التداخل بين فوسينوبريل وهيدروكلوروثيازيد وتريامتيرين
فوسينوبريل وهيدروكلوروثيازيد وتريامتيرين: كلتا نشرتَي الوصف تصفان تداخلًا يستدعي عادةً المراقبة أو تغيير الجرعة أو المباعدة بين الجرعات.
يمكن التعامل معه عادةً بالمراقبة أو بتغيير الجرعة. أخبر الصيدلي بأنك تتناول الاثنين.
ما تقوله نشرات FDA
من نشرة تريامتيرين (Dyrenium) · تاريخ السريان 2024-12-05
If the ECG shows no widening of the QRS or arrhythmia in the presence of hyperkalemia, it is usually sufficient to discontinue Dyrenium (triamterene) and any potassium supplementation, and substitute a thiazide alone.
Drug Interactions Caution should be used when lithium and diuretics are used concomitantly because diuretic-induced sodium loss may reduce the renal clearance of lithium and increase serum lithium levels with risk of lithium toxicity.
The effects of the following drugs may be potentiated when given together with triamterene: antihypertensive medication, other diuretics, preanesthetic and anesthetic agents, skeletal muscle relaxants (non-depolarizing).
Potassium-sparing agents should be used with caution in conjunction with angiotensin-converting enzyme (ACE) inhibitors due to an increased risk of hyperkalemia.
من نشرة فوسينوبريل وهيدروكلوروثيازيد (Fosinopril Sodium and Hydrochlorothiazide) · تاريخ السريان 2024-04-28
Symptomatic hypotension is most likely to occur in patients who have been volume- and/or salt-depleted as a result of prolonged diuretic therapy, dietary salt restriction, dialysis, diarrhea, or vomiting.
The thiazide component of fosinopril sodium and hydrochlorothiazide may potentiate the action of other antihypertensive drugs, especially ganglionic or peripheral adrenergic-blocking drugs.
In such patients, fosinopril sodium and hydrochlorothiazide therapy should be started under close medical supervision; they should be followed closely for the first 2 weeks of treatment and whenever the dose of fosinopril or diuretic is increased.
In some studies of hypertensive patients with unilateral or bilateral renal artery stenosis, treatment with ACE inhibitors has been associated with increases in blood urea nitrogen and serum creatinine; these increases were reversible upon discontinuation of ACE inhibitor therapy, concomitant diuretic therapy, or both.
Some ACE-inhibitor-treated hypertensive patients with no apparent preexisting renal vascular disease have developed increases in blood urea nitrogen and serum creatinine, usually minor and transient, especially when the ACE inhibitor has been given concomitantly with a diuretic.
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