Albendazole (Albenza) -- FDA approved but considered investigational to treat hookworms; inhibits microtubule polymerization by binding to cytoplasmic b-tubulin; by affecting intestinal cells of parasite, prevents use of nutrients by parasite, essentially starving it to death.Dosage shown is selectively toxic to parasites because binding to parasite b-tubulin occurs at a much lower concentration than binding to mammalian protein.Because drug acts locally on worms within GI tract, action is not dictated by systemic drug concentration.In children, albendazole appears superior to mebendazole for curing hookworm infestations (cure rates of ~90% for Ancylostoma and 75% for Necator using albendazole)
Adult Dose
For classic hookworm disease and eosinophilic enteritis: 400 mg PO onceFor cutaneous larva migrans: 400 mg PO qd for 3 d
Pediatric Dose
<6>6 years: Administer as in adults
Contraindications
Documented hypersensitivity
Interactions
Coadministration with carbamazepine may decrease efficacy; dexamethasone, cimetidine, and praziquantel may increase toxicity
Pregnancy
C - Safety for use during pregnancy has not been established
Precautions
Information based on use to treat patients with hydatid disease and neurocysticercosis, for which the drug is used for prolonged periods (8-30 d for neurocysticercosis and 3 mo for hydatid disease); embryotoxic and teratogenic in pregnant rats and rabbits; no adequate studies in pregnant women, but no deleterious effects were recorded among 10 cases of women who were exposed accidentally to high doses of albendazole for systemic infection during first trimester and followed to term; excreted in animal milk; whether excreted in human milk unknownPatients with abnormal liver function tests (LFTs) should be carefully evaluated before commencing therapy because drug metabolized in liver and associated with hepatotoxicity; most common adverse effect is reversible increase in serum aminotransferases (16%); abdominal pain, diarrhea, nausea, dizziness, and headache occasionally occur (just above 1%); causes reversible reductions in total WBC count in <1% of patients
Tampilkan postingan dengan label Drugs. Tampilkan semua postingan
Tampilkan postingan dengan label Drugs. Tampilkan semua postingan
Jumat, 18 April 2008
Various Usage of Coccaine.
Chewed/eaten
Coca leaves are typically mixed with an alkaline substance (such as lime) and chewed into a wad that is retained in the mouth between gum and cheek (much in the same as chewing tobacco is chewed) and sucked of its juices. The juices are absorbed slowly by the mucous membrane of the inner cheek and by the gastrointestinal tract when swallowed. Alternatively, coca leaves can be infused in liquid and consumed like tea. Ingesting coca leaves generally is an inefficient means of administering cocaine. Advocates of the consumption of the coca leaf state that coca leaf consumption should not be criminalized as it is not actual cocaine, and consequently it is not properly the illicit drug. Because cocaine is hydrolyzed and rendered inactive in the acidic stomach, it is not readily absorbed when ingested alone. Only when mixed with a highly alkaline substance (such as lime) can it be absorbed into the bloodstream through the stomach. The efficiency of absorption of orally administered cocaine is limited by two additional factors. First, the drug is partly catabolized by the liver. Second, capillaries in the mouth and esophagus constrict after contact with the drug, reducing the surface area over which the drug can be absorbed. Nevertheless, cocaine metabolites can be detected in the urine of subjects that have sipped even one cup of coca leaf infusion. Therefore, this is an actual additional form of administration of cocaine, albeit an inefficient one.
Orally administered cocaine takes approximately 30 minutes to enter the bloodstream. Typically, only a third of an oral dose is absorbed, although absorption has been shown to reach 60% in controlled settings. Given the slow rate of absorption, maximum physiological and psychotropic effects are attained approximately 60 minutes after cocaine is administered by ingestion. While the onset of these effects is slow, the effects are sustained for approximately 60 minutes after their peak is attained.Contrary to popular belief, both ingestion and insufflation result in approximately the same proportion of the drug being absorbed: 30 to 60%. Compared to ingestion, the faster absorption of insufflated cocaine results in quicker attainment of maximum drug effects. Snorting cocaine produces maximum physiological effects within 40 minutes and maximum psychotropic effects within 20 minutes, however, a more realistic activation period is closer to 5 to 10 minutes, which is similar to ingestion of cocaine. Physiological and psychotropic effects from nasally insufflated cocaine are sustained for approximately 40 - 60 minutes after the peak effects are attained.
Insufflation
Insufflation is the most common method of ingestion of recreational powdered cocaine in the Western world. Cocaine is not inhaled using this method. The drug coats and is absorbed through the mucous membranes lining the sinuses. When insufflating cocaine, absorption through the nasal membranes is approximately 30–60%, with higher doses leading to increased absorption efficiency. Any material not directly absorbed through the mucous membranes is collected in mucus and swallowed (this "drip" is considered pleasant by some and unpleasant by others). In a study of cocaine users, the average time taken to reach peak subjective effects was 14.6 minutes. Any damage to the inside of the nose is because cocaine highly constricts blood vessels – and therefore blood and oxygen/nutrient flow – to that area.
Injected
Drug injection provides the highest blood levels of drug in the shortest amount of time. Upon injection, cocaine reaches the brain in a matter of seconds, and the exhilarating rush that follows can be so intense that it induces some users to vomit uncontrollably. In a study of cocaine users, the average time taken to reach peak subjective effects was 3.1 minutes. The euphoria passes quickly. Aside from the toxic effects of cocaine, there is also danger of circulatory emboli from the insoluble substances that may be used to cut the drug. As with all injected illicit substances, there is a risk of the user contracting blood-borne infections if sterile injecting equipment is not available or used.
