Furosemide

Furosemide
Introduction
Furosemide is a loop diuretic medication used to treat fluid build-up due to heart failure, liver
scarring, or kidney disease.
It may also be used for the treatment of high blood pressure. It can be taken by injection into a
vein or by mouth. When taken by mouth, it typically begins working within an hour, while
intravenously, it typically begins working within five minutes.
Mechanism of action
Furosemide, like other loop diuretics, acts by inhibiting the luminal Na-K-Cl cotransporter in the
thick ascending limb of the loop of Henle, by binding to the chloride transport channel, thus
causing more sodium, chloride, and potassium to remain in the urine.
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. Because of the large NaCl absorptive capacity of the loop
of Henle, diuresis is not limited by development of acidosis, as it is with the carbonic anhydrase
inhibitors.
Additionally, furosemide is a noncompetitive subtype-specific blocker of GABA-A receptors
Furosemide has been reported to reversibly antagonize GABA-evoked currents of α6β2γ2
receptors at μM concentrations, but not α1β2γ2 receptors.During development, α6β2γ2 receptor
increases in expression in cerebellar granule neurons, corresponding to increased sensitivity to
furosemide.
Pharmacokinetics;
Pharmacokinetics of furosemide is as follow;
Molecular weight;
 Molecular weight (daltons) 330.7
Bioavailability;
 % Bioavailability 47-70%
 Bioavailability with end-stage renal disease 43 – 46%
Protein binding;
 % Protein binding 91–99
Volume of distribution;
 Volume of distribution (L/kg) 0.07 – 0.2
 Volume of distribution may be higher in patients with cirrhosis or nephrotic syndrome
Excretion
 % Excreted in urine (% of total dose) 60 – 90
 % Excreted unchanged in urine (% of total dose) 53.1 – 58.8
 % Excreted in feces (% of total dose) 7 – 9
 % Excreted in bile (% of total dose) 6 – 9
Metabolism
 Approximately 10% is metabolized by the liver in healthy individuals, but this percentage
may be greater in individuals with severe kidney failure
Elimination
 Elimination half-life (hours)
 Prolonged in congestive heart failure (mean 3.4 hours)
 Prolonged in severe kidney failure (4 – 6 hours) and anephric patients (1.5-9 hours)
Peak Concentration
Time to peak concentration (hours)
 Intravenous administration 0.3
 Oral solution 0.83
 Oral tablet 1.45
Uses;
Furosemide is primarily used for the treatment of edema, but also in some cases of hypertension
(where there is also kidney or heart impairment). It is often viewed as a first-line agent in most
people with edema caused by congestive heart failure because of its anti-vasoconstrictor and
diuretic effects.Compared with furosemide, however, torasemide (aka “torsemide”) has been
demonstrated to show improvements to heart failure symptoms, possibly lowering the rates of
rehospitalisation associated with heart failure, with no difference in risk of death. Torsemide may
also be safer than furosemide.
Furosemide is also used for liver cirrhosis, kidney impairment, nephrotic syndrome, in adjunct
therapy for swelling of the brain or lungs where rapid diuresis is required (IV injection), and in
the management of severe hypercalcemia in combination with adequate rehydration.
Kidney disease
In chronic kidney diseases with hypoalbuminemia, furosemide is used along with albumin to
increase diuresis.It is also used along with albumin in nephrotic syndrome to reduce edema.
Other information
Furosemide is mainly excreted by tubular secretion in the kidney. In kidney impairment,
clearance is reduced, increasing the risk of adverse effects Lower initial doses are recommended
in older patients (to minimize side-effects) and high doses may be needed in kidney failure. It
can also cause kidney damage; this is mainly by loss of excessive fluid (i.e., dehydration), and is
usually reversible.
Furosemide acts within 1 hour of oral administration (after IV injection, the peak effect is within
30 minutes). Diuresis is usually complete within 6–8 hours of oral administration, but there is
significant variation between individuals.
Interaction;
Furosemide has potential interactions with these medications:
Aspirin and other salicylates
Other diuretics (e.g. ethacrynic acid, hydrochlorothiazide)
Synergistic effects with other antihypertensives (e.g. doxazosin)
Sucralfate
Potentially hazardous interactions with other drugs:
Analgesics:
increased risk of kidney damage (nephrotoxicity) with nonsteroidal anti-inflammatory drugs;
antagonism of diuretic effect with NSAIDs
Antiarrhythmics:
a risk of cardiac toxicity exists with antiarrhythmics if hypokalemia occurs; the effects of
lidocaine and mexiletine are antagonized.
Antibacterials:
increased risk of ototoxicity with aminoglycosides, polymyxins and vancomycin; avoid
concomitant use with lymecycline.
Antidepressants:
increased risk of hypokalemia with reboxetine; enhanced hypotensive effect with MAOIs;
increased risk of postural hypotension with tricyclic antidepressants
Antiepileptics:
increased risk of hyponatremia with carbamazepine
Antifungals:
increased risk of hypokalemia with amphotericin
Antihypertensives:
enhanced hypotensive effect; increased risk of first dose hypotensive effect with alpha-blockers;
increased risk of ventricular arrhythmias with sotalol if hypokalemia occurs
Side effects;
Furosemide also can lead to gout caused by hyperuricemia. Hyperglycemia is also a common
side effect.
The tendency, as for all loop diuretics, to cause low serum potassium concentration
(hypokalemia) has given rise to combination products, either with potassium or with the
potassium-sparing diuretic amiloride (Co-amilofruse). Other electrolyte abnormalities that can
result from furosemide use include hyponatremia, hypochloremia, hypomagnesemia, and
hypocalcemia.
In the treatment of heart failure, many studies have shown that the long-term use of furosemide
can cause varying degrees of thiamine deficiency, so thiamine supplementation is also suggested
Furosemide is a known ototoxic agent generally causing transient hearing loss but can be
permanent. Reported cases of furosemide induced hearing loss appeared to be associated with
rapid intravenous administration, high dosages, concomitant renal disease and coadministration
with other ototoxic medication.However, a recently reported longitudinal study showed that
participants treated with loop diuretics over 10 years were 40% more likely to develop hearing
loss and 33% more likely of progressive hearing loss compared to participants who did not use
loop diuretics.This suggests the long-term consequences of loop diuretics on hearing could be a
more significant than previously thought and further research is required in this area.
Other precautions include: nephrotoxicity, sulfonamide (sulfa) allergy, and increases free thyroid
hormone effects with large doses.
Reference
https://medlineplus.gov/druginfo/meds/a682858.html
https://en.m.wikipedia.org/wiki/Furosemide

Furosemide

Uploaded by

Copyright:

Available Formats

Furosemide

Uploaded by

Document Information

Original Description:

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Furosemide

Uploaded by

Copyright:

Available Formats

Furosemide

You might also like

Pfad - The Proxy pFad of © 2024 Garber Painting. All rights reserved.