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Absorption: Tamsulosin is absorbed in the small intestine, fasting bioavailability of almost 100%. When administered with food absorption of tamsulosin is reduced it. To achieve the same level of absorption of the drug should be taken daily in doses specified in the instructions, after breakfast. When receiving a long acting capsule 0.4 mg after meals maximum concentration  of the equipoise side effects drug in the plasma is achieved after about 6 hours. Repeated reception of the equilibrium concentration is reached by day 5, when maximum drug concentration in plasma of about 2-3 times higher than for single reception.Although these indicators were evaluated in elderly patients, assuming they have similar younger patients. When single and multiple reception can meet individual variations in plasma concentration of the drug.

 

Metabolism: Tamsulosin is metabolized slowly, the effect of “first pass” insignificant. Tamsulosin slowly biotransformed in the liver with the formation of pharmacologically active metabolites that retain high selectivity for alpha 1-adrenoceptor A. Most of the active substance is present in blood in an unmodified form. In rats revealed slight induction of microsomal caused by tamsulosin. None of the metabolites are not to be more active than tamsulosin.

Excretion: Tamsulosin and its metabolites are primarily excreted by the kidneys, approximately 9% of the dose of the drug – in an unmodified form. The half-life of the drug from plasma was 10 hours with a single reception capsules 0.4 mg, after repeated equipoise side effects hours, the final half-life -. 22 hours When kidney disease dose adjustment is required. Finasteride

Absorption: rapidly absorbed from the gastrointestinal tract after 2 hours reaches a maximum plasma concentration equal to 37 ng / ml. Absorption in the gastro-intestinal tract is completed in 6-8 hours after ingestion. Food intake has no effect on the absorption of finasteride. The bioavailability of finasteride when taken orally is approximately 80%.

Distribution: 90% of circulating finasteride is associated with plasma proteins and has no damaging effect in diseases of the kidneys. Finasteride penetrates the blood-brain barrier and seed is distributed to patients in a small amount of liquid. The volume of distribution was 76 ± 14 l.

Metabolism: Finasteride is extensively metabolised in the liver by oxidative biotransformation. Two of finasteride 5 metabolites have poor activity and are responsible for 20% of inhibition .

Excretion: The average half-life of finasteride is 6 hours equipoise side effects, in men older than 70 years – 8 hours (6-15 hours). When using labeled finasteride, approximately  of the administered dose excreted by the kidneys as metabolites. Unchanged finasteride virtually undetectable in urine. Approximately  of the total dose is excreted through the intestines. Patients with narusheniehM renal function revealed no differences in excretion of finasteride. Finasteride in sperm concentration ranges from undetectable .
Long, 3-7 months receiving 5 mg / day, reduces the concentration of equipoise side effects in the serum by 70%.

Pharmacokinetics in specific patient groups:
In elderly patients Finasteride displays a little slower, but it has no clinical significance and does not require dose adjustment. This also applies to patients with renal insufficiency, as a decrease in renal excretion of metabolites offset by increased excretion of the drug through the intestines. Indicators pharmacokinetics of finasteride has not been studied in patients equipoise side effects with hepatic insufficiency. Since Finasteride is extensively metabolised in the liver, liver diseases require additional monitoring.

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Tamsulosin selectively and competitively blocks postsynaptic alpha-1 adrenergic receptors located in the smooth muscle of the prostate, bladder neck and prostatic urethra , and alpha-1-adrenergic receptors, mainly located in the body of the bladder define equipoise. This leads to a reduction in smooth muscle tone of the prostate, bladder neck and prostatic urethra and detrusor improve function. This reduces the symptoms of obstruction and irritation associated with benign prostatic hyperplasia. Typically, the therapeutic effect is at 2 weeks after the beginning of reception of the preparation, although some patients, a decrease in symptoms observed after the first dose. Tamsulosin ability to influence the alpha-1A adrenoceptors 20 times greater than its ability to interact with alpha-1 adrenoceptors located in vascular smooth muscle. Due to such a high selectivity of the drug does not cause any clinically significant reduction in systemic blood pressure  in both hypertensive patients and in patients with normal baseline .

