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Tuesday 26 June 2012

Tramadol is use for treating

Though some painkillers may bring alternative side effects which are harmful to the general health, people go for this option frequently as this gives rapid solution. Tramadol is such a medication for reducing pain. Tramadol is an efficient analgesic whose mode of actions is quite identical to those of the narcotics. Tramadol is the generic of an analgesic whose brand name ultram. The IUPAC name of Tramadol is rac-(1R, 2R)-2-(dimethylaminomethyl)-1-(3-methoxyphenyl)-cyclohexanol. 

Tramadol is use for treating moderate to rigorous pain of different sources. Some pain may natural part of life and need to take proper care to handle and get relief. And some cases of pain may be so strong that it becomes hard to manage and handle. Taking Tramadol like painkillers is the only solution in such cases. Pain management and eradicating is an essential thing for enjoying the healthy life at fullest without unnecessary sufferings. Pain offers only negative effects on life retarding the body strength, mental stamina and overall peace and general health of us. 
Tramadol is the synthetic typical opioids use for treating severe to moderate pains. Tramadol possesses potential actions on the noradrenergic GABAergic, and serotonergic systems of the body. Tramadol is the precious gift of the German pharmaceutical company GrĂ¼nenthal GmbH to the mankind for eliminating pain and this analgesic is marketed under Tramal trade name. Tramadol is offered in both intravenous and intramuscular forms that can be injected to veins and muscles respectively. Tramadol is also available in oral preparations. 

Tramadol is found as Tramadol hydrochloride (hydrochloride salt) that is traded with brad name of Ultram in the United States of America. Ultracet is another form of Tramadol obtainable in juxtaposition with acetaminophen as. The dosage of Tramadol consumption varies with degree of pain occurred in the patient. Tramadol is more or less 10% as effective as morphine, when injected by IV/IM route whereas oral dosage ranges from 50 to 400 mg daily and even up to 600 mg daily in certain severe cases. 
Tramadol endure hepatic metabolism by way of the cytochrome P450 isozyme CYP2D6, as it is O- and N-demethylated to five particular metabolites. The most adverse drug reactions of Tramadol include vomiting, nausea, Drowsiness, Respiratory depression, and sweating. Though many physicians are referring Tramadol of pain relief in many cases then too the Prescribing Information of Ultram informs that Tramadol "may encourage physical and psychological dependence of morphine-type."

Saturday 23 June 2012

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Tramadol Tablets



Tramadol Tablets

We are engaged in manufacturing and supplying of Tramadol Tablets across the country. Tramadol is a man-made (synthetic) analgesic (pain reliever). Its exact mechanism of action is unknown but is similar to morphine. Like morphine, tramadol binds to receptors in the brain (opioid receptors) that are important for transmitting the sensation of pain throughout the body. Tramadol, like other narcotics used for the treatment of pain, may be abused. Tramadol is not a nonsteroidal anti-inflammatory drug (NSAID) and does not have the increased risk of stomach ulceration and internal bleeding that can occur with NSAIDs.

Prparation
  • ALTRAMA- 100 - 100mg.
  • ALTRADOL-P - 50mg. + Paracetamol 500 mg.

Pack Size : 10 x 10

Packing : Blister

ultram synthetic opioid


developed by the German pharmaceutical company GrĂ¼nenthal GmbH in the late 1970s. Ultiva (Generic name - Remifentanil) OnLine Information - Ultiva (marketed by Abbott as Ultiva®) is a potent ultra short-acting synthetic opioid analgesic drug. It is given to . Dextromethorphan (the stereoisomer of levomethorphan, a semi-synthetic opioid agonist) and its ultram synthetic opioid . Retrieved 10 March 2012. ↑ "Ultram brand of TRAMADOL HYDROCHLORIDE" www.opiods.com ULTRAM ER is a centrally acting synthetic opioid analgesic. Although its mode of action is not completely understood, from animal tests, at least two complementary mechanisms . Tell me what you know about Alfentanil (the hydrochloride salt form of alfentanil, an ultra short-acting, synthetic, opioid agonist with analgesic and local anesthesia . Return. Alfentanil hydrochloride. The hydrochloride salt form of alfentanil, an ultra short-acting, synthetic, opioid agonist with analgesic and local anesthesia enhancing . Ultram Information. Ultram is a brand name for the drug Tramadol. Tramadol is a synthetic opioid and was developed by . ultram synthetic opioid ULTRAM is a centrally acting synthetic opioid analgesic. Although its mode of action is not completely understood, from animal tests, at least two comple mentary mechanisms appear . Tramadol hydrochloride (Ultram, Tramal) is a centrally acting synthetic opioid analgesic used in treating severe pain. The drug has a wide range of applications, including . ULTRAM ER is a centrally acting synthetic opioid analgesic. Although its mode of action is not completely understood, from animal tests, at least two complementary My wife was put into jail due to a failed urine test and all that she has had is Ultram. Remifentanil (marketed by GlaxoSmithKline and Abbott as Ultiva) is a potent ultra short-acting synthetic opioid analgesic drug. It is given to patients during surgery to relieve . ULTRAM ER, a nonscheduled centrally acting synthetic opioid analgesic, is the first US Food and Drug Administration (FDA)-approved, extended-release . ULTRAM contains tramadol, a centrally acting synthetic opioid analgesic. Although its mode of action is not completely understood, from animal tests, at least two complementary .


