Clioquinol-hydrocortisone 3%-0.5% topical cream. Hydrocortisone is a mild corticosteroid that works by reducing the swelling, redness, and itching that occurs. Lidocaine 3%-hydrocortisone 0.5% rectal cream. Imprint No data. This medicine is a cream ‹ Back to Gallery. Lidocaine 3%-hydrocortisone 1% (7 gram) rectal kit. Hydrocortisone Cream 0.5% can be used as continuation therapy in mild cases of seborrhoeic or atopic eczema once the acute inflammatory phase has passed. 4.2 Posology and method of administration Posology.
Hydrocortisone 0.5%. Iodochlorhydroxyquin 3% Cream. 1 oz (28.4 grams) WARNING: Keep out of reach of children. Ireal pro 2019 6 – music book & play along. For external use only. Not for ophthalmic use. Usual Dosage: Apply as a thin film to the affected areas 2 to 4 times daily or as directed by physician. See package insert for full prescribing information.
2012-09-13 04:00:00
Question:
Do you have a formulation for hydrocortisone 100 mg suppositories?
Answer:
Hydrocortisone is a white to almost-white bitter-tasting crystalline powder. It is only very slightly soluble in water (~0.28 mg/mL). Its solubility is less than 25 mg/mL at the most in ethanol and 12.7 mg/mL in propylene glycol. In nonsterile suspension, hydrocortisone’s pH is 5.5 to 7.0. The pKa of hydrocortisone when titrated with NaOH is 11.05 at 25°C.
Products and preparations containing hydrocortisone or its salts or esters are stored in tight containers at controlled room temperature and protected from light. Hydrocortisone acetate suppositories are available as the commercial product Anusol-HC, Anucort-HC, and other generic forms. The formulation for this product (which was on the market pre–Durham-Humphrey, and therefore a “grandfathered” product without NDA) is a fatty acid blend. Using professional judgment, pharmacists can compound the formulation or a variation when the commercially manufactured product is unavailable or not available in time.
One formulation employs hydrocortisone free base rather than hydrocortisone acetate. Patient response to compounded preparations is the usual clinical determinant of efficacy.
Suggested Formulation
Hydrocortisone suppositories 100 mg Calculated to make 12 each (2-mL mold)
Ingredients
Hydrocortisone USP 1.200 g
Silica gel (fumed silica USP/NF) 0.120 g
Fatty acid blend 20.520 g
Supplies
Suppository molds, 2 mL
Hot plate (with a stir bar option)
Water bath; thermometer
Beaker
Stirring rod
Ceramic or Wedgwood mortar and pestle
Suggested Method
1. Weigh or measure ingredients accurately.
2. Combine the powders in the mortar and comminute to fine, uniform consistency.
3. Heat the fatty acid blend in the water bath until completely melted and temperature is 55°C to 60°C.
4. Stir the melted fatty acid blend to form a vortex and sprinkle the powders slowly into the vortex until thoroughly dispersed and the mixture is homogeneous.
5. Reduce heat and allow the mixture to cool to 45°C to 50°C.
6. Pour into room temperature molds, allow to cool, remove from molds, package, and dispense. Label: Refrigerate, do not freeze.
Note: Fatty acid blend weighs approximately 1.82 g/2 mL. This formulation is for informational purposes only. No claims are made as to the uses, efficacy, safety, or bioavailability of this preparation.
Mr. Erickson is director of professional affairs and director of professional services at Gallipot, a Fagron company.
Do you have a formulation for hydrocortisone 100 mg suppositories?
Answer:
Hydrocortisone is a white to almost-white bitter-tasting crystalline powder. It is only very slightly soluble in water (~0.28 mg/mL). Its solubility is less than 25 mg/mL at the most in ethanol and 12.7 mg/mL in propylene glycol. In nonsterile suspension, hydrocortisone’s pH is 5.5 to 7.0. The pKa of hydrocortisone when titrated with NaOH is 11.05 at 25°C.
Products and preparations containing hydrocortisone or its salts or esters are stored in tight containers at controlled room temperature and protected from light. Hydrocortisone acetate suppositories are available as the commercial product Anusol-HC, Anucort-HC, and other generic forms. The formulation for this product (which was on the market pre–Durham-Humphrey, and therefore a “grandfathered” product without NDA) is a fatty acid blend. Using professional judgment, pharmacists can compound the formulation or a variation when the commercially manufactured product is unavailable or not available in time.
One formulation employs hydrocortisone free base rather than hydrocortisone acetate. Patient response to compounded preparations is the usual clinical determinant of efficacy.
