Lidocaine HCl 3.88%

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Overview

What is Lidocaine HCl 3.88%?

Contains Lidocaine HCl 3.88% in a mild acidic vehicle. Lidocaine is chemically designated as acetamide, 2-(diethylamino)-N-(2,6-dimethylphenyl), and has the following structure:

Ingredients:

Lidocaine HCl 3.88% Cream

What does Lidocaine HCl 3.88% look like?

What are the available doses of Lidocaine HCl 3.88%?

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What should I talk to my health care provider before I take Lidocaine HCl 3.88%?

Sorry No records found

How should I use Lidocaine HCl 3.88%?

For temporary relief of pain and itching associated with minor burns, sunburn, minor cuts, scrapes, insect bites, and minor skin irritation.

Apply a thin film to the affected area two or three times daily or as directed by a physician.

What interacts with Lidocaine HCl 3.88%?

Tuberculous or fungal lesions of skin vaccinia, varicella and acute herpes simplex and in persons who have shown hypersensitivity to any of its components. Lidocaine is contraindicated in patients with a known history of hypersensitivity to local anesthetics of the amide type.

What are the warnings of Lidocaine HCl 3.88%?

Mild cases of pseudomembranous colitis usually respond to drug discontinuation alone. In moderate to severe cases, consideration should be given to management with fluids and electrolytes, protein supplementation and treatment with an antibacterial drug clinically effective against colitis.

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Keep out of reach of children.

What are the precautions of Lidocaine HCl 3.88%?

If irritation of sensitivity occurs or infection appears, discontinue use and institute appropriate therapy. should be used with caution in ill, elderly, debilitated patients and children who may be more sensitive to the systemic effects of lidocaine.

Carcinogenesis, Mutagenesis, and Impairment of Fertility:

Use in Pregnancy:

Nursing Mothers:

Pediatric Use:

What are the side effects of Lidocaine HCl 3.88%?

During or immediately after treatment, the skin at the site of treatment may develop erythema or edema or may be the locus of abnormal sensation.

What should I look out for while using Lidocaine HCl 3.88%?

Tuberculous or fungal lesions of skin vaccinia, varicella and acute herpes simplex and in persons who have shown hypersensitivity to any of its components. Lidocaine is contraindicated in patients with a known history of hypersensitivity to local anesthetics of the amide type.

Keep out of reach of children.

What might happen if I take too much Lidocaine HCl 3.88%?

Sorry No Records found

How should I store and handle Lidocaine HCl 3.88%?

Lidocaine HCl 3.88% Cream3 oz (85 g) tube - NDC 69621-371-07Lidocaine HCl 3.88% Cream3 oz (85 g) tube - NDC 69621-371-07Lidocaine HCl 3.88% Cream3 oz (85 g) tube - NDC 69621-371-07

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Clinical Information

Chemical Structure

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Clinical Pharmacology

Mechanism of Action:

Lidocaine HCl 3.88% Cream

Pharmacokinetics:

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 conjungation. N-dealkylation, a major pathway of biotransformation, yields the metabolites monoethylglycinexylidide and glycinexlidide. 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 concentration 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. 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.

Non-Clinical Toxicology

Tuberculous or fungal lesions of skin vaccinia, varicella and acute herpes simplex and in persons who have shown hypersensitivity to any of its components. Lidocaine is contraindicated in patients with a known history of hypersensitivity to local anesthetics of the amide type.

Keep out of reach of children.

Catecholamine-depleting drugs (e.g., reserpine) may have an additive effect when given with beta-blocking agents or monoamine oxidase (MAO) inhibitors. Observe patients treated with metoprolol tartrate plus a catecholamine depletor for evidence of hypotension or marked bradycardia, which may produce vertigo, syncope, or postural hypotension. In addition, possibly significant hypertension may theoretically occur up to 14 days following discontinuation of the concomitant administration with an irreversible MAO inhibitor.

Both digitalis glycosides and beta-blockers slow atrioventricular conduction and decrease heart rate. Concomitant use can increase the risk of bradycardia. Monitor heart rate and PR interval.

