Tonorma film-coated tablets No. 30

Instructions for Tonorma film-coated tablets No. 30

Composition

active ingredients: atenolol, chlortalidone, nifedipine.

1 tablet contains: atenolol 100 mg, chlorthalidone 25 mg, nifedipine 10 mg;

excipients: light magnesium carbonate, potato starch, hypromellose, colloidal anhydrous silicon dioxide, sodium lauryl sulfate, croscarmellose sodium, microcrystalline cellulose, magnesium stearate, polyethylene glycol, titanium dioxide (E 171), sunset yellow FCF (E 110).

Dosage form

Film-coated tablets.

Main physicochemical properties: tablets, coated, yellow-orange in color, round in shape, with a biconvex surface, with a score, white inclusions are allowed on the surface.

Pharmacotherapeutic group

Selective β1-adrenergic blockers in combination with other antihypertensive agents. ATC code C07F B03.

Pharmacological properties

Pharmacodynamics.

Tonorma® is a combined antihypertensive drug containing atenolol, nifedipine and chlorthalidone. The antihypertensive effect of the drug is due to the mechanism of action of its components, primarily the main one - atenolol.

Atenolol is a cardioselective β1-adrenergic blocker. It has antihypertensive, antianginal and antiarrhythmic effects. It has no intrinsic sympathomimetic activity and membrane-stabilizing action. It blocks mainly β-adrenergic receptors of the heart and reduces the stimulating effect on the heart of the sympathetic nervous system and catecholamines circulating in the blood, as a result of which the automatism of the sinus node decreases, the heart rate decreases, atrioventricular conduction slows down, myocardial contractility decreases, and myocardial oxygen demand decreases.

Chlorthalidone is a long-acting thiazide-like diuretic. Blocks the reabsorption of sodium ions, chlorine and, accordingly, fluid in the distal tubules of the nephron. Increases the excretion of potassium and magnesium ions from the body. Delays the excretion of calcium ions and uric acid. Reduces blood pressure by reducing the volume of circulating blood, reducing cardiac output, and reducing total peripheral vascular resistance with prolonged use.

Nifedipine is a 1,4-dihydropyridine type calcium antagonist. It inhibits the transmembrane flow of calcium ions through slow calcium channels into the cell. It acts on myocardial cells and smooth muscle of the coronary arteries and peripheral vessels. In the heart, nifedipine dilates the coronary arteries, especially large blood vessels, and even intact segments of the walls of partially stenosed vessels. In addition, nifedipine reduces the tone of the smooth muscles of the coronary arteries, which leads to an increase in coronary blood flow and prevents angiospasm. With long-term use, it prevents the development of atherosclerotic plaques in the vascular wall. Reduces the need for myocardial oxygen by reducing afterload. Reduces the tone of the smooth muscles of the arterioles, thereby reducing the increased resistance of peripheral vessels, which leads to a decrease in blood pressure. Nifedipine increases the excretion of sodium and fluid from the body. The antihypertensive effect is especially pronounced in patients with arterial hypertension.

Pharmacokinetics.

The active ingredients of the drug do not interact with each other, so the metabolism of each component takes its own path. After oral administration, its main component, atenolol, is absorbed in the gastrointestinal tract in an amount of 50–60%. Less than 5% of the drug binds to blood plasma proteins, the volume of distribution is 0.7 l/kg. Penetrates the placental barrier and into breast milk. Atenolol practically does not penetrate the blood-brain barrier. The half-life (T½) is 6–9 hours and may be prolonged in case of impaired renal function. The pharmacological effects of atenolol continue for a long period of time - up to 24 hours. 85% of the dose taken is excreted in the urine unchanged.

Nifedipine is rapidly absorbed after oral administration. The maximum concentration in the blood plasma is detected 30 minutes after administration. The half-life (T½) is 3–4 hours. Approximately 80% is excreted by the kidneys in the form of inactive metabolites, almost 15% - with feces.

