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With the availability of numerous drugs for the treatment of psychiatric
disorders, it can sometimes be difficult to choose from amongst them. Therefore, the rationale of prescribing has to be based on: 1.
Patient’s profile, e.g. age, underlying medical problems, previous history of drug response and allergy; and
The benzodiazepine anxiolytics are currently the most widely-used and
prescribed drugs in the world. However, in recent years there has been growing concern regarding the problem of dependence and abuse. Concurrent prescription of selective serotonin reuptake inhibitor and BZD with gradual withdrawal of BZD has become a common practice. When anxiety is a symptom of another psychiatric disorder such as depression, the specific treatment with antidepressants is generally more effective in relieving the anxiety than using BZD in the long term mangement.
When BZD are chosen to treat generalized anxiety disorders (GAD), the
principle of treatment is to ensure adequate anxiolysis throughout the day without the need for frequent doses. Short-acting BZD often cause withdrawal symptoms in between doses; therefore BZD with intermediate or long duration of action may be more suitable for generalized anxiety. Examples of these BZD are diazepam and chlordiazepoxide.
When choosing a BZD for treatment of panic attacks, the key principle is that
the BZD must have a rapid onset in aborting the attack. A high potency agent like alprazolam would then be more appropriate.
BZD act on specific BZD receptors and potentiate the action of gamma-
aminobutyric acid (GABA) in the brain and spinal cord. GABA is an inhibitory
neurotransmitter and potentiation of GABA leads to neural inhibition resulting in
muscle relaxation as well as reduced arousal. Pharmacokinetics
BZD are well absorbed orally. The onset of action is partly dependent on the
lipid solubility. Most of them are lipid soluble and have rather rapid CNS effect.
Plasma concentration of BZD and their active metabolites correlate to a
certain extent with clinical response, although this relationship is complicated by the development of tolerance. That explains why patients who are chronic BZD users do not become sedated even after usual therapeutic doses.
BZD bind extensively to plasma proteins which means they are difficult to
remove from the body by dialysis in case of overdose. BZD are metabolized in the liver microsomal enzyme system. Many are broken down into active metabolites. The metabolic pathways are influenced by factors such as age, liver disease and the co-administration of other drugs that affect the liver.
Table 1. Common Benzodiazepines
Adverse Effects of BZD
1. Sedation is the most common adverse effect. It may be more severe in the
elderly and increases the risk of falls.
2. Anterograde amnesia. Some patients have an inability to remember events for
periods of up to a few hours after taking the drugs. It is more common after intravenous administration.
3. Respiratory and cardiac functions are not usually affected by normal therapeutic
doses of BZD although it causes a slowing down of respiration and heart rate in anxious persons.
4. Rare adverse psychological effects such as irritability and behavioural
5. Tolerance does develop in some patients with BZD usage. Larger doses are
required and physical dependence occurs with time. When BZD are abruptly discontinued, patients experience anxiety and withdrawal symptoms (e.g. prolonged sleep latency, interrupted sleep with vivid dreams, nausea or vomiting, muscle cramps, irritability and, rarely, convulsions). These withdrawal symptoms may be especially common after discontinuation of shorter-acting BZD.
The efficacy of all available AD are almost similar. The adverse drug effects
are different. The choice of AD depends on the efficacy and the tolerability of the adverse effects in each individual patient.
This group of drugs acts by blocking the reuptake of noradrenaline or
serotonin in the presynaptic neurons. The tricyclic AD (e.g. imipramine, amitriptyline,
dothiepin, clomipramine) are still useful first generation AD drugs. These AD are inexpensive but they cause dose-dependent anticholinergic, orthostatic hypotensive and cardiotoxic effects. Therefore, if patients have close-angle glaucoma, cardiac arrhythmia, prostatic hypertrophy or chronic constipation, these drugs are not suitable.
Relatively newer drugs in this class of AD are amoxapine and maprotiline.
Although maprotiline has less cardiotoxic effect, it is quite sedating and has anticholinergic side effects. Because tricyclic AD often cause drowsiness, fatigue and lethargy initially, patients should be informed at the beginning of the treatment in order to minimize non-compliance. 2.
