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The dose is titrated to achieve the desired reduction in blood pressure by increasing in increments of 1µg/kg/min every 20 to 60 minutes purchase accutane 20mg fast delivery acne out biotrade. The dose is titrated to achieve the desired effect or until headache or nausea appear by increasing in increments of 0 order 5 mg accutane with visa skin care qvc. Usual dose is 3µg/kg/min; maximum dose buy accutane 5mg amex acne 22 years old, 10µg/kg/min Pharmacokinetics Onset of action: less than 2 minutes (hypotensive effect) Half-life: parent drug cheap accutane 40 mg amex skin care ingredients, less than 10 minutes; thiocyanate, 2. Monitor closely for signs of cyanide and thiocyanate oxicity (see Poisoning Information), including acid-base status, blood cyanide level (especially patients with hepatic dysfunction), and blood thiocyanate level. Adverse Effects Cardiovascular: excessive hypotensive response, palpitations, reflex tachycardia, substernal chest pain Respiratory: tachypnea or respiratory distress (from metabolic acidosis caused by cyanide toxicity), hypoxemia Central nervous system: disorientation, restlessness, headache, psychosis, elevated intracranial pressure Gastrointestinal: nausea, vomiting 106 S. Neuromuscular and skeletal: weakness, muscle spasm Endocrine/metabolic: thyroid suppression Hematological: thiocyanate toxicity Other: diaphoresis, tinnitus Precautions Because both the liver and kidney contribute to removal of nitroprusside’s breakdown products, use with caution in patients with either hepatic or renal dysfunction. Patients with renal dysfunction are at increased risk of thiocy- anate toxicity, and patients with hepatic dysfunction are at increased risk of cyanide toxicity. Drug-Drug Interactions The addition of nitroprusside to treatment regimens that include other agents that reduce blood pressure can lead to excessive hypotension. Poisoning Information Toxicity from nitroprusside can occur either by cyanide toxicity or thiocy- anate toxicity. Thiocyanate toxicity is manifested by psy- chosis, hyperreflexia, confusion, weakness, tinnitus, dilated pupils, seizures, and coma. Patients with hepatic dysfunction or anemia should have blood cyanide levels measured. If toxicity develops, in addition to discontinuing nitroprusside administra- tion, therapies include: Table 4-3. Reference ranges for blood thiocyanate and cyanide levels Thiocyanate Cyanide Therapeutic: 6–29µg/mL Normal: < 0. Because light causes nitroprusside to break down to form cyanide, it must be protected from light (e. The solution is stable at room temperature for up to 24 hours if protected from light. Blood Cyanide and Thiocyanate Concentrations Produced by Long-Term Therapy with Sodium Nitroprusside. Systemic Vasodilators: Phenoxybenzamine and Phentolamine Phenoxybenzamine Indication Phenoxybenzamine is a nonspecific, long-acting, α-adrenergic antagonist used in pediatric patients for the treatment of arterial hypertension, particularly when secondary to pheochromocytoma,1 and in the acute post- operative course of congenital or acquired cardiac anomalies. In some pediatric cardiac centers, it is considered to be an essential drug in the armamentarium for the treatment of low cardiac output state after weaning from cardiopulmonary bypass. Mechanism of Action Phenoxybenzamine forms a permanent and irreversible covalent bond with nitrogen atoms on the surface of α-adrenoceptors, thereby blocking epinephrine and norepinephrine from binding with these receptors. This causes systemic vasodilation, and to some extent, pulmonary vasodilation because of a reduction in vascular resistances. These activities are beneficial in controlling the effects of endogenously released catecholamines in the periop- erative stress response. By affecting postsynaptic membrane adrenoceptors in the sympathetic nervous pathway, phenoxybenzamine also acts on α1 and α2 receptors, reducing sympathetic activity. This resulting “chemical sympathectomy” induces fur- ther general vasodilation, miosis, an increase in gastrointestinal tract motility, secretions, and glycogen synthesis. In addition to the α-blockade effect, phenoxybenzamine irreversibly inhibits responses to 5-hydroxytryptamine (serotonin), histamine, and acetylcholine. Phenoxybenzamine is a noncompetitive (irreversible) antagonist, meaning that receptor blockade cannot be overcome by addition of agonist drugs. Dosing Phenoxybenzamine should be slowly titrated to the desired effect after a small initial dose and under close hemodynamic monitoring. It may be progressively increased to 