Chlorthalidone is well absorbed when taken orally, in the systemic bloodstream it is absorbed on the surface of erythrocytes, binds less to plasma proteins. The diuretic effect begins 2–4 hours after administration and lasts for 1 day or more, sometimes up to 3 days. The half-life (T½) is long – 30–40 hours. It is excreted in the urine (approximately 25%) and feces (almost 75%). A feature of the action of chlorthalidone is the relative duration of the diuretic effect, which is due to its slow excretion by the kidneys.

Indication

Arterial hypertension, in cases where therapy with one or two of the components of the drug is ineffective.

Contraindication

Hypersensitivity to atenolol, chlorthalidone, nifedipine, other dihydropyridines and β-blockers or to other components of the drug.

Myocardial infarction and the first month after myocardial infarction.

Unstable angina.

Acute heart failure.

Heart failure (NYHA III-IV).

Sick sinus syndrome.

Atrioventricular block II and III degree.

Sinoatrial block.

Clinically significant aortic stenosis.

Arterial hypotension (systolic pressure less than 90 mm Hg).

Cardiogenic shock.

Severe peripheral circulatory disorders.

Bronchial asthma, bronchoobstructive syndrome.

Metabolic acidosis.

Untreated pheochromocytoma.

Ileostomy, colostomy.

Porphyria.

Gout.

Severe hepatic and/or renal failure (glomerular filtration rate less than 30 ml/min), anuria.

Precoma associated with Addison's disease.

Hypokalemia, hyponatremia, hypercalcemia.

Intoxication with cardiac glycoside drugs.

Concomitant use with lithium preparations, MAO inhibitors (except MAO-B inhibitors), rifampicin.

Inflammatory bowel disease or Crohn's disease.

The drug is contraindicated in patients who have received verapamil within the last 48 hours.

Interaction with other medicinal products and other types of interactions

When used simultaneously with other medicines, it is possible:

with non-selective monoamine reuptake inhibitors – dangerous decrease in blood pressure; increased effect of chlorthalidone, which is part of the drug; do not use simultaneously without medical supervision;

with antiarrhythmics, blockers of "slow" calcium channels, blockers of β-adrenoceptors - increased severity of negative chrono-, ino- and dromotropic effects. This can cause severe arterial hypotension, pronounced bradycardia and heart failure. Blockers of "slow" calcium channels should not be used intravenously within 48 hours after the withdrawal of β-adrenoceptors;

with inhalation anesthesia agents (e.g. halothane, methoxyflurane), the risk of myocardial depression and the development of arterial hypotension increases, therefore, a few days before anesthesia, it is necessary to stop taking the drug or choose an anesthetic agent with minimal negative inotropic effect;

with fentanyl - arterial hypotension may occur. At least 36 hours before elective surgery with fentanyl anesthesia, nifedipine should be discontinued;

with cardiac glycosides - the occurrence of tachycardia or bradycardia, arrhythmias, as well as increased hypokalemia when used simultaneously with digitalis preparations, therefore, laboratory parameters should be monitored. Digitalis preparations and atenolol slow down the heart rate, worsen atrioventricular conduction. You should also be careful when prescribing the drug to patients who take digitalis preparations together with an inadequate diet (which does not provide the body's need for potassium), or those who have gastrointestinal diseases;

with hydralazine and prazosin – the antihypertensive effect is enhanced, their combination leads to a greater decrease in blood pressure than when taking only one drug;

with dihydropyridines (e.g. nifedipine) – increased hypotensive effect, heart failure in patients with chronic heart failure, heart rhythm disturbances;

with reserpine, guanethidine, guanfacine, clonidine - the occurrence of bradycardia. When using these drugs simultaneously, clonidine can be stopped only a few days after stopping the drug. β1-blockers can exacerbate "ricochet" hypertension, which can occur after clonidine withdrawal. When used simultaneously with catecholamines (for example, reserpine), arterial hypotension and/or bradycardia were observed during studies, which can lead to dizziness, syncope or orthostatic hypotension;

