Corzide (Nadolol and bendroflumethiazide)

Corzide is a combination of nadolol (a non-selective beta-blocker) and bendroflumethiazide (a thiazide diuretic). It is used in the treatment of hypertension.

Corzide (Nadolol and bendroflumethiazide) Uses:

  • Hypertension:

    • Used for management of hypertension (not for initial therapy)

Corzide (Nadolol and bendroflumethiazide) Dose in Adults

Corzide dose in the treatment of Hypertension: 

Note: Not for initial therapy. Dose must be individualized.

  • Initial:
  • Nadolol 40 mg/bendroflumethiazide 5 mg OD orally
  • May increase to nadolol 80 mg/bendroflumethiazide 5 mg OD orally based on patient response.

Corzide (Nadolol and bendroflumethiazide) Dose in Childrens

Not recommended for use in children.

Pregnancy Risk Factor C

  • This combination has not been used in animal reproduction studies.
  • Talk to individual agents.

Corzide use during breastfeeding:

  • Breast milk contains bendroflumethiazide and naprolol.
  • According to the manufacturer breast-feeding during therapy should be considered in light of the risks to the infant as well as the benefits to the mother. Refer to individual agents.

Corzide Dose in Kidney Disease:

  • CrCl >50 mL/minute/1.73 m²:

    • Administer dose q 24 hours
  • CrCl 31 to 50 mL/minute/1.73 m²:

    • Administer dose q 24 to 36 hours
  • CrCl 10 to 30 mL/minute/1.73 m²:

    • Administer dose q 24 to 48 hours
  • CrCl <10 mL/minute/1.73 m²:

    • Administer dose q 40 to 60 hours

Corzide Dose in Liver disease:

  • The manufacturer's labelling does not mention dosage modifications.
  • Use with caution since changes to the electrolyte and fluid balance can lead to hepatic coma.

Side Effects of Corzide (Nadolol and bendroflumethiazide)

See individual agents (Nadolol and bendroflumethiazide)

Contraindications to Corzide (Nadolol and bendroflumethiazide):

  • Hypersensitivity to bendroflumethiazide, drugs derived from sulfonamides, or any other component of the formulation
  • Bronchial asthma
  • Sinus bradycardia
  • Heart block of greater than the first degree is possible (except for patients who have a working artificial pacemaker).
  • Cardiogenic shock
  • Uncompensated cardiac Failure
  • Anuria

Notification:

  • Although the FDA-approved product labelling warns that this medication should not be taken with other groups of drugs that contain sulfonamides, the scientific validity of this claim has been questioned.
  • For more information, go to "Warnings/Precautions."

Warnings/Precautions

  • Anaphylactic reactions

    • Avoid using this product if you have had severe allergic reactions to allergens in the past.
    • Beta-blockers can make patients more sensitive to repeated challenges.
    • Patients taking beta-blockers might experience anaphylaxis (e.g., epinephrine), which can be ineffective or cause undesirable side effects.
  • Electrolyte disturbances:

    • Thiazides can cause hypokalemia, hypochloremic acidkalosis, hypomagnesemia and hyponatremia.
    • Correct electrolyte disturbances as appropriate before initiating.
  • Photosensitivity

    • Photosensitization can occur.
  • Allergy to sulfonamide ("sulfa")

    • Wide-ranging contraindications for patients who have previously experienced an adverse reaction to sulfonamides are listed on FDA-approved product labels for drugs that contain sulfonamide chemical groups.
    • Cross-reactivity between members of a class is conceivable (eg two antibiotic sulfonamides).
    • Concerns about cross-reactivity have been expressed for all substances with the sulfonamide structure.
    • A fuller understanding of allergic pathways shows that it may not be possible for non-antibiotic or antibiotic sulfonamides to cross-react with each other.
    • Sulfonamides that are not antibiotics are not likely to trigger mechanisms of cross-reaction from antibody formation or anaphylaxis (anaphylaxis).
    • Less is known about type IV T-cell reactions, such as maculopapular skin rash. Based on what is known at the moment, it is difficult to rule out this possibility.
    • Some clinicians opt to avoid these classes in cases of severe reactions (Stevens Johnson syndrome/TEN).
  • Bronchospastic disease

