Monopril pills 20 mg 28 pcs
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Active ingredients
Fozinopril
Release form
Pills
Composition
Fosinopril sodium 20 mg adjuvants: anhydrous lactose - 126 mg, microcrystalline cellulose - 40 mg, crospovidone - 7 mg, povidone - 4 mg, sodium fumarate - 3 mg.
Pharmacological effect
ACE inhibitor. Fosinopril sodium is chemically the sodium salt of the ester of the pharmacologically active compound fosinoprilat. Once in the human body, fosinopril undergoes enzymatic hydrolysis and turns into fosinoprilat. Fosinoprilat, due to the presence of the phosphinate group, is a specific competitive ACE inhibitor. Due to ACE inhibition, fosinoprilat prevents the conversion of angiotensin I to angiotensin II, which has a vasoconstrictor effect. Inhibition of ACE leads to a decrease in the concentration of angiotensin II in the blood plasma, which causes a decrease in its vasopressor activity and a decrease in the secretion of aldosterone. Reduced aldosterone secretion can lead to a slight increase in serum potassium ions (average of 0.1 meq / l) and a decrease in sodium ions and fluid volume. Phozinoprilat slows down the metabolism of bradykinin, which has a powerful vasodilating effect; due to this, its antihypertensive effect increases. Reduction of blood pressure is not accompanied by changes in the BCC, cerebral and renal blood flow, blood supply to the internal organs, skeletal muscles, skin, and myocardial reflex activity. After ingestion, the antihypertensive effect develops within 1 hour, reaches a maximum after 2-6 hours and lasts for 24 hours. The antihypertensive effect of the drug appears to the same extent in the position of the patient standing and lying down. Orthostatic hypotension and tachycardia are sometimes noted in patients with hypovolemia or on a salt-free diet. It may take several weeks to achieve the maximum therapeutic effect. The antihypertensive effects of fosinopril and thiazide diuretics complement each other. The effectiveness of the antihypertensive effect does not depend on age, gender and body weight. The drug does not have withdrawal syndrome even with an abrupt cessation of treatment. In chronic heart failure, the positive effect of Monopril is achieved mainly due to inhibition of the renin-angiotensin-aldosterone system.Suppression of ACE leads to a decrease in both preload and afterload on the myocardium. The drug helps to increase exercise tolerance, reducing the severity of chronic heart failure.
Pharmacokinetics
Absorption After oral absorption from the gastrointestinal tract is about 30-40%. The degree of absorption does not depend on food intake, but its speed may slow down when taking the drug during a meal. Cmax of fosinoprilat in plasma is reached after 3 hours and does not depend on the dose taken. Distribution: Plasma protein binding is ≥95%. Phozinoprilat has a relatively small Vd and is slightly associated with cellular components of blood. MetabolismPerucative hydrolysis of fosinopril with the formation of fosinoprilat occurs mainly in the liver and the mucous membrane of the gastrointestinal tract. normal kidney function and liver T1 / 2 fosinoprilat is about 11.5 hours. With chronic heart failure, T1 / 2 is 14 hours. Pharmacokinetics in sobyh clinical sluchayahU patients with impaired renal function (creatinine clearance <80 mL / min / 1.73 m2) fozinoprilata total clearance from the body is approximately twice lower than in patients with normal renal function. At the same time, absorption, bioavailability and protein binding are not markedly changed. Reduced excretion by the kidneys is compensated for by increased excretion through the intestines with bile. A moderate increase in plasma AUC values (less than doubled compared to the norm) is observed in patients with various degrees of renal failure, including end-stage renal failure (CC <10 ml / min / 1.73 m2). Freninoprilar adhesion during hemodialysis and peritoneal dialysis on average is 2% and 7%, respectively (relative to the values of urea clearance). In patients with impaired liver function (with alcohol or biliary cirrhosis), the rate of hydrolysis of fosinopril can be reduced, but the degree of hydrolysis is appreciable manner is not altered. The overall clearance of fosinoprilat from these patients is about half compared with patients with normal liver function.