Mechanism of action

Simplified model of NMDAR activation and various types of NMDAR blockers.
The NMDA receptor is an ionotropic receptor that allows for the transfer of electrical signals between neurons in the brain and in the spinal column. For electrical signals to pass, the NMDA receptor must be open. To remain open, glutamate and glycine must bind to the NMDA receptor. An NMDA receptor that has glycine and glutamate bound to it and has an open ion channel is called "activated."
Chemicals that deactivate the NMDA receptor are called antagonists. NMDAR antagonists fall into four categories: Competitive antagonists, which bind to and block the binding site of the neurotransmitter glutamate; glycine antagonists, which bind to and block the glycine site; noncompetitive antagonists, which inhibit NMDARs by binding to allosteric sites; and uncompetitive antagonists, which block the ion channel by binding to a site within it

Examples

Competitive antagonists

  • AP5 (APV, R-2-amino-5-phosphonopentanoate)
  • AP7 (2-amino-7-phosphonoheptanoic acid)
  • CPPene (3-[(R)-2-carboxypiperazin-4-yl]-prop-2-enyl-1-phosphonic acid)
  • Selfotel: an anxiolytic, anticonvulsant but with possible neurotoxic effects.

Uncompetitive channel blockers

  • Amantadine: used for treating Parkinson's disease and influenza and Alzheimer's.
  • Dextrallorphan: a more potent analogue of dextromethorphan.
  • Dextromethorphan: a common antitussive found in cough medicines.
  • Dextrorphan: active metabolite of dextromethorphan.
  • Dizocilpine (MK-801): an experimental drug used in scientific research.
  • Ethanol: also known as alcohol, a widely used legal intoxicant.
  • Eticyclidine: a Schedule I controlled substance in the United States.
  • Gacyclidine: an experimental drug developed for neuroprotection.
  • Ibogaine: a Schedule I controlled substance in the United States
  • Magnesium
  • Memantine: treatment for Alzheimer's disease.
  • Methoxetamine: a novel designer drug sold on the internet.[citation needed]
  • Nitrous oxide: used for anesthesia, particularly in dentistry.
  • Phencyclidine: a Schedule II controlled substance in the United States.
  • Rolicyclidine: a Schedule I controlled substance in the United States.
  • Tenocyclidine: a Schedule I controlled substance in the United States.
  • Methoxydine: 4-meo-pcp
  • Tiletamine: an animal anesthetic.
  • Xenon: an anesthetic.
  • Neramexane: a memantine analogue with nootropic, antidepressant properties. Also a nicotinic acetylcholine antagonist.
  • Eliprodil: an anticonvulsant with neuroprotective drug.
  • Etoxadrol: a potent dissociative similar to PCP.
  • Dexoxadrol: similar to etoxadrol.
  • WMS-2539: potent fluorinated derivative of dexoxadrol.
  • NEFA: a moderate affinity antagonist.
  • Remacemide: a low affinity antagonist also a sodium-channel blocker.
  • Delucemine: also a SSRI with neuroprotective properties.
  • 8A-PDHQ: a high affinity PCP structural analogue.

The mechanism of action

Opioid analgesics : The mechanism of action

opioid mechanismInteractions with one or more subtypes of opioid receptors, in example mu-, delta-, kappa-, sigma and epsilon at supraspinal, spinal and peripheral levels, causing analgesia, and many other effects. Opioid analgesics can be full agonists of opioid receptors, namely μ (mu)-receptor partial μ-agonist and mixed agonist-antagonists have opposite effects.



Opioids act by:


• presynaptic inhibition of production of neurotransmitters C-fiber endings,
• postsynaptic suppression of evoked activity in nociceptive path or remove the remaining parts of the regulation of inhibition of nociceptive impulses.
• increased transmission of the descending inhibition of spinal nociceptive conduction.

tramadol mechanism of action

It is an atypical opioid which is a centrally acting analgesic, used for treating moderate to severe pain. Its exact mechanism of action is unknown but is thought to be similar . Tramadol hydrochloride (trademarked as Conzip, Ryzolt, Ultracet, Ultram in the USA,Ralivia in Canada) is a centrally acting synthetic analgesic used to treat moderate to . Tramadol Mechanism Of Action articles, reference materials. Need more on Tramadol Mechanism Of Action? We suggest these original texts: The Story of Tramadol Mechanism Of . Opioid and nonopioid components independently contribute to the mechanism of action of tramadol, an 'atypical' opioid analgesic. While the mechanism of action of Ultram is not completely known, it is believed to work through modulation of
the noradrenergic and serotonergic systems in Mechanism of action. Tramadol acts as a ?-opioid receptor agonist, [50] [51] serotonin releasing agent, [3] [4] [52] [53] norepinephrine reuptake inhibitor, [51] NMDA receptor antagonist, [54] 5 . Mechanism of Action The mechanism of action exerted by Neurontin (gabapentin) is unknown. Gabapentin is structurally related to the neurotransmitter GABA, but i. Mechanism of action The mode of action of tramadol has yet to be fully understood, but it is believed to work through modulation of the noradrenergic and serotonergic systems in . Vorlage:Infobox Chemikalie/Summenformelsuche vorhanden. Tramadol ist ein vollsynthetischer Arzneistoff aus der Gruppe der Opioide und wird zur Behandlung mĂ¤ĂŸig starker bis . TRICYCLIC COMPOUNDS; CARBAMAZEPINE/TAPENTADOL; TRAMADOL. MECHANISM OF ACTION Tramadol and tricyclic compounds, including carbamazepine, may lower the seizure threshold.(1 . 2 Mechanism of action; 3 Metabolism; 4 Adverse effects; 5 Pregnancy and breastfeeding . The mode of action of tramadol has yet to be fully understood, but it is believed to work . Tramadol mechanism of action, side effects. Tramadol compared to other analgesics. Tramadol acts as a μ-opioid receptor agonist, serotonin releasing agent, norepinephrine reuptake inhibitor, NMDA receptor antagonist, 5-HT 2C receptor antagonist, (α7) 5 . TRAMADOL (9/20/10) Classification Analgesics Dosage, Timing, Route 50mg IVTT q 8hrs Indication Moderate to moderately severe pain Mechanism of Action tramadol mechanism of action 1. J Pharmacol Exp Ther. 1992 Jan;260(1):275-85. tramadol mechanism of action Opioid and nonopioid components independently contribute to the mechanism of action of tramadol, an 'atypical' opioid analgesic.