    • Patients with bronchospastic diseases should not be given beta-blockers.
    • If you do use it, please be careful and keep an eye on it.
  • Conductive abnormality

    • Be mindful of any existing disorders, such as sick sinus syndrome, before beginning nadolol.
  • Diabetes:

    • Patients with DM should be cautious
    • Hypoglycemia may be potentiated and/or mask symptoms (eg diaphoresis and tachycardia).
    • Also, may reduce insulin secretion when hyperglycemia occurs
    • It may be necessary to adjust anti-diabetic medications.
  • Gout

    • In some people with a history of gout or who are at risk for chronic renal failure, thiazide diuretics can cause gout.
  • Heart failure (HF):

    • Patients with compensated heart disease should be cautious and monitored for any possible complications. Noradrolol's efficacy in HF has not yet been proven to work.
  • Hepatic impairment

    • Patients with impaired liver function or progressive liver disease should be cautious.
    • Thiazides can alter fluid and electrolyte equilibrium, which could lead to hepatic coma.
  • Hypercalcemia:

    • Thiazides could decrease renal calcium excretion
    • Patients with hypercalcemia should be advised to stop using it.
  • Hypercholesterolemia:

    • Patients with high or moderate cholesterol should be cautious
    • Thiazides have been linked to an increase in cholesterol and triglyceride.
  • Myasthenia gravis:

    • Patients with myasthenia gravis should be treated with caution.
  • Parathyroid disease

    • Thiazide diuretics reduce calcium excretion.
    • Long-term use has been associated with pathologic changes in parathyroid glands, including hypophosphatemia and hypercalcemia.
    • Do not discontinue testing for parathyroid function.
  • Raynaud and peripheral vascular disease (PVD).

    • It can cause or exacerbate arterial insufficiency symptoms in patients with Raynaud and PVD.
    • Be cautious and monitor for arterial obstruction.
  • Untreated Pheochromocytoma

    • Before any beta-blocker can be used, it is necessary to have adequate alpha-blockade.
  • Psoriasis:

    • Although beta-blocker usage has been linked to psoriasis exacerbation or induction, cause and effect are not clear.
  • Renal impairment

    • Patients with impaired renal function should be cautious
    • Dosage adjustments may be required.
    • Stop using if you have progressive renal impairment
    • Patients with impaired renal function may experience cumulative effects, including azotemia.
    • Patients with chronic kidney disease could be at greater risk of developing acute renal failure due to thiazides.
    • Patients with anuria are not advised to use this product.
  • Systemic lupus erythematosus (SLE):

    • SLE activation or exacerbation may occur.
  • Thyroid disease:

    • Hyperthyroidism may be disguised (eg, Tachycardia).
    • Thyrotoxicosis should be treated and monitored if it is suspected.
    • Rapid withdrawal can worsen hyperthyroidism symptoms or cause a thyroid storm.

Nadolol and bendroflumethiazide: Drug Interaction

Risk Factor C (Monitor therapy)

Acetylcholinesterase Inhibitors

May enhance the bradycardic effect of Beta-Blockers.

Ajmaline

Sulfonamides might make ajmaline more harmful or poisonous. In particular, there may be an elevated risk for cholestasis.

Alcohol (Ethyl)

Increases the effectiveness of thiazide and thiazide-like diuretics in lowering orthostatic blood pressure.

Alfuzosin

The hypotensive effects of blood pressure-lowering medications may be strengthened.

Allopurinol

The possibility of allergic or hypersensitive reactions to allopurinol may be increased by thiazide and thiazide-like diuretics. The serum concentration of Allopurinol may rise in response to thiazides and thiazide-like diuretics. In particular, Thiazide Diuretics may raise Oxypurinol's levels, an active metabolite of Allopurinol.

