Q. Are there legal drugs that I could list as taken which would cause a false positive?
A. There are more than 250 over-the-counter medications and prescription drugs that could cause a False Positive. Filling out the lab test form to include over the counter medications that cause the same positive results as the illegal drug that might be consumed would be a good idea. If a positive result occurs on the test, a basis will have been laid for an appeal. Remember that the negative error rate is just as large or larger than the positive error rate. Many people using drugs escape detection. Pain relievers such as Advil, Nuprin, Motrin, Midol, Trendar and Ibuprofen are known to cause false positives for Marijuana use. Second hand smoke inhalation from a rock concert or from being with someone who is smoking marijuana could also cause a false positive for THC. Hemp seed products, such as hemp burgers or food products containing hemp oil will also cause false positives for THC. Twelve ounces of hemp seed products ingested before a test will cause you to fail your test and has held up as a defense in at least two federal court cases. Dristan Nasal Spray, Neosynephren, Vicks Nasal Spray, Sudafed and other medications containing ephedrine or phenypropanolamine could cause a false positive reading for Amphetamines. Vicks Formula 44M containing Dextromethorphan, and Primatene-M containing perylamine as well as the pain reliever Demerol, Quinine water, poppy seeds and prescription anti-depressant Elavil will cause a false positive for opiates. Nyquil Nighttime Cold Medicine will cause a false positive for Methadone. Antibiotics such as Ampicillin and Amoxicillin will cause a false positive for cocaine. Diasepam as well as Dextromethorophan (an ingredient in some cough medicines) will cause a false positive for PCP.
Q. am interested in the Fecal Occult Blood Test which you list at $3.59. My question is: After using the test, how do I get it evaluated? Do you also do the lab work? If not, where do I send the sample and what is the fee?
A. No, you don't need to send specimen for evaluation. Developer included in the package.
Q. Last week, I ordered and received some of your Multi Drug 5 Panel Test Urine kits. Two weeks ago, my son was discovered using marijuana. He, of course, claims not to have used since, but we have discussed and agreed to implement routine testing. My question is, how soon should I begin testing? Am not sure if the use 2 weeks ago will show up now, or if any positive result would indicate more recent use. Any advise?
A. At first I recommend you always have a stock of Drug Tests and let know about it to your son. Second thing, do not test him by regular schedule. Third, you need to have also adulteration tests to look about any attempts to cheat the test. And finally, the marijuana usage appears in the urine in 12-24 hours and still detectable for slim/athletic people with light usage up to 7-8 days. For this reason maybe twice a month will be enough.
Q. How safe to pay on your web sites with a credit cards?
A. Don't worry about your personal information. Our system not allowed even see your credit card information and never stored in our server.
Q. How long does Nicotine stay in your system. We purchased a tobacco test and tested her on Friday. She was positive for nicotine use and then was positive again on Tuesday. Could this positive test on Tuesday still be a result of her smoking on Friday? What should be the amount of time between tests to not have the results be skewed?
A. It is very personal, but usually:
Nicotine is a short-acting drug that is eliminated from the body relatively quickly (i.e., within a day or so). However, the effects of acute nicotine withdrawal can be felt for as much as two weeks or more. In addition, the byproducts of nicotine can be detected in the blood for up to a month after
you stop smoking. This is only of concern if you are in a situation where someone else might want to test you for the presence of nicotine or nicotine byproducts in your system.
Most people can quit "cold turkey" without any ill effects other than feeling irritable, restless, and craving cigarettes. However, if you have any medical condition for which you are (or should be) receiving treatment, it's a good idea to check with your doctor first. He or she can also support
your efforts to quit and discuss nicotine replacement options if you choose to slowly wean yourself off nicotine.
Q. What is TCA?
A. TCA are tricyclic group of antidepressants, as exmple we will describe the NORPRAMINÂ® (desipramine hydrochloride USP).<BR>CLINICAL PHARMACOLOGY
Mechanism of Action
Available evidence suggests that many depressions have a biochemical basis in the form of a relative deficiency of neurotransmitters such as norepinephrine and serotonin. Norepinephrine deficiency may be associated with relatively low urinary 3-methoxy-4-hydroxyphenyl glycol (MHPG) levels, while serotonin deficiencies may be associated with low spinal fluid levels of 5-hydroxyindoleacetic acid.
