Loop Diuretics

Loop Diuretics

Q. 1

All the following adverse effects can be caused by Loop Diuretics EXCEPT:

 A Hypercalcemia
 B

Hyperglycemia

 C Hypomagnesemia
 D

Hyperuricemia

Q. 1

All the following adverse effects can be caused by Loop Diuretics EXCEPT:

 A Hypercalcemia
 B

Hyperglycemia

 C Hypomagnesemia
 D

Hyperuricemia

Ans. A

Explanation:

Hypercalcemia REF: WI 6’h edition page 567

“Loop diuretics on chronic use cause hypocalcaemia while thiazides cause hypercalcemia” 

Adverse effect specific to Loop Diuretics:

  • Hearing loss
  • Hypocalcaemia
  • Excess use causes dehydration & fall in bp .

Adverse effect specific to thiazide Diuretics-.

  • Hypercalcernia

Adverse effects common to both loop St thiazide diuretics:

  • Hypokalemia
  • Hypomagne setnia
  • Hyperglycemia
  • Hyperlipidelnia
  • Hyperuricemia

Q. 2

The usual maximum dose of furosemide and spironolactone in patients with cirrhosis and portal hypertension is:

 A

Furosemide 160 mg and spironolactone 400 mg

 B

Furosemide 80 mg and spironolactone 400 mg

 C

Furosemide 160 mg and spironolactone 200 mg

 D

Furosemide 80 mg and spironolactone 200 mg

Q. 2

The usual maximum dose of furosemide and spironolactone in patients with cirrhosis and portal hypertension is:

 A

Furosemide 160 mg and spironolactone 400 mg

 B

Furosemide 80 mg and spironolactone 400 mg

 C

Furosemide 160 mg and spironolactone 200 mg

 D

Furosemide 80 mg and spironolactone 200 mg

Ans. A

Explanation:

Usual maximum doses of diuretic for the treatment of ascites in decompensated cirrhosis are 400 mg/day of spironolactone and 160 mg/day of furosemide.

Furosemide can be temporarily withheld in patients presenting with hypokalemia, which is very common in the setting of alcoholic hepatitis.
 
Ref: HEPATOLOGY, June 2009.

Q. 3

Which of the following is not an adverse effect of Furosemide?

 A

Hyper uricemia

 B

Hypokalemia

 C

Ototoxicity

 D

Hypercalcemia

Q. 3

Which of the following is not an adverse effect of Furosemide?

 A

Hyper uricemia

 B

Hypokalemia

 C

Ototoxicity

 D

Hypercalcemia

Ans. D

Explanation:

Furosemide is a loop diuretic which acts by inhibiting Na-K-Cl cotransport in the thick ascending limb of Loop of Henle.

It increases calcium excretion and cause hypocalcemia.

Other side effects of furosemide are hypokalemia, ototoxicity, hyperuricemia and hypomagnesemia.


Q. 4

Which of the following is the mechanism of action of bumetanide?

 A

Angiotensin converting enzyme inhibitor

 B

Carbonic anhydrase inhibitor

 C

Loop diuretic

 D

Potassium sparing diuretic

Q. 4

Which of the following is the mechanism of action of bumetanide?

 A

Angiotensin converting enzyme inhibitor

 B

Carbonic anhydrase inhibitor

 C

Loop diuretic

 D

Potassium sparing diuretic

Ans. C

Explanation:

Bumetanide is a loop diuretic. It inhibits the sodium, potassium, chloride cotransporter in the thick ascending limb of the loop of Henle.
 
Angiotensin converting enzyme inhibitors include benazepril, captopril and lisinopril. They interfere with the conversion of angiotensin I to angiotensin II.
 
Carbonic anhydrase inhibitors, such as acetazolamide, act in the proximal convoluted tubule. They cause a self-limited sodium bicarbonate diuresis. They are used to alkalinize the urine, and for the treatment of metabolic alkalosis and glaucoma.
 
Potassium-sparing diuretics such as spironolactone, triamterene, and amiloride inhibit the action of aldosterone. They are used in the treatment of hyperaldosteronism and potassium depletion.
 