Pharmacodynamics finasteride

Finasteride – a synthetic 4-azasteroid, a specific inhibitor of the intracellular enzyme 5-alpha-reductase type II. Last converts testosterone into the more active androgen – 5-alpha-dihydrotestosterone .The normal function and growth of the prostate gland, including its hypertrophied tissue is dependent on the conversion of testosterone to define equipoise. Finasteride has no effect on the androgenic receptors. In healthy volunteers, proliferation and apoptosis of prostate cells are balanced due to the interaction of factors that inhibit and stimulate growth. Although the etiological factors, on a molecular level causing prostatic hyperplasia are not yet known, probable that in this process  plays a role. Specific inhibitors of type II 5-alpha-reductase reduce the concentration  in the prostate and promote regression of prostate hyperplasia. According to clinical studies, treatment with finasteride rapidly reduces the concentration  in the plasma by 70%, resulting in a decrease in prostate volume. At constant reception statistically significant effects recorded after 3 months (decrease prostate volume by about 20%) and 7 months (decrease in severity of symptoms associated with benign prostatic hyperplasia).

In humans, there are two kinds of 5-alpha reductase inhibitor: I and P. Their distribution in tissues differently: in prostate, testis and epididymis, glans penis, scrotum, seminal vesicle, liver, and the chest occurs type II isozyme; Type I is found mainly in the skin of the head, back and chest, sebaceous glands, in the liver, kidney and adrenal glands. Finasteride inhibits primarily type II isozyme, is responsible for most of the  in the blood. A single dose of finasteride quickly and significantly change the concentration of define equipoise in plasma. A single dose of 5 mg of finasteride reducing DHT concentration in plasma is 75%, which is 24 o’clock reaches its minimum, and then returns to its original level within 7 days.

Repeated reception finasteride is effective. Finasteride decreases the concentration  in the prostate itself to <15% and provides a corresponding increase in testosterone in the prostate. Compared with surgical or chemical castration, treatment with finasteride is accompanied by a significantly greater decrease in the level  in the prostate. Prostate-specific antigen  – a sensitive and specific marker of prostate carcinoma androgenozavisimy. In most cases, after a few months of treatment with finasteride, a rapid decrease in  levels, and then setting it to low values. After 1 year receiving finasteride 5 mg average concentration  is reduced by 50%.

Finasteride does not exhibit affinity for androgen receptors and has no other hormonal action. Following the discovery of the 5-alpha-reductase deficiency syndrome and the description of the 5-alpha-reductase type II (male hermaphroditism type) the role of androgens in benign prostatic hyperplasia was again revised.

Prostate development is dependent ondefine equipoise strong androgen. When failure of 5-alpha-reductase in the background of normal or high testosterone levels in adulthood there is atrophy of the prostate.  Activates the androgen receptor to form after the accession to the dimers, which are entering into a relationship with  directly or indirectly, contribute to cell proliferation by changing the expression of genes responsible for proliferation and apoptosis. In the intact prostate apoptosis and proliferation processes are in equilibrium. Despite the fact that the factors that trigger prostate hyperplasia at the molecular level, are not known, the role of the  is very likely. Specific inhibitors of 5-alpha-reductase type II can reduce the concentration define equipoisein the prostate and promote regression of hyperplastic prostate.

Pharmacokinetics

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After oral tamsulosin is rapidly and almost completely absorbed from the gastrointestinal tract. The bioavailability of the drug – about 100%. After a single oral administration at a dose equipoise steroid of the active substance in plasma is reached after 6 hours.

Distribution
At equilibrium  of the active substance in plasma at 60-70% higher than the after a single dose.

Binding to plasma proteins – 99%. Tamsulosin has a slight volume of distribution (approximately 0.2 l / kg).

Metabolism
Tamsulosin is not subject to the effect of “first pass” and slowly biotransformed in the liver with the formation of pharmacologically active metabolites that retain a high selectivity to the α 1Aadrenoretseptoram. Most of the active substance is present in blood in an unmodified form.

Excretion
Tamsulosin excreted by equipoise steroid the kidneys, 9% of the dose is excreted unchanged.

T1 / 2 at a single dose of tamsulosin -10 hours after multiple dose -13 h, the final half-life – 22 hours.

Indications
Treatment dizuricheskih disorders caused by benign prostatic hyperplasia.

Contraindications:
Hypersensitivity to tamsulosin hydrochloride or any other component of the formulation.

Precautions: chronic renal failure (creatinine clearance below 10 ml / min), hypotension (including orthostatic..), Severe liver failure.

Dosing and Administration
Inside, after eating, 1 capsule per day, at one and the same time of day, drinking plenty of water. The capsule should not be any broken into parts or chew because equipoise steroid wherein the broken sustained release of the active substance.

Side effects:
Rarely – headache, dizziness, fatigue, sleep disturbances (insomnia or drowsiness), retrograde ejaculation, decreased libido, pain, back pain, rhinitis; in rare cases -ortostaticheskaya hypotension, tachycardia, palpitations, chest pain.