Smoked
Smoking freebase or crack cocaine is most often accomplished using a pipe made from a small glass tube, often taken from "Love roses," small glass tubes with a paper rose that are promoted as romantic gifts. These are sometimes called "stems", "horns", "blasters" and "straight shooters". A small piece of clean heavy copper or occasionally stainless steel scouring pad – often called a "brillo" (actual Brillo pads contain soap, and are not used), or "chore", named for Chore Boy brand copper scouring pads, – serves as a reduction base and flow modulator in which the "rock" can be melted and boiled to vapor. In a pinch, crack smokers sometimes smoke though a soda can with small holes in the bottom instead of a crack pipe. Also, the bottoms of small glass liquor bottles can be removed, and the bottles neck can then be stuffed with chore to use as a makeshift crack pipe.Crack is smoked by placing it at the end of the pipe; a flame held close to it produces vapor, which is then inhaled by the smoker. The effects, felt almost immediately after smoking, are very intense and do not last long – usually five to fifteen minutes. In a study performed on crack cocaine users, the average time taken for them to reach their peak subjective "high" was 1.4 minutes.
Coca leaf infusions
Coca herbal infusion (also referred to as Coca tea) is used in coca-leaf producing countries much as any herbal medicinal infusion would elsewhere in the world. The free and legal commercialization of dried coca leaves under the form of filtration bags to be used as "coca tea" has been actively promoted by the governments of Peru and Bolivia for many years as a drink having medicinal powers. Visitors to the city of Cuzco in Peru, and La Paz in Bolivia are greeted with the offering of coca leaf infusions (prepared in tea pots with whole coca leaves) purportedly to help the newly-arrived traveler overcome the malaise of high altitude sickness. The effects of drinking coca tea are a mild stimulation and mood lift. It does not produce any significant numbing of the mouth nor does it give a rush like snorting cocaine. In order to prevent the demonization of this product, its promoters publicize the unproven concept that much of the effect of the ingestion of coca leaf infusion would come from the secondary alkaloids, as being not only quantitatively different from pure cocaine but also qualitatively different.
The cocaine metabolite benzoylecgonine can be detected in the urine of people a few hours after drinking one cup of coca leaf infusion.
Oral
Cocaine has been used medically and informally as an oral anesthetic. Many users rub the powder along the gum line, or onto a cigarette filter which is then smoked, which numbs the gums and teeth - hence the colloquial names of "numbies", "gummies" or "cocoa puffs" for this type of administration. This is mostly done with the small amounts of cocaine remaining on a surface after insufflation. Another oral method is to wrap up some cocaine in rolling paper and swallow it. This is sometimes called a "snow bomb."
Coca leaves are typically mixed with an alkaline substance (such as lime) and chewed into a wad that is retained in the mouth between gum and cheek (much in the same as chewing tobacco is chewed) and sucked of its juices. The juices are absorbed slowly by the mucous membrane of the inner cheek and by the gastrointestinal tract when swallowed. Alternatively, coca leaves can be infused in liquid and consumed like tea. Ingesting coca leaves generally is an inefficient means of administering cocaine. Advocates of the consumption of the coca leaf state that coca leaf consumption should not be criminalized as it is not actual cocaine, and consequently it is not properly the illicit drug. Because cocaine is hydrolyzed and rendered inactive in the acidic stomach, it is not readily absorbed when ingested alone. Only when mixed with a highly alkaline substance (such as lime) can it be absorbed into the bloodstream through the stomach. The efficiency of absorption of orally administered cocaine is limited by two additional factors. First, the drug is partly catabolized by the liver. Second, capillaries in the mouth and esophagus constrict after contact with the drug, reducing the surface area over which the drug can be absorbed. Nevertheless, cocaine metabolites can be detected in the urine of subjects that have sipped even one cup of coca leaf infusion. Therefore, this is an actual additional form of administration of cocaine, albeit an inefficient one.
Orally administered cocaine takes approximately 30 minutes to enter the bloodstream. Typically, only a third of an oral dose is absorbed, although absorption has been shown to reach 60% in controlled settings. Given the slow rate of absorption, maximum physiological and psychotropic effects are attained approximately 60 minutes after cocaine is administered by ingestion. While the onset of these effects is slow, the effects are sustained for approximately 60 minutes after their peak is attained.Contrary to popular belief, both ingestion and insufflation result in approximately the same proportion of the drug being absorbed: 30 to 60%. Compared to ingestion, the faster absorption of insufflated cocaine results in quicker attainment of maximum drug effects. Snorting cocaine produces maximum physiological effects within 40 minutes and maximum psychotropic effects within 20 minutes, however, a more realistic activation period is closer to 5 to 10 minutes, which is similar to ingestion of cocaine. Physiological and psychotropic effects from nasally insufflated cocaine are sustained for approximately 40 - 60 minutes after the peak effects are attained.