Indications
- arterial hypertension (monotherapy or in combination with other antihypertensive drugs, in particular with thiazide diuretics); - heart failure (as part of combination therapy).
Contraindications
- hereditary angioedema and idiopathic angioedema in the history (including after taking other ACE inhibitors); - congenital lactose intolerance, lactase deficiency, glucose-galactose malabsorption; - pregnancy; - lactation (breastfeeding) period; 18 years old (efficacy and safety have not been established); - hypersensitivity to fosinopril or any other substance that is a part of the preparation; - hypersensitivity to any other ACE inhibitor in history. it is necessary to prescribe a drug for renal failure; hyponatremia (risk of dehydration, arterial hypotension, chronic renal failure); bilateral stenosis of the renal arteries or stenosis of the artery of a single kidney; aortic stenosis; condition after kidney transplantation; desensitization; systemic connective tissue diseases (including SLE, scleroderma) due to an increased risk of developing neutropenia or agranulocytosis; with hemodialysis; with cerebrovascular diseases (including cerebrovascular insufficiency); CHD; chronic heart failure III-IV functional class (according to the NYHA classification); diabetes; oppression of bone marrow hematopoiesis; hyperkalemia; in elderly patients; gout, on the background of a salt-restricted diet; in conditions accompanied by a decrease in BCC (including diarrhea, vomiting, prior treatment with diuretics).
Precautionary measures
During treatment, psoriasis may worsen. During pheochromocytoma, propranolol can only be used after taking an alpha blocker. After a long course of treatment, propranolol should be discontinued gradually, under the supervision of a physician. during anesthesia, you must stop taking propranolol or find a remedy for anesthesia with minimal negative inotropic effects.The impact on the ability to drive vehicles and control mechanisms of patients whose activities require increased attention, the question of the use of propranolol on an outpatient basis should be addressed only after evaluating the individual response of the patient.
Use during pregnancy and lactation
Monopril is contraindicated in pregnancy. The use of the drug in the II and III trimesters of pregnancy causes damage or death of the developing fetus. Since fosinoprilat is excreted in breast milk, if you need to use Monopril during lactation, breastfeeding should be discontinued. For newborns whose mothers took ACE inhibitors during pregnancy, careful monitoring is recommended to timely detect arterial hypotension, oliguria and hyperkalemia. The use of ACE inhibitors during pregnancy can cause a developmental disorder or fetal death. If pregnancy is established during treatment with Monopril, it should be canceled as soon as possible. If (in rare cases) there is no alternative to ACE inhibitors for treating the patient, you should inform her of the potential harm of treatment for the development of the fetus and conduct a thorough ultrasound examination to identify the pathology of the fetus. When oligohydroamnion is detected, treatment with Monopril is not canceled only if it is carried out for health reasons. It should, however, be borne in mind that oligohydroamnion is sometimes detected only in the presence of irreversible damage to the fetus. In newborns whose mothers took ACE inhibitors during pregnancy, hypotension, oliguria, hyperkalemia was noted. pregnancy should be carefully examined for hypotension, oliguria and hyperkalemia. If oliguria is present in a newborn, efforts should be directed towards monitoring blood pressure and supporting renal perfusion. Replacement transfusions or dialysis may be necessary to restore blood pressure and replace impaired renal function. Fosinopril is slowly eliminated from the circulating blood in adults during hemodialysis and peritoneal dialysis.There is no experience in removing fosinopril from the circulating blood in newborns. Since fosinopril is found in breast milk, the drug should not be used during breastfeeding.