Alpha1-Blockers

Alpha1Blockers' orthostatic hypotensive action may be strengthened by beta-blockers. Ophthalmic products likely carry a lower level of risk than systemic ones.

Aminolevulinic Acid (Topical)

Aminolevulinic Acid's photosensitizing impact may be enhanced by photosensitizing agents (Topical).

Amiodarone

May enhance the bradycardic effect of Beta-Blockers. Possibly to the point of cardiac arrest. Amiodarone may increase the serum concentration of Beta-Blockers.

Amphetamines

May diminish the antihypertensive effect of Antihypertensive Agents.

Angiotensin-Converting Enzyme Inhibitors

Angiotensin-Converting Enzyme Inhibitors' hypotensive effects may be enhanced by thiazide and thiazide-like diuretics. Angiotensin-Converting Enzyme Inhibitors' nephrotoxic effects may be increased by thiazide and thiazide-like diuretics.

Anticholinergic Agents

May raise the levels of thiazide and thiazide-like diuretics in the blood.

Antidiabetic Agents

The therapeutic value of anti-diabetic agents may be diminished by thiazide and thiazide-like diuretics.

Antidiabetic Agents

The therapeutic benefit of anti-diabetic agents may be reduced by hyperglycemia-associated agents.

Antipsychotic Agents (Second Generation [Atypical

Antipsychotic drugs' hypotensive effects may be enhanced by blood pressure-lowering medications (Second Generation [Atypical]).

Barbiturates

Increases the effectiveness of thiazide and thiazide-like diuretics in lowering orthostatic blood pressure.

Barbiturates

May enhance the hypotensive effect of Blood Pressure Lowering Agents.

Benperidol

May enhance the hypotensive effect of Blood Pressure Lowering Agents.

Bradycardia-Causing Agents

May enhance the bradycardic effect of other Bradycardia-Causing Agents.

Bretylium

May enhance the bradycardic effect of Bradycardia-Causing Agents. Bretylium may also enhance atrioventricular (AV) blockade in patients receiving AV blocking agents.

Brigatinib

May diminish the antihypertensive effect of Antihypertensive Agents. Brigatinib may enhance the bradycardic effect of Antihypertensive Agents.

Brimonidine (Topical

May enhance the hypotensive effect of Blood Pressure Lowering Agents.

Bupivacaine

Beta-Blockers may increase the serum concentration of Bupivacaine.

Calcium Channel Blockers (Nondihydropyridine)

May enhance the hypotensive effect of BetaBlockers. Bradycardia and signs of heart failure have also been reported. Calcium Channel Blockers (Nondihydropyridine) may increase the serum concentration of Beta-Blockers. Exceptions: Bepridil.

Calcium Salts

The excretion of calcium salts may be decreased by thiazide and thiazide-like diuretics. Metabolic alkalosis can also be brought on by continued concurrent usage.

CarBAMazepine

Thiazide and Thiazide-Like Diuretics may intensify CarBAMazepine's negative/toxic effects. Particularly, there could be a higher risk of hyponatremia.

Cardiac Glycosides

Beta-Blockers may enhance the bradycardic effect of Cardiac Glycosides.

Cardiac Glycosides

Cardiac Glycosides may have an increased negative or toxic effect when used with thiazide and thiazide-Like Diuretics. Particularly, the hypokalemic and hypomagnesemic impact of thiazide diuretics may worsen cardiac glycoside toxicity.

Cholinergic Agonists

Beta-Blockers may make Cholinergic Agonists' harmful or toxic effects worse. The possibilities for bronchoconstriction and aberrant cardiac conduction are of special concern. Management: Use cautious while combining these drugs, and keep an eye out for conduction issues. Because methacholine may cause further bronchoconstriction when used with any beta blocker, avoid using it.

Corticosteroids (Orally Inhaled)

Thiazide and Thiazide-Like Diuretics might have an enhanced hypokalemic impact.

Corticosteroids (Systemic)

Thiazide and Thiazide-Like Diuretics might have an enhanced hypokalemic impact.

