Anxiety Disorder: Pharmacology

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Introduction. Pathophysiology of Anxiety Disorder

Anxiety causes fear, insomnia, chronic pain, premonition, difficulty concentrating, the effectiveness of selective serotonin reuptake inhibitors (SSRIs), and more.
The key point – sympathoadrenal, is associated with hypothalamic-pituitary-adrenal hyperreactivity.
An increase in the concentration of ACTH and cortisol (Anxiety disorder).
Anxiety decreases the brain-derived neurotrophic factor (BDNF).

Treatment should not be self-administered
The disorder regulatory effect on neurotransmitter systems, mainly serotonin (Anxiety disorder).
Together with the norepinephrine and dopamine systems, the concentration of ACTH and cortisol provides an adequate emotional response to the body.
Usually, 9-12 months of therapy is required to achieve complete remission
The appointment of medicines begins with half the starting dose with a gradual increase in dosage after a week to the standard dose

Drugs of selective serotonin reuptake inhibitors (SSRIs) help in anxiety treatment (Anxiety disorder).
SSRIs have a pathogenetic therapeutic focus.
Tranquilizers: maximum two weeks at the start of therapy.
Prescribing tranquilizers is warranted for a maximum of 2 weeks when initiating SSRI treatment to avoid increased anxiety during the first week of SSRIs (Anxiety disorder).
Medicines prescribed by a doctor.

Examples of SSRIs: citalopram (Celexa), fluoxetine (Prozac).
Celexa stimulates synaptogenesis processes, restoring autophagy signals, and improving tissue immunoregulation with inhibition of immunogenic cytotoxicity of macrophages (Citalopram).
An analog is Prozac, the mechanism of action in the central nervous system, which block the reverse neuronal uptake of serotonin selectively (Fluoxetine).
Examples of tranquilizers: alprazolam (Xanax), clonazepam (Klonopin).
Xanax has a sedative, central muscle relaxant, anticonvulsant, hypnotic, anxiolytic, effect. It reduces the impact of motor, vegetative, emotive and helps the body in falling asleep (Alprazolam).
The anxiolytic effect of Klonopin is obtained as a result of the impact on the amygdala complex of the limbic system (Clonazepam). It is manifested in decreased fear, emotional stress, weakening and general anxiety.

Celexa dissolves in the liver.
The action of the drug occurs because of central inhibition of serotonin reuptake.
Celexa has a strong effect on the heart and gastrointestinal tract, thus requires for ECG and/or monitoring of electrolytes.
Approved for use during pregnancy and lactation.
It has side effects include poor feeding, colic, and unusual drowsiness, irritability, or restlessness in a minimal number of children.

Absorbed from the gastrointestinal tract.
Delays the reverse capture of serotonin.
Monitoring is required.
Approved for use during pregnancy and lactation.
It increases the risk of genetic heart defects in the fetus, premature birth, and weight loss in a baby (Fluoxetine).

Absorbed from the gastrointestinal tract.
Binds γ-aminobutyric acid (GABA) type A receptors (GABA AR).
Completely individual dosage, therefore, requires monitoring and consultation with a doctor.
Alprazolam has a harmful effect on the fetus and raises the possibility of congenital malformations when used in the first three months of pregnancy, thus, prohibited during pregnancy (Alprazolam).
May cause drowsiness in newborns.
Makes breastfeeding difficult.

Plasma protein binding.
The activity of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) in the central nervous system.
Completely individual dosage, therefore, requires monitoring and consultation with a doctor.
Pregnancy and lactation are contraindicated.

Each drug has its characteristics and contraindications, so one needs to consult a doctor.
General contraindications include allergy, heart problems, problems with the gastrointestinal tract.
Tranquilizers are prohibited if a person has glaucoma and diseases of the respiratory system.
Long-term use is not justified because of the possibility of drug dependence.
In addition, after the abolition of drugs in this group, the return of painful symptoms occurs since the main pathophysiological mechanisms associated with impaired serotonin mediation are not resolved.