Diuretics Flashcards

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 Cadecreased 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

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

A

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

22
Q

Loop Diuretics

Side effects

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

Potassium Sparing Diuretics

Classification

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

A

LATE distal tubule and Collecting duct

25
Q

Spironolactone and Eplerenone

Administered

A

Orally

26
Q

Spironolactone and Eplerenone

Inactivation

A

By liver

27
Q

Spironolactone

MOA

A

NON-selective Aldosterone receptor antagonist

Anatgonize aldosterone→ spiranolactone-receptor complex (inactive)→cant produce mediator proteins→NO reabsroption of Na and secretion of H and K (K sparing)

28
Q

Inactive spironolactone-receptor complex causes

A
  1. Decreased Na reabsorption
  2. Decreased K secretion→K sparing
29
Q

Spiranolactone

Therapeutic uses

A
  • Combined with thiazides and loop diuretics (K losing) to preserve K balance.
  • Secondary hyperaldosteronism: as occurs in hepatic cirrhosis
    • حتى برايمري
30
Q

Spironolactone

Side effects

A
  • Hyperkalemia→metabolic acidosis
  • Gynaecomastia
  • Testicular atrophy
31
Q

Eplerenone

MOA

A

Selective mineralocotricoid receptor antagonist→blocks binding of aldosterone→ Inhibits Na reabsorption

32
Q

Eplerenone indicated for

A
  • HTN
  • FIRST LINE for heart failure secondary to MI
33
Q

Eplerenone

Side Effects

A

LESS than spiranolactone

34
Q

Triamterene and Amiloride

Site of Action

A

Collecting tubules and ducts

35
Q

Triamterene and Amiloride

MOA

A
  • Block Na channels→ Inhibit Na reabsorption and decrease K excretion
  • Reduce Na/H exchange→ INHIBIT H excretion→ METABOLIC ACIDOSIS
36
Q

Triamterene and Amiloride

Administered

A

ORALLY

37
Q

Triamterene and Amiloride

Therapeutic uses

A

Preserves K balance

38
Q

Triamterene and Amiloride

Side Effect

A

HYPERKALEMIA

39
Q

Osmotic Diuretics Include

A

Mannitol

40
Q

Mannitol

Administered

A

IV INJECTION

41
Q

Mannitol

USES

A

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
Q

Mannitol

MOA

A

Freely filtered at glomerulus with little reabsorption.

Increases osmotic pressure in tubules→reduces water reabsorption→diuresis

43
Q

Mannitol

Side Effect

A

HYPOnatremia

44
Q

Carbonic Anhydrase inhibitor

A

Acetazolamide

45
Q

Acetazolamide

Site of Action

A

PCT

46
Q

Acetazolamide

MOA

A

Inhibits CA in PCT→ icnreased excretion of HCO3, Na, K, H2O→ increase flow of alkaline urine (mild metabolic acidosis)

47
Q

Acetazolamide

Adminstered

A

Direct IV preferred

48
Q

Acetazolamide

USES

A

Mainly for non renal uses

Treats glaucoma by decreasing the formation of aqueous humor

49
Q

Acetazolamide

Adverse effects

A
  • Metabolic acidosis
  • Hypokalemia