Lupine Publishers | Journal of Medical Sciences
Abstract
Psychiatric symptoms are
very frequent in medical practice, up to 40% of the people that have physical
problems present anxiety or depressive symptoms associated to physical illness.
Due to this, psychiatric liaison is an important part of hospital attention and
many people usually have psychiatric drugs associated to other treatments. In
the second half of the last century, many clinicians mostly psychoanalytically
oriented-have opposed the use of psychoactive drugs for the treatment of mental
illness, particularly in the course of psychotherapy, arguing that they
suppress conflicts and states of mind considered essential for the
understanding of suffering. Furthermore, psychoactive drugs were supposed to
have a negative influence on psychotherapy by making it less effective. In
reality, in 1974 research demonstrated that integrated therapy (i.e. combined
use of medication and psychotherapy) is not harmful to the patient but is
actually useful. However, the conflict between pharmacotherapy and psychotherapy
had already made a great disservice to patients, sometimes delaying the
required drug treatment (e.g. the importance of duration of untreated psychosis
for the prognosis of schizophrenia) or other avoiding effective psychological
interventions that could lead to a better quality of life and reduce the risk
of suicide. This may be the case when considering dialectical behavior therapy
(DBT) or exposure and response prevention (ERP) techniques in cognitive
behavioral therapy (CBT) for borderline personality disorder (BPD) and
obsessive-compulsive disorder (OCD), respectively. Unfortunately, today,
despite a much-vaunted integration of treatments, on the one hand we often deal
with reductionist attitudes that judge psychotherapy as irrelevant and consider
drug therapy alone sufficient for treatment. On the other hand, we deal with
extreme psychological assumptions that consider psychiatric illness as a social
problem and treatable solely and only-through psychosocial interventions,
including psychotherapy. Over time, psychiatry seems to move from a
“brainlessness” approach to a “mindlessness” one. In fact, before the
introduction of psychoactive drugs the psychiatrist’s attention was almost
exclusively on unconscious and intrapsychic conflicts supposed to affect the
mind (as separate from the brain). After 1956, attention moved to
neurotransmitters and other aspects of the brain, consequently with an
extensive use of drugs and less interest for the exploration of the life
stories of patients and focused on symptoms. Therefore, a biological model of
mental illness prevailed, causing an important crisis for psychotherapy. In my
opinion, the cause of this crisis is simple: psychiatry reductionists, using
data from scientific research, support the biological causes of psychiatric
illness (e.g. excess dopamine, serotonin deficiency, etc.), and therefore were
supposed to be able to say when, how and why a treatment protocol is effective,
describing the mechanisms of action, therapeutic effects, limitations and side
effects.
Keywords: Psychiatric
drugs; Psychotherapy; Psychosis; Dialectical behavior therapy; Cognitive
behavioral therapy; Obsessive compulsive disorder
Abbreviations: DBT:
Dialectical Behavior Therapy; ERP: Exposure and Response Prevention; CBT:
Cognitive Behavioral Therapy; BPD: Borderline Personality Disorder; OCD:
Obsessive-Compulsive Disorder; SSRI: Serotonine Selective Reuptake Inhibitors;
AP: Antipsychotics
Introduction
Psychiatric drugs
usually are classified into six great families depending on their principal
focus of action or their use in the main psychiatric disorders:
Antidepressants
These drugs act on
depressive illness through the action on various neurotransmitter systems:
serotonine, noradrenaline and dopamine. The most used of these are SSRI
(serotonine selective reuptake inhibitors), because of their efficacy and good
profile of side effects.
Antipsychotics
They are used in the
control of psychotic symptoms and as major tranquilizers. Antipsychotics are
classified on first generation and second generation. The first of them act
upon dopamine receptors and the second ones upon serotonine and dopamine
receptors to have antipsychotic effects. These second-generation substances
have less side effects and a different profile of action.
Anxiolytics
The most widely used are
benzodiacepines, which act upon a specific GABA receptor. This family of drugs
has a very quick effect, but they aren’t recommended for a long time use
because they can produce dependence and their effects are limited. They are
also used like anticonvulsants.
Antiepileptics
This group of drugs is
used in psychiatry for the maintenance and control of bipolar disorders, and
they are useful too like anti aggressive drugs. The therapeutic drug monitoring
is necessary when some of these substances are administrated because of their
potential toxicity and the pharmacological interactions with other treatments.