On the part of the digestive system: rarely – nausea, vomiting, constipation or diarrhea. In very rare cases, hypersensitivity reactions – skin rash, itching, angioedema.

Overdose
Cases of acute overdose have not been described.

Symptoms: theoretically possible occurrence of acute hypotension, compensatory tachycardia.

Treatment: The patient should be put to restore blood pressure and normalize heart rate. Spend kardiotropnyh therapy. It is necessary to monitor renal function and to apply the general supportive therapy.

If the symptoms persist, you should enter obemozameschayuschie solutions vasoconstrictor drugs. To prevent further absorption of tamsulosin may gastric lavage, activated charcoal or osmotic laxative.Dialysis is not effective as tamsulosin binds strongly to plasma proteins.

Interaction with other drugs
Cimetidine increases the concentration of tamsulosin in plasma furosemide reduces the (substantial clinical significance has not, change the dosing is not required).

Diclofenac and indirect anticoagulants equipoise steroid increases the excretion of tamsulosin.

Diazepam, propranolol, trichloromethiazide, chlormadinone, amitriptyline, diclofenac, glibenclamide, simvastatin and warfarin does not alter tamsulosin free fraction in human plasma in vitro. In turn, tamsulosin does not change the free fractions of diazepam, propranolol, trichlormethiazide and chlormadinone.

In in vitro studies found no interaction at the level of hepatic metabolism with amitriptilipom, salbutamol, glibenclamide and finasteride.

Other alpha 1-blockers, acetylcholinesterase inhibitors, alprostadil, anesthetics, diuretics, levodopa, antidepressants, beta-blockers, blockers “slow” calcium channel blockers, nitrates and ethanol may exacerbate the severity of the hypotensive effect of tamsulosin.

Cautions
As with other α1-blockers tamsulosin may cause a decrease in blood pressure, rarely causing faint. At the first signs of orthostatic hypotension (dizziness, weakness), you must sit down or put the patient until symptoms disappear.

Treatment with tamsulosin must be preceded by a preliminary examination of the patient in order to exclude any other disease, flowing with the same symptoms as benign prostatic hyperplasia. Treatment should be preceded by a pre-digital rectal examination of the prostate and measuring the level of prostate specific antigen (PSA), which later, in the course of treatment is repeated regularly.

In the period of treatment should refrain equipoise steroid from activities potentially hazardous activities that require high concentration and psychomotor speed reactions. stabol

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Drowsiness, confusion, urinary retention, disorientation, coma, areflexia, hyperreflexia, dry mouth, nasal congestion, postural hypotension, respiratory center clinical equipoise depression, convulsions, hypothermia. Treatment is symptomatic, aimed at reducing the suction and the acceleration of excretion of the drug. Gastric lavage solution of activated charcoal, laxatives (eg magnesium sulfate). Introduction isotonic solutions.Control function of the cardiovascular and respiratory systems. If you want to consistently perform artificial respiration and monitoring functions of the cardiovascular system, prevent the development of metabolic acidosis. There is no specific antidote.

Interaction with other drugs
The synergy of action with general anesthetics, opioids, barbiturates, ethanol, atropine. It enhances the hepatotoxic effects of antidiabetic drugs. With amphetamine –  clinical equipoise acts antagonistically. Since levodopa – reduced antiparkinsonian action. The use of adrenaline – can lead to a sudden and pronounced reduction in blood pressure. With guanetidinom reduces the antihypertensive effect of the latter, but enhances the effect of other antihypertensive drugs, which increases the risk of a significant orthostatic hypotension. It reduces the effect of anticoagulants. Action sonapaks can weaken anticonvulsants, cimetidine.Quinidine – cardiodepressive potentiates the action. Ephedrine – contributes to a paradoxical decrease in blood pressure. Sympathomimetics – reinforce arrhythmogenic effect. Probucol, astemizole, cisapride, disopyramide, erythromycin, pimozide, quinidine, procainamide, and contribute to further prolongation of the  interval, which increases the risk of ventricular tachycardia. Antithyroid drugs increase the risk of agranulocytosis. Reduces means reducing appetite (except for fenfluramine). Reduces the effectiveness of the action of the emetic apomorphine enhances its inhibitory effect on the central nervous system. Increases concentration of plasma prolactin and bromocriptine prevents action.

