Interactions between Avapro and Prazosin

Prazosin has a moderate potential interaction with Autonomic Neuropathy.

Peripheral alpha 1- adrenergic receptor blocking agents (aka alpha 1- blockers) cause vasodilation and can produce marked hypotension, especially orthostatic hypotension with syncope or other postural symptoms such as dizziness, lightheadedness, and palpitations. Orthostatic effects are most common during initiation of therapy and often occur within 90 minutes after the first dose. However, they can also occur following a dosage increase or resumption of therapy after an interruption of more than a few days. Agents with alpha 1a specificity, such as tamsulosin, act primarily on the prostate but are not devoid of hypotensive effects. Therapy with peripheral alpha-1 blockers should be administered cautiously in patients with or predisposed to hypotensive or syncopal episodes. Caution is also advised in patients who are dehydrated (e.g., due to severe or prolonged diarrhea or vomiting), since they may be more sensitive to the hypotensive effect of the drugs. Therapy should be initiated with the lowest dosage possible and titrated gradually based on patient response and tolerance in accordance with the individual product package labeling. During initiation or reinstitution of therapy and following an increase in dosage, patients should be advised not to rise abruptly from a sitting or recumbent position and to avoid situations where injury could result if syncope occur. Concomitant use of alcohol, extensive periods of standing, prolonged or intense exercise, and exposure to heat can also precipitate orthostatic hypotension and should be minimized. If dizziness, lightheadedness or palpitations occur, the patient should sit or lie down, and seek medical attention if symptoms are recurrent or bothersome.

Prazosin has a moderate potential interaction with Biliary Obstruction.

Little data exist concerning the pharmacokinetic disposition of prazosin in patients with liver disease. Prazosin is known to be metabolized by the liver and subsequently excreted in the bile, primarily as metabolites. Some of the metabolites are pharmacologically active and possess 10% to 25% of the hypotensive activity of prazosin. Therapy with prazosin should be administered cautiously in patients with significantly impaired hepatic or biliary function, since drug and/or metabolite accumulation may occur.

The irbesartan in Avapro has a major potential interaction with Dehydration.

Angiotensin II receptor (AR) antagonists can cause symptomatic hypotension in patients with an activated renin-angiotensin system, such as volume- and/or sodium-depleted patients. Therapy with AR antagonists should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if high doses were used or if recently instituted; those on dietary salt restriction; renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with AR antagonists, and the patient should be hemodynamically stable. Ideally, patients at risk for excessive hypotension should initiate AR antagonist therapy under close medical supervision, preferably with a lower dose, and followed closely for the first 2 weeks of treatment and whenever the dosage of AR antagonist or diuretic is increased.

Prazosin has a moderate potential interaction with Dehydration.

Peripheral alpha 1- adrenergic receptor blocking agents (aka alpha 1- blockers) cause vasodilation and can produce marked hypotension, especially orthostatic hypotension with syncope or other postural symptoms such as dizziness, lightheadedness, and palpitations. Orthostatic effects are most common during initiation of therapy and often occur within 90 minutes after the first dose. However, they can also occur following a dosage increase or resumption of therapy after an interruption of more than a few days. Agents with alpha 1a specificity, such as tamsulosin, act primarily on the prostate but are not devoid of hypotensive effects. Therapy with peripheral alpha-1 blockers should be administered cautiously in patients with or predisposed to hypotensive or syncopal episodes. Caution is also advised in patients who are dehydrated (e.g., due to severe or prolonged diarrhea or vomiting), since they may be more sensitive to the hypotensive effect of the drugs. Therapy should be initiated with the lowest dosage possible and titrated gradually based on patient response and tolerance in accordance with the individual product package labeling. During initiation or reinstitution of therapy and following an increase in dosage, patients should be advised not to rise abruptly from a sitting or recumbent position and to avoid situations where injury could result if syncope occur. Concomitant use of alcohol, extensive periods of standing, prolonged or intense exercise, and exposure to heat can also precipitate orthostatic hypotension and should be minimized. If dizziness, lightheadedness or palpitations occur, the patient should sit or lie down, and seek medical attention if symptoms are recurrent or bothersome.

Prazosin has a moderate potential interaction with Diarrhea.