Lithium
It is a salt used for
control of manic symptoms and maintenance of bipolar disorders. Its action
mechanism is unknown, despite its usefulness and generalized utilization. It’s
necessary to control its plasmatic level into a tight range to avoid toxicity
and to achieve its function.
Other drugs widely used
in psychiatric disorders: methadone, anticholinesterases, stimulants, alcohol
aversive are also important due to their side effects and their pharmacologic
interactions [1].
Antidepressants
First antidepressant
drugs were a casual finding and they affect to various neurotransmitters
systems. Usually these old drugs produce many secondary effects. Afterwards,
some hypotheses have emerged about the neurotransmission implicated in
depression (monoamines: serotonin, noradrenalin and dopamine). Drug development
progresses in parallel to this investigation so more selective drugs appeared
as Selective Serotonin Reuptake Inhibitors, (from now on SSRIs), ameliorating
secondary effects. Antidepressant classification depends on the assumption of
their action mechanism. Following that schema, there are eight different
pharmacological mechanisms at least. Most of the antidepressants block
monoamine reuptake, but others block alpha-2 receptors or monoaminoxidase
enzyme [2].
Monoamine reuptake inhibitors
Tricyclic and tetracyclic antidepressants (TCA)
The tricyclic and
tetracyclic branch of antidepressants has a demonstrated and high efficacy,
only limited by their sedative and anticholinergic effects. They act on a huge
number of receptors, and are cardiotoxic in case of overdoses, as
anticholinergic toxicity and convulsions.
a) Pharmacological actions: A significant part is absorbed totally after oral
administration. They have a significant metabolism by first-pass. Maximum
plasmatic concentration is reached in 2-48 hours, but equilibrium appears after
5-7 days. Their long halflife allows them to be used once in a day. Clearance
of tricyclics is dependent primarily on hepatic cytochrome P450 (CYP) oxidative
enzymes.
Main therapeutic indications
a) Depression: Treatment
of one major depressive episode and prophylaxis of one major depressive episode
(main directions); depression in Bipolar type I disorder (in resistant cases,
with many precautions to prevent swinging: associated with anticonvulsants or
lithium); one depressive episode with psychotic manifestations almost always
requires the simultaneous administration of an antipsychotic drug and an
antidepressant; Disorder mood due to a general medical disease with depressive
features.
· i. Panic disorder.
· ii. Generalized
anxiety disorder
· iii. Obsessive-compulsive
disorder: clomipramine especially. None of the others seems so effective.
· iv. Others:
Alimentary conduct disorder and pain disorder.
Serotonin Selective Reuptake Inhibitors
(SSRIS)
Serotonin is a
neurotransmitter especially relevant in neurobiological basis in affective
disorders, compulsive-obsessive disorder, and aggressive behavior. SSRIs block
the serotonin reuptake bombs action, augmenting serotonin concentration in
synapsis and post synapsis receptors’ occupation. Though this effect appears
early during treatment, clinical effects delay 3-6 weeks. They are metabolized
at liver, present a low affinity except for serotonin receptors, are enough
sure in overdoses, change sleep structure (reduce latency and total amount of
REM sleep) and might be avoid used with MAOIs, due to the risk of
serotoninergic syndrome.
a) Therapeutic indications: Depression; Anxiety disorders, including
Obsessive-Compulsive Disorder, Bulimia nervosa, Psychosomatic disorders [3].
Noradrenalin selective reuptake inhibitors
It selectively inhibits
the reuptake of norepinephrine, but it has little effect on the reuptake of
serotonin or dopamine. It is structurally related to fluoxetine. It has little
affinity for muscarinic receptors or cholinergic and does not interact with the
alfa1, alpha2, adrenergic beta, serotonergic, dopaminergic or histaminergic
receptors. Therefore, SSRIs and reboxetine have some complementarity effects
and are used together in the clinic in some resistant depressions.
a) Medical indications: Depressive disorders and social phobia. Adverse reactions:
the most common are: faltering urination, headache, constipation, nasal
congestion, sweating, dizziness, dry mouth, decreased libido, insomnia.
Hypertension and tachycardia can appear at high doses, as well as psychomotor
retardation if it is taken with alcohol. The syndrome of inappropriate
secretion of antidiuretic hormone is exceptional. Precautions: contraindicated
in pregnancy and breastfeeding. The doses must be reduced in elderly patients
and serious renal impairment.