Tramadol opioid receptors

Gillen, C., M. Haurand, D. J. Kobelt, and S. Wnendt, 2000, "Affinity, potency and efficacy of tramadol and its metabolites at the cloned human mu-opioid receptor," Naunyn . Tramadol's primary active metabolite, O-desmethyltramadol, is a considerably more potent μ-opioid receptor agonist than tramadol tramadol opioid receptors itself, and is so much more so . 1. Eur J Pharmacol. 1996 Dec 5;316(2-3):369-72. Tramadol, M1 metabolite and enantiomer affinities for cloned human opioid receptors expressed in transfected HN9.10 . Opioid Receptors: What are the mechanisms of opioid-induced respiratory depression . components independently contribute to the mechanism of action of tramadol, an 'atypical' opioid . Tramadol is effective in the management of pain (8), although the affinity of tramadol to opioid μ-receptors makes it less ideal than morphine and/or peptide-like agonists . Tramadol acts as a μ-opioid receptor agonist, serotonin releasing agent, norepinephrine reuptake inhibitor, NMDA receptor antagonist, 5-HT2C receptor antagonist,(α7)5 . However, the low affinity of tramadol for opioid receptors – 60-fold less than d-propoxyphene and 10-fold less than codeine (Raffa et al., 1992) – and the minimal withdrawal . Tramadol's primary active metabolite, O-desmethyltramadol, is a considerably more potent μ-opioid receptor agonist than tramadol itself. Thus, tramadol is in part a prodrug to O . The contribution of non-opioid activity is demonstrated by the analgesic effects of tramadol not being fully antagonised by the μ-opioid receptor antagonist naloxone. Opioide (von gr. ὄπιον [ˈɔpiÉ”n] und εἶδος, . wodurch ein komplexes Wirkmuster entsteht (multiple receptor . Tramadol: 0,1-0,2: 240! 4 h: Agonist: nicht . . mixed mode of action that also counteracts neuropathic pain, particularly tramadol or . Each group of opioid receptors elicits a distinct set of neurological responses, with the . Tramadol acts as a ?-opioid receptor agonist, [50] [51] serotonin releasing agent, [3] [4] [52] [53] norepinephrine reuptake

tramadol opioid receptors

inhibitor, [51] NMDA receptor antagonist, [54] 5-HT 2C receptor . 1. Anesthesiology. 2003 Feb;98(2):420-7. Respiratory depression by tramadol in the cat: involvement of opioid receptors. Teppema LJ, Nieuwenhuijs D, Olievier CN, Dahan A. Opioid Narcotics: Tramadol . MLWhitworth, MD Feb 2012. Classification: Weak narcotic . Receptors: Weak mu opioid receptor agonist with second mechanism of action probably . der Orphan-Rezeptor (ORL fĂ¼r opioid receptor like) ist ebenfalls eine jĂ¼ngere Entdeckung; der σ-Rezeptor wird heute nicht mehr zu den Opioidrezeptoren gezählt.

Saturday 2 June 2012

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Wish List


Wish List
We want to make sure the families have what they need to make their stay as comfortable as possible.  Just like any other House, we need items but in bigger quantities.
Conduct a wish list drive at your school, work place or church to help the Houses in their every day needs
High needed items (marked in red much needed)
  • Lightbulbs (40 watts)
  • White or copy paper
  • Stamps
  • Trash bags
  • Laundry detergent
  • Pack and Play (portable cribs)
  • Alarm Clocks for the bedrooms (28)
  • Clorox
  • Desinfecting products
  • Hand sanitizer or sanitizer wipes
  • Cleaning products (Fantastik, Windex, Comet)
  • Napkins
  • Plastic forks, knifes and spoons
  • Disposable plates
  • Paper towels
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    Description:

    Once it concerns body pain, one of the most beneficial ways of addressing it is to discover an effective alleviation that could provide you with immediate results. Tramadol, a well-known pain pill, mostly prescribed to patients who suffer from modest to acute pain. Tramadol as a pill is actually a semisynthetic agent as 4-phenyl-piperidine analog of codeine. That peculiar medication is also known to function like a morphia.

    For Tramadol to assist you getting rid of the pain, it acts by crossing the brain sense organs which are responsible for transmitting the message of pain in the physical structure. It's safe to take that medication once it's used for short time periods and under the doctor's direction. A lot of health professionals suggest that that medication should only be used during emergency conditions and for modest to acute pain only.