In a joint application with tricyclic antidepressants, maprotiline, clinical equipoise inhibitors, antihistamines may lengthening and strengthening of sedative and anticholinergic effects. With thiazide diuretics – strengthening of hyponatremia. With lithium medications – reducing the absorption in the gastrointestinal tract, increasing the rate of excretion of the lithium ions by the kidneys, increased severity of extrapyramidal disorders, early signs of lithium toxicity (nausea and vomiting) may be masked antiemetic effect of perphenazine. In combination with beta-blockers enhances the hypotensive effect, it increases the risk of irreversible retinopathy, arrhythmias, and tardive dyskinesia.

Cautions
In the period of treatment is necessary to monitor the morphological composition of the blood; refrain from the use of ethanol and activities potentially hazardous activities that require high concentration and psychomotor speed reactions.
Effects on ability to road management and maintenance clinical equipoise machinery in motion.
Sonapaks weakens motor coordination, and reduces the reaction, especially at the beginning of the treatment, so the period of drug treatment should refrain from driving vehicles and moving machinery maintenance. buy legal anabolic steroids online

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Absorption – high, time of onset of the maximum concentration  in plasma – 1-4 hours after ingestion. About 90% of the drug binds to plasma proteins. It is metabolized in the liver with the formation of active metabolites (mesoridazine and sulforidazin).  Equipoise cycle – pharmacologically more active than the starting material, has a greater  less bound to proteins, free concentration higher than that of thioridazine. Excretion in unchanged form and as metabolites – the kidneys (35%) in the bile. Provided with breast milk.

Indications
Schizophrenia, manic-depressive psychosis; neuroses, accompanied by fear, anxiety, agitation, tension, depressed mood, sleep disturbances, intrusive state; psychotic disorders, accompanied by hyperactivity and excitement; severe behavioral disorders associated with psychotic disorders or neurological diseases involving aggression, inability to long-term focus; abstinence syndrome (drug addiction, alcoholism); agitation of various origins; moderate and severe depression in adults; Huntington’s disease, tics; skin conditions with a strong and painful itching; in child psychiatry is used for behavioral disorders with increased psychomotor activity.

Contraindications:
Hypersensitivity, acute depression, comatose states from any cause, traumatic brain injuries, progressive system of the brain and spinal cord diseases; severe heart failure, severe hypotension, pheochromocytoma, porphyria, blood disorders (hypo-and aplastic processes). Pregnancy, lactation, children’s age (up to 4 years).

Precautions
When alcoholism equipoise cycle (predisposition to hepatotoxicity), pathological changes in the blood (impaired hematopoiesis), breast cancer (as a result of induced phenothiazine prolactin increases the potential risk of disease progression and resistance to the treatment of endocrine and cytotoxic drugs), angle-closure glaucoma, prostatic hyperplasia with clinical manifestations, liver and / or renal failure, gastric ulcer and duodenal ulcer (in the period of exacerbation); diseases accompanied by an increased risk of thromboembolic complications; Parkinson’s disease (amplified extrapyramidal effects); epilepsy; myxedema;chronic diseases accompanied by respiratory disorders (especially in children); Reye syndrome (increased risk of hepatotoxicity in children and adolescents); cachexia, vomiting (antiemetic effect of phenothiazines may mask vomiting associated with overdoses of other drugs). Elderly age.

Dosing and Administration
Inside. An individual dosage regimen. Adult equipoise cycle Acute psychosis, mania, schizophrenia and depression azhitatsionnyh: an outpatient basis – 150-400 mg per day; hospital – 250-800 mg per day. Treatment is usually started with a low dosage of 25-75 mg per day, gradually increasing to an optimal therapeutic dose, which is usually achieved within 7 days, and the antipsychotic effect is observed after 10-14 days.The course of treatment is several weeks. Maintenance daily dose: 75-200 mg once daily at bedtime. In the treatment of the elderly are usually used low doses: 30-100 mg per day. The drug should be withdrawn gradually. In light of mental and emotional disorders – 30-75 mg per day, with moderate disorders – 50-200 mg per day. To begin treatment with low doses of gradually increasing doses until the optimal therapeutic. In psychosomatic disorders: 10-75 mg per day. To suppress the strong itch, dose set individually, and it should not exceed 200 mg. Children 4 to 7 years – 10-20 mg sutki.Kratnost reception – 2-3 times a day. From 8 to 14 years – 20 30 mg per day. Multiplicity of reception – 3 times a day. From 15 to 18 years – 30-50 mg per day. Multiplicity of reception – 3 times a day. buy anabolic steroids online bruce lee’s workout anabolic steroids online uk