Insufflation
Insufflation is the most common method of ingestion of recreational powdered cocaine in the Western world. Cocaine is not inhaled using this method. The drug coats and is absorbed through the mucous membranes lining the sinuses. When insufflating cocaine, absorption through the nasal membranes is approximately 30–60%, with higher doses leading to increased absorption efficiency. Any material not directly absorbed through the mucous membranes is collected in mucus and swallowed (this "drip" is considered pleasant by some and unpleasant by others). In a study of cocaine users, the average time taken to reach peak subjective effects was 14.6 minutes. Any damage to the inside of the nose is because cocaine highly constricts blood vessels – and therefore blood and oxygen/nutrient flow – to that area.
Injected
Drug injection provides the highest blood levels of drug in the shortest amount of time. Upon injection, cocaine reaches the brain in a matter of seconds, and the exhilarating rush that follows can be so intense that it induces some users to vomit uncontrollably. In a study of cocaine users, the average time taken to reach peak subjective effects was 3.1 minutes. The euphoria passes quickly. Aside from the toxic effects of cocaine, there is also danger of circulatory emboli from the insoluble substances that may be used to cut the drug. As with all injected illicit substances, there is a risk of the user contracting blood-borne infections if sterile injecting equipment is not available or used.
Smoked
Smoking freebase or crack cocaine is most often accomplished using a pipe made from a small glass tube, often taken from "Love roses," small glass tubes with a paper rose that are promoted as romantic gifts. These are sometimes called "stems", "horns", "blasters" and "straight shooters". A small piece of clean heavy copper or occasionally stainless steel scouring pad – often called a "brillo" (actual Brillo pads contain soap, and are not used), or "chore", named for Chore Boy brand copper scouring pads, – serves as a reduction base and flow modulator in which the "rock" can be melted and boiled to vapor. In a pinch, crack smokers sometimes smoke though a soda can with small holes in the bottom instead of a crack pipe. Also, the bottoms of small glass liquor bottles can be removed, and the bottles neck can then be stuffed with chore to use as a makeshift crack pipe.Crack is smoked by placing it at the end of the pipe; a flame held close to it produces vapor, which is then inhaled by the smoker. The effects, felt almost immediately after smoking, are very intense and do not last long – usually five to fifteen minutes. In a study performed on crack cocaine users, the average time taken for them to reach their peak subjective "high" was 1.4 minutes.
Coca leaf infusions
Coca herbal infusion (also referred to as Coca tea) is used in coca-leaf producing countries much as any herbal medicinal infusion would elsewhere in the world. The free and legal commercialization of dried coca leaves under the form of filtration bags to be used as "coca tea" has been actively promoted by the governments of Peru and Bolivia for many years as a drink having medicinal powers. Visitors to the city of Cuzco in Peru, and La Paz in Bolivia are greeted with the offering of coca leaf infusions (prepared in tea pots with whole coca leaves) purportedly to help the newly-arrived traveler overcome the malaise of high altitude sickness. The effects of drinking coca tea are a mild stimulation and mood lift. It does not produce any significant numbing of the mouth nor does it give a rush like snorting cocaine. In order to prevent the demonization of this product, its promoters publicize the unproven concept that much of the effect of the ingestion of coca leaf infusion would come from the secondary alkaloids, as being not only quantitatively different from pure cocaine but also qualitatively different.
The cocaine metabolite benzoylecgonine can be detected in the urine of people a few hours after drinking one cup of coca leaf infusion.
Oral
Cocaine has been used medically and informally as an oral anesthetic. Many users rub the powder along the gum line, or onto a cigarette filter which is then smoked, which numbs the gums and teeth - hence the colloquial names of "numbies", "gummies" or "cocoa puffs" for this type of administration. This is mostly done with the small amounts of cocaine remaining on a surface after insufflation. Another oral method is to wrap up some cocaine in rolling paper and swallow it. This is sometimes called a "snow bomb."
Senin, 14 April 2008
Medicinal Use of Foxgloves
Medicines from foxgloves are called "Digitalin". The use of Digitalis purpurea extract containing cardiac glycosides for the treatment of heart conditions was first described by William Withering, in 1785, which is considered the beginning of modern therapeutics (Silverman) It is used to increase cardiac contractility (it is a positive inotrope) and as an antiarrhythmic agent to control the heart rate, particularly in the irregular (and often fast) atrial fibrillation. It is therefore often prescribed for patients in atrial fibrillation, especially if they have been diagnosed with heart failure.
A group of pharmacologically active compounds are extracted mostly from the leaves of the second year's growth, and in pure form are referred to by common chemical names such as digitoxin or digoxin, or by brand names such as Crystodigin and Lanoxin, respectively. The two drugs differ in that Digoxin has an additional hydroxyl group at the C-3 position on the B-ring (adjacent to the pentane). Both molecules include a lactone and a triple-repeating sugar called a glycoside.
Digitalis works by inhibiting sodium-potassium ATPase. This results in an increased intracellular concentration of sodium, which in turn increases intracellular calcium by passively decreasing the action of the sodium-calcium exchanger in the sarcolemma. The increased intracellular calcium gives a positive inotropic effect. It also has a vagal effect on the parasympathetic nervous system, and as such is used in reentrant cardiac arrhythmias and to slow the ventricular rate during atrial fibrillation. The dependence on the vagal effect means that digitalis is not effective when a patient has a high sympathetic nervous system drive, which is the case with acutely ill persons, and also during exercise.
