Captopril Stella 25 mg treatment for hypertension, congestive heart failure, myocardial infarction (10 blisters x 10 tablets)

Long -term prevention of heart failure: Symptoms: Indications for patients with clinical stability with disordered left ventricular disorders (blood expulsion ≤ 40%) after myocardial infarction to improve survival, slowing symptoms, reducing the risk of hospitalization due to heart failure, reducing recurrent myocardial infarction and coronary recurrent procedure.

Treatment of kidney disease due to diabetes with high urinary protein (micronutrient albumin> 30 mg/day), to prevent the progression of kidney disease and reduce related clinical events such as separation, kidney transplant and death.

Captopril can be used individually or in combination with other anti -hypertension drugs.

Pharmacokology

captopril is an enzyme inhibitor in the form of angiotensin, used to treat hypertension and heart failure. The hypotension effect of the drug is related to the inhibition of the Renin-Anotensin-Aldosteron system. Angiotensin I is an inactive decapeptid. Thanks to the catalyst of the enzyme, the Angiotensin I transformed into Angiotensin II has a very strong vascular effect. Angiotensin II stimulates the adrenal shells of aldosteron secretion, which holds sodium and water.

Effects on the Renin-Anotensin-Aldosteron System:

Captopril prevents Angiotensin I transformed into angiotensin II by inhibiting ACE competition. ACE inhibits reduces angiotensin II concentration and increases lyin activity in plasma. Reducing angiotensin II reduces vascular contractions, reducing aldosteron secretion should increase sodium and water and retain a small amount of potassium.

However, in some patients with aldosteron concentration in plasma does not decrease during the treatment of ACE inhibitors with normal doses and can return to the level before treatment when long -term treatment. Live renin activity may be due to the kidneys that are not inhibited from reverse release and/or due to stimulation of reflexes through pressure receptors (due to reduced blood pressure). Captopril has the effect of lowering blood pressure in patients with high or normal renin concentrations.

Captopril also works to reduce blood pressure on the spot on the wall of the vessel. The effect of reducing the blood pressure of captopril is longer than ACE inhibits in the blood, but it is not known whether Ace is inhibited longer in the endothelium compared to the blood.

Effects on catecholamine:

Captopril does not affect the circulating norepinephrin levels in plasma and does not inhibit the increase in norepinephrin levels in plasma due to posture reflexes. However, due to the inhibition of Angiotensin II formation, captopril can affect the release and reabsorption of norepinephrin in noradrenergic nerves and/or may reduce blood vessel sensitivity to hypertension medications.

Because ACE can decompose Bradykinin is a vasodilator, inhibiting ACE because captopril can make Bradykinin accumulate in plasma or in tissue and dilate vascular.

Cardiovascular effects:

In people with hypertension, captopril reduces blood pressure by reducing peripheral artery resistance, does not increase or increases heart frequency, systolic volume, cardiac efficiency. These effects do not depend on blood pressure or cardiac efficiency before treatment.

Aortic expansion medication and maybe even veins. Systolic and diastolic blood pressure usually decreased by about 15-25% (in a standing position as well as lying). Hypotension and a fast heartbeat (less occur but more common in people who lack salt or decrease in the amount of circulating). After taking a single dose, hypotension appears immediately after 15 minutes, reaching a maximum of 1 -1.5 hours after drinking.

Dosage time depends on the dose: 6 - 12 hours. In people who respond to drugs, blood pressure returns to normal about 15 days to 1 month of treatment and maintenance. Stop treatment does not increase blood pressure suddenly. The drug increases the elasticity of the artery, increases the blood flow through the kidneys without reducing the amount of glomerular filtration and reduces left ventricular hypertrophy.

In people with congestion heart failure, captopril reduces many obstacles of peripheral vascular system and blood pressure (posterior burden) of pulmonary artery pressure (money) and pulmonary artery resistance, increasing cardiac efficiency and increasing tolerance time. Hemodynamic and clinical effects appear after the first and prolonged doses during treatment.

Effects on the kidneys:

The blood flow through the kidneys may increase but the glomerular filtration rate usually does not change during treatment. Sometimes blood urea nitrogen and creatinine levels in plasma increase, often found in patients with kidney damage before, or under treatment in combination with a diuretics or congestive heart failure.

Creatinine clearance coefficient changes when renal perfusion pressure 70 mmHg.

pharmacokinetics

absorption:

In healthy people or hypertension, when taking a dose of captopril when hungry, about 60-75% of the dose is absorbed quickly through the gastrointestinal tract. Food absorbs up to 25-40% but does not affect the effect. After taking a single dose of 100 mg of captopril when hungry, the average peak concentration in the blood is 800 nanogam/ml, achieved within 1 hour.