Also Know:
Loop diuretics inhibit a specific ion transport protein, the Na+-K+-2Cl– symporter on the apical membrane of renal epithelial cells in the ascending limb of the loop of Henle to increase Na+ and fluid delivery to distal nephron segments. These drugs also enhance K+ secretion, particularly in the presence of elevated aldosterone levels, as is typical in CHF.
 
Ref: Maron B.A., Rocco T.P. (2011). Chapter 28. Pharmacotherapy of Congestive Heart Failure. In L.L. Brunton, B.A. Chabner, B.C. Knollmann (Eds), Goodman & Gilman’s The Pharmacological Basis of Therapeutics, 12e.

Q. 5

Which of the following is NOT known as adverse drug reaction of furosemide?

 A

Hyperkalemia

 B

Acidosis

 C

Hyperuricemia

 D

Hypomagnesemia

Q. 5

Which of the following is NOT known as adverse drug reaction of furosemide?

 A

Hyperkalemia

 B

Acidosis

 C

Hyperuricemia

 D

Hypomagnesemia

Ans. A

Explanation:

Toxicity of frusemide includes:

  • Hypokalemic metabolic alkalosis
  • Ototoxicity
  • Hyperuricemia
  • Hypomagnesemia
  • Allergic and other reactions
Ref: Katzung, 11th edition, Chapter 15.

Q. 6

Which of the following metabolic abnormality is seen with long term use of loop diuretics?

 A

Metabolic acidosis

 B

Metabolic alkalosis

 C

Hyperkalemia

 D

None of the above

Q. 6

Which of the following metabolic abnormality is seen with long term use of loop diuretics?

 A

Metabolic acidosis

 B

Metabolic alkalosis

 C

Hyperkalemia

 D

None of the above

Ans. B

Explanation:

By inhibiting salt reabsorption in the TAL, loop diuretics increase delivery to the collecting duct.

Increased delivery leads to increased secretion of K+ and H+ by the duct, causing hypokalemic metabolic alkalosis.

This toxicity is a function of the magnitude of the diuresis and can be reversed by K+ replacement and correction of hypovolemia.

Ref: Katzung, 11th edition, Chapter 15.

Q. 7

Which one of the following is most likely to result in contraction alkalosis?

 A

Laxatives

 B

Infant formula

 C

Loop diuretics

 D

Acetazolamide

Q. 7

Which one of the following is most likely to result in contraction alkalosis?

 A

Laxatives

 B

Infant formula

 C

Loop diuretics

 D

Acetazolamide

Ans. C

Explanation:

The term “contraction alkalosis” refers to the development of metabolic alkalosis (excess plasma HCO3-) when there is a loss of extracellular fluid volume (hypovolemia). Hypovolemia evokes numerous homeostatic reflexes that act to normalize extracellular fluid volume, including stimulation of the renin-angiotensin-aldosterone system. In the kidney, elevated levels of angiotensin II and aldosterone increase Na reabsorption through processes that are ultimately coupled to hydrogen secretion. Consequently, volume regulation results in a net increase in plasma HCO3-. Correction is obtained when the lost volume is replenished through intake of water and sodium.
 
Loop diuretics such as furosemide act primarily on the thick segment of the medullary and cortical ascending limbs of Henle’s loop. They inhibit the coupled transport of Na+ and Cl- that results in the production of large volumes of relatively iso osmotic urine. Excessive use of these drugs can result in hypovolemia and contraction alkalosis.
 
Antacid and infant formula can result in metabolic alkalosis but not as a result of hypovolemia. In patients with renal insufficiency, antacids containing calcium carbonate can increase the plasma HCO3- concentration. Infant formulas that contain sodium but very little chloride enhance Na+ reabsorption in the renal tubule and, like volume contraction, this results in an increase in urinary H+ secretion.

Administration of laxatives or acetazolamide promotes metabolic acidosis. Laxatives result in the loss of intestinal fluids that are relatively alkaline and contain large amounts of HCO3-. Acetazolamide inhibits the enzyme carbonic anhydrase. As a result, acetazolamide reduces the reabsorption of HCO3- in the renal tubule. Acetazolamide is often used in combination with loop diuretics to correct the alkalosis caused by these compounds.