While the precise mechanism of action of the tricyclic antidepressants is unknown, a leading theory suggests that they restore normal levels of neurotransmitters by blocking the re-uptake of these substances from the synapse in the central nervous system. Evidence indicates that the secondary amine tricyclic antidepressants, including NORPRAMIN, may have greater activity in blocking the re-uptake of norepinephrine. Tertiary amine tricyclic antidepressants, such as amitriptyline, may have greater effect on serotonin re-uptake.
NORPRAMIN (desipramine hydrochloride) is not a monoamine oxidase (MAO) inhibitor and does not act primarily as a central nervous system stimulant. It has been found in some studies to have a more rapid onset of action than imipramine. Earliest therapeutic effects may occasionally be seen in 2 to 5 days, but full treatment benefit usually requires 2 to 3 weeks to obtain.
Tricyclic antidepressants, such as desipramine hydrochloride, are rapidly absorbed from the gastrointestinal tract. Tricyclic antidepressants or their metabolites are to some extent excreted through the gastric mucosa and reabsorbed from the gastrointestinal tract. Desipramine is metabolized in the liver, and approximately 70% is excreted in the urine.
The rate of metabolism of tricyclic antidepressants varies widely from individual to individual, chiefly on a genetically determined basis. Up to a 36-fold difference in plasma level may be noted among individuals taking the same oral dose of desipramine. The ratio of 2-hydroxydesipramine to desipramine may be increased in the elderly, most likely due to decreased renal elimination with aging.
Certain drugs, particularly the psychostimulants and the phenothiazines, increase plasma levels of concomitantly administered tricyclic antidepressants through competition for the same metabolic enzyme systems. Concurrent administration of cimetidine and tricyclic antidepressants can produce clinically significant increases in the plasma concentrations of the tricyclic antidepressants. Conversely, decreases in plasma levels of the tricyclic antidepressants have been reported upon discontinuation of cimetidine, which may result in the loss of the therapeutic efficacy of the tricyclic antidepressant. Other substances, particularly barbiturates and alcohol, induce liver enzyme activity and thereby reduce tricyclic antidepressant plasma levels. Similar effects have been reported with tobacco smoke.
Research on the relationship of plasma level to therapeutic response with the tricyclic antidepressants has produced conflicting results. While some studies report no correlation, many studies cite therapeutic levels for most tricyclics in the range of 50 to 300 nanograms per milliliter. The therapeutic range is different for each tricyclic antidepressant. For desipramine, an optimal range of therapeutic plasma levels has not been established.
INDICATIONS AND USAGE
NORPRAMIN (desipramine hydrochloride) is indicated for the treatment of depression.
Desipramine hydrochloride should not be given in conjunction with, or within 2 weeks of, treatment with an MAO inhibitor drug; hyperpyretic crises, severe convulsions, and death have occurred in patients taking MAO inhibitors and tricyclic antidepressants. When NORPRAMIN (desipramie hydrochloride) is substituted for an MAO inhibitor, at least 2 weeks should elapse between treatments. NORPRAMIN should then be started cautiously and should be increased gradually.
The drug is contraindicated in the acute recovery period following myocardial infarction. It should not be used in those who have shown prior hypersensitivity to the drug. Cross-sensitivity between this and other dibenzazepines is a possibility.
Extreme caution should be used when this drug is given in the following situations:
a. In patients with cardiovascular disease, because of the possibility of conduction defects, arrhythmias, tachycardias, strokes, and acute myocardial infarction.
b. In patients with a history of urinary retention or glaucoma, because of the anticholinergic properties of the drug.
c. In patients with thyroid disease or those taking thyroid medication, because of the possibility of cardiovascular toxicity, including arrhythmias.
d. In patients with a history of seizure disorder, because this drug has been shown to lower the seizure threshold.