Distribution:

Animal research shows that captopril is distributed into most body tissues, except for the central nervous system. Captopril through the placenta and breast milk with a concentration of about 1% of the concentration of drugs in the mother's blood. About 25 - 30% of captopril attached to plasma proteins, mainly albumin.

Era:

Sell spaces of cagoPril is not metabolized for less than 2 hours in patients with normal kidney function. The sale time of captopril and metabolites correlated with creatinine clearance and increased to about 20-40 hours in patients with creatinine clearance below 20 ml/minute and up to 6.5 days in patients with auria.

About half of the absorption dose is rapidly metabolized, mainly into Collil-Cystein Disulfid and Dimercestril Disulfid. The drug can metabolize stronger in people with kidney function damaged than people with normal kidney function.

captopril and metabolites excreted into urine. The kidneys excreted captopril without trips mainly through the renal tubules. In people with normal renal function, over 95% of the absorption dose is excreted in urine for 24 hours; About 40 - 50% of the excreted drug in urine is non -metabolic captlil and the rest are mainly captopril -cystein disulfid and dimercesril Disulfid. In healthy people, about 20% of CodePril doses have been found in feces for 5 days, is an non -metabolic drug.

captopril can be removed by hemolysis.

History of veins related to the use of angiotensin enzyme inhibitors. Genetic or spontaneous edema.

After myocardial infarction (if hemodynamic is unstable).

Evaluation in the limb, face, lips, mucosa, tongue, bar or larynx can occur at patients treated with ACE inhibitors, especially in the first weeks of treatment. However, rare cases of heavy angioed angi can progress after prolonged treatment with ACE inhibitors. Should stop treatment immediately.

Thiche related to the tongue, bar or larynx can be fatal. Need emergency treatment immediately. The patient should be taken to the hospital and monitored at least 12 - 24 hours and should not be discharged until the symptoms are completely resolved.

ho:

cough has been reported when using ACE inhibitors. Characterized by dry cough, persistent and ending after treatment.

Double Renin-Anotensin-Aldosteron (RAAS):

Concentrated use of ACE inhibitors, Angiotensin II or Aliskiren receptor drugs may cause an increased risk of hypotension, hyperkalemia and reduced kidney function (including acute renal failure). Therefore, it is not recommended to combine ACE inhibitors, Angiotensin II or Aliskiren.

If really needed, a doctor's supervision and regular monitoring of kidney function, electrolytes and blood pressure. Ace ACE and Angiotensin II should not be used simultaneously in patients with diabetic kidney disease.

Hepatic failure:

ACE inhibitors may be involved in the starting syndrome of jaundice and progress to dark liver necrosis, sometimes deadly (though very rare). It is recommended to stop taking the drug in patients with the symptoms of jaundice or increasing liver enzyme significantly when taking ACE inhibitors and appropriate medical monitoring.

Hyperbonemia:

Hyetics have been seen in patients treated with ACE inhibitors, including captopril. In patients with the risk of hyperkalemia, including people with kidney failure, diabetes, or use in combination with diuretics to keep potassium, potassium supplements or salt -containing salt substitutes; Or patients taking other drugs related to serum hyperpassing (like heparin). If you need to use the above medications, regularly monitor serum.

Lithi:

Do not recommend coordination of lithium and captlil.

proteinuria:

can occur especially in patients who are impaired kidney function or high doses of ACE inhibitors. In most cases, proteinuria decreases or completely out of about 6 months whether continuing or not continuing to use captopril.

Parameters of kidney function such as blood urea nitrogen and creatinine rarely change in patients with proteinuria, in patients with signs of previous kidney disease should assess proteinuria (embedded in the urine in the first morning) before treatment and periodic treatment later.

Anaphylactic reaction in the treatment of sensitive solution:

Rarely respond to life -threatening anaphylaxis in patients who are treating hypersensitivity to the venom of insect wings while taking other ACE inhibitors, in those patients, they can avoid these reactions when they temporarily stop using ACE inhibitors, but will reappear when accidentally taking the drug again. Therefore, caution should be careful in patients treated with ACE inhibitors while conducting such sensitivity.

Anaphylactic reaction during the process of separating with high absorbent/ contacting lipoprotein plastering membrane: Therefore, avoid combining. Consider using other types of separation, filters or other drug groups.

Patients with diabetes:

Should monitor the blood glucose level of diabetes patients taking oral hypoglycemic or insulin in the first month of treatment with ACE inhibitors.

Neutral leukemia/ grain leukemia:

Neutral leukemia/grain leukemia, thrombocytopenia and anemia may occur in patients with ACE inhibitors, including captopril, normal kidney function and no other complicated factors. Caode CaPril should be used in patients with previous renal function, blood vessel collagen, immunosuppressive therapy, treatment with allopurinol or process, or in combination with these complication factors.