    Action:

    This medicinal drug is administrated to relieve modest pain. It's similar to narcotic pain drugs. It acts on particular nerves in the head that manage how you feel pain. Apart from pain control, Tramadol can as well be taken by people who have chronic pain conditions or by sick people who just had dental surgical operation. Tramadol could also assist alleviating the pain brought by sick headache, sprains, bust ligaments, habitual pain, acute back pain, carcinoma pain and a whole lot more. With all the following data, you'll decidedly have an idea on what Tramadol is and what it could do to the physical structure.

    Taking Soma

    Use the remedy orally with or with no food as prescribed by the health care provider. If you've got sickness, you could take that medication with food. Confer with your health care provider or druggist about other directions to minify sickness (e.g., antihistamines, resting one to two hours with as little head motion as possible).

    The dose is based on the health disorder and reaction to therapy. To alleviate the danger of side effects, your health care provider may tell you to step by step multiply your dosage when commencing Tramadol.

    The max suggested dosage is four hundred milligrams daily. If you've got serious renal disorders (for instance, if you're on dialysis), the max suggested dosage is a hundred milligrams each twelve hours. If you've got grievous liver ailment (for instance, cirrhosis of the liver), the max suggested dosage is fifty milligrams each twelve hours. If you're older than seventy-five years, the max suggested dosage is three hundred milligrams daily.

    Pain drugs act best if they're taken as the first symptoms of pain (or sick headache) happen. If you delay till the pain has aggravated, the remedy may not act as well. Observe your doctor's or pharmacist's direction for the safe usage of non-narcotic pain allayers (e.g., Panadol, Motrin). Ask the health care provider or druggist for more inside information concerning your therapy.

    That remedy might induce withdrawal responses, peculiarly if it has been taken on a regular basis for a while or in high dosages. In such disorders, secession symptoms (such as anxiousness, perspiring, insomnia, shaking, looseness of the bowels, fast respiring) might happen if you abruptly cease using that remedy. To foreclose secession responses, your health care provider may reduce your dosage step by step. Besides, if you're using regular dosages of narcotic drugs for ongoing pain (for instance, carcinoma pain), starting Tramadol might induce a withdrawal response. Consult your health care provider or druggist for more details, and report any drug withdrawal reactions instantly.

    Seldom, abnormal drug- searching demeanor (dependency) is possible with that remedy. Don't multiply your dosage, take it more often, or take it for a longer time than administrated. Decently stop the medication once so directed.

    List of drugs included in the TCAs class


    Tertiary Amines
    Amitriptyline (Elavil, Endep, Vanatrip)
    Imipramine (Tofranil)
    Clomipramine (Anafranil)
    Doxepin (Adapin)
    Butriptyline (Evadene, Evadyne)
    Dosulepin (Prothiade)
    Lofepramine (Feprapax, Gamanil, Lomont)
    Trimipramine (Surmontil)
    Secondary Amines
    Desipramine (Norpramin, Pertofrane)
    Nortriptyline (Aventyl, Nortrilen, Pamelor)
    Protriptyline (Vivactil)

    List of SNRIs

    Venlafaxine (Effexor XR, Effexor)
    Desvenlafaxine (Pristiq)
    Duloxetine(Cymbalta)

    Mind map of TCAs and SNRI pharmacological properties

    serotonin-norepinephrine-reuptake-inhibitors-tricyclic-antidepressants

    Diseases Treated With Tricyclic antidepressant


    List of diseases, sicknesses, maladies or medical conditions cured, healed or treated by Tricyclic antidepressant. List includes any and all diseases, viruses, chronic and non-chronic disorders that can be treated or cured by Tricyclic antidepressant. This list of what diseases are cured by Tricyclic antidepressant or treated by Tricyclic antidepressant is sorted alphabetically and can be sorted by any column. The major illnesses that require Tricyclic antidepressant treatment are listed below along with symptoms that may be healed by Tricyclic antidepressant. (8 Items)

    Differences between tricyclic antidepressants and SNRIs mechanism of action



    Serotonin-norepinephrine reuptake inhibitors are a class of drugs used for the treatment of depression in patients in whom SSRIs are ineffective. Since they have little activity on  histaminic, muscarinic and alpha 1postsynaptic receptors; they lack of most of tricyclic antidepressants (TCAs) side effects .
    Note: the terms Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs) and Selective Serotonin-Norepinephrine Reuptake Inhibitors (SSNRIs) are used interchangeably in this text.

    Serotonin norepinephrine reuptake inhibitors and tricyclic antidepressants share aspects of their mechanism of action

    5- HT (serotonin) and norepinephrine (noradrenaline) are released from the nerve terminal to the synaptic cleft and bind to post-synaptic receptors. Drugs like venlafaxine, duloxetine, and the newer desvenlafaxine – all of them Serotonin-Norepinephrine Reuptake Inhibitors- block proteins in the pre-synaptic neuron that act as re-uptakers. This increases the concentration of both neurotransmitters at the synaptic cleft.
    Drug_SNRI
    Image Source:
    Tricyclic antidepressants (TCAs) are an important group of antidepressants in clinical practice; this drug class includes imipramine, amitriptyline, clomipramine, and desipramine. The main pharmacological effect on presynaptic 5-HT and norepinephrine receptors is the same that SNRIs. This is, they block the reuptake protein that acts as transporter in the nerve terminal. TCAs have very little effect on dopamine reuptake.
    Drug Uptake inhibition

    Norepinephrine Serotonin
    Selective serotonin re-uptake inhibitor

    Fluoxetine none ++++
    Selective serotonin/norepinephrine re-uptake inhibitor:


    Venlafaxine ++ ++++
    Duloxetine ++++ ++++
    Tricyclic antidepressant

    Imipramine ++++ +++
    From: Lippincott Illustrated reviews: Pharmacology, 4ed. Lippincott Williams and Wilkins.