with methyldopa – increased hypotensive effect and occurrence of bradycardia;

with nonsteroidal anti-inflammatory drugs (e.g. ibuprofen, indomethacin), estrogens, α- and β-adrenomimetics, aminophylline, theophylline – weakening of the effect of atenolol, which is part of the drug;

with inducers of the cytochrome P450 3A4 system (in particular, phenytoin, carbamazepine, phenobarbital) - weakening of the effect of nifedipine. The use of nifedipine may lead to an increase in the concentration of carbamazepine and phenytoin in the blood serum. Patients who are already taking nifedipine and phenytoin or carbamazepine simultaneously should be under constant medical supervision. In case of signs of toxicity or an increase in the concentration of carbamazepine and phenytoin in the blood serum, the dose of these drugs should be reduced;

with antihypertensive agents of various groups, ACE inhibitors, AT-1 receptor antagonists, diuretics, peripheral vasodilators (PDE-5 inhibitors), nitrates, tricyclic antidepressants, antiepileptic agents, barbiturates, phenothiazines, baclofen - increased hypotensive effect;

with antidepolarizing muscle relaxants – enhancing the effect of the latter;

with digoxin - the concentration of digoxin in the blood plasma may increase. It is necessary to monitor the concentration of digoxin in the blood plasma and adjust the dose at the beginning of treatment with nifedipine in case of increasing the dose and stopping treatment with nifedipine;

with magnesium sulfate - nifedipine may enhance the toxic effect of magnesium sulfate, leading to neuromuscular blockade. The simultaneous use of nifedipine and magnesium sulfate is dangerous and can threaten the patient's life, therefore, the use of these drugs together is not recommended;

with amiodarone there is a risk of impaired sinus or atrioventricular node function, automaticity, conduction and contractility of the heart;

with cimetidine - the clearance of atenolol decreases, which causes an increase in its level in the blood plasma and an increase in the therapeutic effect;

with propafenone – enhancing the effect of atenolol, which is part of the drug;

with nicotine – increased effect of atenolol as a result of reduced metabolism and increased blood levels of the drug;

with drugs containing potassium - weakening of the effect of the latter;

with drugs that depress the central nervous system – increased sedative effect;

with lithium – enhancing the effect of the latter;

with narcotic analgesics – increased narcotic effect; dangerous inhibition;

with adrenaline, noradrenaline – increased effect of the latter, with subsequent bradycardia;

with sympathomimetic agents – decreased bronchodilator activity;

with anticoagulants such as coumarin - an increase in prothrombin time may be observed after administration of nifedipine. The significance of this interaction has not been fully investigated;

with indirect anticoagulants – potentiation of the effect of the latter;

with oral hypoglycemic agents, insulin - increased effect of the latter; with simultaneous use of these drugs, blood plasma glucose levels should be monitored;

with anticholinesterase agents, angiotensin-converting enzyme inhibitors (captopril, enalapril, lisinopril) - increased potassium levels in the blood;

with quinolones, cimetidine – increased bioavailability of atenolol;

with lidocaine – decreased excretion (increased plasma concentration) and increased risk of toxic effects;

with tacrolimus - increased plasma concentration, and with theophylline - may increase, decrease or remain unchanged. Their plasma concentration should be carefully monitored and, if necessary, the dose adjusted;

with quinidine - a decrease in the concentration of the latter in the blood plasma, while quinidine may increase the patient's sensitivity to the action of nifedipine. When using these drugs simultaneously, blood pressure should be monitored and attention should be paid to the undesirable effects of nifedipine. Before starting treatment and after discontinuation of the drug, the concentration of quinidine should be carefully monitored and, if necessary, its dose should be adjusted. If a patient already taking quinidine is started on nifedipine, attention should be paid to the undesirable effects of nifedipine;

with quinupristin, dalfopristin – plasma levels of nifedipine may increase;

Caution should be exercised when prescribing a β1-adrenergic blocker in combination with class I antiarrhythmics (desopyramide), as the cardiodepressive effect may be additive.