Dosage and administration
The drug is prescribed inside. The dose is set individually. In case of arterial hypertension, the recommended initial dose is 10 mg 1 time / day. The dose should be selected depending on the dynamics of lowering blood pressure. Doses vary from 10 to 40 mg 1 time / day. In the absence of a sufficient hypotensive effect, additional diuretics may be prescribed. If treatment with Monopril is started on the background of diuretic therapy, its initial dose should be no more than 10 mg with regular medical monitoring of the patient's condition. The maximum daily dose is 40 mg. In chronic heart failure, the recommended the initial dose is 10 mg 1 time / day. Treatment begins under mandatory medical supervision. If the drug is well tolerated when taken in the initial dose, the dose can be gradually increased at weekly intervals, up to 40 mg 1 time / day (maximum daily dose). The drug should be prescribed in combination with a diuretic. Simultaneous use of digoxin is optional. Since the drug is eliminated from the body in two ways, dose adjustment for patients with impaired renal or liver function is usually not required. There is no difference in efficacy and safety of Monopril treatment in patients 65 years of age and older and younger patients, therefore, there is no correction doses for elderly patients are usually not required. However, we cannot exclude a greater susceptibility in some elderly patients to the drug, due to the possible effects of overdose due to delayed elimination of the drug.
Side effects
Since the cardiovascular system: pronounced decrease in blood pressure, orthostatic hypotension, tachycardia, syncope, arrhythmia, feeling of heartbeat, angina, myocardial infarction, flushing of the skin of the face, impaired cardiac conduction, increased blood pressure, sudden death, cardiac arrest, peripheral edema. From the urinary system: renal failure, proteinuria, prostate gland disease (hyperplasia, adenoma), polyuria,oligouria. From the side of the central nervous system and peripheral nervous system: stroke, cerebral ischemia, dizziness, imbalance, headache, weakness, memory impairment; sleep disorders, anxiety, depression, confusion, drowsiness, paresthesias. On the part of the sense organs: hearing and vision impairment, ear pain, tinnitus, taste change. On the part of the digestive system: nausea, diarrhea, intestinal obstruction, pancreatitis, hepatitis , cholestatic jaundice, abdominal pain, vomiting, constipation, anorexia, stomatitis, glossitis, dysphagia, flatulence, loss of appetite, changes in body weight, dryness of the oral mucosa, bleeding. From the respiratory system: pneumonia, dry cough, pulmonary infiltrates, bronchospasm, shortness of breath, rhinorrhea, sinusitis, laryngitis, pharyngitis, tracheobronchitis, dysphonia, nasal bleeding. Two patients had a symptom complex: bronchospasm, cough, eosinophilia. On the lymphatic system: inflammation of the lymph nodes. On the musculoskeletal system: arthritis, myalgia, musculoskeletal pain, muscle weakness in the extremities. On the side of metabolism: exacerbation of the course of gout Allergic reactions: skin rash, pruritus, angioedema, dermatitis. Others: increased body temperature, hyperhidrosis, impaired sexual function. For laboratory indicators: hypercreatininemia, increased concentration of Evin, elevated liver enzymes, hyperbilirubinemia, hyperkalemia, hyponatremia; decrease in hemoglobin and hematocrit, increased ESR, leukopenia, neutropenia, eosinophilia. Effect on the fetus: impaired development of the fetal kidneys, reduced fetal blood pressure and newborns, impaired renal function, hyperkalemia, hypoplasia of the skull bones, oligohydramnion, contracture of the extremities, hypoplasia of the lungs.
Overdose
Symptoms: pronounced decrease in blood pressure, bradycardia, shock, impaired water-electrolyte state, acute renal failure, stupor. Treatment: the drug should be stopped, gastric lavage, sorbent administration (eg, activated carbon), vasopressor agents, infusion of sodium 0.9% are indicated. chloride and further symptomatic and supportive treatment. The use of hemodialysis is ineffective.