Digitalis toxicity (Digitalis intoxication) results from an overdose of digitalis and causes anorexia, nausea, vomiting and diarrhea, as well as sometimes resulting in xanthopsia (jaundiced or yellow vision) and the appearance of blurred outlines (halos). Bradycardia also occurs. Because a frequent side effect of digitalis is reduction of appetite, some individuals have abused the drug as a weight loss aid.
Digitalis is a classic example of a drug derived from a plant formerly used by folklorists and herbalists: herbalists have largely abandoned its use because of its narrow therapeutic index and the difficulty of determining the amount of active drug in herbal preparations. Once the usefulness of digitalis in regulating pulse was understood, it was employed for a variety of purposes, including the treatment of epilepsy and other seizure disorders, now considered inappropriate.
Jumat, 11 April 2008
Coccaine
From Wikipedia, the free encyclopedia
Systematic (IUPAC) name methyl (1R,2R,3S,5S)-3- (benzoyloxy)-8-methyl-8-azabicyclo[3.2.1] octane-2-carboxylate
The word "cocaine" was made from "coca" + the suffix "-ine"; from its use as a local anaesthetic a suffix "-caine" was extracted and used to form names of synthetic local anaesthetics.
Cocaine (benzoylmethyl ecgonine) is a crystalline tropane alkaloid that is obtained from the leaves of the coca plant. The name comes from "coca" in addition to the alkaloid suffix -ine, forming cocaine. It is both a stimulant of the central nervous system and an appetite suppressant. Specifically, it is a dopamine reuptake inhibitor. Because of the way it affects the mesolimbic reward pathway, cocaine is addictive. Nevertheless, cocaine is used in medicine as a topical anesthetic, even in children, specifically in eye, nose and throat surgery.
Formula C17H21NO4; Mol. mass303.353 g/mol
Melt. point 195 °C (383 °F); Solubility in water1800 mg/mL (20 °C)
Bioavailability Oral: 33% Nasal: 19% (11%–26%)
Cocaine as a local anesthetic
Cocaine was historically useful as a topical anesthetic in eye and nasal surgery, although it is now predominantly used for nasal and lacrimal duct surgery. The major disadvantages of this use are cocaine's intense vasoconstrictor activity and potential for cardiovascular toxicity. Cocaine has since been largely replaced in Western medicine by synthetic local anaesthetics such as benzocaine, proparacaine, lignocaine/xylocaine/lidocaine, and tetracaine though it remains available for use if specified. If vasoconstriction is desired for a procedure (as it reduces bleeding), the anesthetic is combined with a vasoconstrictor such as phenylephrine or epinephrine. In Australia it is currently prescribed for use as a local anesthetic for conditions such as mouth and lung ulcers. Some ENT specialists occasionally use cocaine within the practice when performing procedures such as nasal cauterization. In this scenario dissolved cocaine is soaked into a ball of cotton wool, which is placed in the nostril for the 10-15 minutes immediately prior to the procedure, thus performing the dual role of both numbing the area to be cauterized and also vasoconstriction. Even when used this way, some of the used cocaine may be absorbed through oral or nasal mucosa and give systemic effects.
Synthesis
Synthetic cocaine would be highly desirable to the illegal drug industry, as it would eliminate the high visibility and low reliability of offshore sources and international smuggling, replacing them with clandestine domestic laboratories, as are common for illicit methamphetamine. However, natural cocaine remains the lowest cost and highest quality supply of cocaine.
Actual full synthesis of cocaine is rarely done. Formation of inactive enantiomers and synthetic by-products limits the yield and purity.
Note, names like 'synthetic cocaine' and 'new cocaine' have been misapplied to phencyclidine (PCP) and various designer drugs.
The Digitalis Toxicity
Depending on the species, the digitalis plant may contain several deadly physiological and chemically related cardiac and steroidal glycosides. Thus, the digitalis has earned several more sinister monikers: Dead Man’s Bells, and Witches’ Gloves.
The entire plant is a poison (including the roots and seeds), although the leaves of the upper stem are particularly potent, with just a nibble being enough to potentially cause death. Early symptoms of ingestion include nausea, vomiting, anorexia, diarrhea, abdominal pain, wild hallucinations, delirium, and severe headache. Depending on the severity of the toxicosis the victim may later suffer irregular and slow pulse, tremors, various cerebral disturbances, especially of a visual nature (unusual color visions with objects appearing yellowish to green, and blue halos around lights), convulsions, and deadly disturbances of the heart. For a case description, see the paper by Lacassie
There have been instances of people confusing digitalis with the harmless Symphytum (comfrey) plant (which is often brewed into a tea) with fatal consequences. Other fatal accidents involve children drinking the water in a vase containing digitalis plants. Drying does not reduce the toxicity of the plant. The plant is toxic to animals including all classes of livestock, as well as cats and dogs.