Concomitant administration of a beta-adrenergic antagonist with a calcium channel blocker may produce an additive reduction in myocardial contractility because of negative chronotropic and inotropic effects.

Some inhalation anesthetics may enhance the cardiodepressant effect of beta-blockers. (See ).

Potent inhibitors of the CYP2D6 enzyme may increase the plasma concentration of metoprolol tartrate which would mimic the pharmacokinetics of CYP2D6 poor metabolizer (see section). Increase in plasma concentrations of metoprolol would decrease the cardioselectivity of metoprolol. Known clinically significant potent inhibitors of CYP2D6 are antidepressants such as fluvoxamine, fluoxetine, paroxetine, sertraline, bupropion, clomipramine, and desipramine; antipsychotics such as chlorpromazine, fluphenazine, haloperidol, and thioridazine; antiarrhythmics such as quinidine or propafenone; antiretrovirals such as ritonavir; antihistamines such as diphenhydramine; antimalarials such as hydroxychloroquine or quinidine; antifungals such as terbinafine.

Concomitant administration of hydralazine may inhibit presystemic metabolism of metoprolol leading to increased concentrations of metoprolol.

Antihypertensive effect of alpha-adrenergic blockers such as guanethidine, betanidine, reserpine, alpha-methyldopa or clonidine may be potentiated by beta blockers including metoprolol tartrate. Beta-adrenergic blockers may also potentiate the postural hypotensive effect of the first dose of prazosin, probably by preventing reflex tachycardia. On the contrary, beta adrenergic blockers may also potentiate the hypertensive response to withdrawal of clonidine in patients receiving concomitant clonidine and beta-adrenergic blocker.

If a patient is treated with clonidine and metoprolol tartrate concurrently, and clonidine treatment is to be discontinued, stop metoprolol tartrate several days before clonidine is withdrawn. Rebound hypertension that can follow withdrawal of clonidine may be increased in patients receiving concurrent beta-blocker treatment.

Concomitant administration with beta-blockers may enhance the vasoconstrictive action of ergot alkaloids.

In general, administration of a beta-blocker should be withheld before dipyridamole testing, with careful monitoring of heart rate following the dipyridamole injection.

If irritation of sensitivity occurs or infection appears, discontinue use and institute appropriate therapy. should be used with caution in ill, elderly, debilitated patients and children who may be more sensitive to the systemic effects of lidocaine.

Carcinogenesis, Mutagenesis, and Impairment of Fertility:

Use in Pregnancy:

Nursing Mothers:

Pediatric Use:

During or immediately after treatment, the skin at the site of treatment may develop erythema or edema or may be the locus of abnormal sensation.

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Reference

This information is obtained from the National Institute of Health's Standard Packaging Label drug database.
"https://dailymed.nlm.nih.gov/dailymed/"

While we update our database periodically, we cannot guarantee it is always updated to the latest version.

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Professional

Clonazepam Description Each single-scored tablet, for oral administration, contains 0.5 mg, 1 mg, or 2 mg Clonazepam, USP, a benzodiazepine. Each tablet also contains corn starch, lactose monohydrate, magnesium stearate, microcrystalline cellulose, and povidone. Clonazepam tablets USP 0.5 mg contain Yellow D&C No. 10 Aluminum Lake. Clonazepam tablets USP 1 mg contain Yellow D&C No. 10 Aluminum Lake, as well as FD&C Blue No. 1 Aluminum Lake. Chemically, Clonazepam, USP is 5-(o-chlorophenyl)-1,3-dihydro-7-nitro-2H-1,4-benzodiazepin-2-one. It is a light yellow crystalline powder. It has the following structural formula: C15H10ClN3O3 M.W. 315.72

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Interactions

A total of 440 drugs (1549 brand and generic names) are known to interact with Imbruvica (ibrutinib). 228 major drug interactions (854 brand and generic names) 210 moderate drug interactions (691 brand and generic names) 2 minor drug interactions (4 brand and generic names) Show all medications in the database that may interact with Imbruvica (ibrutinib).

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