2mg/kg once or twice a day in patients younger than 12 years, or 1 mg/kg once or twice a day in patients older than 12 years Adults: Oral: 5 to 10 mg P. G twice a day; dose may be increased every other day to 20 to 80 mg two or three times a day Note: In patients with pheochromocytoma, if persistent or excessive tachy- cardia occurs, the use of a concomitant β-blocker may be necessary Pharmacokinetics Onset of action: rapid Absorption: when administered orally, 20 to 30% of the drug is absorbed in the active form13 Duration: 3 to 4 days Metabolism: hepatic Half-life: the half-life of oral phenoxybenzamine is not well known; intra- venously, the half-life is approximately 24 hours, and effects may persist for 3 to 4 days. The duration of action is dependent not only on the presence of the drug, but also on the rate of synthesis of α-receptors Elimination: renal and biliary 4. Vasodilators 109 Contraindications Phenoxybenzamine is contraindicated in patients with hy- persensitivity to the drug or any of its components. Compounds that stimulate both types of receptors may produce an exaggerated hypotensive response with reflex tachycardia. Adverse Effects Cardiovascular: tachycardia, arrhythmias, hypotension (mostly in patients with intravascular volume depletion), shock Gastrointestinal: vomiting Metabolic: water and sodium retention Central nervous system: dizziness, drowsiness, postural hypotension Neuromuscular and skeletal: weakness Ophthalmological: miosis Other: nasal congestion, irritation, fatigue, lethargy Drug-Drug Interactions Phenoxybenzamine interacts with compounds that stimulate both α- and β-adrenergic receptors to produce severe hypotension and tachycardia. Phenoxybenzamine blocks the hyperthermia produced by norepinephrine and blocks the hypothermia produced by reserpine. Poisoning Information Overdosage of phenoxybenzamine produces symptoms of sympathetic nervous system blockade; symptoms and signs include hypoten- sion, tachycardia, dizziness or fainting, vomiting, lethargy, and shock. Treat- ment of overdosage consists of the following: ● Drug withdrawal ● Recumbent position with leg elevation ● I. Epinephrine is contraindicated because it stimulates both α- and β-receptors, and, because α-receptors are blocked, epinephrine may produce further hypotension via β-receptor stimulation ● Antagonism with vasopressin has been described as effective, particu- larly for the treatment of phenoxybenzamine-induced side effects in patients after the Norwood procedure14 References 1. Preoperative blood pressure management of children with cathecho- lamine-secreting tumors: time for a change. Combined use of phenoxybenzamine and dopamine for low cardiac output syndrome in children at withdrawal from cardiopulmonary bypass. Radial artery graft treatment with phenoxybenzamine is clinically safe and may reduce perioperative myocardial injury. Combination of low-dose phenoxybenzamine and sodium nitroprusside in children undergoing cardiac surgery. Combination of phenoxybenzamine and nitroglycerin: effective control of pulmonary artery pressures in children undergoing cardiac surgery. Comparison of phenoxybenzamine to sodium nitroprusside in infants undergoing surgery. Comparison of phenoxybenzamine to sodium nitroprusside in infants undergoing surgery. Effects of vasodilators on rates of change of nasopharyngeal temperature and systemic vascular resistance during cardiopulmonary bypass in anaesthetized dogs. Practical use of alpha blockade strategy in the management of hypoplastic left heart syndrome following stage one palliation with a Blalock-Taussig shunt. Vasopressin reversal of phenoxybenzamine-induced hypotension after the Norwood procedure. Combination of phenoxybenzamine and nitroglycerin: effective control of pulmonary artery pressures in children undergoing cardiac surgery. In: Goodman & Gillman, The Pharmacological Basis of Therapeutics, 6th Edition, New York, MacMillan Publishing Co, 1980. Vasopressin reversal of phenoxybenzamine-induced hypotension after the Norwood procedure. Phentolamine Indication Phentolamine is a reversible, competitive, nonselective, α-adrener- gic antagonist that has similar affinities for α1 and α2 receptors. Its effects on the cardiovascular system are very similar to those of phenoxybenzamine, 4. The primary application for phentolamine is for the control of hypertensive emergencies, most notably caused by pheochromocytoma. It has also been used to treat hypertensive crises secondary to monoamine oxidase inhibitor-sympathomimetic amine interactions and for withdrawal of clonidine, propranolol, or other antihypertensives.