Inhibitors of the reuptake of serotonin and
norepinephrine
Venlafaxine
It is a potent inhibitor
of the reuptake of serotonin, at higher doses inhibits the reuptake of
noradrenaline and slightly inhibits the reuptake of dopamine. The absorption is
good at digestive level and suffer important hepatic metabolism, by CYP 2D6
isoenzyme, so some SSRIs isozyme inhibitor drugs may increase plasma levels of
venlafaxine, giving effects at low doses which are resolved once the inhibitor
drug is withdrawn.
Duloxetine
Like venlafaxine, it
inhibits the reuptake of both serotonin and norepinephrine, Duloxetine has a
minimal affinity for dopamine and histamine receptors. It has significant
hepatic metabolism, with many metabolites. It’s a moderate inhibitor of CYP
2D6. Its excretion is renal [4].
Inhibitors of the reuptake of norepinephrine and dopamine
(bupropion)
It is usually more
effective on symptoms of depression than anxiety and quite useful in
combination with SSRIs. It has some dopaminergic effects and therefore can
induce mild psychostimulant effects. The mechanism of action is not known with
accuracy. It seems that weakly inhibits the reuptake of dopamine, raising
levels of it in the nucleus accumbens. This increase in dopamine levels in the
“area of reward” of the brain may be responsible for the use of bupropion in
the cessation. Some data indicate that it exerts its antidepressant effects
increasing the
functional efficiency of the noradrenergic systems. Apparently, it has no
effect on the serotonin system, so it is not effective to block panic attacks.
Serotoninergic modulators: Trazodone
Its mechanism of action
is the modulation of serotonergic neurotransmission; it is a relatively
specific inhibitor of the reuptake of serotonin. It does not cause any
anticholinergic effects. It has Alfa1 adrenergic antagonism and
antihistaminergic activity, so has more sedative effects than other
antidepressants. The sedative effects appear to one hour after administration
and antidepressant effects at 2-4 weeks.
Monoamine Oxidase Inhibitors (MAOIs)
They inhibit the enzyme
MAO, who is responsible for the oxidative deamination of neurotransmitters such
as serotonin, norepinephrine, or dopamine. There are two ways for MAO enzyme:
MAOa and MAOb. The MAOa metabolizes the monoaminergic neurotransmitters more
closely associated with depression (norepinephrine and serotonin). The MAOb
acts upon some aminergic substrates, called protoxins, toxins that can cause
neural damage. Therefore, the inhibition of the MAOa is associated both
hypertensive effects and therapeutic effects. Inhibition of the MAOb is
associated with the prevention of neurodegenerative disorders, such as
Parkinson’s disease processes. The MAO is widely distributed in the body. The
blockade of the MAOa in the gastrointestinal tract is responsible for the
“cheese effect”. It consists of a severe hypertensive crisis that occurs in
patients who are taking MAOIs and ingest food containing tyramine. Tyramine is
usually metabolized in the digestive tract but the blocking of the MAOa allowed
their passage into general circulation. So, patients in treatment with IMAOs
must follow a tyramine-restricted diet. They exert their effects primarily in
the CNS. They act on the mood, decreased sleep and insomnia and daytime
sleepiness. They are characterized by a significant reduction of REM sleep. The
MAOIs are not considered antidepressants in frontline due to restrictions in
the diet, its pharmacological interactions and its broad side effect profile.
Classic and second-generation antipsychotics
Classic antipsychotics
Among classis
antipsychotics (AP) there is no one that has a clear superiority over the
others, so choice must be made depending on previous response or side effects
profile. The AP are well absorbed orally, although their bioavailability is
altered with the intake of certain foods, coffee, calcium antacids and
excessive consumption of nicotine, which can reduce the absorption from the
intestinal tract. They have great solubility and easily cross the blood-brain
barrier. Classic antipsychotics include: Clorpromacine, levomepromacine,
flufenacine, perfenacine, trifluoperacine, haloperidol, zuclopentixol,
molindone, and pimocide. The AP show a great affinity for plasma proteins
(85-90%), which involves risk of toxicity when other drugs that also bind to
proteins are running simultaneously. On the other hand, given that they pass
easily through the blood-brain barrier, concentrations achieved in CNS doubles
those that are quantified in the peripheral circulation. They also cross the
placental barrier, reaching to the fetus during pregnancy. Due to their
lipophilic properties, antipsychotics are stored in the peripheral fat, so
dialysis is ineffective in cases of overdose. Traditional antipsychotic drugs
are metabolized in the liver via hydroxylation and demethylation in cytochrome
P450 processes. Some, such as haloperidol, suffer an additional glucuronidation
and remain active as dopamine antagonists. Major isozymes in the metabolism of
these drugs are the 2D6 and the 3A4. It is estimated that between 5 and 10% of
individuals in white, and one much higher proportion of black individuals are
slow track metabolizers of cytochrome P450 2D6, so it is predictable that
submit side effects with a greater frequency and severity. The AP are removed
primarily by urine and feces, through bile, but also by the saliva, tears,
sweat, and breast milk. The elimination halflife varies between 18 and 40
hours. In the elderly, who often have impaired kidney function to a greater or
lesser extent, physician should proportionally reduce the dose.
