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Questions and Answers
Loop diuretics inhibit Na+/K+/2Cl― co-transport system in the distal convoluted tubule of the nephron.
Loop diuretics inhibit Na+/K+/2Cl― co-transport system in the distal convoluted tubule of the nephron.
False (B)
The absorption of bumetanide is erratic.
The absorption of bumetanide is erratic.
False (B)
Diuretics are used to treat edema due to lymphatic obstruction.
Diuretics are used to treat edema due to lymphatic obstruction.
False (B)
Loop diuretics increase the excretion of Ca2+ in the urine.
Loop diuretics increase the excretion of Ca2+ in the urine.
Non-steroidal anti-inflammatory drugs (NSAIDs) enhance the effect of loop diuretics.
Non-steroidal anti-inflammatory drugs (NSAIDs) enhance the effect of loop diuretics.
Loop diuretics are used to treat acute hypercalcemia without saline.
Loop diuretics are used to treat acute hypercalcemia without saline.
Loop diuretics cause vasoconstriction of the pulmonary vascular bed.
Loop diuretics cause vasoconstriction of the pulmonary vascular bed.
The effect of loop diuretics on renal PGE2 and PGI2 production leads to a decrease in RBF and GFR.
The effect of loop diuretics on renal PGE2 and PGI2 production leads to a decrease in RBF and GFR.
Furosemide is usually given in non-emergency situations
Furosemide is usually given in non-emergency situations
Hyponatremia increases the sensitivity of vascular smooth muscles to circulating catecholamines
Hyponatremia increases the sensitivity of vascular smooth muscles to circulating catecholamines
Thiazide diuretics inhibit Na+/Cl― co-transport system in the proximal part of the PCT
Thiazide diuretics inhibit Na+/Cl― co-transport system in the proximal part of the PCT
Metabolic acidosis is caused by an increase in H+ ion excretion.
Metabolic acidosis is caused by an increase in H+ ion excretion.
Primary hyperaldosteronism is an example of secondary hyperaldosteronism.
Primary hyperaldosteronism is an example of secondary hyperaldosteronism.
Furosemide causes peripheral vasodilation due to the production of prostaglandins in many vascular beds
Furosemide causes peripheral vasodilation due to the production of prostaglandins in many vascular beds
Thiazide diuretics are absorbed from the liver
Thiazide diuretics are absorbed from the liver
K+ sparing diuretics can cause hypokalemia.
K+ sparing diuretics can cause hypokalemia.
Furosemide can cause reversible hearing loss
Furosemide can cause reversible hearing loss
Loop diuretics can cause metabolic alkalosis.
Loop diuretics can cause metabolic alkalosis.
Combining loop diuretics with K+ sparing diuretics can minimize the risk of electrolyte imbalance.
Combining loop diuretics with K+ sparing diuretics can minimize the risk of electrolyte imbalance.
Ethacrynic acid is a derivative of sulfonamides
Ethacrynic acid is a derivative of sulfonamides
All cases of edema are caused by hyperaldosteronism.
All cases of edema are caused by hyperaldosteronism.
Thiazide diuretics produce diuresis within 6-8 hours
Thiazide diuretics produce diuresis within 6-8 hours
K+ sparing diuretics are used to treat all cases of edema.
K+ sparing diuretics are used to treat all cases of edema.
Combining loop diuretics with K+ sparing diuretics can minimize the risk of acid-base imbalance.
Combining loop diuretics with K+ sparing diuretics can minimize the risk of acid-base imbalance.
All diuretics are absorbed from the GIT.
All diuretics are absorbed from the GIT.
Spironolactone is a direct inhibitor of Na+ channels in the distal part of the DCT.
Spironolactone is a direct inhibitor of Na+ channels in the distal part of the DCT.
Amiloride is metabolized by the liver.
Amiloride is metabolized by the liver.
Triamterene and amiloride have a fast onset of action.
Triamterene and amiloride have a fast onset of action.