Interaction with other drugs
The simultaneous use of antacids (including aluminum or magnesium hydroxide), as well as simethicone can reduce the absorption of fosinopril, therefore, these drugs should be taken at least 2 hours apart. When using ACE inhibitors with lithium salts at the same time, serum lithium and the risk of lithium intoxication may increase, so at the same time apply Monopril and lithium preparations with caution. Careful monitoring of serum lithium levels is recommended. It is known that NSAIDs indomethacin can reduce the antihypertensive effect of ACE inhibitors, especially in patients with arterial hypertension and low plasma renin activity. Other NSAIDs, for example, acetylsalicylic acid, and selective COX-2 inhibitors may have a similar effect. In patients older than 65 years of age, with hypovolemia (including with diuretic therapy), with impaired renal function, the simultaneous administration of NSAIDs (including selective COX-2 inhibitors) and ACE inhibitors (including fosinopril) can worsen renal function, up to acute renal failure. Usually this condition is reversible. Kidney function should be carefully monitored in patients taking fosinopril and NSAIDs. When using Monopril with diuretics at the same time, especially in the beginning of diuretic therapy, as well as in combination with a strict diet that limits salt intake, or dialysis, a pronounced decrease in blood pressure can develop. especially in the first hour after taking the initial dose of Monopril. Potassium preparations, potassium-sparing diuretics (amiloride, spironolactone, triamteren) increase the risk of hyperkalemia. In patients with heart failure, diabetes mellitus, simultaneously taking potassium-saving diuretics, potassium, potassium-containing salt substitutes, or other agents that cause hyperkalemia (for example, heparin), ACE inhibitors increase the risk of an increase in the content of potassium ions in the blood serum. , the risk of leukopenia with simultaneous use with allopurinol, cytotoxic drugs, immunosuppressants,Procainamide. Estrogens weaken the antihypertensive effect of the drug Monopril because of its ability to retain water. propantheline bromide, digoxin and warfarin does not change.
special instructions
Before starting treatment, it is necessary to analyze the previously conducted antihypertensive therapy, the degree of increase in blood pressure, salt and / or fluid restriction of the diet and other clinical circumstances. If possible, the previous antihypertensive therapy should be stopped several days before the treatment with Monopril. In order to reduce the likelihood of hypotension, diuretics should be canceled 2-3 days before the treatment with Monopril. the content of potassium ions, creatinine, urea, the concentration of electrolytes and the activity of liver enzymes in the blood. Angioneurotic edema. The development of angioedema of the extremities, face, lips, mucous membranes, tongue, pharynx, or larynx was reported in patients using Monopril. With swelling of the tongue, pharynx, or larynx, an airway obstruction may develop with possible death. In such cases, it is necessary to stop taking the drug and carry out urgent measures, including subcutaneous administration of the solution of epinephrine (adrenaline) (1: 1000), as well as taking other measures of emergency treatment. In most cases, swelling of the face, oral mucosa, lips and extremities, discontinuation of the drug resulted in normalization of the condition; however, appropriate therapy was sometimes required. Swelling of the intestinal mucosa. Swelling of the intestinal mucosa was rarely observed while taking ACE inhibitors. Patients complained of abdominal pain (with nausea and vomiting could not be), in some cases, swelling of the intestinal mucosa occurred without swelling of the face, the activity of C1 esterase was normal. Symptoms disappeared after stopping the use of ACE inhibitors.Swelling of the intestinal mucosa should be included in the differential diagnosis of patients taking ACE inhibitors, complaining of abdominal pain. Anaphylactic reactions during dialysis using high-permeable membranes. Anaphylactic reactions can develop in patients taking ACE inhibitors during hemodialysis using high-permeable membranes, as well as during the apheresis of low-density lipoproteins with adsorption on dextran sulfate. In these cases, you should consider the possibility of using dialysis membranes of another type or the use of antihypertensive drugs of another class. Anaphylactic reactions during desensitization. Two patients during desensitization with hymenoptera venom against the background of taking an ACE inhibitor enalapril had life-threatening anaphylactoid reactions. In the same patients, these reactions were avoided by the timely suspension of the ACE inhibitor; however, they reappeared after unintentionally resuming the use of an ACE inhibitor. Special care should be taken when desensitizing patients who are taking ACE inhibitors. Neutropenia / agranulocytosis. Perhaps the development of agranulocytosis and suppression of bone marrow function during treatment