    TCAs adverse effects are determined by they blockade on cholinergic, adrenergic and histamine transmission

    What gives TCAs a different adverse effects profile is their ability to block muscarinic, alpha 1 adrenergic and histamine H1 receptors. The blockade of these receptors gives as a result:
    Anticholinergic (atropine-like) effects: blurred vision, xerostomia, urinary retention, constipation and narrow angle glaucoma.
    Sympatholytic effects (alpha 1 blockade): postural hypotension, dizziness and reflex tachicardia.
    Histamine (H1) antagonism: sedation.
    Image source: CNSforum.com
    Image source:

    Mechanism in pain modulation

    As the title of the image below explains, multiple neurotransmitters modulate pain processing in the spinal cord. Pain is only in part modulated by 5-HT (serotonin) and norepinephrine (NE). In adition, there are higher centers involved in pain processing ( periaqueductal grey matter, nucleus raphe magnus, thalamus and the brain cortex itself) that are not shown in the picture.

    Tricyclic Antidepressants

    About Tricyclic Antidepressants

    Tricyclic antidepressants (TCAs) are an old class of antidepressive drugs, much older than Prozac and other SSRIs. The first TCA imipramine was discovered back in the 1950s, when psychopharmacology was still a new science. The name "tricyclic" comes from their molecular structure which contains three rings of atoms.

    The TCAs are effective antidepressants, but because they tend to cause more side effects than newer drugs, they are rarely used to treat depression any more. They are, however, still commonly used in the treatment of chronic pain, sleep disorders and some other conditions, usually in doses much smaller than would be used for depression.

    The SSRIs are fairly selective for serotonin, as their name, selective serotonin reuptake inhibitors, implies. TCAs on the other hand are far from selective. They increase brain levels of serotonin, but also norepinephrine (noradrenaline). In addition they block histamine receptors, muscarinic acetylcholine receptors and alpha adrenergic receptors and have some other actions.

    How TCAs work
    Tricyclic antidepressants (TCAs) inhibit the reabsorption (reuptake) of serotonin and norepinephrine by brain cells. To a lesser extent, TCAs also inhibit reabsorption of dopamine. These antidepressants also block other cell receptors, which accounts for many of their side effects. TCAs are called tricyclic because of their chemical structure. They were among the earliest antidepressants developed and remained the first line of treatment for depression before newer antidepressants arrived.

    Image and video hosting by TinyPic

    Antidepressants, in general, may also work by playing a neuroprotective role in how they relieve anxiety and depression. It's thought that antidepressants may increase the effects of brain receptors that help nerve cells keep sensitivity to glutamate — an organic compound of a nonessential amino acid — in check. This increased support of nerve cells lowers glutamate sensitivity, providing protection against the glutamate overwhelming and exciting key brain areas related to anxiety and depression.

    Therapeutic effects of antidepressants may vary in people, due in part to each person's genetic makeup. It's thought that people's sensitivity to antidepressant effects, especially selective serotonin reuptake inhibitor effects, can vary depending on:
    • How each person's serotonin reuptake receptor function works
    • His or her alleles — the parts of chromosomes that determine inherited characteristics, such as height and hair color, which combine to make each person unique

    Antidepressant medications are often the first treatment choice for adults with moderate or severe depression, sometimes along with psychotherapy. Although antidepressants may not cure depression, they can help you achieve remission — the disappearance or nearly complete reduction of depression symptoms.

    TCA and Clinical Depression
    For many years the TCAs were the first choice for pharmacological treatment of clinical depression. Although they are still considered to be highly effective, they have been increasingly replaced by the SSRIs and other newer antidepressants. Notably, however, a recent Cochrane review of the efficacy of the SSRIs concluded that they were only slightly more effective than placebo for the treatment of people with depression. Other indications of SSRIs were not tested. Newer antidepressants are thought to have fewer and less intense side effects and are also thought to be less likely to result in injury or death if used in a suicide attempt, as the doses required for clinical treatment and potentially lethal overdose are far wider in comparison.

    Image and video hosting by TinyPic

    Nonetheless, the TCAs are still occasionally used for treatment-resistant depression that has failed to respond to therapy with newer antidepressants. They are not considered addictive and are somewhat preferable to the monoamine oxidase inhibitors (MAOIs). The side effects of the TCAs usually come to prominence before the therapeutic benefits against depression and/or anxiety do, and for this reason, they may potentially be somewhat dangerous, as volition can be increased, possibly giving the patient a greater desire to attempt or commit suicide.

    TCAs approved to treat depression
    Here are the TCAs approved by the Food and Drug Administration specifically to treat depression, with their generic, or chemical, names followed by available brand names in parentheses:
    • Amitriptyline
    • Amoxapine
    • Desipramine (Norpramin)
    • Doxepin (Sinequan)
    • Imipramine (Tofranil, Tofranil-PM)
    • Nortriptyline (Pamelor)
    • Protriptyline (Vivactil)
    • Trimipramine (Surmontil)
    Some of these medications come in forms that must be injected or as oral solutions that must be mixed with liquids, such as water or juice.
    Some of these medications may also be used to treat conditions other than depression.