Peripheral alpha 1- adrenergic receptor blocking agents (aka alpha 1- blockers) cause vasodilation and can produce marked hypotension, especially orthostatic hypotension with syncope or other postural symptoms such as dizziness, lightheadedness, and palpitations. Orthostatic effects are most common during initiation of therapy and often occur within 90 minutes after the first dose. However, they can also occur following a dosage increase or resumption of therapy after an interruption of more than a few days. Agents with alpha 1a specificity, such as tamsulosin, act primarily on the prostate but are not devoid of hypotensive effects. Therapy with peripheral alpha-1 blockers should be administered cautiously in patients with or predisposed to hypotensive or syncopal episodes. Caution is also advised in patients who are dehydrated (e.g., due to severe or prolonged diarrhea or vomiting), since they may be more sensitive to the hypotensive effect of the drugs. Therapy should be initiated with the lowest dosage possible and titrated gradually based on patient response and tolerance in accordance with the individual product package labeling. During initiation or reinstitution of therapy and following an increase in dosage, patients should be advised not to rise abruptly from a sitting or recumbent position and to avoid situations where injury could result if syncope occur. Concomitant use of alcohol, extensive periods of standing, prolonged or intense exercise, and exposure to heat can also precipitate orthostatic hypotension and should be minimized. If dizziness, lightheadedness or palpitations occur, the patient should sit or lie down, and seek medical attention if symptoms are recurrent or bothersome.

The irbesartan in Avapro has a moderate potential interaction with Heart Failure.

Angiotensin II receptor (AR) antagonists can cause renal impairment in patients whose renal function depends on the activity of the renin-angiotensin-aldosterone system. In addition, symptomatic hypotension can occur in susceptible individuals, which may compromise renal and myocardial perfusion. In patients with severe congestive heart failure (CHF), treatment with AR antagonists has been associated with oliguria and/or progressive azotemia and, rarely, renal failure, myocardial ischemia, and death. Therapy with AR antagonists should be initiated cautiously in patients with severe CHF, especially when accompanied by volume and/or sodium depletion. In patients who experience a decline in renal function, discontinuation of AR antagonist therapy is usually not required provided there is symptomatic improvement of the heart failure and renal deterioration is well-tolerated. Transient hypotension is also not a contraindication to further treatment with AR antagonists, since therapy can usually be reinstated without difficulty after blood pressure stabilizes.

The irbesartan in Avapro has a major potential interaction with Hemodialysis.

Angiotensin II receptor (AR) antagonists can cause symptomatic hypotension in patients with an activated renin-angiotensin system, such as volume- and/or sodium-depleted patients. Therapy with AR antagonists should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if high doses were used or if recently instituted; those on dietary salt restriction; renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with AR antagonists, and the patient should be hemodynamically stable. Ideally, patients at risk for excessive hypotension should initiate AR antagonist therapy under close medical supervision, preferably with a lower dose, and followed closely for the first 2 weeks of treatment and whenever the dosage of AR antagonist or diuretic is increased.

The irbesartan in Avapro has a moderate potential interaction with Hyperkalemia.

Drugs that inhibit the renin-angiotensin, such as angiotensin II receptor antagonist system can cause hyperkalemia. Concomitant use of these agents with drugs that increase potassium levels may increase the risk of hyperkalemia. Use caution when using these agents together and monitor serum potassium periodically.

The irbesartan in Avapro has a major potential interaction with Hyponatremia.

Angiotensin II receptor (AR) antagonists can cause symptomatic hypotension in patients with an activated renin-angiotensin system, such as volume- and/or sodium-depleted patients. Therapy with AR antagonists should be administered cautiously in such patients and in those predisposed to hypovolemic or hyponatremic states (e.g., patients on diuretic therapy, especially if high doses were used or if recently instituted; those on dietary salt restriction; renal dialysis patients). Volume and/or sodium depletion should be corrected prior to initiating therapy with AR antagonists, and the patient should be hemodynamically stable. Ideally, patients at risk for excessive hypotension should initiate AR antagonist therapy under close medical supervision, preferably with a lower dose, and followed closely for the first 2 weeks of treatment and whenever the dosage of AR antagonist or diuretic is increased.

Prazosin has a moderate potential interaction with Hypotension.

Peripheral alpha 1- adrenergic receptor blocking agents (aka alpha 1- blockers) cause vasodilation and can produce marked hypotension, especially orthostatic hypotension with syncope or other postural symptoms such as dizziness, lightheadedness, and palpitations. Orthostatic effects are most common during initiation of therapy and often occur within 90 minutes after the first dose. However, they can also occur following a dosage increase or resumption of therapy after an interruption of more than a few days. Agents with alpha 1a specificity, such as tamsulosin, act primarily on the prostate but are not devoid of hypotensive effects. Therapy with peripheral alpha-1 blockers should be administered cautiously in patients with or predisposed to hypotensive or syncopal episodes. Caution is also advised in patients who are dehydrated (e.g., due to severe or prolonged diarrhea or vomiting), since they may be more sensitive to the hypotensive effect of the drugs. Therapy should be initiated with the lowest dosage possible and titrated gradually based on patient response and tolerance in accordance with the individual product package labeling. During initiation or reinstitution of therapy and following an increase in dosage, patients should be advised not to rise abruptly from a sitting or recumbent position and to avoid situations where injury could result if syncope occur. Concomitant use of alcohol, extensive periods of standing, prolonged or intense exercise, and exposure to heat can also precipitate orthostatic hypotension and should be minimized. If dizziness, lightheadedness or palpitations occur, the patient should sit or lie down, and seek medical attention if symptoms are recurrent or bothersome.

