Its a antidiruetic drug.

1. Antidiruetic Drug
By Muhammad Sufyan Akram B.S MLT (2)
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Sargodha Institute Of Health Sciences

2. Introduction
Antidiruetic are the agent that reduce the urine
volume opposing diuresis.
(or)
Acting on kidney to reduce the water excretion.

3. Classification of Antidiruetic Drug:
These drug can be classified in following steps.
 Hydrochlorothiazide
 Furosemide
 Acetazolamide

4. Hydrochlorothiazide
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5. Content
 Hydrochlorothiazide
Dosage Forms & TradeNames
Pharmacokinetics Ι & ΙΙ
Mechanism of action
 Action
Therapeutic uses
Adverse effects
Contraindication & Drug Interaction
 Overdose
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6. Hydrochlorothiazide
HCTZ,HCT,or HZT
 The thiazides are the most widely used diuretics.
They are sulfonamidederivatives.
Sometimes called “low ceiling diuretics” because
increasing the dose above normal therapeutic doses
doesn't promote further diureticresponse.
 Because the site of action of the thiazide derivatives is
on the luminalmembrane, these drugs mustbe
excreted intothetubularlumentobe effective.
Therefore, with decreased renal function,thiazide
diureticslose efficacy.
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7. Dosage Forms&TradeNames
Trade Names: Microzide, HydroDiuril, Hydro, Esidrix
Dosage Forms: Tablet, Capsule,Solution.
Tablet/Capsule: 12.5 mg, 25 mg, 50mg
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Co-Diovan: Valsartan –Hydrochlorothiazide (ARB+Thiazide)

8. Pharmacokinetics 𝚰
The drugs are effectiveorally.
 Most thiazides take 1 to 3 weeks to produce a
stable reduction inblood pressure.
They exhibit a prolonged half-life.
 All thiazides are secreted by the organic acid
secretory systemof the kidney.
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9. Pharmacokinetics 𝚰𝚰
 Absorption
 Onset: Diuresis, ~2hr;hypertension, 3-4 days
 Peak plasma time:1-2.5hr
 Peak effect: Diuresis, 4-6hr
 Bioavailability: 65-75%
 Distribution
 Protein bound: 40-68%
 Vd: 3.6-7.8L/kg
 Metabolism
 Minimally metabolized
 Elimination
 Half-life: 5.6-14.8hr
 Dialyzable: Hemodialysis,no
 Excretion: Urine
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10. Mechanism of action
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Hydrochlorothiazide belongs to Thiazide class of
diuretics. It reduces blood volume by acting on the kidneys
to reduce sodium (Na+) reabsorption in the distal
convoluted tubule. ... Additionally, by other
mechanisms, HCTZ is believed to lower peripheral vascular
resistance.
 Thiazide increase the reabsorption of calcium in this
segment in a manner unrelated to sodium transport.
Excretion: Primarily kidney (>95% as unchang...
Formula: C7H8ClN3O4S2
Molar mass: 297.74 g/mol g·mol−1

11. Action
Increased excretion of Na+and Cl−.
LossofK+.
Lossof Mg++:The mechanism for the magnesuria
is not understood.
Decreased urinarycalcium excretion.
Reduced peripheral vascular resistance: An initial
reduction in blood pressureresults from a
decrease in blood volume and, therefore, a
decrease in cardiacoutput.
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12. Therapeutic uses
Chronic edema
Mild & moderate cardiac edema.
Ascites due to cirrhosis.
Hypertension:
Decrease intravascularvolume
Decrease PVRdue to decrease responsivenessof vascular
smoothmuscle to noradrenaline.
Heartfailure.
Hypercalciuria:
InhibiturinaryCa2+ excretion
Idiopathic hypercalciuria
Calcium oxalate stones.
Diabetesinsipidus:
Hyperosmolarurine.
Nephrogenic diabetes insipidus.
The urine volume of such individuals may drop from11L/dto
about 3L/dwhen treated with the drug.
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13. Adverse effects
Potassiumdepletion:
Digoxinto ventriculararrhythmias.
 Hyponatremia:
Elevation of ADH as a result of hypovolemia.
 Hyperuricemia:
Decreasing the amount of acid excreted by the organic
acid secretorysystem.
Volume depletion:
Orthostatic hypotension.
 Hypercalcemia:
Inhibit the secretion ofCa2+.
 Hyperglycemia:
Glucose intolerance
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14. Contraindication &Drug
Interaction
Contraindication:
Anuria
Hypersensitivity to this product or to othersulfonamide-
derived drugs.
Renal impairment: CrCl <10mL/min:Avoiduse.
noteffective with CrCl <30mL/minunless usedin
combination with loopdiuretic.
DrugInteraction:(Serious- Use Alternative)
Amisulpride
Carbamazepine
Cisapride
Cyclosporine
Dofetilide
Squill
tretinoin
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15. Overdose
Overdose signsand symptoms :
hypokalemia, hyponatremia.
Dehydration.
hypokalemia may accentuate cardiac arrhythmias.
Overdose management:
Normal saline used for volumereplacement.
Dopamine or norepinephrine used to treat hypotension.
Ifdysrhythmia due to decreased potassiumor
magnesium issuspected, replace aggressively.
Emesisshould be inducedor gastric lavage performed.
Ifrequired, give oxygen or artificial respiration for
respiratory impairment.
Lethal Dose:
The oral LD50 of Hydrochlorothiazide is greater than 10
g/kgin the mouseand rat.
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16. Furosemide:
Furosemide: Effective but less desirable: short and brisk
action
Effective in both neurogeneic as well as nephrogenic DI
Mechanism of action
 Similar to salt restriction
 State of sustained electrolyte depletion
 Glomerular filtrate completely reabsorbed iso-osmotically PT
 Urine passing has low solute ……… presented to cortical DT ……….salt
reabsorption decreases
 Less dilute urine presented to CD ……… some is passed out
2) Reduce the Glomerular filtrate rate …..reduced fluid load
on tubules
3) Amiloride:Lithium induced nephrogenic DI
(S
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19. References
 www.drugs.com
 www.reference.medscape.com
 www.nlm.nih.gov
 www.webmd.com
 www.medicinenet.com
 www.youtube.com/watch?v=oh0nAyW5r5Y
₰ www.slideshare.com
₰ wikipedia
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