Академический Документы
Профессиональный Документы
Культура Документы
Types
Antidepressants
Antidepressants are drugs used to treat clinical depression, and they are also often used for anxiety
and other disorders. Most antidepressants will hinder the breakdown of serotonin
or norepinephrine or both. A commonly used class of antidepressants are called selective serotonin
reuptake inhibitors (SSRIs), which act on serotonin transporters in the brain to increase levels of
serotonin in the synaptic cleft.[16] SSRIs will often take 35 weeks to have a noticeable effect, as the
regulation of receptors in the brain adapts. There are multiple classes of antidepressants which have
different mechanisms of action. Another type of antidepressant is a monoamine oxidase inhibitor,
which is thought to block the action of Monoamine oxidase, an enzyme that breaks down serotonin
and norepinephrine. MAOIs are not used as first-line treatment due to the risk of hypertensive
crisis related to the consumption of foods containing the amino acid tyramine.[16][17]
Common antidepressants:
Fluoxetine (Prozac), SSRI
Paroxetine (Paxil, Seroxat), SSRI
Citalopram (Celexa), SSRI
Escitalopram (Lexapro), SSRI
Sertraline (Zoloft), SSRI
Duloxetine (Cymbalta), SNRI
Venlafaxine (Effexor), SNRI
Bupropion (Wellbutrin), NDRI[18]
Mirtazapine (Remeron), NaSSA
Isocarboxazid (Marplan), MAOI
Phenelzine (Nardil), MAOI
Tranylcypromine (Parnate), MAOI
Antipsychotics
Antipsychotics are drugs used to treat various symptoms of psychosis, such as those caused by
psychotic disorders or schizophrenia. Atypical antipsychotics are also used as mood stabilizers in
the treatment of bipolar disorder, and they can augment the action of antidepressants in major
depressive disorder.[16] Antipsychotics are sometimes referred to as neuroleptic drugs and some
antipsychotics are branded "major tranquilizers".
There are two categories of antipsychotics: typical antipsychotics and atypical antipsychotics. Most
antipsychotics are available only by prescription.
Common antipsychotics:
Z-drugs are a group of drugs with effects generally similar to benzodiazepines, which are used in the
treatment of insomnia.
In 1949, the Australian John Cade discovered that lithium salts could control mania, reducing the
frequency and severity of manic episodes. This introduced the now popular drug lithium carbonate to
the mainstream public, as well as being the first mood stabilizer to be approved by the U.S. Food &
Drug Administration. Besides lithium, several anticonvulsants and atypical antipsychotics have mood
stabilizing activity. The mechanism of action of mood stabilizers is not well understood.
Stimulants
A stimulant is a drug that stimulates the central nervous system, increasing arousal, attention and
endurance. Stimulants are used in psychiatry to treat attention deficit-hyperactivity disorder. Because
the medications can be addictive, patients with a history of drug abuse are typically monitored
closely or treated with a non-stimulant.
Common stimulants:
Methylphenidate (Ritalin, Concerta), a norepinephrine-dopamine reuptake inhibitor
Dexmethylphenidate (Focalin), the active dextro-enantiomer of methylphenidate
Mixed amphetamine salts (Adderall), a 3:1 mix of dextro/levo-enantiomers of amphetamine
Dextroamphetamine (Dexedrine), the dextro-enantiomer of amphetamine
Lisdexamfetamine (Vyvanse), a prodrug containing the dextro-enantiomer of amphetamine
Methamphetamine (Desoxyn), a potent but infrequently prescribed amphetamine
Psychopharmacological substances
Alcohol
Alcohol is a depressant, the effects of which may vary according to dosage amount, frequency, and
chronicity. As a member of the sedative-hypnotic class, at the lowest doses, the individual feels
relaxed and less anxious. In quiet settings, the user may feel drowsy, but in settings with increased
sensory stimulation, individuals may feel uninhibited and more confident. High doses of alcohol
rapidly consumed may produce amnesia for the events that occur during intoxication. Other effects
include reduced coordination, which leads to slurred speech, impaired fine-motor skills, and delayed
reaction time. The effects of alcohol on the bodys neurochemistry are more difficult to examine than
some other drugs. This is because the chemical nature of the substance makes it easy to penetrate
into the brain, and it also influences the phospholipid bilayer of neurons. This allows alcohol to have
a widespread impact on many normal cell functions and modifies the actions of several
neurotransmitter systems. Alcohol inhibits glutamate (a major excitatory neurotransmitter in the
nervous system) neurotransmission by reducing the effectiveness at the NMDA receptor, which is
related to memory loss associated with intoxication. It also modulates the function of GABA, a major
inhibitory amino acid neurotransmitter. The reinforcing qualities of alcohol leading to repeated use
and thus also the mechanisms of withdrawal from chronic alcohol use are partially due to the
substances action on the dopamine system. This is also due to alcohols effect on
the opioid systems, or endorphins, that have opiate-like effects, such as modulating pain, mood,
feeding, reinforcement, and response to stress.
