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Anxiety disorders
Anxiety is an emotional state commonly caused by the perception of real or perceived danger that
threatens the security of an individual. Anxiety can produce uncomfortable and potentially debilitating
psychologic (e.g., worry or feeling of threat) and physiologic arousal (e.g., tachycardia or shortness of
breath) if it becomes excessive. Anxiety disorders are among the most frequent mental disorders
encountered in clinical practice. Healthcare professionals often mistake anxiety disorders for physical
illnesses, and only 23% of patients receive appropriate treatment.
Epidemiology
United States, the 1-year prevalence rate for anxiety disorders was 18.1% in persons aged 18 years and
older.
Pathophysiology
anxiety states is associated with multiple regions of the brain and abnormal function in several
neurotransmitter systems, including norepinephrine (NE), gama-aminobutyric acid (GABA), serotonin (5HT), corticotrophin-releasing factor (CRF), and cholesystokinin.
Neurochemical theories
In response to threat or fearful situations, the LC (locus ceruleus) serves as an alarm center, activating
NE release and stimulating the sympathetic and parasympathetic nervous systems. Chronic central
noradrenergic overactivity downregulates -adrenoreceptors in patients with GAD. This receptor is
hypersensitive in some patients with panic disorder. Patients with SAD appear to have a hyperresponsive
adrenocortical response to psychologic stress.
GABA Receptor model
Panic disorder is secondary to a lack of central inhibition that results in uncontrolled elevations in anxiety
during panic attacks.
Serotonin theory
Disregulation of serotoin.
Clinical presentations
SAD is characterized by an intense, irrational, and persistent fear of being negatively evaluated or
scrutinized in at least one social or performance situation.
Panic disorder begins as a series of unexpected (spontaneous) panic attacks involving an intense,
terrifying fear similar to that caused by life-threatening danger
Treatment
Goals of the therapy
 Reduce the severity and duration of the anxiety symptoms and to improve overall functioning.
 The long-term goal in GAD is remission with minimal or no anxiety symptoms, no functional
impairment, and increased QOL
Non Pharmacological therapy
Psychoeducation, Short-term counseling, stress management, psychotherapy, meditation, or exercise.
Pharmacotherapy
The benzodiazepines are the most effective, safe, and commonly prescribed drugs for the rapid relief of
acute anxiety symptoms. Because of the lack of dependency and tolerable adverse effect profile,
antidepressants have emerged as the treatment of choice for the management of chronic anxiety,
especially in the presence of comorbid depressive symptoms. Because of the high risk of adverse effects
and toxicity, barbiturates, antipsychotics, antipsychotic-antidepressant combinations, and antihistamines
generally are not indicated in the treatment of GAD.
Social anxiety disorder
Panic disorders
Post traumatic stress disorder and obsessive compulsive disorder
Post-traumatic stress disorder is a type of anxiety disorder that occur after a person seen or experienced
a traumatic event that involved the threat of injury or death. Recent world events (e.g., wars, terrorist
attacks, hurricanes, and tsunamis) have placed a renewed focus on posttraumatic stress disorder
(PTSD).
Etiology
Genetics may play a role in expression of PTSD and OCD, but environmental factors likely are also
involved.
Pathophysiology
Research findings in the areas of neuroendocrinology, neurobiology, and neuroimaging have advanced a number of
theories on the pathophysiology of anxiety disorders. Neuroendocrine changes in the hypothalamic-pituitary-adrenal
(HPA) axis are implicated in the pathophysiology of PTSD. Data from neurochemical and neuroimaging studies
indicate that the modulation of normal and pathologic anxiety states is associated with multiple regions of the brain
(e.g., amygdala, hippocampus, thalamus, and prefrontal cortex). Abnormal function in several neurotransmitter
systems, including norepinephrine (NE), γ-aminobutyric acid (GABA), glutamate, dopamine (DA), and serotonin
(5-HT) may affect the manifestations of anxiety disorders.
Neuroendocrine theories - The release of corticotrophin releasing factor stimulates cortisol secretion from the
adrenal gland. Both catecholamines and cortisol levels rise in tandem. Cortisol reduces the stress response by
tempering the sympathetic reaction through negative feedback on the pituitary and hypothalamus. These systems
return to normal after a few hours. Patients with PTSD have a hypersecretion of corticotropinreleasing
factor but demonstrate subnormal levels of cortisol at the time of trauma and chronically. Dysregulation of the HPA
axis is postulated to be a risk factor for eventual development of PTSD.
Neurochemical theories- 5-HT and NE are associated with the processing of emotional and somatic contents of
memories in the amygdala. The cortex and hippocampus are involved in storing the facts and related cues of
memory. The noradrenergic theory posits that the autonomic nervous system of anxious patients is hypersensitive
and overreacts to stimuli. The alarm center, the locus ceruleus, releases NE to stimulate the sympathetic and
parasympathetic nervous systems. Patients with PTSD tend to experience sustained elevated heart rates
during trauma and enhanced startle effects starting a month after trauma exposure. Patients with chronic central
noradrenergic over
Clinical Presentation
Obsessive compulsive disorder
OCD usually begins early in life, with 20% of cases occurring in childhood, 29% in adolescence, and 49% of cases
occurring by age 20. The onset of illness is earlier in men than women.
Genetics may play a role in expression of OCD, but environmental factors likely are also involved. OCD has been
characterized as a pediatric autoimmune neuropsychiatric disorder associated with streptococcal infections. In
response to streptococcal infection, antibodies are produced in some individuals that temporally precipitate sudden
onset or exacerbation of symptoms of OCD.
Pathophysiology THOPHYSIOLOGY
Both 5-HT and DA are implicated in the pathogenesis of OCD. Selective and potent serotonergic reuptake inhibitors
have consistently been shown be effective for symptoms of the illness. Results of challenge studies using 5-HT
agonists support a role for this neurotransmitter as well. However, to date there is no specific identified abnormality in
the 5-HT system with OCD. DA dysregulation may contribute to some forms of OCD. Neurologic symptoms (e.g., tics)
are part of the clinical presentation in some patients with OCD. Tourette’s disorder, a disorder of DA dysfunction, is
often a concurrent disease.
Treatment of obsessive- Compulsive Disorder
Pregnancy In general, CBT alone should be used for pregnant patients except in cases in which the risks of
untreated OCD outweigh the risks of drug use (e.g., a pregnant woman who will not eat because of contamination
fears)