    Side effects of TCA
    The most common side effects of tricyclic antidepressants, and ways to deal with them are as follows:
    • Dry mouth -it is helpful to drink sips of water; chew sugarless gum; brush teeth daily. Or use saliva substitutes, which come in liquid and tablet forms and are available without a prescription.
    • Constipation -bran cereals, prunes, fruit, and vegetables should be in the diet.
    • Bladder problems -emptying the bladder completely may be difficult, and the urine stream may not be as strong as usual. Older men with enlarged prostate conditions may be at particular risk for this problem. The doctor should be notified if there is any pain.
    • Sexual problems -sexual functioning may be impaired; if this is worrisome, it should be discussed with the doctor.
    • Blurred vision -this is usually temporary and will not necessitate new glasses. Glaucoma patients should report any change in vision to the doctor.
    • Dizziness -rising from the bed or chair slowly is helpful.
    • Drowsiness as a daytime problem - this usually passes soon. A person who feels drowsy or sedated should not drive or operate heavy equipment. The more sedating antidepressants are generally taken at bedtime to help sleep and to minimize daytime drowsiness.
    • Increased heart rate -pulse rate is often elevated. Older patients should have an electrocardiogram (EKG) before beginning tricyclic treatment.
    • Increased sensitivity to sunlight. Even brief exposure to sun can cause severe sunburn or a rash. While being treated with this tricyclic antidepressants, avoid being in direct sunlight, especially between 10A.M. and 3 P.M.; wear a hat and tightly woven clothing that covers the arms and legs; use a sunscreen with a skin protection factor (SPF) of at least 15; protect the lips with a sun block lipstick; and do not use tanning beds, tanning booths, or sunlamps.
    Image and video hosting by TinyPic

    Special conditions
    People with certain medical conditions or who are taking certain other medicines can have problems if they take tricyclic antidepressants. Before taking these drugs, be sure to let the physician know about any of these conditions:
    -        ALLERGIES. Anyone who has had unusual reactions to tricyclic antidepressants or to carbamazepine (Tegretol), maprotiline (Ludiomil), ortrazodone (Desyrel) in the past should let his or her physician know before taking tricyclic antidepressants. The physician should also be told about anyallergies to foods, dyes, preservatives, or other substances.
    -        PREGNANCY. Problems have been reported in babies whose mothers took tricyclic antidepressants just before delivery. Women who are pregnant or who may become pregnant should check with their physicians about the safety of using tricyclic antidepressants.
    -        BREASTFEEDING. Tricyclic antidepressants pass into breast milk and may cause drowsiness in nursing babies whose mothers take the drugs. Women who are breastfeeding should check with their physicians before using tricyclic antidepressants.
    -        DIABETES. Tricyclic antidepressants may affect blood sugar levels. Diabetic patients who notice changes in blood or urine test results while taking this medicine should check with their physicians

    Suicidal feelings and TCAs
    In some cases, antidepressants may be associated with worsening symptoms of depression or suicidal thoughts or behavior in those ages 18 to 24. These symptoms likely occur in the first one to two months of treatment or when you change your dosage. Be sure to talk to your doctor about any changes in your symptoms. You may need more careful monitoring when beginning treatment or changing dosage, or you may need to stop the medication if your symptoms worsen. Adults age 65 and older taking antidepressants have a decreased risk of suicidal thoughts.

    Work with your doctor or a mental health provider to nix your irritability, sadness or guilt and boost your mood with tricyclics. Feel good again.

    Recommended dosage
    The recommended dosage depends on many factors, including the patient's age, weight, general health and symptoms. The type of tricyclic antidepressant and its strength also must be considered. Check with the physician who prescribed the drug or the pharmacist who filled the prescription for the correct dosage.

    Always take tricyclic antidepressants exactly as directed. Never take larger or more frequent doses, and do not take the drug for longer than directed. Do not stop taking the medicine just because it does not seem to be working. Several weeks may be needed for its effects to be felt. Visit the physician as often as recommended so that the physician can check to see if the drug is working and to note for side effects.

    Do not stop taking this medicine suddenly after taking it for several weeks or more. Gradually tapering the dose may be necessary to reduce the chance of withdrawal symptoms.

    Taking this medicine with food may prevent upset stomach.

    tricyclic antidepressant treatment


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    Tricyclic antidepressant - Wikipedia, the free encyclopedia
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    Controversy

    Several studies have stimulated doubt about the effectiveness of antidepressants. The studies cite that the difference between antidepressants and a placebo is negligible. Antidepressants work only slightly better than placebo, and the Food and Drug Administration has not informed physicians of how little benefit most of these depression drugs offer (Kirsch I, Moore TJ, Scoboria A, Nicholls SS (2002a), The emperor's new drugs: an analysis of antidepressant medication data submitted to the U.S. Food and Drug Administration. Prevention & Treatment 5:Article 23[1]).
    Through a Freedom of Information Act request, two psychologists obtained 47 studies used by the FDA for approval of the six antidepressants prescribed most widely between 1987-99. Overall, antidepressant pills worked 18 % better than placebos, a statistically significant difference, "but not meaningful for people in clinical settings," says University of Connecticut psychologist Irving Kirsch. He and co-author Thomas Moore released their findings in "Prevention and Treatment," an e-journal of the American Psychological Association.
    More than half of the 47 studies found that patients on antidepressants improved no more than those on placebos, Kirsch says. "They should have told the American public about this. The drugs have been touted as much more effective than they are." He says studies finding no benefit have been mentioned only on labeling for Celexa, the most recently approved drug. The others included in his evaluation: Prozac, Paxil, Zoloft, Efexor and Serzone.
    Additional papers have been published regarding the benefits of atypical vs. typical antidepresants. These are timely papers given the need for evidence based medicine, as well as the cost of health care. Discussion of a key paper reviewing this topic titled "Quantitative analysis of sponsorship bias in economic studies of antidepressants" can be found at an an on line journal club