Some patients in this group develop severe infections, in a few cases that do not respond to strong antibiotic therapy. If using captopril for these patients, counting the number of white blood cells and distinguishing leukocytes before treatment, every 2 weeks in the first 3 months of treatment and periodic treatment.

During treatment, it is necessary to guide all patients to report any signs of infection (such as sore throat, fever), then it is necessary to distinguish leukocytes. Captopril should be discontinued and other medications simultaneously detected or suspected neutropenia (neutrophils

surgery/ anesthesia:

In patients who are undergoing surgery or during anesthesia with medications that cause hypotension, captopril will inhibit the formation of angiotensin II due to clearing and hypotension but can be adjusted by compensation.

lactose:

Captopril Stella 25 mg contains lactose, so it is not advisable to specify patients with rare genetic problems galactose intolerance, total lactase enzyme deficiency or glucose-galactose.

Race:

The effect of hypotension of captopril in black people is worse than other skin -colored people, possibly due to low renin situation accounting for a higher proportion in the black -blooded black population.

The ability to drive and operate machinery

The ability to drive and operate machinery can be reduced when starting treatment, when changing the dosage and when used simultaneously with alcohol, but these effects depend on the sensitivity of each individual.

Pregnancy

Use captopril or other ACE inhibitors in the three months and the last 3 months of pregnancy can cause damage to the fetus and infants such as lowering blood pressure, reducing newborn skulls, urology, renal failure recovery or non -recovery and death.

Lack of amniotic fluid may be due to reduced fetal kidney function. Protestant pregnancy, premature birth and arterioscleros have occurred. So contraindicated captopril during pregnancy.

The period of breastfeeding

captopril excreted into milk, causing many harmful effects for breastfed babies, so do not use captopril on this object.

Interactive drug

diuretics (diuretics or diuretics):

Previous treatment with high -dose dietary drugs can lead to a decrease in circulatory volume and the risk of hypotension when starting treatment with captopril. Hypotension effects may be reduced when diuretics stop taking diuretics, increasing the volume of circulatory, supplementing with salt or starting treatment with Captopril in low doses.

Potassium diuretics or potassium supplements:

ACE inhibitors reduce potassium loss due to diuretics. Potassium diuretics (triamteren, amilorid and spironolacton), salt -containing substances containing potassium or potassium supplements can significantly increase serum potassium. If indicated, these drugs are indicated due to obvious hypokalemia, caution should be used and regularly monitor serum potassium.

Other anti -hypertension drugs:

Timidant use of these drugs may increase the hypotension effect of captopril. Caution should be used when treated with nitroglycerin and other nitrates, or other vasodilators (such as minoxidil).

Lithi:

Increased lithium concentration and increased toxicity recovery when used simultaneously lithium with ACE inhibitors. If combining thiazid diuretics can increase the risk of lithium toxicity and increase the risk of lithium toxicity when used with ACE inhibitors. It is not recommended to use captopril with lithium, but if it is necessary to combine should carefully monitor the lithium concentration in serum.

Non -steroid anti -inflammatory drugs (NSAIDs) (such as indomethacin, ibuprofen):

Combined with ACE inhibitors that cause combination effects on increased serum potassium concentration while renal function may be reduced and often recovered. In some rare cases, acute renal failure may occur, especially in patients with impaired renal function such as elderly or dehydrated people. For long -term use NSAIDs can reduce the effect of lowering the blood pressure of the ACE breast.

clonidin:

Anti -hypertension effect of captopril may be delayed when patients treated with clonidin to use captopril.

Allopurinol, processaamid, cell medications or immunosuppressive inhibitors:

Used in combination with ACE inhibitors can lead to an increased risk of leukopenia, especially when using ACE inhibitors at a higher dosage than the current recommended dose.

Probenecid:

The kidney clearance of captopril decreases when the presence of probenecid.

3 -round antidepressants/psychotic drugs:

ACE inhibitors can increase the hypotension effect of some 3 -round antidepressants and psychotic disorder. Lower blood pressure can occur.

Sympathetic drugs:

can reduce the effect of lowering the blood pressure of ACE inhibitors, so monitor patients carefully.

anti -diabetic drugs:

ACE inhibitors, including captopril, can increase the effect of hypoglycemia of insulin and oral hypoglycemic drugs like sulphonylure in diabetes patients. This interaction rarely occurs, may need to reduce the dose of anti -diabetes when treated simultaneously with ACE inhibitors.

Testing:

captopril can cause false positive reactions when testing acetone in urine.

Double Renin-Anotensin-Aldosteron (RAAS):

Combining ACE inhibitors, Angiotensin II or Aliskiren anti -receptor drugs that increase the risk of unwanted effects such as hypotension, hyperkalemia and reduced kidney function (including acute renal failure) compared to solitary use.