Cyclophosphamide

Thiazide and Thiazide-Like Diuretics may intensify Cyclophosphamide's harmful or hazardous effects. Particularly, granulocytopenia could be worsened.

Dexketoprofen

Sulfonamides' harmful or poisonous effects could be amplified.

Dexmethylphenidate

Can lessen an antihypertensive drug's therapeutic impact.

Diacerein

Could make diuretics' therapeutic effects stronger. Particularly, there may be a higher chance of hypokalemia or dehydration.

Diazoxide

Thiazide and Thiazide-Like Diuretics may intensify Diazoxide's harmful or toxic effects.

Diazoxide

The hypotensive effects of blood pressure-lowering medications may be strengthened.

Dipyridamole

Could make beta-blockers' bradycardic impact stronger.

Disopyramide

Could make beta-blockers' bradycardic impact stronger. Beta-blockers might make Disopyramide's adverse inotropic impact worse.

DULoxetine

The hypotensive impact of DULoxetine may be enhanced by blood pressure lowering medications.

EPINEPHrine (Nasal)

The hypertensive impact of EPINEPHRINE may be enhanced by beta-blockers like Nonselective (Nasal).

EPINEPHrine (Oral Inhalation)

The hypertensive impact of EPINEPHRINE may be enhanced by beta-blockers like Nonselective (Oral Inhalation).

Epinephrine (Racemic)

Epinephrine's hypertensive action may be enhanced by beta-blockers like Nonselective (Racemic).

EPINEPHrine (Systemic)

The hypertensive impact of EPINEPHRINE may be enhanced by beta-blockers like Nonselective (Systemic).

Erdafitinib

P-glycoprotein/ABCB1 Substrates serum levels can rise.

Herbs (Hypertensive Properties)

May diminish the antihypertensive effect of Antihypertensive Agents.

Herbs (Hypotensive Properties)

May enhance the hypotensive effect of Blood Pressure Lowering Agents.

Hypotension-Associated Agents

Blood Pressure Lowering Agents may enhance the hypotensive effect of Hypotension-Associated Agents.

Insulins

Beta-Blockers may enhance the hypoglycemic effect of Insulins.

Ipragliflozin

The toxic and harmful effects of thiazide and thiazide-like diuretics may be increased. In particular, there may be an elevated risk for intravascular volume depletion.

Ivabradine

The arrhythmogenic impact of ivabradine may be enhanced by thiazide and thiazide-like diuretics.

Ivabradine

Bradycardia-Causing Agents may enhance the bradycardic effect of Ivabradine.

Lacosamide

Bradycardia-Causing Agents may enhance the AV-blocking effect of Lacosamide.

Levodopa-Containing Products

Blood Pressure Lowering Agents may enhance the hypotensive effect of Levodopa-Containing Products.

Licorice

The arrhythmogenic impact of ivabradine may be enhanced by thiazide and thiazide-like diuretics.

Lidocaine (Systemic)

Thiazide and Thiazide-Like Diuretics might have an enhanced hypokalemic impact.

Lidocaine (Topical)

Beta-blockers might boost the level of lidocaine in the blood (Systemic).

Lormetazepam

Beta-blockers might boost the level of lidocaine in the blood (Topical).

Lumacaftor

May lower the level of P-glycoprotein/ABCB1 Substrates in the serum. The serum concentration of P-glycoprotein/ABCB1 Substrates may rise when using lumacaftor.

Mepivacaine

Mepivacaine's serum levels may rise after taking beta-blockers.

Methoxyflurane

May enhance the hypotensive effect of Beta-Blockers.

Methylphenidate

May diminish the antihypertensive effect of Antihypertensive Agents.

Midodrine

May enhance the bradycardic effect of Bradycardia-Causing Agents.

Molsidomine

The hypotensive effects of blood pressure-lowering medications may be strengthened.

Multivitamins/Fluoride (with ADE)

May intensify the effects of thiazide and thiazide-like diuretics on hypercalcemia.

