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Diuretics Flashcards

(49 cards)

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1
Q

Goal of Diuretics

A

Adjust volume and or composition of body fluids in conext of HTN, Heart failure, renal failure

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2
Q

Generalization on how diuretics act

A

They block the active transport that is required to reabsorb electrolytes

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3
Q

Different classes of diuretics

A
  1. Thiazide diuretics
  2. Loop diuretics
  3. Potassium sparing diuretics
  4. Osmotic diuretics
  5. Carbonic Anhydrase Inhibitors
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4
Q

Thiazide diuretics include

A
  • Chlorothiazide
  • Hydrochlorothiazide
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5
Q

Thiazide like diurteics

A
  • Chlorthalidone
  • Indapamide
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6
Q

Thiazide diuretics range of use

A

Most widely used

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7
Q

Strength of thiazide diuretics

A

Moderatelty powerful

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8
Q

Thiazide diuretics site of action

A

Early distal tubule

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9
Q

Thiazide diuretics pharmacokinetics

A
  • Effective orally
  • Well absorbed from GIT
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10
Q

Thiazide diuretics

MOA

A

Inhibit NCC (Na/Cl co transporter) on luminal membrane of tubules→ decrease active transport of Na and Cl→increase concentration of Na and Cl in tubular fluid

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11
Q

Thiazide diuretics

Actions

A
  1. Increase excretion of Na and Cl
  2. Loss of K
  3. Promote reabsorption of Ca→decreased excretion of Ca
    • ​​IN CONTRAST TO LOOP DIURETICS
  4. Antihypertensive
    • Initially→ due to diuresis induced decrease in blood volume and therefore decreased cardiac output
    • Continued therapy→ due to reduced peripheral vasuclar resistance due to relaxation of arteriolar smooth muscles
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12
Q

Thiazide diuretics

Therapeutic uses

A
  1. Hypertension: if used alone or with other antihypertensives
  2. Hypercalciuria: inhibit urinary Ca excretion→ prevent stone formation
    • esp in pt with calcium oxalate stones in urinary tract (nephtolithiasis)
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13
Q

Thiazide diuretics

Side effects

A
  • Hypokalemia: because thiazides increase Na in the filtrate of the distal tubule, you end up having more to exchange for K→K lost→hypokalemia (what about activation of RAAS)
    • supplemet K by diet or salt supplements
  • Hyperuricaemia: uric acid deposits in jounts→GOUT
  • HYperglycemia: due to inhibition of insulin secretion→decreased glucose uptake
  • Hyponatremia
  • Hypotension
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14
Q

Loop diuretics include

A
  • Furosemide
  • Ethacrynic acid
  • Bumetanide
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15
Q

Loop diuretics efficacy

A
  • Greatest efficay of all diuretics
  • Max secretion: 15-25% of filtered Na
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16
Q

Loop diuretics pharmacokinetics

A

Absorbed from GIT

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17
Q

Loop diuretics administration

A
  • Orally (since absorbed from GIT)
  • Injection
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18
Q

Loop diuretics site of action

A

TALH

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19
Q

Loop diuretics

MOA

A

Inhibit NKCC2→inhibit reabsorbtion of Na, K, Cl→ increased NaCl concentration in tubular fluid reaching distal tubule, collectig ducts→decreased H2O reabsorption in distal nephron.

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20
Q

Loop diuretics

Actions

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A
  1. High levels of Na reaching collecting tubule enhances loss of K and H→METABOLIC ALKALOSIS
  2. Increased excretion of Mg and Ca
  3. May precipitate gout (similar to thizaides)
21
Q

Loop diuretics

Therapeutic use

Study These Flashcards
A

DRUG OF CHOICE in reducing the acute pulmonary and peripheral edema caused by heart or renal failure

22
Q

Loop Diuretics

Side effects

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A
  • Ototoxicity
  • Hyperurecemia
  • Hypotension
  • Hypokalemia: can be treated by K sparing diuretics or K supllement
  • Hypomagnesemia
23
Q

Potassium Sparing Diuretics

Classification

Study These Flashcards
A

A. ALDOSTERONE ANTAGONITS

  1. ​​Spironolactone
  2. Eplerenone

B. Na Channel Blockers

  1. Triamterene
  2. Amiloride
24
Q

Aldosterone Antagonist (K sparing)

Site of Action

Study These Flashcards
A

LATE distal tubule and Collecting duct

25
Spironolactone and Eplerenone Administered
Orally
26
Spironolactone and Eplerenone Inactivation
By liver
27
Spironolactone MOA
**NON-selective** Aldosterone receptor antagonist ## Footnote Anatgonize aldosterone→ *spiranolactone-receptor complex (inactive)*→cant produce mediator proteins→NO reabsroption of Na and secretion of H and K (**K sparing)**
28
Inactive spironolactone-receptor complex causes
1. Decreased Na reabsorption 2. Decreased K secretion→**K sparing**
29
Spiranolactone Therapeutic uses
* Combined with thiazides and loop diuretics (K losing) to **preserve K balance.** * **Secondary hyperaldosteronism:** as occurs in hepatic cirrhosis * حتى برايمري
30
Spironolactone Side effects
* Hyperkalemia→metabolic acidosis * Gynaecomastia * Testicular atrophy
31
Eplerenone MOA
**Selective** mineralocotricoid receptor antagonist→blocks binding of aldosterone→ Inhibits Na reabsorption
32
Eplerenone indicated for
* HTN * **FIRST LINE** for heart failure secondary to MI
33
Eplerenone Side Effects
**LESS** than spiranolactone
34
Triamterene and Amiloride Site of Action
**Collecting** tubules and ducts
35
Triamterene and Amiloride MOA
* Block Na channels→ Inhibit Na reabsorption and **decrease K excretion** * *Reduce Na/H exchange*→ INHIBIT H excretion→ METABOLIC ACIDOSIS
36
Triamterene and Amiloride Administered
ORALLY
37
Triamterene and Amiloride Therapeutic uses
Preserves K balance
38
Triamterene and Amiloride Side Effect
HYPERKALEMIA
39
Osmotic Diuretics Include
Mannitol
40
Mannitol Administered
IV INJECTION
41
Mannitol USES
**RARE BECAUSE NOT AS EFFECTIVE AS OTHERS** * Cerebral edema as it reduces ICP * Glaucoma (lowers IOP) * Prevents ARF **NOTE:** it gets filtered, exerts its effect, and that effect ends as soon as its excreted
42
Mannitol MOA
Freely filtered at **glomerulus** with little reabsorption. Increases **osmotic pressure in tubules**→reduces water reabsorption→diuresis
43
Mannitol Side Effect
HYPOnatremia
44
Carbonic Anhydrase inhibitor
Acetazolamide
45
Acetazolamide Site of Action
PCT
46
Acetazolamide MOA
Inhibits CA in PCT→ icnreased excretion of HCO3, Na, K, H2O→ increase flow of alkaline urine (mild metabolic acidosis)
47
Acetazolamide Adminstered
Direct IV preferred
48
Acetazolamide USES
**Mainly for non renal uses** Treats **glaucoma** by decreasing the formation of *aqueous humor*
49
Acetazolamide Adverse effects
* Metabolic acidosis * Hypokalemia

Renal (9 decks)

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