Digitalis poisoning can cause heart block and bradycardia (lowered heart rate) and tachycardia (increased heart rate). It can cause either, depending on the dose and the condition of one's heart. It should however be noted, that electric cardioversion (to "shock" the heart) is generally not indicated in ventricular fibrillation in digitalis toxicity, as it can increase the dysrhythmia in digitalis toxicity. Also, the classic drug of choice (www.erc.edu) for VF (ventricular fibrillation) in emergency setting, amiodarone (cordarone(R)) can worsen the dysrhythmia caused by digitalis, therefore, the second choice drug Lidocaine (100mg) is to be used.[citation needed]
The entire plant is a poison (including the roots and seeds), although the leaves of the upper stem are particularly potent, with just a nibble being enough to potentially cause death. Early symptoms of ingestion include nausea, vomiting, anorexia, diarrhea, abdominal pain, wild hallucinations, delirium, and severe headache. Depending on the severity of the toxicosis the victim may later suffer irregular and slow pulse, tremors, various cerebral disturbances, especially of a visual nature (unusual color visions with objects appearing yellowish to green, and blue halos around lights), convulsions, and deadly disturbances of the heart. For a case description, see the paper by Lacassie
There have been instances of people confusing digitalis with the harmless Symphytum (comfrey) plant (which is often brewed into a tea) with fatal consequences. Other fatal accidents involve children drinking the water in a vase containing digitalis plants. Drying does not reduce the toxicity of the plant. The plant is toxic to animals including all classes of livestock, as well as cats and dogs.
Digitalis poisoning can cause heart block and bradycardia (lowered heart rate) and tachycardia (increased heart rate). It can cause either, depending on the dose and the condition of one's heart. It should however be noted, that electric cardioversion (to "shock" the heart) is generally not indicated in ventricular fibrillation in digitalis toxicity, as it can increase the dysrhythmia in digitalis toxicity. Also, the classic drug of choice (www.erc.edu) for VF (ventricular fibrillation) in emergency setting, amiodarone (cordarone(R)) can worsen the dysrhythmia caused by digitalis, therefore, the second choice drug Lidocaine (100mg) is to be used.[citation needed]
How Aspirin Works
by Lucas Hoffman, MD PhD
Have you ever had a headache? Chances are you have; almost all of us do once in a while. And chances are you took some kind of medicine to ease your headache. That medicine was most likely a relative of aspirin.
You may also have taken aspirin or its relatives for other problems, like inflammation (swelling of joints or other parts of the body) or fever. But did you know that about 80 billion aspirin tablets are taken per year for these problems, as well as many others? For example, millions of people take aspirin to help prevent heart attacks. There are good reasons a doctor might say, "Take two aspirin and call me in the morning."
In this article, Dr. Luke Hoffman leads an exploration of aspirin. You will learn about the many benefits of aspirin, as well as some good reasons not to take this medication. You will also come to understand why Bayer has called aspirin "the wonder drug that works wonders."
Aspirin is a member of a family of chemicals called salicylates. These chemicals have been known to people interested in medicine for centuries.
One of the first and most influential physicians, Hippocrates, wrote about a bitter powder extracted from willow bark that could ease aches and pains and reduce fevers as long ago as the fifth century B.C. In the 1700s, the scientist Reverend Edmund Stone wrote about the success of the bark and the willow in the cure of the "agues," or fevers with aches. With a bit of chemical detective work, scientists found out that the part of willow bark that was (1) bitter and (2) good for fever and pain is a chemical known as salicin.
This chemical can be converted (changed) by the body after it is eaten to another chemical, salicylic acid. It was a pharmacist known as Leroux who showed in 1829 that salicin is this active willow ingredient, and for many years it, salicylic acid (made from salicin for the first time by Italian chemist Piria), and close relatives were used at high doses to treat pain and swelling in diseases like arthritis and to treat fever in illnesses like influenza
From : HowStuffWorks.com
Antidepressants
What are antidepressants?
Antidepressants are medicines used to help people who have depression. Most people with depression get better with treatment that includes these medicines.
How do antidepressants work?
Most antidepressants are believed to work by slowing the removal of certain chemicals from the brain. These chemicals are called neurotransmitters. Neurotransmitters are needed for normal brain function. Antidepressants help people with depression by making these natural chemicals more available to the brain.
How long will I have to take an antidepressant?
Antidepressants are typically taken for at least 4 to 6 months. In some cases, patients and their doctors may decide that antidepressants are needed for a longer time.
What are the different kinds of antidepressants?
Antidepressants are put into groups based on which chemicals in the brain they affect. There are many different kinds of antidepressants, including:
Selective serotonin reuptake inhibitors (SSRIs)
citalopram (brand name: Celexa)
escitalopram (brand name: Lexapro)
fluoxetine (brand name: Prozac)
paroxetine (brand names: Paxil, Pexeva)
sertraline (brand name: Zoloft)
These medicines tend to have fewer side effects than other antidepressants. Some of the side effects that can be caused by SSRIs include dry mouth, nausea, nervousness, insomnia, sexual problems and headache.
Tricyclics
amitriptyline (brand name: Elavil)
desipramine (brand name: Norpramin)
imipramine (brand name: Tofranil)
nortriptyline (brand name: Aventyl, Pamelor)
Common side effects caused by these medicines include dry mouth, blurred vision, constipation, difficulty urinating, worsening of glaucoma, impaired thinking and tiredness. These antidepressants can also affect a person's blood pressure and heart rate.
Serotonin and norepinephrine reuptake inhibitors (SNRIs)
venlafaxine (brand name: Effexor)
duloxetine (brand name: Cymbalta)
Some common side effects caused by these medicines include nausea and loss of appetite, anxiety and nervousness, headache, insomnia and tiredness. Dry mouth, constipation, weight loss, sexual problems, increased heart rate and increased cholesterol levels can also occur.