 
Ref: Barrett K.E., Barman S.M., Boitano S., Brooks H.L. (2012). Chapter 35. Gas Transport & pH. In K.E. Barrett, S.M. Barman, S. Boitano, H.L. Brooks (Eds),Ganong’s Review of Medical Physiology, 24e. 
 

Q. 8

Loop diuretics acts on ?

 A

Descending limb

 B

Thick ascending limb

 C

Cortical segment

 D

Collecting duct

Q. 8

Loop diuretics acts on ?

 A

Descending limb

 B

Thick ascending limb

 C

Cortical segment

 D

Collecting duct

Ans. B

Explanation:

Ans. is b’ i.e., Thick ascending limb


Q. 9

Which one of the following drug causes increased concentration of Na’ & CI- in urine with normal bicarbonate –

 A

Ethacrynic acid

 B

Furosemide

 C

Acetazolamide

 D

Bumetanide

Q. 9

Which one of the following drug causes increased concentration of Na’ & CI- in urine with normal bicarbonate –

 A

Ethacrynic acid

 B

Furosemide

 C

Acetazolamide

 D

Bumetanide

Ans. A

Explanation:

Ans. is ‘a’ i.e., Ethacrynic Acid

 Ethacrynic acid is a loop diuretic and acts by inhibiting No’ – – 2Ct transport in ascending loop of Nettle. Thus it inhibits reabsorbtion of No’ and Ch ions and promotes excretion of these electrolytes in urine. Unlike other loop diuretics however, it does not inhibit carbonic anhydrase, and therefore it does not cause any increase in WO jexcretion in urine.

 

Remember

o Most marked Kaliuresis (K’ excretion) is caused by : Acetazolamide

o Most marked Natriuresis (Natexcretion) is caused by : Furosemide

o Most marked Chloride excretion is caused by : Ethacrynic acid : Acetazolamide (Pretest)

o Only diuretic which inhibits choride excretion is that is why it causes metabolic acidosis. : Thiazide like diuretics e.g. indapamide, metazoline, chlorthalidone.

o Diuretics which do not promote bicarbonate excretion : Ethacrynic acid

o Diuretics which maximally promotes uric acid excretion : Acetazolamide (by alkalanizing urine)


Q. 10

Following is true about furosemide –

 A

It is given only by IV route

 B

It causes mild diuresis

 C

It is used in pulmonary edema

 D

Acts on PCT

Q. 10

Following is true about furosemide –

 A

It is given only by IV route

 B

It causes mild diuresis

 C

It is used in pulmonary edema

 D

Acts on PCT

Ans. C

Explanation:

Ans. is ‘c’ i.e., It is used in pulmonary edema

o Intravenous administration of furosemide produces prompt relief in acute pulmonary edema and acute heart failure (Acute LVF).

o It is due to vasodilators (venous dilatation) action and not due to diuretic action (in contrast with chronic heart failure, where the symptomatic relieve is due to diuretic action).

o IV furosemide causes prompt increase in systemic venous capictance and decreases left ventricular filling pressure (preload) even before the diuretic action becomes apperent.

About other options

  • Furosemide can be given i.m. also.
  • It has maximum diuretic action (more than other classes of diuretic).

It acts on thick ascending limb of loop of Henle.


Q. 11

Furosemide causes all except –

 A

Hyperuricemia

 B

Ototoxicity

 C

Hypercalcemia

 D

Hypokalemia

Q. 11

Furosemide causes all except –

 A

Hyperuricemia

 B

Ototoxicity

 C

Hypercalcemia

 D

Hypokalemia

Ans. B

Explanation:

Ans. is `b’ i.e., Hypercalcemia

Coniolications of high ceiling (furosamidel diuretics

o Hypokalemia (M. C)                                      o Hyperuricemia                  o GI disturbances

o Acute saline depletion                                   o Hypocalcemia                   o Mental disturbances

o Dilutional hyponatremia                                 o Hyperglycemia                 o Allergic manifestations

o Alkolosis                                                      o Hyperlipidemia

o Hearing loss (ototoxicity)                              o Hypomagnesemia

Thiazides also have same complications except

o Thiazides cause hypercalcemia                 

o Thiazides may aggravate renal insufficiency.

o Thiazides do not cause ototoxicity.