Selective Serotonin Reuptake inhibitors (SSRIs)
Examples of SSRIs include fluoxetine, sertraline, citalopram, paroxetine and
fluvoxamine. As the name suggests they selectively inhibit 5-HT reuptake at presynaptic neurons. They cause fewer anticholinergic adverse effects and are therefore drugs of choice for patients with underlying cardiac problems or in those who are unable to tolerate anticholinergic effects of tricyclic AD. 3.
With the advent of the reversible MAOI, e.g. RIMAs (Reversible Inhibition of
Monoamine Oxidase A), the first generation MAOI such as phenelzine, tranylcypromine are not often used because of drug interactions and the “cheese” effects. RIMAs are able to induce a reversible and specific inhibition on MAO-A and the frequency and severity of drug interactions with other drugs are reduced, although co-administration with tricyclic AD, pethidine and dextromethorphan should be avoided. 4.
Serotonin/Norepinephrine Reuptake Inhibitor (SNRI)
Venlafaxine is the only drug available. At low doses, only serotonin reuptake
inhibition occurs. Norepinephrine and dopamine reuptake inhibition occur at higher doses. It does not have anticholinergic effects. 5
Other new antidepressants such as nefazodone and mirtazepine.
Nefazodone has pharmacological actions of a SSRI and a 5HT2 blocker. It is thus less likely than SSRIs to cause sexual dysfunction.
Mirtazepine blocks presynaptic alpha 2 and post synaptic 5HT2 and 5HT3
receptors. It causes weight gain and sedation, which is related to its antihistamine action.
Table 2. Antidepressants
Tetracyclic e.g. maprotiline Inhibits the reuptake of NE Dose dependent sedation.
The use of tricyclic AD, SSRI or pethidine in patients on MAOI may lead to
delirium, coma and death. Therefore, when changing prescription from a tricyclic to a MAOI, a drug-free interval of five days to one week is recommended. However, when changing from fluoxetine to a MAOI, the recommended wash-out period is five weeks or longer because fluoxetine has a very long-acting active metabolite.
The terms antipsychotics and neuroleptics are used interchangeably although
“antipsychotic” has a clearer meaning. They are used to treat psychoses including schizophrenic, paranoid and other delusional disorders as well as mania.
The antipsychotic drugs are not specific in action. In addition to blocking
postsynaptic D2 receptors, they also block α1 receptors (causing sedation and postural hypotension), cholinergic receptors, 5-HT receptors (affecting appetite and sexual functions) and histamine receptors.
Table 3. Common Typical Antipsychotic Drugs
*Extrapyramidal side effects, i.e. EPSE, are related to the antidopaminergic action in the basal ganglia. The high-potency drugs are more likely to produce EPSE.
Table 4. Adverse Effects of Typical Antipsychotic Drugs
Table 5. Extrapyramidal Side Effects
New generation antipsychotics
This group of drugs has been termed “atypical”, as they are less likely to
cause EPSE as compared to the typical antipsychotics. They generally block 5HT2A receptors in addition to dopamine, histamine and adrenergic receptors. In addition, they attenuate both the positive and negative symptoms of schizophrenia. Clozapine is the first to be discovered as an “atypical” antipsychotic. It causes a rare adverse effect of agranulocytosis and its use is therefore limited to patients who are resistant to conventional treatment and those who suffered severe EPSE. Other “atypical” drugs are risperidone, olanzapine, quetiapine and ziprasidone.
Lithium (Li) carbamazepine (CBZ) and valproate are commonly referred to as
“mood-stabilising” agents because of their primary action of preventing mood swings in patients with mood disorders.
The mechanism of mood stabilizing effects remains “unknown” although a
multitude of effects have been suggested. One of the recent findings on the mode of action of Li is its effect on the cell membrane. CBZ has also neuronal membrane stabilizing effect. Probably, the basic mechanism of mood stabilization of these agents is to modulate neurotransmission.
The plasma therapeutic range of Li is 0.4 meq/L to 1.2 meq/L. Regular
monitoring of plasma concentration must be carried out because of the low
therapeutic index for Li plasma. References
Tyrer P. Drugs in Psychiatric Practice
. London: Butterworths, 1982.
Reeves SM, Scheepers BDM. Drugs in Psychiatry: A pocket guide
. Quay Publishing and Lancaster, 1991.
Brian E Leonard. Fundamentals of Psychopharmacology,
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