When used simultaneously with euphylline or theophylline, mutual inhibition of therapeutic effects is possible.

Concomitant use of diuretics (chlorthalidone, which is part of the drug) with lithium preparations reduces the renal clearance of lithium.

Simultaneous use with glucocorticosteroids, amphotericin, furosemide contributes to increased potassium excretion.

with rifampicin - may be accompanied by a decrease in the concentration of nifedipine in the blood plasma and, as a result, a decrease in its therapeutic effect. In the event of angina attacks or increased blood pressure during the simultaneous use of nifedipine and rifampicin, the dose of nifedipine should be increased;

with vincristine – a decrease in vincristine excretion is observed;

with cephalosporin – increased plasma levels of cephalosporin;

with methacholine - the bronchial response to methacholine may change. Nifedipine treatment should be discontinued before a nonspecific bronchoprovocation test with methacholine is performed (if possible);

Grapefruit juice inhibits the cytochrome P450 3A4 system. Concomitant use of the drug with grapefruit juice leads to an increase in the concentration of nifedipine in the blood plasma and a prolongation of its effect due to a decrease in metabolism. This may lead to an increase in the hypotensive effect.

Other types of interaction.

The use of nifedipine may cause falsely elevated spectrophotometric values of vanillylmandelic acid in blood plasma. However, when determined using the high-performance liquid chromatography method, such an effect is not observed.

Ethyl alcohol potentiates the effect of the drug.

Quitting smoking increases the therapeutic effect of atenolol as a result of reducing its metabolism and increasing the level of the drug in the blood.

Application features

Treatment with the drug should be carried out under the supervision of a doctor.

The drug should be used with caution in patients with impaired liver and kidney function, atrioventricular block of the 1st degree, heart failure (NYHA ΙΙ), peripheral circulatory disorders (Raynaud's syndrome, obliterating vascular diseases of the lower extremities), Prinzmetal's angina, water and electrolyte balance disorders, pulmonary emphysema, psoriasis, depression, digestive tract diseases, diabetes mellitus, hypoglycemia; elderly patients.

Heart failure.

The drug reduces heart rate. In case of slowing of heart rate, dose adjustment should be performed.

Sympathetic nervous system stimulation is necessary to maintain circulatory function in chronic heart failure. Blockade of β1-receptors poses a potential risk of further depression of myocardial contractility and leads to more severe heart failure.

At the first signs of decompensated heart failure, you should stop using the drug and consult a doctor.

Use with caution in patients with chronic heart failure controlled by digitalis and/or diuretics, as digitalis and atenolol slow atrioventricular conduction.

Ischemic heart disease.

The drug should not be used if there is a possibility of a relationship between previous use and ischemic pain.

Withdrawal of the drug should be carried out gradually, since with some β1-blockers in patients with coronary heart disease, angina may worsen and in some cases, myocardial infarction may occur more quickly (withdrawal syndrome). Therefore, in such patients, therapy with this drug should be discontinued with caution and only under medical supervision.

In patients with angina pectoris, attacks may occur more frequently and their duration and intensity may increase, especially at the beginning of treatment. Use is contraindicated in patients with an acute attack of angina pectoris.

Even in the absence of existing angina, discontinuation of the drug should be carried out under the supervision of a physician gradually, reducing the dose over 7–10 days and limiting physical activity to a minimum.

Because coronary heart disease is common and may be unrecognized, it is advisable not to discontinue drug therapy abruptly, even in patients who have been treated for arterial hypotension.

In the treatment of coronary angiospasm in the post-infarction period, treatment should be started approximately 3–4 weeks after myocardial infarction and only if coronary circulation is stabilized.

Arterial hypertension and hypotension.

When using the drug with other antihypertensive agents, postural arterial hypertension may occur. Blood pressure levels in patients should be monitored.