This drug is capable of blocking the antihypertensive effect of guanethidine and similarly acting compounds.
The patient should be cautioned that this drug may impair the mental and/or physical abilities required for the performance of potentially hazardous tasks such as driving a car or operating machinery.
In patients who may use alcohol excessively, it should be borne in mind that the potentiation may increase the danger inherent in any suicide attempt or overdosage.
It is important that this drug be dispensed in the least possible quantities to depressed outpatients, since suicide has been accomplished with this class of drug. Ordinary prudence requires that children not have access to this drug or to potent drugs of any kind; if possible, this drug should be dispensed in containers with child-resistant safety closures. Storage of this drug in the home must be supervised responsibly.
If serious adverse effects occur, dosage should be reduced or treatment should be altered.
NORPRAMIN (desipramine hydrochloride) therapy in patients with manic-depressive illness may induce a hypomanic state after the depressive phase terminates.
The drug may cause exacerbation of psychosis in schizophrenic patients.
Both elevation and lowering of blood sugar levels have been reported.
Leukocyte and differential counts should be performed in any patient who develops fever and sore throat during therapy; the drug should be discontinued if there is evidence of pathologic neutrophil depression.
Clinical experience in the concurrent administration of ECT and antidepressant drugs is limited. Thus, if such treatment is essential, the possibility of increased risk relative to benefits should be considered.
This drug should be discontinued as soon as possible prior to elective surgery because of possible cardiovascular effects. Hypertensive episodes have been observed during surgery in patients taking desipramine hydrochloride.
Q. How dangerous is PROZAC, and how possible is addiction to PROZAC?
A. Prozac Â® (fluoxetine hydrochloride) is a psychotropic drug for oral administration. CLINICAL PHARMACOLOGY
The antidepressant, antiobsessive-compulsive, and antibulimic actions of fluoxetine are presumed to be linked to its inhibition of CNS neuronal uptake of serotonin. Studies at clinically relevant doses in man have demonstrated that fluoxetine blocks the uptake of serotonin into human platelets. Studies in animals also suggest that fluoxetine is a much more potent uptake inhibitor of serotonin than of norepinephrine.
Antagonism of muscarinic, histaminergic, and (alpha) 1 -adrenergic receptors has been hypothesized to be associated with various anticholinergic, sedative, and cardiovascular effects of classical tricyclic antidepressant (TCA) drugs. Fluoxetine binds to these and other membrane receptors from brain tissue much less potently in vitro than do the tricyclic drugs.
Metabolism --Fluoxetine is extensively metabolized in the liver to norfluoxetine and a number of other unidentified metabolites. The only identified active metabolite, norfluoxetine, is formed by demethylation of fluoxetine. In animal models, S -norfluoxetine is a potent and selective inhibitor of serotonin uptake and has activity essentially equivalent to R - or S -fluoxetine. R -norfluoxetine is significantly less potent than the parent drug in the inhibition of serotonin uptake. The primary route of elimination appears to be hepatic metabolism to inactive metabolites excreted by the kidney. General
Anxiety and insomnia --In US placebo-controlled clinical trials for major depressive disorder, 12% to 16% of patients treated with Prozac and 7% to 9% of patients treated with placebo reported anxiety, nervousness, or insomnia.
In US placebo-controlled clinical trials for OCD, insomnia was reported in 28% of patients treated with Prozac and in 22% of patients treated with placebo. Anxiety was reported in 14% of patients treated with Prozac and in 7% of patients treated with placebo.
In US placebo-controlled clinical trials for bulimia nervosa, insomnia was reported in 33% of patients treated with Prozac 60 mg, and 13% of patients treated with placebo. Anxiety and nervousness were reported, respectively, in 15% and 11% of patients treated with Prozac 60 mg and in 9% and 5% of patients treated with placebo.