Remember

o Hypokalemia is less common with loop diuretics than with thiazides.

o Hypokalemia is prevented and treated by


Q. 12

All the following adverse effects can be caused by Loop Diuretics EXCEPT –

 A

Hypercalcemia

 B

Hyperglycemia

 C

Hypomagnesemia

 D

Hyperuricemia

Q. 12

All the following adverse effects can be caused by Loop Diuretics EXCEPT –

 A

Hypercalcemia

 B

Hyperglycemia

 C

Hypomagnesemia

 D

Hyperuricemia

Ans. A

Explanation:

Ans. is ‘a’ i.e., Hypercalcemia


Q. 13

Ethacrynic acid is not used due to ‑

 A

Renal toxicity

 B

Ototoxicity

 C

GI toxicity

 D

Pulmonary toxicity

Q. 13

Ethacrynic acid is not used due to ‑

 A

Renal toxicity

 B

Ototoxicity

 C

GI toxicity

 D

Pulmonary toxicity

Ans. B

Explanation:

Ans. is ‘b’ i.e., Ototoxicity

Ethacrynic acid is most ototoxic loop diuretic.


Q. 14

Following drug interact with cefotaxime –

 A

Digoxin

 B

Paracetamol

 C

Loop diuretics

 D

Nifedipine

Q. 14

Following drug interact with cefotaxime –

 A

Digoxin

 B

Paracetamol

 C

Loop diuretics

 D

Nifedipine

Ans. C

Explanation:

Ans. is ‘c’ i.e., Loop diuretics

o Nephrotoxicity of cephalosporins is accentuated by concurrent administration of a loop diuretic.


Q. 15

All of the following are true about Hypercalcemia, except:

 A

Management of primary cause

 B

Management of primary cause

 C

IV fluid with furosemide is given

 D

Pamidronate is not effective

Q. 15

All of the following are true about Hypercalcemia, except:

 A

Management of primary cause

 B

Management of primary cause

 C

IV fluid with furosemide is given

 D

Pamidronate is not effective

Ans. D

Explanation:

Answer is D (Pamidronate is not effective):

Pamidronate is a second generation hiphosphonate that is approved for intravenous use in the treatment of hypercalcemia.


Q. 16

Drug of choice for acute left ventricular failure:

September 2006

 A

Rapid digitalization

 B

I/V Aminophylline

 C

I/V Morphine

 D

I/V Furosemide

Q. 16

Drug of choice for acute left ventricular failure:

September 2006

 A

Rapid digitalization

 B

I/V Aminophylline

 C

I/V Morphine

 D

I/V Furosemide

Ans. D

Explanation:

Ans. D: I/V Furosemide

Diuretics remain the mainstay of therapy and current standard of care for acute heart failure.

Intravenous administration of a loop diuretic (furosemide, bumetanide, torsemide) is preferred initially due to potential poor absorption of the oral forms in the presence of bowel edema.

Treatment of Symptomatic Left Ventricular Systolic Dysfunction

First Line (Class I recommendation)

  • Diuretics and fluid restriction in patients who have evidence of fluid retention.
  • ACE inhibitor – all patients, unless contraindicated (eg. renal artery stenosis, unstable renal function, hypotension)
  • Beta-adrenergic blockade in all stable patients, unless contraindicated (eg. no or minimal evidence of fluid retention, no recent inotropic agent, no bronchospasm)
  • Digitalis for the treatment of symptoms of Heart Failure, unless contraindicated (eg. renal insufficiency)
  • Withdrawal of drugs known to adversely affect the clinical status of patients (e.g., nonsteroidal anti-inflammatory drugs, most antiarrhythmic drugs, and most calcium channel blocking drugs)

Q. 17

Furosemide mechanism of action in LVF is:

September 2010

 A

Inhibitor of Na-K-Cl ion symport

 B

Aldosterone antagonist

 C

Mercurial derivative

 D

Carbonic anhydrase inhibitor

Q. 17

Furosemide mechanism of action in LVF is:

September 2010

 A

Inhibitor of Na-K-Cl ion symport

 B

Aldosterone antagonist

 C

Mercurial derivative

 D

Carbonic anhydrase inhibitor

Ans. A

Explanation:

Ans. A: Inhibitor of Na-K-Cl ion symport

Like other loop diuretics, furosemide acts by inhibiting the Na-K-2C1 symporter in the thick ascending limb of the loop of Henle.