The drug should be used with extreme caution in patients with malignant hypertension and hypovolemia who are on hemodialysis, as a significant decrease in blood pressure may occur due to vasodilation.

It is contraindicated to prescribe the drug in case of very low blood pressure (severe arterial hypotension with systolic blood pressure below 90 mm Hg), as well as in case of severe weakness of cardiac activity (decompensated heart failure).

Concomitant use of calcium channel blockers.

May cause bradycardia, increased diastolic blood pressure (when β1-blockers are used with verapamil or diltiazem), atrioventricular block, and death. Patients with pre-existing intraatrial conduction disorders or left ventricular dysfunction are particularly sensitive to the drug.

Renal and hepatic failure.

In case of impaired liver and/or kidney function, the dynamics of their functional state should be monitored, since the drug can provoke azotemia. Given that a cumulative effect may develop with reduced renal insufficiency, and if renal function continues to deteriorate, treatment with the drug should be discontinued.

Use with caution in patients with impaired liver function. In patients with impaired liver function or progressive liver disease, a slight change in fluid and electrolyte balance may lead to hepatic coma.

Therefore, this drug should be prescribed with caution to such patients.

Metabolism and endocrine disorders.

The drug should be used with caution in patients with diabetes mellitus due to the possibility of masking the symptoms of hypoglycemia (tachycardia, dizziness, sweating, etc.)

At recommended doses, atenolol does not potentiate insulin-dependent hypoglycemia and, unlike non-selective β1-blockers, does not delay the restoration of blood glucose to normal levels.

The need for insulin for diabetics may be increased, decreased, or unchanged.

Latent diabetes mellitus may become manifest during treatment with chlorthalidone.

The drug should be used with caution during prolonged fasting and heavy physical exertion (severe hypoglycemic state may occur). Blood plasma sugar levels should be monitored.

Consideration should be given to discontinuing treatment or to closely monitoring patients suspected of developing thyrotoxicosis, as β-blockers may mask some clinical symptoms of hyperthyroidism, such as tachycardia. Abrupt discontinuation of treatment may precipitate exacerbation of the disease.

The drug should not be used before conducting studies of parathyroid function, since thiazides reduce calcium excretion.

During long-term thiazide therapy, patients experienced pathological changes in the parathyroid gland with hypercalcemia and hypophosphatemia, but general complications of hyperparathyroidism, such as nephrolithiasis, bone atrophy, and gastric ulcer, were not observed.

Any chloride deficiency during thiazide therapy is usually minor and does not require specific treatment except in exceptional circumstances (e.g., liver or kidney disease).

Hyperuricemia or acute gout may occur in some patients receiving thiazide therapy. The hypotensive effects of thiazides may be increased in post-sympathectomy patients.

In the event of withdrawal syndrome, treatment with the drug should be resumed.

Untreated pheochromocytoma.

The drug should not be used in patients with untreated pheochromocytoma. When prescribing the drug to patients with pheochromocytoma, α-adrenergic blockers should be prescribed in advance to prevent the development of hypertensive crisis.

Water and electrolyte balance.

Plasma and urine electrolyte levels should be determined periodically to detect possible electrolyte imbalances (e.g., hyponatremia, hypochloremic alkalosis, and hypokalemia), and creatinine levels should be monitored, especially in patients with intractable vomiting or receiving parenteral fluids. Signs or symptoms of fluid and electrolyte imbalance include dry mouth, thirst, weakness, lethargy, drowsiness, nervousness, muscle pain or cramps, muscle weakness, hypotension, oliguria, tachycardia, and gastrointestinal disturbances such as nausea and vomiting.

Potassium levels should be measured periodically, especially in elderly patients, in patients taking digitalis preparations for the treatment of heart failure, in patients with an unbalanced diet, or in patients with complaints of digestive tract disorders.

Hypokalemia may develop especially in patients with accelerated diuresis, in the presence of severe cirrhosis, or during concomitant use of corticosteroids or adrenocorticotropic hormone.

