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Pharmacology Test #3 > 11.21 Duretics > Flashcards

11.21 Duretics Flashcards

1
Q

osmotic diuretic

A

mannitol

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2
Q

-Given i.v., 90% recovered unchanged in urine after 24 hr
• Promote diuresis during acute renal failure
• Reduction of intracranial pressure of cerebral edema
• Promote excretion of toxic substances

A

Mannitol

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3
Q
  • Not commonly used (weak action)
  • Inhibit carbonic anhydrase that converts HCO3-, into
    H2O and CO2, and back
  • Net effect: ↓water, Na+ and HCO3- reabsorption in
    proximal tubule
A

-carbonic anhydrase inhibitors (proximal tubule)

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4
Q

• Glaucoma: reduce aqueous humor formation
• Nausea and vomiting associated with acute mountain
sickness (↓intracranial secretion)
• Epilepsy: adjunctive agent; retards abnormal, excessive
discharge of CNS neurons
• Reversal of metabolic alkalosis
• Potential adverse effect: Metabolic acidosis

A

Acetazolamide (carbonic anhydrase inhibitor)

-acts in the proximal tubule

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5
Q
  • Active Na+ reabsorption (25% of filtered load) by Na+/K+/2Cl- co- transporter
  • Na+ reabsorption leads to dilution of the tubular fluid
  • Ca++ and Mg++ are reabsorbed via a paracellular pathway
A

Furosemide (acts on the thick ascending loop of Henle)

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6
Q

Descending loop of Henle

A
  • No active pumps
  • Water leaves tubule by osmosis
  • Na+ and urea concentrations outside the tubule (medullary interstitium) increase from 400 to 1200 mOsmol from the top to the bottom of the loop, respectively.
  • As the fluid in the lumen of the tubule moves down the tubule, the fluid osmolarity increases in a concomitant fashion (i.e., 400 to 1200 mOsmol).
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7
Q

loop diuretics

A
  • they are the most powerful agents
  • congestive heart failure front line agents
  • Inhibition of the coupled Na+/Cl-/K+ transport system in thick ascending loop of Henle. Net effect: increased excretion of Na+, Ca++, Mg++, K+
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8
Q

when would a loop diuretic be used?

A
  • Edema with hepatic cirrhosis, renal disease
  • Edema associated with congestive heart failure
  • Ascites due to malignancy, lymphedema, idiopathic edema • Hypertension (oral forms)
  • Acute hypercalcemia
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9
Q

adverse effects/drug interactions with loop diuretics

A
  • Excessive diuresis/dehydration, depletion of Ca++, Mg++, K+, decreased blood volume (orthostasis, shock)
  • Transient/reversible ototoxicity (i.e. hearing loss)
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10
Q

distal convoluted tubule

A

• Active Na+ reabsorption (10% of filtered load) by Na+/Cl- co- transporter
• Relatively impermeable to water, therefore Na+ reabsorption further dilutes the tubular fluid.
• Ca++ is reabsorbed by an apical Ca++ channel and a basolateral Na+/Ca++ exchanger
-thiazide diuretics

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11
Q

thiazide diuretics

A

-distal convoluted tubule
Inhibiton of the Na+/Cl- cotransporter system
Thiazides: moderately effective since 85% of the filtered load of Na+ has been reabsorbed in earlier parts of the nephron.
-CALCIUM RETENTION

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12
Q
  • Hypertension (1st)
  • Adjunctive therapy for edema of various types, including CHF
  • Prevention of kidney stones due to hypercalciuria; thiazides have a direct effect to increase Ca++ reabsorption thus decrease urine Ca++ • Nephrogenic diabetes insipidus (action in proximal tubular)
A

Chlorothiazide (Diuril®),

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13
Q

Adverse effects / Drug interactions of thiazides (Chlorothiazide)

A
  • Hypokalemia - increased delivery of Na+ to distal tubule reduces reabsorption of K+ (potassium supplements added to treatment)
  • Hypercalcemia - due to increased Ca++ reabsorption.
  • Hyperuricemia - longterm reduces uric acid secretion (gout)
  • Glucose intolerance
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14
Q

collecting tubule

A
  • Site of active Na+ reabsorption (2-5% of filtered load)
  • Final site for determining Na+ concentration of the urine
  • Site of K+ release into the tubular luman through K+ channels
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15
Q

aldosterone does what in the collecting tubule?