Norepinephrine and dopamine reuptake inhibitors (NDRIs)
bupropion (brand name: Wellbutrin)
Some of the common side effects in people taking NDRIs include agitation, nausea, headache, loss of appetite and insomnia. It can also cause increase blood pressure in some people.
Combined reuptake inhibitors and receptor blockers
trazodone (brand name: Desyrel)
nefazodone (brand name: Serzone)
maprotiline
mirtazpine (brand name: Remeron)
Common side effects of these medicines are drowsiness, dry mouth, nausea and dizziness. If you have liver problems, you should not take nefazodone. If you have seizures, you should not take maprotiline.
Monamine oxidase inhibitors (MAOIs)
isocarboxazid (brand name: Marplan)
phenelzine (brand name: Nardil)
tranlcypromine (brand name: Parnate)
MAOIs are used less commonly than the other antidepressants. They can have serious side effects, including weakness, dizziness, headaches and trembling. Taking an MAOI antidepressant while you're taking another antidepressant or certain over-the-counter medicines for colds and flu can cause a dangerous reaction. Your doctor will also tell you what foods and alcoholic beverages you should avoid while you are taking an MAOI. You should not take an MAOI unless you clearly understand what medications and foods to avoid. If you are taking an MAOI and your doctor wants you to start taking one of the other antidepressants, he or she will have you stop taking the MAOI for a while before you start the new medicine. This gives the MAOI time to clear out of your body.
Will antidepressants affect my other medicines?
Antidepressants can have an effect on many other medicines. If you're going to take an antidepressant, tell your doctor about all the other medicines you take, including over-the-counter medicines and herbal health products (such as St. John's wort). Ask your doctor and pharmacist if any of your regular medicines can cause problems when combined with an antidepressant.
by familydoctor.org editorial staff. American Academy of Family Physicians
Antidepressants are medicines used to help people who have depression. Most people with depression get better with treatment that includes these medicines.
How do antidepressants work?
Most antidepressants are believed to work by slowing the removal of certain chemicals from the brain. These chemicals are called neurotransmitters. Neurotransmitters are needed for normal brain function. Antidepressants help people with depression by making these natural chemicals more available to the brain.
How long will I have to take an antidepressant?
Antidepressants are typically taken for at least 4 to 6 months. In some cases, patients and their doctors may decide that antidepressants are needed for a longer time.
What are the different kinds of antidepressants?
Antidepressants are put into groups based on which chemicals in the brain they affect. There are many different kinds of antidepressants, including:
Selective serotonin reuptake inhibitors (SSRIs)
citalopram (brand name: Celexa)
escitalopram (brand name: Lexapro)
fluoxetine (brand name: Prozac)
paroxetine (brand names: Paxil, Pexeva)
sertraline (brand name: Zoloft)
These medicines tend to have fewer side effects than other antidepressants. Some of the side effects that can be caused by SSRIs include dry mouth, nausea, nervousness, insomnia, sexual problems and headache.
Tricyclics
amitriptyline (brand name: Elavil)
desipramine (brand name: Norpramin)
imipramine (brand name: Tofranil)
nortriptyline (brand name: Aventyl, Pamelor)
Common side effects caused by these medicines include dry mouth, blurred vision, constipation, difficulty urinating, worsening of glaucoma, impaired thinking and tiredness. These antidepressants can also affect a person's blood pressure and heart rate.
Serotonin and norepinephrine reuptake inhibitors (SNRIs)
venlafaxine (brand name: Effexor)
duloxetine (brand name: Cymbalta)
Some common side effects caused by these medicines include nausea and loss of appetite, anxiety and nervousness, headache, insomnia and tiredness. Dry mouth, constipation, weight loss, sexual problems, increased heart rate and increased cholesterol levels can also occur.
Norepinephrine and dopamine reuptake inhibitors (NDRIs)
bupropion (brand name: Wellbutrin)
Some of the common side effects in people taking NDRIs include agitation, nausea, headache, loss of appetite and insomnia. It can also cause increase blood pressure in some people.
Combined reuptake inhibitors and receptor blockers
trazodone (brand name: Desyrel)
nefazodone (brand name: Serzone)
maprotiline
mirtazpine (brand name: Remeron)
Common side effects of these medicines are drowsiness, dry mouth, nausea and dizziness. If you have liver problems, you should not take nefazodone. If you have seizures, you should not take maprotiline.
Monamine oxidase inhibitors (MAOIs)
isocarboxazid (brand name: Marplan)
phenelzine (brand name: Nardil)
tranlcypromine (brand name: Parnate)
MAOIs are used less commonly than the other antidepressants. They can have serious side effects, including weakness, dizziness, headaches and trembling. Taking an MAOI antidepressant while you're taking another antidepressant or certain over-the-counter medicines for colds and flu can cause a dangerous reaction. Your doctor will also tell you what foods and alcoholic beverages you should avoid while you are taking an MAOI. You should not take an MAOI unless you clearly understand what medications and foods to avoid. If you are taking an MAOI and your doctor wants you to start taking one of the other antidepressants, he or she will have you stop taking the MAOI for a while before you start the new medicine. This gives the MAOI time to clear out of your body.
Will antidepressants affect my other medicines?