Oral electrolyte supplementation may also contribute to hypokalemia. Hypokalemia may increase the sensitivity or enhance the cardiac response to the toxic effects of digitalis drugs (e.g., increase ventricular sensitivity).

Hypokalemia can be corrected or treated by taking potassium supplements or eating foods high in potassium.

Any chloride deficiency during thiazide therapy is usually minor and does not require specific treatment except in exceptional circumstances (e.g., liver or kidney disease).

Dilutional hyponatremia may occur in patients with edema in hot weather. Appropriate therapy is fluid restriction rather than salt restriction, except in rare cases when hyponatremia is life-threatening.

Anesthesia and surgery.

Before surgery with general anesthesia, it may be necessary to stop taking the drug. In such cases, 48 hours should elapse between the last dose of the drug and anesthesia. If treatment is ongoing, caution should be exercised when using anesthetic agents - choose a drug for general anesthesia with minimal negative inotropic effect. If vagal dominance occurs, it can be eliminated with atropine (1-2 mg intravenously).

However, the drug should be used with caution in combination with anesthetic agents due to attenuation of reflex tachycardia and increased risk of arterial hypotension.

β1-blockers are competitive inhibitors of β1-receptor agonists, and their effects on the heart can be completely reversed when agents such as dobutamine or isoproterenol are administered.

Bronchoobstructive syndrome.

The drug should not be used in patients with bronchoobstructive syndrome, other bronchospastic diseases, and acute attacks of stable angina.

However, since the drug is a selective β1-adrenergic blocker, it can be used with caution in patients with bronchoobstructive syndrome in the absence of response to treatment or tolerance to other antihypertensive therapy. Since the selectivity of β1-adrenergic blockers is not absolute, the drug should be used in the lowest possible doses and with the possibility of using β2-adrenergic agonists. If the dosage needs to be increased, the dose should be divided to achieve lower maximum blood levels of the drug.

Hypersensitivity reactions may occur in patients with a history of bronchial asthma and who are receiving thiazides.

Allergic reactions.

The drug should be used with extreme caution in patients with a history of severe hypersensitivity reactions and in patients receiving desensitization therapy to reduce adrenergic counteraction.

Gastrointestinal tract.

The drug should be used with caution in patients with severe narrowing of the gastrointestinal tract due to the possibility of obstructive symptoms. Bezoars may occur, which may require surgical intervention.

In isolated cases, obstructive symptoms have been described in the absence of a history of gastrointestinal disorders.

Not to be used in patients with an ileostomy (post-proctocolectomy ileostomy).

General violations.

Separate in vitro experiments have revealed a relationship between the use of calcium antagonists, in particular nifedipine, and reversible biochemical changes in spermatozoa, which impair their ability to fertilize.

The use of the drug may lead to false-positive results in X-ray examinations using barium contrast media (for example, filling defects are interpreted as polyps) and in spectrophotometric determination of the concentration of vanillylmandelic acid in urine (however, this effect is not observed when using the high-performance liquid chromatography method).

A positive doping test reaction is possible when using the drug.

There have been reports of exacerbation of systemic lupus erythematosus.

During treatment with atenolol, changes in the results of some laboratory tests are possible: increased levels of lipoproteins, cholesterol and potassium in the blood serum, levels of catecholamines and their metabolic products in the urine and blood.

Although the relationship between atenolol and depression has not been established, the drug should be used with caution in these patients.

Elderly patients are prescribed atenolol in lower doses, especially if they have impaired kidney function.

During treatment, you should stop drinking alcohol.

Excipients.

This medicinal product contains sodium compounds. Caution should be exercised when administered to patients on a controlled sodium diet.

This medicine contains propylene glycol - may cause symptoms similar to those caused by alcohol consumption.

This medicine contains yellow FCF (E 110) which may cause allergic reactions.

Use during pregnancy or breastfeeding

The drug is contraindicated during pregnancy or breastfeeding.

