered IV and has less side effects than vasopressin.

31
Q

What are the clinical uses of V1 receptor agonists?

A

Given IV to treat:

  • post operative ileus,
  • reduce bleeding in esophageal varices, and to
  • reduce bleeding during acute hemorrhagic gastritis.
32
Q

What is SIADH?

A

Excessive production of ADH resulting in impaired

water excretion and plasma Hypoosmolarity (Hyponatremia).

33
Q

What are some drugs that cause SIADH?

A
  • Psychotropics: SSRI, haloperidol & tricyclic anti depressants.
  • Sulfonylureas: chloropropamide.
  • Vinca Alkaloids: (Vincristine and vinblastine).
34
Q

When is SIADH treated?

A
  • Patient is asymptomatic if plasma osmolarity is 125-132 mM and Water restriction is enough.
  • Generally treatment is ignited when plasma Na+ falls below 120 mM
35
Q

How is SIADH treated?

A
  • Water restriction, IV hypertonic saline is used with extreme care in severe or acute SYMPTOMATIC hyponatremia.
  • Loop diuretics (interfere with kidney concentrating ability)
  • Demeclocycline: antagonizes ADH at V2 receptors.
  • Vaptans
36
Q

What are some other water retaining conditions?

A

• In CHF, cirrhosis, or nephrotic syndrome, effective blood volume is reduced; hypovolemia exacerbated by diuretics.

• Hypovolemia stimulates AVP release; patients may become
hyponatremic owing to vasopressin-mediated retention of water.

• Orally active V2 R antagonists provides a new therapeutic
strategy in patients with SIADH and hyponatremia in patients with heart failure, liver cirrhosis, and nephrotic syndrome.

37
Q

What is Tolvaptan?

A

ADH receptor antagonist that is 29X more selective for the V2R than the V1aR.

38
Q

When is Tolvaptan used?

A

Significant hypervolemic and euvolemic hyponatremia

[serum sodium

39
Q

Metabolism of Tolvaptan?

A

completely metabolized by CYP3.

40
Q

Side effects of Tolvaptan?

A

Hyperglycemia, GI disturbances and clotting problems.

41
Q

What is Conivaptan? What is it used for?

A
  • Less selective for the V2R than tolvaptan.

* Given IV for acute treatment of hyponatremia in hospital setting only.

42
Q

Side effects of Conivaptan?

A

Numerous side effects: such as infusion site reaction.

• Too rapid correction of hyponatremia (e.g., >12 mEq/L/24 hours) can cause osmotic demyelination resulting in dysarthria, mutism, dysphagia, lethargy, affective changes, spastic quadriparesis, seizures, coma and death.

In susceptible patients, including those with severe malnutrition, alcoholism or advanced liver disease, slower rates of correction may be advisable.

43
Q

Metabolism of Conivaptan?

A

Metabolized by CYP3A4.

Renal Week 1 (20 decks)

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