Among the most common adverse events associated with discontinuation (incidence at least twice that for placebo and at least 1% for Prozac in clinical trials collecting only a primary event associated with discontinuation) in US placebo-controlled fluoxetine clinical trials were anxiety (2% in OCD), insomnia (1% in combined indications and 2% in bulimia), and nervousness (1% in major depressive disorder) ( see Table 3).
Altered appetite and weight --Significant weight loss, especially in underweight depressed or bulimic patients may be an undesirable result of treatment with Prozac.
In US placebo-controlled clinical trials for major depressive disorder, 11% of patients treated with Prozac and 2% of patients treated with placebo reported anorexia (decreased appetite). Weight loss was reported in 1.4% of patients treated with Prozac and in 0.5% of patients treated with placebo. However, only rarely have patients discontinued treatment with Prozac because of anorexia or weight loss ( see also Pediatric Use under PRECAUTIONS ).
DRUG ABUSE AND DEPENDENCE
Controlled substance class --Prozac is not a controlled substance.
Physical and psychological dependence --Prozac has not been systematically studied, in animals or humans, for its potential for abuse, tolerance, or physical dependence. While the premarketing clinical experience with Prozac did not reveal any tendency for a withdrawal syndrome or any drug seeking behavior, these observations were not systematic and it is not possible to predict on the basis of this limited experience the extent to which a CNS active drug will be misused, diverted, and/or abused once marketed. Consequently, physicians should carefully evaluate patients for history of drug abuse and follow such patients closely, observing them for signs of misuse or abuse of Prozac (e.g., development of tolerance, incrementation of dose, drug-seeking behavior).
Worldwide exposure to fluoxetine hydrochloride is estimated to be over 38 million patients (circa 1999). Of the 1578 cases of overdose involving fluoxetine hydrochloride, alone or with other drugs, reported from this population, there were 195 deaths.
Among 633 adult patients who overdosed on fluoxetine hydrochloride alone, 34 resulted in a fatal outcome, 378 completely recovered, and 15 patients experienced sequelae after overdosage, including abnormal accommodation, abnormal gait, confusion, unresponsiveness, nervousness, pulmonary dysfunction, vertigo, tremor, elevated blood pressure, impotence, movement disorder, and hypomania. The remaining 206 patients had an unknown outcome. The most common signs and symptoms associated with non-fatal overdosage were seizures, somnolence, nausea, tachycardia, and vomiting. The largest known ingestion of fluoxetine hydrochloride in adult patients was 8 grams in a patient who took fluoxetine alone and who subsequently recovered. However, in an adult patient who took fluoxetine alone, an ingestion as low as 520 mg has been associated with lethal outcome, but causality has not been established.
Among pediatric patients (ages 3 months to 17 years), there were 156 cases of overdose involving fluoxetine alone or in combination with other drugs. Six patients died, 127 patients completely recovered, 1 patient experienced renal failure, and 22 patients had an unknown outcome. One of the six fatalities was a 9-year-old boy who had a history of OCD, Tourette's syndrome with tics, attention deficit disorder, and fetal alcohol syndrome. He had been receiving 100 mg of fluoxetine daily for 6 months in addition to clonidine, methylphenidate, and promethazine. Mixed-drug ingestion or other methods of suicide complicated all 6 overdoses in children that resulted in fatalities. The largest ingestion in pediatric patients was 3 grams which was non-lethal.
Other important adverse events reported with fluoxetine overdose (single or multiple drugs) include coma, delirium, ECG abnormalities (such as QT interval prolongation and ventricular tachycardia, including torsades de pointes-type arrhythmias), hypotension, mania, neuroleptic malignant syndrome-like events, pyrexia, stupor, and syncope.
Q. How dangerous drugs of abuse addiction in a workplace. How it is looks in numbers?
A. Ten percent of the U.S. workforce abuses drugs which costs employers more than $110,000,000,000,000.00 every year. Companies that lack corporate drug testing programs suffer repercussions in cost and safety including: higher employee turnover and absenteeism, workplace violence, increased on-the-job accidents, elevated employee theft and inventory shrinkage, as well as higher workers compensation rates and healthcare benefit utilization.