The action on the distal tubules is independent of any inhibitory effect on carbonic anhydrase or aldosterone; it also abolishes the corticomedullary osmotic gradient and blocks negative as well as positive free water clearance.


Q. 18

Which drug is excreted unchanged in urine ‑

 A

Verapamil

 B

Furosemide

 C

Propranolol

 D

Thiopentone

Q. 18

Which drug is excreted unchanged in urine ‑

 A

Verapamil

 B

Furosemide

 C

Propranolol

 D

Thiopentone

Ans. B

Explanation:

Ans. is ‘b’ i.e., Furosemide

Furosemide pharmacokinetics

  • Furosemide is rapidly absorbed orally but bioavailability is about 60%.
  • Lipid solubility is low and it is highly bound to plasma proteins.
  • It is party conjugated by glucuronic acid and is mainly excreted unchanged by glomerular filtration and tubular secretion.

Q. 19

ECG image,U wave seen, patient is on furosemide & beta blocker. Diagnosis

 A

Hypocalcemia

 B

Hypokalemia

 C

Hyperkalemia

 D

Hypercalcemia

Q. 19

ECG image,U wave seen, patient is on furosemide & beta blocker. Diagnosis

 A

Hypocalcemia

 B

Hypokalemia

 C

Hyperkalemia

 D

Hypercalcemia

Ans. B

Explanation:

Ans. is ‘b’ i.e., Hypokalemia

E.C.G. manifestations of electrolyte disorders

Hvperkalemia

  • A tall peaked and symmetrical T-waves is the first change seen on ECG in patients with hyperkalemia. o RR interval lengthens and QRS duration increases.
  • Flattening or disappearance of P wave.
  • ST elevation.
  • Widening of the QRS complexes due to a severe conduction delay and may become ‘sine wave’.
  • The progresion and the severity of the E. C. G change do not correlate well with the serum potassiam concentration.

Hvpokalemia

  • Similar to hyperkalemia, hypokalemia produce changes on the E. C. G which are not necessary related to serum potassiam level.
  • Depression of the ST segment
  • Decrease in amplitude of T waves
  • Increase in amplitude of U waves
  • U and T wave merge in some cases to form a T-U wave which may be misdiagnosed as prolonged QT interval.
  • P wave can become larger and wider and PR interval prolong slightly.
  • QRS duration may increase when hypokalemia becomes more severe.

Hvpocalcemia

  • Prolongation of the QT interval
  • Due to prolongation of the phase 2 of the ventricular action potential and lengthening of the ST segment while the T wave (which correlate with time for repolarisation remains unaltered).

Hvpercalcemia

  • Shortening of the QT interval
  • (Primarily due to a decrease in phase 2 of the ventricular action potential and resultant decrease in ST segment duration).

Iltpothermia

  • Causes slow impulse conduction through all cardial tissues resulting in :‑

Prolongation of all the ECG intervals

  • RR
  • PR
  • QRS’
  • QT
  • There is also “elevation of the J point” (Only if the ST segment is unaltered producing characteristics T or osborne wave.)