with ACE inhibitors. These cases are more common in patients with impaired renal function, especially in the presence of systemic connective tissue diseases (SLE or scleroderma). Before initiating therapy with ACE inhibitors and in the course of treatment, the determination of leukocytes and leukocyte formula is carried out (1 time per month in the first 3-6 months of treatment and in the first year of use of the drug in patients with an increased risk of neutropenia). Arterial hypotension. Patients with an uncomplicated form of arterial hypertension may develop arterial hypotension in connection with the use of the drug Monopril. Symptomatic arterial hypotension develops in patients with ACE inhibitors more often in patients with intensive treatment with diuretics, diet associated with limitation of salt, or during dialysis. Transient arterial hypotension is not a contraindication to use the drug after carrying out measures to restore BCC. In patients with chronic heart failure, treatment with ACE inhibitors can cause an excessive antihypertensive effect that can lead to oliguria or azotemia and in rare cases to acute renal failure with a fatal outcome .Therefore, in the treatment of chronic heart failure with Monopril, it is necessary to carefully monitor patients, especially during the first 2 weeks of treatment, as well as with any increase in the dose of Monopril or diuretic. It may be necessary to reduce the diuretic dose in patients with normal or low blood pressure who previously received diuretic therapy means or having hyponatremia. As such, arterial hypotension is not a contraindication for further use of the drug Monopril in chronic heart failure. Some reduction in systemic blood pressure is a common and desirable effect at the beginning of the drug in chronic heart failure. The extent of this decline is maximum in the early stages of treatment and stabilizes within one or two weeks from the start of treatment. BP usually returns to baseline without a decrease in therapeutic efficacy. Violation of liver function. In rare cases, the use of ACE inhibitors marked syndrome, the first manifestation of which is cholestatic jaundice. This is followed by fulminant hepatic necrosis, sometimes fatal. The mechanism of development of this syndrome has not been studied. With the appearance of noticeable yellowness and a pronounced increase in the activity of liver enzymes, treatment with Monopril should be stopped and appropriate treatment should be prescribed. In patients with impaired liver function, increased plasma concentrations of fosinopril may be noted. With cirrhosis of the liver (including alcoholic), the apparent total clearance of fosinoprilat is reduced, and the AUC is about 2 times higher than in patients without liver dysfunction. Renal failure. In patients with arterial hypertension with single or bilateral renal artery stenosis or single kidney artery stenosis, during treatment with ACE inhibitors, the concentration of blood urea nitrogen and serum creatinine may increase. These effects are usually reversible and disappear after discontinuation of treatment. It is necessary to control renal function in these patients in the first weeks of treatment. In some patients, an increase in the concentration of nitrogen in the blood urea and serum creatinine (usually small and transient) can be observed even without obvious impairment of renal function with simultaneous use of the drug Monopril and diuretics.It may be necessary to lower the dose of Monopril. In patients with severe chronic heart failure, renal function may depend on the activity of the renin-angiotensin-aldosterone system, therefore treatment with ACE inhibitors may be accompanied by oliguria and / or progressive azotemia, and in rare cases to acute renal failure and fatal outcome. Hyperkalemia. There have been cases of an increase in the content of potassium ions in the blood serum of patients taking ACE inhibitors, including fosinopril. The risk group in this regard is made up of patients with renal insufficiency, type 1 diabetes, as well as receiving potassium-saving diuretics, potassium-containing dietary supplements or other drugs that increase the content of potassium ions in serum (for example, heparin). Cough. When using ACE inhibitors, including fosinopril, there was an unproductive, persistent cough that passes after discontinuation of therapy. When coughing occurs in patients taking ACE inhibitors, this therapy should be considered as a possible cause as part of the differential diagnosis. Surgical interventions / general anesthesia. ACE inhibitors can enhance the antihypertensive effect of agents used for general anesthesia. Before surgery (including dentistry), it is necessary to warn the physician / anesthesiologist about the use of ACE inhibitors. Caution should be exercised when performing physical exercises or in hot weather due to the risk of dehydration and arterial hypotension due to a decrease in BCC. Impact on the ability to drive vehicles and machinery. Care must be taken when driving or doing other work requiring increased attention, as dizziness may occur. .