A

• Increases activity of membrane Na+ and K+ channels, and Na+/K+ ATPase pump Na+ reabsorption and K+ excretion

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16
Q

ADH/vasopressin

A

• Absence of ADH tubule impermeable to water reabsorption
→ Diabetes Insipidus results in the production of as much as 20L/d of dilute urine
- Central - inadequate ADH release from posterior pit. - Nephrogenic - absence of tubular response to ADH

17
Q

intercalated cells:

A

site for proton secretion into urine

18
Q

potassium sparing diuretics

A

spironolactone and Triamterene

19
Q
  • Competitive receptor antagonist of aldosterone
  • Inhibition of Na+ and K+ channels (decreased K+ excretion) • Seldom used alone (low potency), used in combination with K+ depleting agents; esp. in antihypertensive therapy.
A

Spironolactone (Aldactone®)

20
Q
  • Inhibition of Na+ and K+ channels (decreased K+ excretion) • Seldom used alone (low potency), valuable in combination with K+ depleting agents, esp. in antihypertensive therapy.
  • Adverse effects: hyperkalemia and photosensitivity
A

Triamterene

21
Q

adverse effects of spironolactone

A
  • Hyperkalemia

* Estrogen-like effects (steroidal structure) • NSAIDs interaction, carcinogenic in rats

22
Q

Diabetes Insipidus - Treatment, Central DI

A

(decreased release of AVP)

  • Desmopressin (DDAVP): more selective for V2- (antidiuresis) than V1-receptor (vasoconstriction)
  • action 6-24 hrs (intranasal, oral, iv, im, sc)
  • Chlorpropamide: enhance AVP action
  • others: Clofibrate (↑release), Carbamazepine (↑rel. & action)
  • Thiazides and NSAIDs (ie. Indomethacin)
23
Q

Diabetes Insipidus - Treatment Nephrogenic DI

A

(decreased response to AVP)

  • Thiazides and mild salt restriction
  • NSAIDs: PGs increase medullary blood flow and diminish medullary solute reabsorption, NSAIDs inhibit this
  • AVP, DDAVP or agents that increase AVP release are generally ineffective
24
Q

Diabetes Insipidus - Treatment

• Primary Polydipsia

A

(increased fluid intake)

  • need to reduce fluid intake
  • avoid above therapies, may cause water intoxication - may use short-acting AVP at night
25
Q

Diuresis

A

water loss

26
Q

natriuresis

A

salt loss

27
Q

potential adverse effect: metabolic acidosis

A

acetazolamide

28
Q

collecting tubule

A
  • site of active Na+ reabsorption (2-5% of filtered load)
  • final site for determining Na+ concentration of the uringe
  • site of K+ release into the tubular luman through K+ channels
29
Q

aldosterone

A

-increases activity of membrane Na+ and K+ channels and Na+/K+ ATPase pump which leads to Na+ reabsorption and K+ excretion

30
Q

ADH

A
  • Antidiuretic hormone (vasopression)
  • absence of ADH tubule impermeable to water reabsorption
  • Diabetes insipidus results in the production of as much as 20 L/day of dilute uring
  • central di =inadequate ADH release from posterior pit
  • Nephrogenic di=absence of tubular response to ADH
31
Q

central di =

A

central di =inadequate ADH release from posterior pit

32
Q

-Nephrogenic di=

A

central di =inadequate ADH release from posterior pit

-Nephrogenic di=absence of tubular response to ADH

33
Q

Diabetes Insipidus - Water deprivation test

A 
Fluid restriction (6-18 hrs) followed by AVP administration
In normal and polydipsia patients, dehydration causes maximum AVP release. Thus, administration of exogenous AVP will have no further effect on urine Osm

Pharmacology Test #3 (9 decks)

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