Multivitamins/Minerals (with ADEK, Folate, Iron)

The effect of multivitamins and minerals on hypercalcemia may be enhanced by thiazide and thiazide-like diuretics (with ADEK, Folate, Iron).

Multivitamins/Minerals (with AE, No Iron)

The serum concentration of multiple vitamins and minerals may rise after taking thiazide and thiazide-like diuretics (with AE, No Iron). Particularly, thiazide diuretics may reduce calcium excretion, and long-term concurrent usage may result in metabolic alkalosis.

Naftopidil

The hypotensive effects of blood pressure-lowering medications may be strengthened.

Neuromuscular-Blocking Agents (Nondepolarizing)

The neuromuscular-blocking action of neuromuscular-blocking agents may be enhanced by thiazide and thiazide-like diuretics (Nondepolarizing).

Nicergoline

The hypotensive effects of blood pressure-lowering medications may be strengthened.

Nicorandil

The hypotensive effects of blood pressure-lowering medications may be strengthened.

NIFEdipine

May enhance the hypotensive effect of Beta-Blockers. NIFEdipine may enhance the negative inotropic effect of Beta-Blockers.

Nitroprusside

Blood Pressure Lowering Agents may enhance the hypotensive effect of Nitroprusside.

Nonsteroidal Anti-Inflammatory Agents

May diminish the antihypertensive effect of BetaBlockers.

Nonsteroidal Anti-Inflammatory Agents

Nonsteroidal Anti-Inflammatory Agents' nephrotoxic effects may be intensified by thiazide and thiazide-like diuretics. Thiazide and Thiazide-Like Diuretics may have less of a therapeutic impact when used with nonsteroidal anti-inflammatory drugs.

Opioid Agonists

Could make diuretics' harmful or toxic effects worse. Opioid antagonists may reduce diuretics' therapeutic benefit.

Opioids (Anilidopiperidine

May enhance the bradycardic effect of Beta-Blockers. Opioids (Anilidopiperidine) may enhance the hypotensive effect of Beta-Blockers.

Oxcarbazepine

Thiazide and Thiazide-Like Diuretics may intensify OXcarbazepine's negative/toxic effects. Particularly, there could be a higher risk of hyponatremia.

Pentoxifylline

The hypotensive effects of blood pressure-lowering medications may be strengthened.

P-glycoprotein/ABCB1 Inducers

May lower the level of Pglycoprotein/ABCB1 Substrates in the serum. P-glycoprotein inducers may also further restrict the distribution of p-glycoprotein substrates to particular cells, tissues, and organs that have high levels of p-glycoprotein (e.g., brain, T-lymphocytes, testes, etc.).

P-glycoprotein/ABCB1 Inhibitors

Pglycoprotein/ABCB1 Substrates serum levels can rise. Additionally, p-glycoprotein inhibitors may improve the distribution of pglycoprotein substrates to particular cells, tissues, and organs where high levels of p-glycoprotein are present (e.g., brain, T-lymphocytes, testes, etc.).

Pholcodine

Pholcodine's hypotensive impact may be strengthened by blood pressure lowering medications.

Phosphodiesterase 5 Inhibitors

The hypotensive effects of blood pressure-lowering medications may be strengthened.

Porfimer

The photosensitizing effect of Porfimer may be strengthened by photosensitizing agents.

Prostacyclin Analogues

The hypotensive effects of blood pressure-lowering medications may be strengthened.

Quinagolide

The hypotensive effects of blood pressure-lowering medications may be strengthened.

Ranolazine

P-glycoprotein/ABCB1 Substrates serum levels can rise.

Reboxetine

Thiazide and Thiazide-Like Diuretics might have an enhanced hypokalemic impact.

Regorafenib

Could make beta-blockers' bradycardic impact stronger.

Reserpine

May strengthen beta-blockers' hypotensive effects.

Ruxolitinib

Bradycardia-Causing Agents' bradycardic effect might be enhanced. Management: The Canadian product labelling for roxolitinib advises against using it in conjunction with medications that can cause bradycardia whenever feasible.