Antidepressants can have an effect on many other medicines. If you're going to take an antidepressant, tell your doctor about all the other medicines you take, including over-the-counter medicines and herbal health products (such as St. John's wort). Ask your doctor and pharmacist if any of your regular medicines can cause problems when combined with an antidepressant.
by familydoctor.org editorial staff. American Academy of Family Physicians
Sabtu, 05 April 2008
Tetracycline
Systematic (IUPAC) name
2-(amino-hydroxy-methylidene)-4-dimethylamino-6,10,11,12a-tetrahydroxy-6-methyl 4,4a,5,5a-tetrahydrotetracene-1,3,12-trioneOR4-(dimethylamino)-1,4,4a,5,5a,6,11,12a-octahydro-3,6,10,12,12a-pentahydroxy-1,11dioxo-naphthacene-2carboxamide
Chemical data
Formula C22H24N2O8
Mol. mass 444.435 g/mol
Pharmacokinetic data
Bioavailability 60-80% Oral while fasting <40%>Metabolism Not metabolized
Half life 6-11 hours
Excretion Fecal and Renal Therapeutic considerations
Tetracycline (is a broad-spectrum polyketide antibiotic produced by the Streptomyces bacterium, indicated for use against many bacterial infections. It is commonly used to treat acne. It is sold under the brand names Sumycin, Terramycin, Tetracyn, and Panmycin, among others. Actisite is a thread-like fiber form, used in dental applications. It is also used to produce several semi-synthetic derivatives, which together are known as the Tetracycline antibiotic group.
It works by inhibiting action of the prokaryotic 30S ribosome, by binding aminoacyl-tRNA. However, bacteria strains can aquire resistance against tetracycline and its derivates by encoding a resistance operon.
In eukaryotic cells, toxicity may be result of inactivation of mitochondrial 30S ribosomes.
History
The tetracyclines are a large family of antibiotics that were discovered as natural products by Benjamin Minge Duggar and first described in 1948.[1] Tetracycline was then discovered by Lloyd Conover in the research departments of Pfizer. The patent for tetracycline, U.S. Patent 2,699,054 , was first issued in 1950. However, Nubian mummies have been studied in the 1990s and were found to contain significant levels of tetracycline; there is evidence that the beer brewed at the time could have been the source.[2] Tetracycline sparked the development of many chemically altered antibiotics and in doing so has proved to be one of the most important discoveries made in the field of antibiotics. It is used to treat many gram-positive and gram-negative bacteria and some protozoa.
Cautions, contraindications, side effects
Are as those of the tetracycline antibiotics group:
Can stain developing teeth (even when taken by the mother during pregnancy)
Inactivated by Ca2+ ion, not to be taken with milk or yogurt
Inactivated by aluminium, iron and zinc, not to be taken at the same time as indigestion remedies
Inactivated by common antacids and over-the-counter heartburn medicines.
Skin photosensitivity; exposure to the Sun or intense light is not recommended
Drug-induced lupus, and hepatitis
Tinnitus
When used for acne vulgaris, skin can be extremely dry and flaky if overused
May interfere with methotrexate by displacing it from the various protein binding sites
Indication
Tetracycline's primary use is for the treatment of acne vulgaris and rosacea.
It is also used to treat a very wide range of infections; see tetracycline antibiotics for details.
Other uses
Since tetracycline is absorbed into bone, it is used as a marker of bone growth for biopsies in humans, and as a biomarker in wildlife to detect consumption of medicine- or vaccine-containing baits.[3] The presence of tetracycline in bone is detected by its fluorescence.[4]
From : Wikipedia
2-(amino-hydroxy-methylidene)-4-dimethylamino-6,10,11,12a-tetrahydroxy-6-methyl 4,4a,5,5a-tetrahydrotetracene-1,3,12-trioneOR4-(dimethylamino)-1,4,4a,5,5a,6,11,12a-octahydro-3,6,10,12,12a-pentahydroxy-1,11dioxo-naphthacene-2carboxamide
Chemical data
Formula C22H24N2O8
Mol. mass 444.435 g/mol
Pharmacokinetic data
Bioavailability 60-80% Oral while fasting <40%>Metabolism Not metabolized
Half life 6-11 hours
Excretion Fecal and Renal Therapeutic considerations
Tetracycline (is a broad-spectrum polyketide antibiotic produced by the Streptomyces bacterium, indicated for use against many bacterial infections. It is commonly used to treat acne. It is sold under the brand names Sumycin, Terramycin, Tetracyn, and Panmycin, among others. Actisite is a thread-like fiber form, used in dental applications. It is also used to produce several semi-synthetic derivatives, which together are known as the Tetracycline antibiotic group.
It works by inhibiting action of the prokaryotic 30S ribosome, by binding aminoacyl-tRNA. However, bacteria strains can aquire resistance against tetracycline and its derivates by encoding a resistance operon.
In eukaryotic cells, toxicity may be result of inactivation of mitochondrial 30S ribosomes.
History
The tetracyclines are a large family of antibiotics that were discovered as natural products by Benjamin Minge Duggar and first described in 1948.[1] Tetracycline was then discovered by Lloyd Conover in the research departments of Pfizer. The patent for tetracycline, U.S. Patent 2,699,054 , was first issued in 1950. However, Nubian mummies have been studied in the 1990s and were found to contain significant levels of tetracycline; there is evidence that the beer brewed at the time could have been the source.[2] Tetracycline sparked the development of many chemically altered antibiotics and in doing so has proved to be one of the most important discoveries made in the field of antibiotics. It is used to treat many gram-positive and gram-negative bacteria and some protozoa.