Antidepressants
Monoamine oxidase inhibitors (MAOIs) are the oldest class of antidepressants. They
inhibit monoamine oxidase, the enzyme that metabolizes the monoamine neurotransmitters in the
presynaptic terminals that are not contained in protective synaptic vesicles. The inhibition of the
enzyme increases the amount of neurotransmitter available for release. It increases norepinephrine,
dopamine, and 5-HT and thus increases the action of the transmitters at their receptors. MAOIs have
been somewhat disfavored because of their reputation for more serious side effects. [1]
Tricyclic antidepressants (TCAs) work through binding to the presynaptic transporter proteins and
blocking the reuptake of norepinephrine or 5-HT into the presynaptic terminal, prolonging the
duration of transmitter action at the synapse.
Selective serotonin reuptake inhibitors (SSRIs) selectively block the reuptake of serotonin (5-HT)
through their inhibiting effects on the sodium/potassium ATP-dependent serotonin transporter in
presynaptic neurons. This increases the availability of 5-HT in the synaptic cleft. [6] The main
parameters to consider in choosing an antidepressant are side effects and safety. Most SSRIs are
available generically and are relatively inexpensive. Older antidepressants, such as the TCAs and
MAOIs usually require more visits and monitoring, and this may offset the low expense of the drugs.
The SSRIs are relatively safe in overdose and better tolerated than the TCAs and MAOIs for most
patients.[6]
Antipsychotics
All proven antipsychotics are postsynaptic dopamine receptor blockers (dopamine antagonists). For
an antipsychotic to be effective, it generally requires a dopamine antagonism of 60%-80% of
dopamine D2 receptors.[6]
Second-generation (atypical) antipsychotics: The concept of atypicality is from the finding that the
second generation antipsychotics (SGAs) had a greater serotonin/dopamine ratio than did earlier
drugs, and might be associated with improved efficacy (particularly for the negative symptoms of
psychosis) and reduced extrapyramidal side effects. Some of the efficacy of atypical antipsychotics
may be due to 5-HT2 antagonism or the blockade of other dopamine receptors. Agents that purely
block 5-HT2 or dopamine receptors other than D2 have often failed as effective antipsychotics.[6]
Benzodiazepines
Benzodiazepines are often used to reduce anxiety symptoms, muscle tension, seizure disorders,
insomnia, symptoms of alcohol withdrawal, and panic attack symptoms. Their action is primarily on
specific benzodiazepine sites on the GABA A receptor. This receptor complex is thought to mediate
the anxiolytic, sedative, and anticonvulsant actions of the benzodiazepines.[6] Use of
benzodiazepines carries the risk of tolerance (necessitating increased dosage), dependence, and
abuse. Taking these drugs for a long period of time can lead to withdrawal symptoms upon abrupt
discontinuation.[7]
Hallucinogens
Hallucinogens cause perceptual and cognitive distortions without delirium. The state of intoxication is
often called a trip. Onset is the first stage after an individual ingests (LSD, psilocybin, or mescaline)
or smokes (dimethyltryptamine) the substance. This stage may consist of visual effects, with an
intensification of colors and the appearance of geometric patterns that can be seen with ones eyes
closed. This is followed by a plateau phase, where the subjective sense of time begins to slow and
the visual effects increase in intensity. The user may experience synesthesia, a crossing-over of
sensations (for example, one may see sounds and hear colors). In addition to the sensory-
perceptual effects, hallucinogenic substances may induce feelings of depersonalization, emotional
shifts to a euphoric or anxious/fearful state, and a disruption of logical thought. Hallucinogens are
classified chemically as either indoleamines (specifically tryptamines), sharing a common structure
with serotonin, or as phenethylamines, which share a common structure with norepinephrine. Both
classes of these drugs are agonists at the 5-HT2 receptors; this is thought to be the central
component of their hallucinogenic properties. Activation of 5-HT 2Amay be particularly important for
hallucinogenic activity. However, repeated exposure to hallucinogens leads to rapid tolerance, likely
through down-regulation of these receptors in specific target cells.[1]
Hypnotics
Hypnotics are often used to treat the symptoms of insomnia, or other sleep disorders.