Selective Serotonin Reuptake Inhibitors

The hyponatremic effects of thiazide and thiazide-like diuretics may be enhanced.

Sulfonylureas

Beta-Blockers may enhance the hypoglycemic effect of Sulfonylureas. Cardioselective beta-blockers (eg, acebutolol, atenolol, metoprolol, and penbutolol) may be safer than nonselective beta-blockers. All beta-blockers appear to mask tachycardia as an initial symptom of hypoglycemia. Ophthalmic beta-blockers are probably associated with lower risk than systemic agents.

Terlipressin

May enhance the bradycardic effect of Bradycardia-Causing Agents.

Tofacitinib

May enhance the bradycardic effect of Bradycardia-Causing Agents.

Toremifene

Toremifene's hypercalcemic impact may be enhanced by thiazide and thiazide-like diuretics.

Verteporfin

Verteporfin's photosensitizing effect may be strengthened by photosensitizing agents.

Vitamin D Analogs

The hypercalcemic impact of vitamin D analogues may be enhanced by thiazides and thiazide-like diuretics.

Yohimbine

May diminish the antihypertensive effect of Antihypertensive Agents.

Risk Factor D (Consider therapy modification)

Alpha2-Agonists

May enhance the AV-blocking effect of Beta-Blockers. Sinus node dysfunction may also be enhanced. Beta-Blockers may enhance the rebound hypertensive effect of Alpha2Agonists. This effect can occur when the Alpha2-Agonist is abruptly withdrawn. Management: Closely monitor heart rate during treatment with a beta blocker and clonidine. Withdraw beta blockers several days before clonidine withdrawal when possible, and monitor blood pressure closely. Recommendations for other alpha2-agonists are unavailable. Exceptions: Apraclonidine.

Amifostine

Blood Pressure Lowering Agents may enhance the hypotensive effect of Amifostine. Management: When amifostine is used at chemotherapy doses, blood pressure lowering medications should be withheld for 24 hours prior to amifostine administration. If blood pressure lowering therapy cannot be withheld, amifostine should not be administered.

Bile Acid Sequestrants

The absorption of thiazide and thiazide-like diuretics may be reduced. Also reduced is the diuretic reaction.

Ceritinib

Bradycardia-Causing Agents may enhance the bradycardic effect of Ceritinib. Management: If this combination cannot be avoided, monitor patients for evidence of symptomatic bradycardia, and closely monitor blood pressure and heart rate during therapy. Exceptions are discussed in separate monographs.

Dofetilide

The QTc-prolonging action of dofetilide may be enhanced by thiazide and thiazide-like diuretics. The blood concentration of Dofetilide may rise in response to thiazide and thiazide-like diuretics. Management: Despite the fact that hydrochlorothiazide is clearly listed as being contraindicated, the risk certainly applies to all thiazide and thiazide-like diuretics and may even be larger when using chlorthalidone or bendroflumethiazide. When feasible, take into account alternatives.

Dronedarone

May enhance the bradycardic effect of Beta-Blockers. Dronedarone may increase the serum concentration of Beta-Blockers. This likely applies only to those agents that are metabolized by CYP2D6. Management: Use lower initial beta-blocker doses; adequate tolerance of the combination, based on ECG findings, should be confirmed prior to any increase in betablocker dose.

Ergot Derivatives

Beta-Blockers may enhance the vasoconstricting effect of Ergot Derivatives. Exceptions: Nicergoline.

Fingolimod

Beta-Blockers may enhance the bradycardic effect of Fingolimod. Management: Avoid the concomitant use of fingolimod and beta-blockers if possible. If coadministration is necessary, patients should have overnight continuous ECG monitoring conducted after the first dose of fingolimod. Monitor patients for bradycardia.

Grass Pollen Allergen Extract (5 Grass Extract)

Beta-Blockers may enhance the adverse/toxic effect of Grass Pollen Allergen Extract (5 Grass Extract). More specifically, Beta-Blockers may inhibit the ability to effectively treat severe allergic reactions to Grass Pollen Allergen Extract (5 Grass Extract) with epinephrine. Some other effects of epinephrine may be unaffected or even enhanced (e.g., vasoconstriction) during treatment with Beta-Blockers.