Atypical or Second-Generation Antipsychotics
(SGA)
Clozapine produces a
total blockade of D2 receptors, so it does not cause extrapyramidal symptoms.
Properties of clozapine are due to the combination of a low affinity for the
D2receptors along with strong affinity to serotonergic 5HT2A and 5HT1C, adrenergic
and cholinergic receptors. Clozapine joins less intensely this receiver, which
is displaced by endogenous dopamine. This property is present in many SGA, not
only clozapine, so these drugs cause fewer movement disorders as side effects.
The indication of clozapine is the treatment of schizophrenia in patients who
do not respond (after at least two months of treatment at appropriate doses) or
that they do not tolerate the AP, although occasionally prescribed for other
purposes such as the treatment of psychosis by L-DOPA in Parkinson’s disease
patients with mania. It can produce leukopenia, so it’s important to control it
weekly during the first six months of treatment and every fifteen days from
then. However, it should be noted that this risk is low, less than 1%. Other
adverse effects are orthostatic hypotension and tachycardia, increased
sedation, and the decline of the seizure threshold with the consequent risk of
convulsions in 5-10% of cases. Some patients develop a symptomatic complex
called metabolic syndrome which consists of weight gain, increased insulin
resistance, increased risk of diabetes type 2, and elevation of plasma lipids.
Clozapine may increase plasma levels of enzymes such as transaminases GOT and
GPT (alanino aminotransferase and aspartate aminotransferase), alkaline
phosphatase, gamma glutamiltranspeptidasa (GGT) and lactate dehydrogenase.
Risperidone
Its mechanism of action is mediated by its high affinity for D2 receptors, 5HT2A
receptors and the adrenergic α1 and α2 receptors. Unlike
haloperidol shows a low affinity for muscarinic receptors for which leads to
fewer anticholinergic effects. With a similar effectiveness or even something
greater than haloperidol, involves a greater tolerance, although risperidone at
high doses can also cause extrapyramidal symptoms. It is considered an SGA
first line in the treatment of psychoses with particular effectiveness in the
prevention of recurrences. It has been used in child psychiatry in the
treatment of aggressive and serious behavior disorders. There is an increase in
brain-vascular accidents in connection with the use of risperidone and
olanzapine in elderly patients with dementia, a complication which advised the
prescription of this drug with much caution in such patients. There is a
long-acting form of risperidone that can be used twice a month in injection for
maintenance treatment.
Olanzapine
Its main indication has been the treatment of schizophrenia, acute
episodes of mania and maintenance of bipolar affective disorder. Its structure
is similar to clozapine and its mechanism of action is unknown, although it has
a stronger affinity for the receptor 5HT2A than by the dopamine receptor D2. Olanzapine also acts
at various levels, interacting with D1 and D2 dopaminergic, 5HT2A serotoninergic, H1 histaminergic, and
muscarinic receptors. Among his include anorexia nervosa, post-traumatic stress
disorder and borderline personality disorder where, at low doses, it seems to improve
objectives such as aggression and impulsiveness parameters. Olanzapine is
metabolized in the liver by oxidation and glucuronidation by cytochrome P450
isoenzyme 1A2. In smokers it must be important to adjust the
dose, since the consumption of cigarettes induce 1A2 isozyme and
increases drug elimination. The main adverse effect that occurs in patients in
treatment with olanzapine is weight gain, so, an important risk that must be
considered in relation to this and other drugs which produce significant weight
gain is the metabolic syndrome. Other side effects of olanzapine are: sedation,
elevation of prolactin, leukopenia (without agranulocytosis), and decrease the
seizure threshold. Olanzapine carries a lower risk of episodes of Parkinsonism,
dystonia and tardive dyskinesia.