    Alternative medicine

    Despite controversy, alternative treatments for depression such as the herbal remedy St John's wort and the amino acid derivative SAM-e have also gained popularity in recent years, although their effectiveness varies. Clinical trials have shown SAM-e to be as effective as standard antidepressant medication, with many fewer side effects (Delle Chiaie et al., 2002; Mischoulon and Fava, 2002). Most studies conclude that St. John's wort is usually as effective against depressions as other modern medication, again with fewer side effects, and it is widely prescribed for depression in Europe. However, a recent study showed St. John's wort to be no more effective than a placebo in cases of severe depression (Hypericum Depression Trial Study Group, 2002). Tryptophan dietary supplements, although banned in many countries due to impurities that caused a blood disease, have also been used as natural antidepressants. Dietary supplements of 5-HTP, a chemical the body forms from tryptophan and uses to make serotonin, have shown some promising research results but need further study.

    References

    • Roberto Delle Chiaie, Paolo Pancheri and Pierluigi Scapicchio. (2002). Efficacy and tolerability of oral and intramuscular S-adenosyl- L-methionine 1,4-butanedisulfonate (SAMe) in the treatment of major depression: comparison with imipramine in 2 multicenter studies. Am J Clin Nutr, 76 (5): 1172S-1176S
    • Mischoulon D, Fava M. (2002). Role of S-adenosyl-L-methionine in the treatment of depression: a review of the evidence. Am J Clin Nutr, 76 (5): 1158S-61S.
    • Hypericum Depression Trial Study Group (2002). Effect of Hypericum perforatum (St John's Wort) in Major Depressive Disorder: A Randomized Controlled Clinical Trial. JAMA, 287 (14):1807-1814


    Side effects and risks

    Choosing

    It is risky to take antidepressants without a prescription. The selection of an antidepressant and the dosage suitable for a certain case and a certain person is a lengthy and complicated process, requiring the knowledge of a professional. Certain antidepressants can initially make depression worse, can induce anxiety, or can make a patient aggressive, dysphoric or acutely suicidal. In certain cases, an antidepressant can induce a switch from depression to mania or hypomania, can accelerate and shorten a manic cycle (i.e. promote a rapid-cycling pattern), or can induce the development of psychosis (or just the re-activation of latent psychosis) in a patient with depression who wasn't psychotic before the antidepressant. Additionally, MAO inhibitors can produce a lethal hypertensive reaction if taken with foods that contain high levels of tyramine, such as cheese and wine. Likewise, lethal reactions to both prescription and over the counter medications have occurred. While more recent antipdepressant groups are considered safer, ongoing monitoring by a physician is essential.
    Antidepressants can often cause side effects, and an inability to tolerate these is the most common cause of discontinuing the medication.
    Although recent drugs may have fewer or less severe side effects, patients sometimes report severe side effects associated with their discontinuation, particularly with paroxetine. Additionally, a certain percentage of patients do not respond to certain antidepressant drugs, and require more than one attempt to find a suitable medication.
    Antidepressants often make the manic component of bipolar disorder worse, and should be used with great care in the treatment of that disorder, usually in conjunction with a mood stabilisers.

    Addiction

    Antidepressants do not seem to have all of the same addictive qualities as other substances such as nicotine, caffeine, cocaine, or other stimulants. There is, however, ongoing controversy on the definition of addiction. While some antidepressants may cause dependence and withdrawal they do not seem to cause uncontrollable urges to increase the dose due to euphoria or pleasure. For example, if an SSRI medication is suddenly discontinued, it may produce both somatic and psychological withdrawal symptoms, a phenomenon known as "SSRI discontinuation syndrome" (Tamam & Ozpoyraz, 2002). When the decision is made to stop taking antidepressants it is common practice to “wean” off of them by slowly decreasing the dose over a period of several weeks.

    Suicide

    It has been noted that the most dangerous period for suicide in a patient with depression is immediately after treatment has commenced. Antidepressants reduce the symptoms of depression such as psychomotor retardation or lack of motivation before the mood starts to improve, heightening the person's physical well-being before their mental well-being similarly improves.
    Although this appears to be a paradox, studies indicate the suicidal ideation is a relatively common component of the initial phases of antidepressant therapy, and it may be even more prevalent in younger patients such as pre-adolescents and teenagers.
    It is strongly recommended that other family members and loved ones monitor the young patient's behavior, especially in the first eight weeks of therapy, for any signs of suicidal ideation or behaviors.

    Sexual

    Sexual dysfunction is a very common side effect, especially with SSRIs. Bupropion, a NDRI, in many cases results in a moderately increased libido. Some clinicians have found that adding bupropion to a regimen of SSRI medications can sometimes alleviate some degree of sexual dysfunction. However, the mechanism of action for bupropion appears to be unique and quite different from other mood elevators, among these being a stimulant-like effect and concurrent insomnia, especially in the first few weeks of use. Moreover, some patients, as seen with most psycho-active drugs, cannot tolerate it at all.