Green Tea

May decrease the serum concentration of Nadolol. Management: Advise patients to minimize green tea consumption during nadolol treatment. The impact of separating nadolol doses from green tea consumption has not been investigated.

Lithium

The excretion of lithium may be reduced by thiazide and thiazide-like diuretics.

Obinutuzumab

May enhance the hypotensive effect of Blood Pressure Lowering Agents. Management: Consider temporarily withholding blood pressure lowering medications beginning 12 hours prior to obinutuzumab infusion and continuing until 1 hour after the end of the infusion.

Siponimod

Bradycardia-Causing Agents may enhance the bradycardic effect of Siponimod. Management: Avoid coadministration of siponimod with drugs that may cause bradycardia.

Sodium Phosphates

Diuretics may enhance the nephrotoxic effect of Sodium Phosphates. Specifically, the risk of acute phosphate nephropathy may be enhanced. Management: Consider avoiding this combination by temporarily suspending treatment with diuretics, or seeking alternatives to oral sodium phosphate bowel preparation. If the combination cannot be avoided, hydrate adequately and monitor fluid and renal status.

Theophylline Derivatives

Beta-Blockers (Nonselective) may diminish the bronchodilatory effect of Theophylline Derivatives.

Topiramate

The hypokalemic impact of topiramate may be enhanced by thiazide and thiazide-like diuretics. The blood concentration of topiramate may rise in response to thiazide and thiazide-like diuretics. When using a thiazide diuretic, monitor for elevated topiramate levels and any negative consequences (such as hypokalemia). Serum potassium levels should be closely watched when receiving concurrent treatment. There may be a need to lower topiramate dosage.

Risk Factor X (Avoid combination)

Aminolevulinic Acid (Systemic)

Aminolevulinic Acid's photosensitizing impact may be enhanced by photosensitizing agents (Systemic).

Beta2-Agonists

Beta-Blockers (Nonselective) may diminish the bronchodilatory effect of Beta2Agonists.

Bromperidol

Blood Pressure Lowering Agents may enhance the hypotensive effect of Bromperidol. Bromperidol may diminish the hypotensive effect of Blood Pressure Lowering Agents.

Floctafenine

May enhance the adverse/toxic effect of Beta-Blockers.

Levosulpiride

Thiazide and Thiazide-Like Diuretics may intensify Levosulpiride's negative/toxic effects.

Mecamylamine

Sulfonamides may intensify Mecamylamine's harmful or hazardous effects.

Methacholine

Beta-Blockers might make methacholine's harmful or toxic effects worse.

Promazine

Promazine's ability to prolong QTc may be enhanced by thiazide and thiazide-like diuretics.

Rivastigmine

Could make beta-blockers' bradycardic impact stronger.

Monitoring parameters:

  • Blood pressure
  • Heart rate
  • Fluid and electrolyte balance
  • Serum glucose regularly (in patients with diabetes)
  • Renal function

How to administer Corzide (Nadolol and bendroflumethiazide)?

P/O

  •  Administer without regard to meals.

Mechanism of action of Corzide (Nadolol and bendroflumethiazide):

  • Nadolol is a competitive inhibitor of beta1- and Beta2-adrenergic stimulation.
  • Bendroflumethiazide prevents sodium from being reabsorbed in the distal tubules, leading to an increase in sodium, water, potassium, and hydrogen ion excretion.

Also, see individual agents.

Bioavailability:

  • Bendroflumethiazide: When used in this combination, bioavailability is increased 30% compared to single-agent administration.

International Brands of Nadolol and bendroflumethiazide:

  • Corzide
  • Corgaretic
  • Corgaretic-40
  • Corgaretic-80

Nadolol and bendroflumethiazide Brand Names in Pakistan

No Brands Available in Pakistan.