Quetiapine
It has clozapine similar profile, with a moderate affinity to D2
receptors and moderate-intense to 5HT2 serotoninergic receptors. It is a
partial agonist of 5HT1A receptors, which increase dopamine
concentrations in mesocortical area, improving cognitive and negative
schizophrenics symptoms. It produces few extrapyramidal symptoms and risk of
tardive dyskinesia. These features make it the choice for the treatment of
disorders of behavior in Parkinson’s patients and patients treated within the
framework of liaison psychiatry. Undesirable side effects are sedation and
weight gain with alteration of glucose and lipid metabolism. However, it does
not produce a significant increase in prolactin levels Quetiapine is metabolized
in the liver by the cytochrome P450 3A4 enzyme, so drugs that produce a large
inhibition of the isozyme (such as erythromycin) may increase their serum
levels. Carbamazepine and phenytoin reduce levels of quetiapine as behave as
enzyme inducers forcing adjust the dose to avoid possible relapse in patients
who are simultaneously being treated with these drugs.
Ziprasidone
It has high antagonism of 5HT2A, 5HT1D, 5HT2C serotoninergic and D2 dopaminergic
receptors. It has a low tendency to cause extrapyramidal effects because them
high ratio 5HT2A / D2 and its low
affinity for adrenergic, muscarinic and histaminergic receptors. Ziprasidone is
metabolized in the liver by isoenzymes 3A4 of the P450, through a process of
reduction effect of aldehyde oxidase. Its bioavailability increases when
ziprasidone is administrated along with food. This compound intensely joins
proteins and has not been shown to see displaced by other drugs with similar
affinity. In addition to the indication in the acute treatment and maintenance
of schizophrenia, given that it exists in injectable presentation, you can use
in patients who do not collaborate in the taking of oral medication and in
emergency situations characterized by agitation or serious behavior disorders.
It is the antipsychotic with a lesser influence upon weight. The most frequent
adverse effects are drowsiness, insomnia, constipation and nausea. Normally
these effects tend to be temporary and, in general, ziprasidone is well
tolerated.
Amisulpiride
While it has no affinity for subtypes D1, D4 and D5 presents affinity
on the D2 and D3 of the dopamine
receptor subtypes. Unlike other AP, it has no affinity for serotonergic,
adrenergic, cholinergic and H1 histaminergic receptors. An important feature
that distinguishes it from other antipsychotic group is its low liver
metabolism which must be taken into account within the framework of the
psychiatric consultations when treating patients with liver failure that you do
not need to adjust the dose. Their degree of plasma protein binding is low
(around 16%). The drug is eliminated through the kidneys in 90% during the
first 24 hours. In patients with severe kidney disease dosages should be
reduced.
Aripiprazol
This is a partial
agonist of dopamine receptor D2, D3 and serotonergic 5HT1A and works as a 5HT2A
serotonin receptor antagonist. In some situations, aripiprazole would act as an
antagonist and in others as agonist. That way there would be a selfregulation
of dopamine, so the drug would act as antidopamine at the mesolimbic via and as
prodopamine at the mesocortical via, without significantly affecting the
nigroestriada or the tuberoinfundibular paths. Its theoretical advantages would
be improvement in cognitive aspects and motor effects in the long term such as
tardive dyskinesia. It is metabolized in the liver by isoenzymes of the
cytochrome P450 3A4, and 2D6 so that compounds which interact at this level
(carbamazepine, quinidine, ketoconazole, fluoxetine and paroxetine) could alter
the plasma concentrations of aripiprazole. It is a well-tolerated drug that
does not affect significantly the weight or the levels of prolactin for
patients, or metabolism of glucose and lipids. The most frequent side effect is
drowsiness.
Paliperidone
It is an active
metabolite of risperidone. It presents a great affinity for 5HT2A receptors and
moderated by the D2 receptors, with a lower lipophilicity than risperidone. The
pharmacological activity of this compound is similar to another high-power SGA.
The receptor binding profile is similar to risperidone and ziprasidone, though
unlike risperidone and another SGA it has a low rate of hepatic metabolism. Its
adverse effects are similar to the risperidone although they produce a greater
increase in the rate of hyperprolactinemia [5].