Suggested Formulation
Hydrocortisone suppositories 100 mg Calculated to make 12 each (2-mL mold)
Ingredients
Hydrocortisone USP 1.200 g
Silica gel (fumed silica USP/NF) 0.120 g
Fatty acid blend 20.520 g
Supplies
Suppository molds, 2 mL
Hot plate (with a stir bar option)
Water bath; thermometer
Beaker
Stirring rod
Ceramic or Wedgwood mortar and pestle
Suggested Method
1. Weigh or measure ingredients accurately.
2. Combine the powders in the mortar and comminute to fine, uniform consistency.
3. Heat the fatty acid blend in the water bath until completely melted and temperature is 55°C to 60°C.
4. Stir the melted fatty acid blend to form a vortex and sprinkle the powders slowly into the vortex until thoroughly dispersed and the mixture is homogeneous.
5. Reduce heat and allow the mixture to cool to 45°C to 50°C.
6. Pour into room temperature molds, allow to cool, remove from molds, package, and dispense. Label: Refrigerate, do not freeze.
Note: Fatty acid blend weighs approximately 1.82 g/2 mL. This formulation is for informational purposes only. No claims are made as to the uses, efficacy, safety, or bioavailability of this preparation.
Mr. Erickson is director of professional affairs and director of professional services at Gallipot, a Fagron company.
MECHANISM OF ACTION:
0/5 Slope
Product releases lidocaine to stabilize the neuronal membrane by inhibiting the ionic fluxes required for initiation and conduction of impulses, thereby effecting local anesthetic action. Hydrocortisone acetate provides relief of inflammatory and pruritic manifestations of corticosteroid responsive dermatoses. Lidocaine is chemically designated as acetamide, 2-(diethylamino)-N-(2,6-dimethylphenyl), and has the following structure:
Hydrocortisone acetate has a chemical name pregn-4-ene-3, 20-dione, 21-(acetyloxy)-11,17- dihydroxy-(11ß)-. It has the following structural formula:
PHARMACOKINETICS:
Lidocaine may be absorbed following topical administration to mucous membranes, its rate and extent of absorption depending upon the specific site of application, duration of exposure, concentration, and total dosage. In general, the rate of absorption of local anesthetic agents following topical application occurs most rapidly after intratracheal administration. Lidocaine is also well-absorbed from the gastrointestinal tract, but little intact drug appears in the circulation because of biotransformation in the liver.
Lidocaine is metabolized rapidly by the liver, and metabolites and unchanged drug are excreted by the kidneys. Biotransformation includes oxidative N-dealkylation, ring hydroxylation, cleavage of the amide linkage, and conjugation. N-dealkylation, a major pathway of biotransformation, yields the metabolites monoethylglycinexylidide and glycinexylidide. The pharmacological/toxicological actions of these metabolites are, similar to but less potent than, those of lidocaine. Approximately 90% of lidocaine administered is excreted in the form of various metabolites, and less than 10% is excreted unchanged. The primary metabolite in urine is a conjugate of 4-hydroxy-2, 6-dimethylaniline. The plasma binding of lidocaine is dependent on drug concentration, and the fraction bound decreases with increasing concentration. At concentrations of 1 to 4 g of free base per mL, 60 to 80 percent of lidocaine is protein bound. Binding is also dependent on the plasma concentration of the alpha-1-acid glycoprotein. Lidocaine crosses the blood-brain and placental barriers, presumably by passive diffusion.
0-5 Military Rank
Studies of lidocaine metabolism following intravenous bolus injections have shown that the elimination half-life of this agent is typically 1.5 to 2 hours. Because of the rapid rate at which lidocaine is metabolized, any condition that affects liver function may alter lidocaine kinetics. The half-life may be prolonged two-fold or more in patients with liver dysfunction. Renal dysfunction does not affect lidocaine kinetics but may increase the accumulation of metabolites. Factors such as acidosis and the use of CNS stimulants and depressants affect the CNS levels of lidocaine required to produce overt systemic effects. Objective adverse manifestations become increasingly apparent with increasing venous plasma levels above 6 g free base per mL. In the rhesus monkey arterial blood levels of 18-21 g/mL have been shown to be threshold for convulsive activity.
Ipulse 3 0 5 Hydrocortisone Cream Usp
The extent of percutaneous absorption of topical corticosteroids is determined by many factors including the vehicle, the integrity of the epidermal barrier, and the use of occlusive dressings.
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Winclone pro 6 6 1 4. Topical corticosteroids can be absorbed from normal intact skin. Inflammation and/or other disease processes in the skin increase percutaneous absorption. Occlusive dressings substantially increase the percutaneous absorption of topical corticosteroids. Thus, occlusive dressings may be a valuable therapeutic adjunct for treatment of resistant dermatoses.
Once absorbed through the skin, topical corticosteroids are handled through pharmacokinetic pathways similar to systemically administered corticosteroids. Corticosteroids are bound to plasma protein in varying degrees. Affinity publisher 1 8 17. Corticosteroids are metabolized primarily in the liver and are then excreted by the kidneys. Some of the topical corticosteroids and their metabolites are also excreted into the bile.