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Hepatic Insufficiency: Elevations of hepatic enzymes and hepatic failure have been reported in association with dipyridamole administration 20 mg accutane sale acne on buttocks. Cholinesterase Inhibitors: Dipyridamole may counteract the anticholinesterase effect of cholinesterase inhibitors cheap accutane 40mg amex acne studios, thereby potentially aggravating myasthenia gravis proven 30mg accutane acne after stopping birth control. Dermatological System: Rash order 5 mg accutane otc skin care now pueblo co, urticaria Haematological System: Thrombocytopaenia Dipyridamole! Ectopic Activity: Dobutamine may precipitate or exacerbate ventricular ectopic activity, but only rarely causes ventricular tachycardia. The vasodilation in these vascular beds is accompanied by increased glomerular filtration rate, renal blood flow, sodium excretion and urine flow. An increase in urinary output produced by dopamine is usually not associated with a decrease in osmolality of the urine. There is little, if any, stimulation of the beta2-adrenoceptors (peripheral vasodilation). Blood flow to the peripheral vascular beds may decrease while mesenteric flow increases due to increased cardiac output. Total peripheral resistance (alpha effects) at low and intermediate doses is usually unchanged. At higher rates of infusion (10-20 mcg/kg/min), there is some effect on alpha- adrenoceptors, with consequent vasoconstrictor effects and a rise in blood pressure. The vasoconstrictor effects are first seen in the skeletal muscle vascular beds, but with increasing doses, they are also evident in the renal and mesenteric vessels. At very high rates of infusion (above 20 mcg/kg/min), stimulation of alpha-adrenoceptors predominates and vasoconstriction may compromise the circulation of the limbs and override the dopaminergic effects of dopamine, reversing renal dilation and natriuresis. The overall prevalence of sulphite sensitivity in the general population is unknown and probably low. Sulphite sensitivity is seen more frequently in asthmatic than in non-asthmatic people. At lower infusion rates, if hypotension occurs, the infusion rate should be rapidly increased until adequate blood pressure is obtained. If hypotension persists, dopamine should be discontinued and a more potent vasoconstrictor agent such as noradrenaline should be added. Concurrent administration of low-dose dopamine and diuretic agents may produce an additive or potentiating effect on urine flow. It is suggested that in patients receiving dopamine, alternatives to phenytoin should be considered if anticonvulsant therapy is needed. Other: Gangrene of the extremities has occurred when high doses were administered for prolonged periods or in patients with occlusive vascular disease receiving low doses of dopamine. Priapism: Doxazosin may cause priapism; if this occurs, urgent urological advice is required. Congestive heart failure or left ventricular dysfunction after myocardial infarction 3. Hypersensitivity to enalapril or any other angiotensin-converting enzyme inhibitor (e. If angioedema involves the tongue, glottis or larynx, airway obstruction may occur and be fatal. Swelling confined to the face, mucous membranes of the mouth, lips and extremities has usually resolved with discontinuation of enalapril; some cases required medical therapy. These patients presented with abdominal pain (with or without nausea or vomiting); in some cases there was no prior history of facial angioedema and C-1 esterase levels were normal. Hypotension in Heart Failure Patients Caution should be observed when initiating therapy in patients with heart failure. Patients with heart failure given enalapril commonly have some reduction in blood pressure. In most cases these were isolated values which resolved despite continued therapy. As most procedures happen during daylight hours, prescribing enoxaparin at night reduces the risk of procedural bleeding secondary to enoxaparin) Therapeutic enoxaparin: The standard treatment doses of enoxaparin (weight adjusted) are either 1mg/kg twice daily or 1. These patients should be dosed on a mg/kg basis in the same way as patients of normal bodyweight, with adjustment for renal impairment if needed. It is not recommended that Xa levels are taken prior to this, as they are unable to be interpreted. Patients receiving enoxaparin for less than 48 hours do not need Anti Xa monitoring. Trough measurements • Measuring trough Anti Xa activity routinely is not recommended as the correlation between bleeding risk and trough Anti Xa has not been clearly established. For twice daily dosing, the sample should be taken 12 hours after a dose, immediately preceding the next dose, and should be ≤ 0. For once daily dosing, the sample should be taken 20 hours after a dose, and should be ≤ 0. Therapeutic range • The therapeutic peak Anti Xa range for treatment dose enoxaparin is 0. Ephedrine may deplete norepinephrine stores in sympathetic nerve endings, so that tachyphylaxis to cardiac and pressor effects of the drug may develop. Ephedrine may induce anginal pain in patients with coronary insufficiency or ischaemic heart disease. The drug also may induce potentially fatal arrhythmias in patients with organic heart disease or who are receiving drugs that sensitise the myocardium Ephedrine! Alpha-adrenergic blocking agents