Q. 20

The site of action of the loop diuretic furosemide is:

 A

Thick ascending limb of loop of Henle

 B

Descending limb of loop of Henle

 C

Proximal convoluted tubule

 D

Distal convoluted tubule

Q. 20

The site of action of the loop diuretic furosemide is:

 A

Thick ascending limb of loop of Henle

 B

Descending limb of loop of Henle

 C

Proximal convoluted tubule

 D

Distal convoluted tubule

Ans. A

Explanation:

Ans. a. Thick ascending limb of loop of Henle


Q. 21

The site of action of the loop diuretic furosemide is:

 A

Thick ascending limb of loop of Henle

 B

Descending limb of loop of Henle

 C

Proximal convoluted tubule

 D

Distal convoluted tubule

Q. 21

The site of action of the loop diuretic furosemide is:

 A

Thick ascending limb of loop of Henle

 B

Descending limb of loop of Henle

 C

Proximal convoluted tubule

 D

Distal convoluted tubule

Ans. A

Explanation:

Ans. a. Thick ascending limb of loop of Henle


Q. 22

Ethacrynic acid is not used due to ‑

 A

Renal toxicity

 B

Ototoxicity

 C

GI toxicity

 D

Pulmonary toxicity

Q. 22

Ethacrynic acid is not used due to ‑

 A

Renal toxicity

 B

Ototoxicity

 C

GI toxicity

 D

Pulmonary toxicity

Ans. B

Explanation:

Ans. is b  i.e., Ototoxicity

Ethacrynic acid is a high efficacy loop diuretic.

  • They have weak carbonic anhydrase inhibitory action except for ethacrynic acid.
  • Ethacrynic acid is most ototoxic loop diuretic.
  • Mersalyl and ethacrynic acid among loop diuretics are not used now.

Loop diuretics

  • Also known as high ceiling or high efficacy diuretics – maximum natriuretic action.
  • Examples – Furosemide, Bumetanide, torasemide, ethacrynic acid and mersalyl.
  • They are fast acting with shorter duration of action.
  • The major site of action is thick ascending limb of loop of Henle where they inhibit Ner2Ct.
  • They are secreted in PT by organic anion transport and reaches AscLH where they act from luminal side of the membrane.
  • They have weak carbonic anhydrase inhibitory action except for ethacrynic acid.
  • In addition to its prominant tubular action, furosemide causes acute changes in renal and systemic haemodynamics
  • After iv injection, renal blood flow is transiently increased and there is redistribution of blood from outer to
  • midcortical zone. These intrarenal hemodynamic changes are due to increased local PG synthesis.
  • IV furosemide also causes prompt increase in systemic venous capacitance (venodilatation) and decreases leftventricular filling pressure quick relief in LVF and pulmonary edema. This action is also PG mediated
  • Furosemide increases Ca’ excretion (contrast thiazides which reduce it).
  • Both furosemide and thiazides increase Mg” excretion.
  • Furosemide decreases tubular secretion of uric acid –> can cause hyperuricaemia.
  • Furosemide also causes hyperglycemia (hyperglycemic and hyperuricaemic actions are less marked than thiazides). 
  • Furosemide is active even in patients with relatively severe renal failure – Diuretic of choice in patients with renal failure.
  • Loop diuretics abolishes the corticomedullary osmotic gradient and blocks positive as well as negative free water clearance. (Free water clearance is the volume of urine excreted per unit time in excess of that required to excrete the contained solute isoosmotically with plasma. It is positive when dilute urine is passed, negative when concentrated urine is passed and zero when isotonic urine is passed).
  • Torasemide (Torsemide) has property similar to furosemide, but 3 times more potent.
  • Bumetanide is the most potent (40 times more potent than furosamide) loop diuretic.
  • Indacrinone can be used in patients of gout because it inhibits reabsorption of uric acid in the nephron (other loop diuretics and thiazides cause hyperuricemia).
  • Ethacrynic acid is most ototoxic loop diuretic.
  • Mersalyl and ethacrynic acid are not used now.

Q. 23

Diuretics of choice for acute pulmonary edema ‑

 A

Loop diuretics

 B

Thiazides

 C

Spironolactone

 D

Mannitol

Q. 23

Diuretics of choice for acute pulmonary edema ‑

 A

Loop diuretics

 B

Thiazides

 C

Spironolactone

 D

Mannitol

Ans. A

Explanation:

Ans. is ‘a’ i.e., Loop diuretics 



Leave a Reply

Free Mini Course on Stomach

Mini Course – Stomach

22 High Yield Topics in Stomach

in Just 2 Hours

Submission received, thank you!

Close Window
%d bloggers like this:
Malcare WordPress Security