    Classes of antidepressants


    • Monoamine oxidase inhibitors (MAOIs)
    • Tricyclic antidepressants
    • Selective serotonin reuptake inhibitors (SSRIs)
    • Serotonin-norepinephrine reuptake inhibitors (SNRIs)
    • Norepinephrine/noradrenaline reuptake inhibitors (NRIs aka NERIs/NARIs)
    • Norepinephrine/dopamine reuptake inhibitors (NDRIs)
    • Dopamine reuptake inhibitors (DRIs)
    • Opioids
    • Selective serotonin reuptake enhancers (SSREs)
    • Tetracyclic antidepressants
    • Norepinephrine reuptake inhibitors

    Common antidepressants

    • Citalopram - Includes Celexa, Cipramil, Talohexane.
    • Escitalopram - Includes Lexapro, Cipralex.
    • Fluvoxamine - Includes Luvox, Faverin.
    • Fluoxetine - Includes Prozac, Sarafem, Fluctin, Fontex, Prodep, Fludep, Lovan.
    • Paroxetine - Includes Paxil, Seroxat, Aropax.
    • Sertraline - Includes Zoloft, Lustral, Apo-Sertral, Asentra, Gladem, Serlift, Stimuloton.
    • Duloxetine - Includes Cymbalta.
    • Venlafaxine - Includes Effexor.
    • Bupropion - Includes Wellbutrin, Zyban.

    How antidepressants work

    Antidepressants are believed to have an effect on neurotransmitters, particularly serotonin and norepinephrine.
    • Selective serotonin reuptake inhibitorss (SSRIs) specifically prevent the reuptake of serotonin (increasing the level of serotonin in the synapses of the brain).
    • Monoamine oxidase inhibitors (MAOIs) block the destruction of neurotransmitters by enzymes which normally break them down.
    • Tricyclic antidepressants (TCAs) prevent the reuptake of various neurotransmitters, including serotonin, norepinephrine, and dopamine.
    Although these drugs are effective in treating depression, exactly how they do it and why is not well understood. Curiously, when a person begins taking antipdepressants, the level in their blood increases to optimal levels in only a few days and begins affecting neurotransmitter activity immediately. Changes in mood, however, often take four weeks or more to appear.

    Antidepressant


    An antidepressant is a medication designed to treat or alleviate the symptoms of clinical depression. Many antidepressants also are used for the treatment of anxiety disorders.

    History 

    Like many psychiatric drugs, antidepressants were discovered by accident. The first useful antidepressant group, Monoamine Oxidase Inhibitors (MAOI) were discovered in the early 1950's, and were originally developed to treat tuberculosis. The next group were the Tricyclic antidepressants. They were effective and safer than the MAOIs but still quite dangerous in overdose. They are still used today but have been largely replaced by Selective Serotonin Reuptake Inhibitors (SSRI). The first SSRI was fluoxetine (Prozac).
    The three main classes of antidepressants have similar abilities to improve depressed mood, but the newer types are generally considered to have less severe side-effects and be less risky if taken in overdose.

    Symptoms

    What Are & How Long Do Tramadol Withdrawal Symptoms Last?

    Tramadol is prescribed for patients with moderate to severe pain from broken bones and other injuries as well as chronic pain in muscles and soft tissue, acid reflux and restless leg syndrome. It is synthetic codeine that is considered less addictive than codeine; however users experience severe physical withdrawal pains when they stop taking it. Psychological withdrawal symptoms also occur, because tramadol works like an opiate and gives a feeling of well-being. For this reason, it may be abused.
    The morphine-type withdrawal symptoms start within a day of stopping the drug. They include muscle aches and pains, nausea, insomnia, restless leg syndrome and headaches which may last for a week. Depression, a psychological symptom, may last for months. However, some of the physical withdrawal symptoms last longer. Insomnia and headaches are reported even months after stopping the drug. The longer tramadol has been taken regularly, the longer the withdrawal symptoms will last.
    The main symptoms of tramadol withdrawal are:
    • Fever and flu-like symptoms
    • Insomnia
    • Seizures
    • Diarrhea
    • Pain
    • Anxiety and Anguish
    • Nausea
    • Hallucinations
    • Sweating and tremors
    • Loss of appetite
    • Mood swings
    • Aggression
    These withdrawal symptoms can cause damage to the heart, lungs, brain, kidneys and liver which may be permanent or last for years depending on how long tramadol was taken. The withdrawal period may be too painful if it is not overseen by medical professionals. This pain is avoidable, and the dependency on tramadol is treatable and reversible.
    Because it works like an opiate, the treatment for withdrawal symptoms is the same as for opiates. Users can stop abruptly and endure the pain while their body detoxifies. For many, this is considered the best approach. They drink lots of fluids, take anti-oxidants and keep busy. It is very difficult for a week or two. The first three days are the worst and then it gets better, but it is considered worth the pain to be completely free of even a small dose of the drug.
    Another possibility is to gradually reduce the dosage over several weeks. A doctor should specify the amount to be reduced. This may work to reduce the dosage taken by a lot, but some experience the last, small dosage is very difficult or impossible to stop. If Tramadol has been taken for many years, it will also take years to completely stop. If it has been taken for the psychological feeling of well-being, it may take addiction treatment therapies to stop any size dose.
    Tramadol withdrawal symptoms can last from one week to several years. It depends on how long and how much of it was taken. It has not been considered a highly addictive drug, and for that reason is prescribed instead of opiates, however users find it difficult to stop even after taking it only for a few weeks. The psychological withdrawal symptoms can exacerbate the physical pain and make the experience even worse.