may reduce the vasopressor response to ephedrine by causing vasodilation. Beta-adrenergic blocking drugs may block the cardiac and bronchodilating effects of ephedrine. For patients with high risk of cardiac arrhythmia infusion should be administered over 2 hours. When further diluted with saline or Hartmanns, solutions should be used within 8 hours. Pseudomembranous colitis: Pseudomembranous colitis has been reported with nearly all antibacterial agents, including erythromycin, and may range in severity from mild to life threatening. Therefore, it is important to consider this diagnosis in patients who present with diarrhoea subsequent to the administration of antibacterial agents! In case of theophylline toxicity and/or elevated serum theophylline levels, the dose of theophylline should be reduced while the patient is receiving concomitant erythromycin therapy. Concomitant administration of erythromycin and digoxin has been reported to result in elevated digoxin serum levels. There have been reports of increased anticoagulant effects when erythromycin and oral anticoagulants were used concomitantly. Increased anticoagulation effects due to interactions of erythromycin with various oral anticoagulents may be more pronounced in the elderly. Erythromycin has been reported to decrease the clearance of triazolam and midazolam and thus may increase the pharmacologic effect of these benzodiazepines. The use of erythromycin in patients concurrently taking drugs metabolized by the cytochrome P450 system may be associated with elevations in serum levels of these other drugs. There have been reports of interactions of erythromycin with carbamazepine, cyclosporin, tacrolimus, hexobarbital, phenytoin, alfentanil, cisapride, disopyramide, lovastatin, bromocriptine, valproate, terfenadine, and astemizole. Serum concentrations of drugs metabolized by the cytochrome P450 system should be monitored closely in patients concurrently receiving erythromycin. Symptoms of hepatitis, hepatic dysfunction and/or abnormal liver function test results may occur.

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Gastric fluid is less acidic in newborns than in adults cheap 30 mg accutane amex acne 6 weeks pregnant, which can affect the absorption of ionizable and acid-labile drugs cheap accutane 30mg without a prescription acne under arms. Decreased enzymatic activity buy cheap accutane 30 mg on line skincarerx, including hepatic first-pass metabolism order accutane 40 mg on line acne on buttocks, is associated with the elderly, which may result in an increased oral bioavailabiliy for drugs subject to the first- pass effect. The effect of the shunt is to increase the presistence of the drug in the body and, provided the concentrations of the drug at its sites of action are sufficiently high, to prolong its duration of action. It is important to remember that although a drug molecule may be predominantly absorbed via one particular route/mechanism, it is also likely that suboptimal transport will occur via alternative routes and mechanisms. Diffusion is driven by a concentration gradient and is inversely related to molecular weight. The junctional complexes begin immediately below the luminal surface and are made up of three components (Section 1. Thus only small hydrophilic molecules, such as, for example, mannitol, are capable of squeezing through the junctional complexes to be absorbed via the paracellular route. The rate of absorption is governed by Fick’s Law and is determined by the physicochemical properties of the drug as well as the concentration gradient across the cells (Section 1. Carrier-mediated transport Amino acid transporters, oligopeptide transporters, glucose transporters, lactic acid transporters, monocarboxylic acid transporters, phosphate transporters, bile acid transporters and other transporters present on the apical membrane of the epithelial cells serve as carriers to facilitate nutrient absorption by the intestine. Drug moieties possessing similar structures to nutrients that are absorbed by such carriers may also be absorbed in this manner. Endocytic processes Considerable evidence has accumulated indicating that macromolecules and microparticulates can be taken up by the intestinal enterocytes, generally via pinocytosis. For example, studies have shown that receptor-mediated endocytosis via enterocytes is a major pathway for the intemalization of certain antisense oligonucleotides. In contrast, endocytic uptake of macromolecules and microparticles is carried out extensively by the M cells of the 144 Peyer’s patches. Transcellular shuttling through the M cells to the underlying Peyer’s patch may involve an adsorptive and/or receptor-mediated process, with membrane-bound vacuoles or vacuoles already present in the apical cytoplasm of the cells (see below, Section 6. Therefore, they are ionized to a certain extent, determined by their pKa and the pH of the biological fluid in which they are dissolved; the extent of ionization can be quantified by the Henderson-Hasselbalch Equation (see Section 1. According to the pH-partition hypothesis, the nonionized form of a drug, with a more favorable oil/water partition coefficient (Ko/w) than the ionized form, is preferentially absorbed. For example, the absorption of salicylic acid, a weakly acidic drug, is approximately twice as high at pH 4 than at pH 7. By