Cautions, contraindications, side effects
Are as those of the tetracycline antibiotics group:
Can stain developing teeth (even when taken by the mother during pregnancy)
Inactivated by Ca2+ ion, not to be taken with milk or yogurt
Inactivated by aluminium, iron and zinc, not to be taken at the same time as indigestion remedies
Inactivated by common antacids and over-the-counter heartburn medicines.
Skin photosensitivity; exposure to the Sun or intense light is not recommended
Drug-induced lupus, and hepatitis
Tinnitus
When used for acne vulgaris, skin can be extremely dry and flaky if overused
May interfere with methotrexate by displacing it from the various protein binding sites
Indication
Tetracycline's primary use is for the treatment of acne vulgaris and rosacea.
It is also used to treat a very wide range of infections; see tetracycline antibiotics for details.
Other uses
Since tetracycline is absorbed into bone, it is used as a marker of bone growth for biopsies in humans, and as a biomarker in wildlife to detect consumption of medicine- or vaccine-containing baits.[3] The presence of tetracycline in bone is detected by its fluorescence.[4]
From : Wikipedia
Kamis, 03 April 2008
Ampicillin
Systematic (IUPAC) name
7-(2-amino-2-phenyl-acetyl)amino-3 ,3-dimethyl-6-oxo-2-thia-5-azabicyclo [3.2.0]heptane-4-carboxylic acid
Formula C16H19N3O4S
Mol. mass 349.406 g/mol
Pharmacokinetic data
Protein binding 15 to 25%
Protein binding 15 to 25%
Metabolism 12 to 50%
Half life approx 1 hour
Excretion 75 to 85% renal
Bioavailability 40% (oral)
Ampicillin is a beta-lactam antibiotic that has been used extensively to treat bacterial infections since 1961. It is considered part of the aminopenicillin family and is roughly equivalent to amoxicillin in terms of spectrum and level of activity.[1] It can sometimes result in allergic reactions that range in severity from a rash (e.g. patients with mononucleosis) to potentially lethal anaphylaxis.
Mechanism of action
Belonging to the penicillin group of beta-lactam antibiotics, ampicillin is able to penetrate Gram-positive and some Gram-negative bacteria. It differs from penicillin only by the presence of an amino group. That amino group helps the drug penetrate the outer membrane of gram-negative bacteria. Ampicillin acts as a competitive inhibitor of the enzyme transpeptidase. Transpeptidase is needed by bacteria to make their cell walls.[1] It inhibits the third and final stage of bacterial cell wall synthesis, which ultimately leads to cell lysis.
All Pseudomonas and most strains of Klebsiella and Aerobacter are considered resistant.
Use in research
Ampicillin is often used as a selective agent in molecular biology to confirm the uptake of genes (e.g., of plasmids) by bacteria (e.g., E. coli). A gene that is to be inserted into a bacterium is coupled to a gene coding for an ampicillin resistance (in E. coli, usually the bla (TEM-1) gene, coding for β-lactamase). The treated bacteria are then grown on a medium containing ampicillin. Only the bacteria that successfully take up the desired genes become ampicillin resistant, and therefore contain the other desired gene as well. It can be used with Cloaxicillin as well.
From : Wikipedia
7-(2-amino-2-phenyl-acetyl)amino-3 ,3-dimethyl-6-oxo-2-thia-5-azabicyclo [3.2.0]heptane-4-carboxylic acid
Formula C16H19N3O4S
Mol. mass 349.406 g/mol
Pharmacokinetic data
Protein binding 15 to 25%
Protein binding 15 to 25%
Metabolism 12 to 50%
Half life approx 1 hour
Excretion 75 to 85% renal
Bioavailability 40% (oral)
Ampicillin is a beta-lactam antibiotic that has been used extensively to treat bacterial infections since 1961. It is considered part of the aminopenicillin family and is roughly equivalent to amoxicillin in terms of spectrum and level of activity.[1] It can sometimes result in allergic reactions that range in severity from a rash (e.g. patients with mononucleosis) to potentially lethal anaphylaxis.
Mechanism of action
Belonging to the penicillin group of beta-lactam antibiotics, ampicillin is able to penetrate Gram-positive and some Gram-negative bacteria. It differs from penicillin only by the presence of an amino group. That amino group helps the drug penetrate the outer membrane of gram-negative bacteria. Ampicillin acts as a competitive inhibitor of the enzyme transpeptidase. Transpeptidase is needed by bacteria to make their cell walls.[1] It inhibits the third and final stage of bacterial cell wall synthesis, which ultimately leads to cell lysis.
All Pseudomonas and most strains of Klebsiella and Aerobacter are considered resistant.
Use in research
Ampicillin is often used as a selective agent in molecular biology to confirm the uptake of genes (e.g., of plasmids) by bacteria (e.g., E. coli). A gene that is to be inserted into a bacterium is coupled to a gene coding for an ampicillin resistance (in E. coli, usually the bla (TEM-1) gene, coding for β-lactamase). The treated bacteria are then grown on a medium containing ampicillin. Only the bacteria that successfully take up the desired genes become ampicillin resistant, and therefore contain the other desired gene as well. It can be used with Cloaxicillin as well.
From : Wikipedia
Langganan:
Postingan (Atom)