Benzodiacepines
Go to
Benzodiacepines (BZD)
are CNS depressors with anxiolytic and hypnotic-sedative properties, and
antiepileptic and muscle relaxing effects. They are more secure in overdoses
than barbiturates and other sedative drugs. They have similar action mechanism
and side effects, and differ in onset time and activity duration, which is
relevant in treatment and indications. Absorption in the gastrointestinal tract
is very good, especially on an empty stomach, so that the oral via is the
choice for these agents. Diazepam and clorazepate are absorbed more quickly
than the others. Other routes of administration are less recommended and should
be reserved only for cases of urgency: the intramuscular absorption is erratic
and intravenous absorption can be dangerous. The BZD are lipophilic agents, so
cross the blood-brain barrier well, exerting their action at the level of the
central nervous system quickly. They also cross the placental barrier and are
excreted through breast milk. Furthermore, their solubility makes that most of
them are accumulated, gradually, in body fat resulting in a high volume of
distribution, which directly influences the duration of the action. The
biotransformation is at hepatic level through a process of oxidation and
conjugation. Some BZD (such as the diacepam or cloracepato) have
pharmacologically active metabolites which, sometimes, even have longer life
than the active ingredient. In addition, should consider that in the healthy
elderly these processes are altered, so you have to choose BZD not metabolized
by microsomal liver enzymes and without active metabolites as oxazepam or
lorazepam. They are eliminated on a majority basis through the kidneys (70-
90%), after their hepatic metabolism. The rest are eliminated through the stool
or bile. All BZD’s action is at CNS, by their ability to enhance the inhibitory
actions of GABA, stimulating the GABA-A receptor. It is believed that their
anxiolytic action is due to the inhibitory action on neurons in the limbic
system, including the amygdala, and serotonergic and noradrenergic neurons of
the CNS. The fact that ethanol, barbiturates, and BZD have similar actions on
the same receptor explains their drug synergy (and therefore the danger of the
combined overdose) and its cross tolerance. This last property is used in the
detoxification of alcoholics with BZD [6].
Drugs used in opioid addiction: Methadone
Methadone is an opioid
analgesic with an outstanding action on the mu receptor. In cases of opioid
dependence methadone is useful for treatment of detoxification, maintenance,
and harm reduction.
Special situations
Opioid analgesics are
generally contraindicated in acute respiratory depression, obstructive
respiratory processes and patients in treatment with opioid antagonists
(naltrexone). They are also contraindicated or should be used with great
caution in alcoholism, seizure disorders, head injuries and processes that have
increased intracranial pressure. They must not be administered to patients in a
coma. In patients with biliary disorders it’s usually recommended to avoid the
use of opiates. Opioid analgesics should be administered with caution or dosage
reduced in patients with: hypothyroidism, adrenocortical insufficiency, asthma,
or decreased respiratory reserve, kidney or liver failure, prostate
hyperplasia, hypotension, shock, inflammatory or obstructive intestinal
disorders and myasthenia gravis. The dose should be reduced in elderly or
debilitated patients. Methadone can prolong cardiac QT interval, increasing the
risk of torsades de pointes, which implies risk of sudden death.
Renal failure and psychoactive drugs
If the drug is
dialyzable, such as lithium, it will experience a sharp decline in its blood
levels after dialysis, so post-dialytic of such drugs levels should be obtained
to determine what amount is provided after the process. Certain drugs that are
metabolized / eliminated by the kidney will accumulate, with the risk of
toxicity, despite not using high doses of these, so that such drugs should be
avoided or give at lower doses. In general, the doses to be used will be
two-thirds of the usual doses of the drug, except drugs with primarily renal
elimination, in which will have to evaluate the clearance of creatinine (ClCr)
as an indicator of renal function and the dose to use of the drug. Plasma
levels of the drug in question must be controlled, at least once a month, and
immediately after the initial dose of medication must provide wherever
possible. In renal failure protein binding is lower than in healthy
individuals, so usually there is a greater amount of free drug in plasma, with
higher therapeutic and side effects. The higher protein binding, the lesser
dialyzable is the drug, what it’s important to prescribe lower doses. In
general, most of the psychotropic substances aren’t dialyzable, except lithium,
gabapentine, pregabaline and others [7].
Conclusion
Psychiatric medicines
have changed the lives of people with mental illnesses for the better and many
people have gone on to live fulfilling lives with the help of these medicines.
Today, there is a wide range of safe and effective medicines available to treat
these illnesses and it is important to know the medicines that your doctor
prescribes to you. Besides knowing what they are and what symptoms they treat,
it is good to be aware of some of the side effects so that you would be able to
talk to your doctor about them. Adhering to medication dosages and schedules is
important. If you wish to adjust the medication routine, please consult your
doctor as abruptly stopping some of these medicines may cause a Discontinuation
Syndrome, with either a worsening of earlier symptoms or the appearance of
other physical or psychological symptoms.
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