Prazosin has a moderate potential interaction with Liver Disease.

Little data exist concerning the pharmacokinetic disposition of prazosin in patients with liver disease. Prazosin is known to be metabolized by the liver and subsequently excreted in the bile, primarily as metabolites. Some of the metabolites are pharmacologically active and possess 10% to 25% of the hypotensive activity of prazosin. Therapy with prazosin should be administered cautiously in patients with significantly impaired hepatic or biliary function, since drug and/or metabolite accumulation may occur.

The irbesartan in Avapro has a moderate potential interaction with Renal Dysfunction.

Changes in renal function including acute renal failure can be caused by drugs that inhibit the renin-angiotensin system and by diuretics. Patients whose renal function may depend in part on the activity of the renin-angiotensin system (e.g., patients with renal artery stenosis, chronic kidney disease, severe congestive heart failure, or volume depletion) may be at particular risk of developing acute renal failure with these agents. Monitor renal function periodically in these patients. Consider withholding or discontinuing therapy in patients who develop a clinically significant decrease in renal function with these agents.

Prazosin has a moderate potential interaction with Syncope.

Peripheral alpha 1- adrenergic receptor blocking agents (aka alpha 1- blockers) cause vasodilation and can produce marked hypotension, especially orthostatic hypotension with syncope or other postural symptoms such as dizziness, lightheadedness, and palpitations. Orthostatic effects are most common during initiation of therapy and often occur within 90 minutes after the first dose. However, they can also occur following a dosage increase or resumption of therapy after an interruption of more than a few days. Agents with alpha 1a specificity, such as tamsulosin, act primarily on the prostate but are not devoid of hypotensive effects. Therapy with peripheral alpha-1 blockers should be administered cautiously in patients with or predisposed to hypotensive or syncopal episodes. Caution is also advised in patients who are dehydrated (e.g., due to severe or prolonged diarrhea or vomiting), since they may be more sensitive to the hypotensive effect of the drugs. Therapy should be initiated with the lowest dosage possible and titrated gradually based on patient response and tolerance in accordance with the individual product package labeling. During initiation or reinstitution of therapy and following an increase in dosage, patients should be advised not to rise abruptly from a sitting or recumbent position and to avoid situations where injury could result if syncope occur. Concomitant use of alcohol, extensive periods of standing, prolonged or intense exercise, and exposure to heat can also precipitate orthostatic hypotension and should be minimized. If dizziness, lightheadedness or palpitations occur, the patient should sit or lie down, and seek medical attention if symptoms are recurrent or bothersome.

Prazosin has a moderate potential interaction with Vomiting.

Peripheral alpha 1- adrenergic receptor blocking agents (aka alpha 1- blockers) cause vasodilation and can produce marked hypotension, especially orthostatic hypotension with syncope or other postural symptoms such as dizziness, lightheadedness, and palpitations. Orthostatic effects are most common during initiation of therapy and often occur within 90 minutes after the first dose. However, they can also occur following a dosage increase or resumption of therapy after an interruption of more than a few days. Agents with alpha 1a specificity, such as tamsulosin, act primarily on the prostate but are not devoid of hypotensive effects. Therapy with peripheral alpha-1 blockers should be administered cautiously in patients with or predisposed to hypotensive or syncopal episodes. Caution is also advised in patients who are dehydrated (e.g., due to severe or prolonged diarrhea or vomiting), since they may be more sensitive to the hypotensive effect of the drugs. Therapy should be initiated with the lowest dosage possible and titrated gradually based on patient response and tolerance in accordance with the individual product package labeling. During initiation or reinstitution of therapy and following an increase in dosage, patients should be advised not to rise abruptly from a sitting or recumbent position and to avoid situations where injury could result if syncope occur. Concomitant use of alcohol, extensive periods of standing, prolonged or intense exercise, and exposure to heat can also precipitate orthostatic hypotension and should be minimized. If dizziness, lightheadedness or palpitations occur, the patient should sit or lie down, and seek medical attention if symptoms are recurrent or bothersome.