contrast, quinine, a weakly basic drug, is absorbed approximately four times higher at pH 7 than at pH 4 (Table 6. The numbers refer to 1, atenolol; 2, practolol; 3, pindolol; 4, metoprolol; 5, oxprenolol; and 6, alprenolol. Generally, the larger the partition coefficient, the more lipophilic is a compound, and the more readily would it partition into biological membranes. By contrast, hydrophilic atenolol, with the smallest partition coefficient, shows the lowest permeability. Some drugs exhibit a lower absorption than expected on the basis of their partition coefficient. This reduced absorption is thought, in some cases, to be due to the P-glycoprotein efflux effect (see above, Section 6. The results shown with the squares represent the relationship between intestinal absorption clearance (ka) observed from the in situ jejunum loop in the presence (■) and absence (□) of cyclosporin A in rats and octanol-buffer (pH 7. The numbers refer to 1, atenolol; 2, nadolol; 3, acetamide; 4, celiprolol; 5, acebutolol; 6, doxorubicin; 7, timolol; 8, sulfathiazole; 9, quinidine; 10, sulfamethoxazole; 11, digoxin; 12, cyclosporin A; 13, vinblastine; 14, b-estradiol; 15, verapamil. The ionized form of a drug displays a higher dissolution rate and greater solubility than the nonionized form (see Section 1. Drug solubility is also a function of the crystalline, hydrate and salt form (see Section 1. For example, the amorphous form of a drug moiety is usually more soluble than the corresponding crystalline form (e. The solubility of a salt form of a lipophilic drug is higher than the free form and conversion of the free base to the corresponding salt represents a common method of increasing drug solubility. Symposium on Drug Absorption, Metabolism and Excretion, Scientific section of the American Pharmaceutical Asso. The Noyes-Whitney equation describes the influence of surface area (S) and other factors on the dissolution rate: (Equation 6. A reduction in particle size results in an increase in the surface area, which facilitates an increase in the dissolution rate and therefore, also, an increase in the rate of absorption. Drugs administered as suspension are generally rapidly absorbed because of the large available surface area of the dispersed solid. For solid dosage forms such as tablets and capsules, decreasing the particle size facilitates dissolution and thus absorption. Peak blood levels occurred much faster with the smaller 148 particles (50 µm) than with large ones (800 µm), confirming that particle size must be considered in order to optimize absorption. For this reason, many poorly soluble, slowly dissolving drugs for oral drug delivery are marketed in a micronized or microcyrstalline form. These include: Wetting agents Wetting agents are surfactants that lower the interfacial tension and contact angle between solid particles and liquid vehicles. These agents are therefore commonly used to improve the wettability of hydrophobic compounds. Polysorbate 80 is the most widely used wetting agent because of its low toxicity and high compatibility with most formulation ingredients. For example, the common pharmaceutical wetting agent, sodium dodecyl sulfate, has been shown to increase the absorption of drugs and peptides across the human intestinal epithelium. Studies have confirmed that such agents enhance absorption via the paracellular pathway. Diluents Diluents are inert substances added to the active ingredient to bulk up the formulation, in order to make a reasonably sized tablet, or to fill a capsule. Carbohydrates are commonly used, such as lactose, dextrose, sucrose, and microcrystalline cellulose. Hydrophilic diluents promote rapid tablet disintegration and therefore liberate the drug quickly from the dosage form, which promotes absorption. Some diluents dissolve very slowly and therefore release of the drug occurs by tablet erosion, rather than tablet disintegration. However, a hydrophobic diluent impedes penetration of gastrointestinal fluids, so that dissolution of drug occurs only from the surface of the plug-shaped mass. Binders (adhesives) In tableting, binders are used to bind powders together in the wet granulation process. These agents coat the drug particles and therefore the rate of binder dissolution can determine the drug release rate. Disintegrants The purpose of a disintegrant is to cause the tablet to disintegrate rapidly, so as to generate an increased surface area which facilitates rapid drug dissolution. An alternative mechanism involves capillary action, in which liquid is drawn up through capillary pathways within the tablet and ruptures the interparticulate bonds, which serves to break the tablet apart. Obviously, disintegrants with high swelling and hydrating capacities promote rapid dissolution and thus a high bioavailability. Lubricants Lubricants act by interposing an intermediate layer between the tablet constituents and the die wall, to prevent adherence of the granules to the punch faces and dies. The most effective lubricants, such as magnesium stearate, are very hydrophobic and can also prevent wetting of powders and hence retard dissolution (Figure 6. Newer technologies may also incorporate additives such as enzyme inhibitors, to prevent premature degradation of enzymatically labile drugs.

Q. Corwyn. Union Theological Seminary.

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