The site of action of these diuretics is the proximal part of the DCT.
The site of action of these diuretics is the proximal part of the DCT.
Spironolactone leads to a decrease in K+ retention.
Spironolactone leads to a decrease in K+ retention.
These diuretics cause a significant loss of Na+ and water.
These diuretics cause a significant loss of Na+ and water.
Triamterene and amiloride increase K+ excretion.
Triamterene and amiloride increase K+ excretion.
Thiazides can reduce urine volume in all cases of nephrogenic diabetes insipidus.
Thiazides can reduce urine volume in all cases of nephrogenic diabetes insipidus.
Thiazides are effective in reducing blood pressure in severe hypertension.
Thiazides are effective in reducing blood pressure in severe hypertension.
Thiazides decrease excretion of halides and H+.
Thiazides decrease excretion of halides and H+.
Spironolactone is a non-steroidal potassium-sparing diuretic.
Spironolactone is a non-steroidal potassium-sparing diuretic.
Triamterene and amiloride are steroidal potassium-sparing diuretics.
Triamterene and amiloride are steroidal potassium-sparing diuretics.
Thiazides are often used as a single agent in the treatment of hypertension.
Thiazides are often used as a single agent in the treatment of hypertension.
Thiazides have a high efficacy in reducing sodium reabsorption.
Thiazides have a high efficacy in reducing sodium reabsorption.
Thiazides can cause hyperkalemia due to their mechanism of action.
Thiazides can cause hyperkalemia due to their mechanism of action.
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Study Notes
Loop Diuretics
- Absorbed from the GIT and secreted into the lumen of the PCT by an organic acid excretory system
- Furosemide absorption is erratic, but bumetanide is complete
- Diuresis occurs within 5 minutes after i.v. administration and within 30 minutes of oral administration
- Mechanism of action: inhibit Na+/K+/2Cl- co-transport system in the thick ascending limb of LOH, leading to inhibition of active reabsorption of Na+, Cl-, and K+
- Effects: increased excretion of Ca2+, Mg2+, halides, and H+; increased renal PGE2 and PGI2 production, leading to vasodilatation and increased RBF and GFR
- Therapeutic uses: edematous conditions, acute pulmonary edema, acute renal failure, acute hypercalcemia, and acute hyperkalemia
- Adverse effects: hypovolemia, hypotension, electrolyte disturbances, hypokalemic metabolic alkalosis, hyperuricemia, and ototoxicity
Thiazide Diuretics
- Classification: true thiazides (derivatives of sulfonamides) and thiazide-like diuretics
- Pharmacokinetics: absorbed from the GIT, secreted into the lumen of the PCT by an organic acid excretory system, and produce diuresis within 1-2 hours
- Mechanism of action: inhibit Na+/Cl- co-transport system in the proximal part of DCT, leading to inhibition of active reabsorption of Na+ and Cl-
- Effects: increased excretion of halides and H+; decreased Ca2+ excretion and enhanced reabsorption
- Therapeutic uses: mild edematous states, essential hypertension, hypercalcuria, and renal Ca2+ stones, and nephrogenic diabetes insipidus
- Adverse effects: hypovolemia, hypotension, electrolyte disturbances, hypokalemic metabolic alkalosis, hyperuricemia, hyperglycemia, and hyperlipidemia
Potassium-Sparing Diuretics
- Classification: spironolactone, triamterene, and amiloride
- Pharmacokinetics: absorbed from the GIT, metabolized by the liver, and have slow onset (days)
- Mechanism of action: spironolactone is a competitive antagonist of aldosterone, while triamterene and amiloride are direct inhibitors of Na+ channels in the distal part of DCT
- Effects: mild Na+ and water loss, hyperkalemia, and metabolic acidosis
- Therapeutic uses: all cases of edema due to hyperaldosteronism, and in combination with loop diuretics or thiazides to minimize the risk of electrolyte and acid-base imbalance
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