Benzodiazepines are still among the most widely prescribed sedative-hypnotics in the United States
today. Certain non-benzodiazepine drugs are used as hypnotics as well. Although they lack the
chemical structure of the benzodiazepines, their sedative effect is similarly through action on the
GABAA receptor. They also have a reputation of being less addictive than
benzodiazepines. Melatonin, a naturally-occurring hormone, is often used over the counter (OTC) to
treat insomnia and jet lag. This hormone appears to be excreted by the pineal gland early during the
sleep cycle and may contribute to human circadian rhythms. Because OTC melatonin supplements
are not subject to careful and consistent manufacturing, more specific melatonin agonists are
sometimes preferred. They are used for their action on melatonin receptors in the suprachiasmatic
nucleus, responsible for sleep-wake cycles. Many barbiturates have or had an FDA-approved
indication for use as sedative-hypnotics, but have become less widely used because of their limited
safety margin in overdose, their potential for dependence, and the degree of central nervous system
depression they induce. The amino-acid L-tryptophan is also available OTC, and seems to be free of
dependence or abuse liability. However, it is not as powerful as the traditional hypnotics. Because of
the possible role of serotonin in sleep patterns, a new generation of 5-HT 2 antagonists are in current
development as hypnotics.[6]
There exist two primary CNS cannabinoid receptors, on which marijuana and the cannabinoids act.
Both the CB1 receptor and CB2 receptor are found in the brain. The CB2 receptor is also found in
the immune system. CB1 is expressed at high densities in the basal
ganglia, cerebellum, hippocampus, and cerebral cortex. Receptor activation can
inhibit cAMPformation, inhibit voltage-sensitive calcium ion channels, and activate potassium ion
channels. Many CB1 receptors are located on axon terminals, where they act to inhibit the release of
various neurotransmitters. In combination, these drug actions work to alter various functions of the
central nervous system including the motor system, memory, and various cognitive processes. [1]
Opiates
The opiate drugs, which include drugs like heroin, morphine, and oxycodone, belong to the class
of narcotic analgesics, which reduce pain without producing unconsciousness, but do produce a
sense of relaxation and sleep, and at high doses, may result in coma and death. The ability of
opiates (both endogenous and exogenous) to relieve pain depends on a complex set of neuronal
pathways at the spinal cord level, as well as various locations above the spinal cord.
Small endorphin neurons in the spinal cord act on receptors to decrease the conduction of pain
signals from the spinal cord to higher brain centers. Descending neurons originating in
the periaqueductal gray give rise to two pathways that further block pain signals in the spinal cord.
The pathways begin in the locus coeruleus (noradrenaline) and the nucleus of raphe (serotonin).
Similar to other abused substances, opiate drugs increase dopamine release in the nucleus
accumbens.[1] Opiates are more likely to produce physical dependence than any other class of
psychoactive drugs, and can lead to painful withdrawal symptoms if discontinued abruptly after
regular use.
Stimulants
Cocaine is one of the more common stimulants, and is a complex drug that interacts with various
neurotransmitter systems. It commonly cause heightened alertness, increased confidence, feelings
of exhilaration, reduced fatigue, and a generalized sense of well-being. The effects of cocaine are
similar to those of the amphetamines, though cocaine tends to have a shorter duration of effect. In
high doses and/or with prolonged use, cocaine can result in a number of negative effects as well,
including irritability, anxiety, exhaustion, total insomnia, and even psychotic symptomatology. Most of
the behavioral and physiological actions of cocaine can be explained by its ability to block the
reuptake of the two catecholamines, dopamine and norepinephrine, as well as serotonin. Cocaine
binds to transporters that normally clear these transmitters from the synaptic cleft, inhibiting their
function. This leads to increased levels of neurotransmitter in the cleft and transmission at the
synapses.[1] Based on in-vitro studies using rat brain tissue, cocaine binds most strongly to the
serotonin transporter, followed by the dopamine transporter, and then the norepinephrine transporter.
[9]
Amphetamines tend to cause the same behavioral and subjective effects of cocaine. Various forms
of amphetamine are commonly used to treat the symptoms of attention deficit hyperactivity
disorder (ADHD) and narcolepsy, or are used recreationally. Amphetamine
and methamphetamine are indirect agonists of the catecholaminergic systems. They block
catecholamine reuptake, in addition to releasing catecholamines from nerve terminals. There is
evidence that dopamine receptors play a central role in the behavioral responses of animals to
cocaine, amphetamines, and other psychostimulant drugs. One action causes the dopamine
molecules to be released from inside the vesicles into the cytoplasm of the nerve terminal, which are
then transported outside by the mesolimbic dopamine pathway to the nucleus accumbens. This
plays a key role in the rewarding and reinforcing effects of cocaine and amphetamine in animals,
and is the primary mechanism for amphetamine dependence.
List of psychiatric medications by condition
treated
Drug dependence therapy
Anxiety disorders
Benzodiazepines
Non-benzodiazepine anxiolytics
Antidepressants
Non-pharmaceutical
INN Common brand names
Tryptophan
Autism
Bipolar disorder
Mood stabilizers
Antipsychotics
Non-pharmaceutical
Insomnia
Benzodiazepines
Z-drugs
Barbiturates
Sedating antidepressants
Antihistamines
Others
Non-pharmaceutical
Mild strength
Strong strength
Other antipsychotics
Adjuncts