Ability to influence reaction speed when driving vehicles or other mechanisms

During treatment, caution should be exercised when driving vehicles or working with complex mechanisms, and in case of dizziness, refrain from potentially hazardous activities that require increased concentration and speed of psychomotor reactions.

Method of administration and doses

The drug should be taken orally by adults during or after meals, without chewing, preferably always at the same time. The dose of the drug and the duration of treatment are determined by the doctor individually. The average dose for adults is 1–2 tablets per day.

Children

The medicine should not be used in children.

Overdose

Symptoms: the clinical picture depends on the degree of intoxication and is manifested mainly by disorders of the cardiovascular and central nervous systems.

Treatment: in case of overdose or a dangerous decrease in heart rate and/or blood pressure, treatment with the drug should be discontinued. In intensive care units, vital signs should be carefully monitored and, if necessary, corrected. Constant monitoring of the function of the cardiovascular and respiratory systems, levels of sugar and electrolytes (potassium, calcium) in the blood plasma, daily diuresis and circulating blood volume is necessary.

In addition to gastric lavage and the use of adsorbents, if necessary, prescribe:

– atropine (0.5–2 mg intravenously as a bolus);

– glucagon: initial dose 1–10 mg intravenously (jet), then 2–2.5 mg/h as a continuous infusion;

– sympathomimetics depending on body weight and effect (dopamine, dobutamine, isoprenaline, oxyprenaline or adrenaline).

If drug treatment of bradycardia is ineffective, electrical cardiostimulation may be performed.

In case of arterial hypotension - administration of plasma or plasma substitutes.

Dobutamine, due to its positive inotropic effect, can also be used to treat hypotension and acute heart failure. The doses indicated are unlikely to be sufficient to control the cardiac symptoms associated with β-blockade in cases of significant overdose. Therefore, if necessary, the dose of dobutamine may be increased until the desired response is achieved according to the patient's clinical condition.

For bronchospasm, prescribe β2-sympathomimetics in the form of an aerosol (if the effect is insufficient, also intravenously) or aminophylline intravenously.

For generalized seizures, administer slow intravenous administration of diazepam.

With significant diuresis, a normal balance of fluid and electrolytes in the body should be maintained.

Since nifedipine is characterized by a high degree of binding to plasma proteins and a relatively small volume of distribution, hemodialysis is ineffective, but plasmapheresis is recommended.

Adverse reactions

On the part of the organs of vision: visual impairment (including temporary blindness at the maximum concentration of nifedipine in the blood serum), temporary retinal ischemia, decreased visual acuity, decreased or increased secretion of tear fluid, conjunctivitis, dry eyes, feeling of pain in the eyes, xanthopsia.

From the side of the organs of hearing and inner ear: tinnitus, balance disorders.

From the respiratory system, chest organs and mediastinum: epistaxis, nasal congestion, cough, shortness of breath, stridor, dyspnea, symptoms of bronchial obstruction; bronchospasm in patients with a history of bronchial asthma, upper respiratory tract infections, cough and nasal congestion.

Gastrointestinal: gastrointestinal disorders, constipation, diarrhea, abdominal pain, nausea, belching; black stools, heartburn, taste disturbance, dyspepsia, flatulence, dry mouth, anorexia, gingival hyperplasia, vomiting, gastroesophageal sphincter insufficiency, dysphagia, bezoar, intestinal obstruction, intestinal ulcer, gastric irritation, spasms, thrombosis of mesenteric arterial vessels, ischemic colitis.

From the liver and biliary tract: hepatotoxicity, including hepatitis, intrahepatic cholestasis, transient increase in liver enzyme activity, jaundice, pancreatitis (predominantly in women), liver dysfunction.

On the part of the kidneys and urinary system: polyuria, dysuria, nocturia, hematuria, difficulty urinating, interstitial nephritis.

Metabolism: hypoglycemia or hyperglycemia (especially in patients with diabetes), impaired carbohydrate tolerance, gout, weight gain, bezoar.

Nervous system: headache, vertigo,