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26 Cards in this Set
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Anxiety disorder
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Fear and anxiety arise in threatening and harmful situations. S&S: arousal, tenseness, increased HR, BP and respiration Epidemiology: Anxiety disorders occur in 10-30% of the population and can take several forms |
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Panic disorder
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Consists of several disabling panic attacks. Occurs in 2-3% of women and 0.5-1.5% of men. Between attacks the person spends time worrying about the next attack, and often engages in avoidance behavior.
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Agorophobia
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Phobic avoidance of persons, places, situations Genetics plays a large role 20% risk among relatives Neuroanatomic links -Locus coeruleus in the brainstem where NE is released and hippocampus, and amygdala in the temporal lobe show increased activity during an attack There may be a reduction of GABA benzodiazepine receptor binding Persons with panic attacks respond to some pharmacologic agents differently than other persons (caffeine, CO2, CCK, NE). Substances with stimulation of the noradrenergic system |
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Signs and symptoms of Agorophobia
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Light headedness, increased HR, difficulty breathing, sweating, weakness and trembling, abdominal distress, chills and hot flashes Symptoms occur spontaneously and vary in length from minutes to an hour |
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Treatment of Agorophobia
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This is highly treatable, up to 80% respond to cognitive behavioral therapy (CBT), antidepressants such as SSRI (paroxetine and sertraline) Tricyclic antidepressants (TCAs like imipramine) Benzodiazepines (BZ) such as alprazolam and clonazepam. Short term side effects of BZ: sedation, ataxia, cognitive impairment. Abrupt BZ withdrawal may produce: diarrhea, photophobia, return to anxiety and insomnia |
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Generalized anxiety disorder (GAD)
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Excessive and persistent worries. Incidence ranges from 4.1 to 6.6%, slightly higher rate in women. GAD emerges in the early 20s with individuals worrying about life events, marital relationships, job performance, health, money, or social status
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Etiology of GAD
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pathophysiology and etiology are poorly understood. There may be alterations in nt and/or receptors. There are reports of decrease in NE and 5HT binding. There is a decrease in peripheral BZ receptors
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S&S of GAD
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restlessness, motor tension, irritability, fatigue, difficulty concentrating, sleep disturbances, depression Symptoms tend to get less severe with age, GAD is diagnosed when a person spends at least 6 months excessively worrying |
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Treatment of GAD
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Behavioral therapy with emphasis on relaxation techniques BZ such as diazepam Long term treatment with buspirone (5HT agonist) is more effective and does not have the side effects of BZ. Unfortunately the response is slow (weeks to months) |
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Post-traumatic stress disorder (PTSD)
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Poorly recognized and diagnosed. Usually associated with exposure to terrifying or traumatic events. This was first described in combat situations as "shell shock" or "war neurosis". Exposure to serious accidents, earthquakes, childhood abuse, kidnapping, rape, or mugging now have been associated with reports of PTSF The traumatic experience is re-experienced through thoughts or dreams. Population estimates are lower in men (0.5%) than in women (1.2%) and it even occurs in children |
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Etiology of PTSD |
Exposure to major stressor involves several neural structures. There have been reports of reduced hippocampal volume. There is blood flow increase in the amygdala and blood flow reduction in the prefrontal cortex
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S&S of PTSD
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Decreased cortisol levels, blunted ATCH response, difficulty sleeping, nightmares and flashbacks. Lack of concentration, exaggerated startle response, hypervigilance, increased HR and BP PTSD is diagnosed when symptoms last longer than 1 month |
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Treatment of PTSD
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Antidepressants (SSRIs, TCS, MAOIs) usually for comorbid conditions and not for PTSD directly Psychotherapy, anxiety management, if you can relieve physical symptoms then it helps to follow up with behavioral therapy Drug puts painful memories to bed, experiments in mice might suggest PTSD treatment |
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Obsessive compulsive disorder (OCD)
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OCD is one of the ten leading causes of disability under anxiety related disorders. Patients have a significant impairment in their quality of life. It is considered a major medical concern
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Etiology of OCD
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Early onset: 20% in childhood, 29% in adolescence, 49% by age of 20. Onset is earlier in women than men. It tends to be chronic. There is a high concordance with monozygotic twins. It has been suggested that OCD is a pediatric autoimmune neuropsychiatric disorder associated with streptococcal infections. Neuroimaging suggest that Abs produce inflammation in the basal ganglia
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S&S of OCD |
A variety of symptoms upon presentation some are obsessive (repetitive thoughts, images, impulses) or they can be compulsive (repetitive activities or mental thoughts Diagnostic criteria require that the obsessions and/or convulsions be excessive enough (>1hr/d) to impair social and occupational functioning. Often see pts with comorbid conditions such as depression, alcohol abuse, or drug dependence Many with OCD are high functioning |
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Treatment of OCD
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Psychotherapy to document symptoms, CBT is the choice for adolescents and in mild cases Many patients resist drug therapy. FDA has approved 5 antidepressants for OCD. Chomipramine, fluoxetine, fluvoxamine, paroxetine, sertraline |
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Eating disorders
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A complex of symptoms involving issues about food, weight, and social relationships. The disorder can jeopardize the person's physical as well as psychosocial health. They develop despite normal functioning of the GI tract, and normal appetite also present
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Anorexia nervosa
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Was first described over 100 years ago. It is a self-starvation syndrome. Persons willingly lose over 15% of original body weight. Hunger is felt, but denied. There is a distorted body image
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Etiology of Anorexia nervosa
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Abnormal HPA-axis. Dysfunctional in serotonin, NE, and DA systems. There is probably a genetic component since there is a 55% concordance rate with monozygotic twins. Studies have focused on polymorphisms in the serotonin 2A receptor. There are psychosocial issues such as family separations, sexual and physical abuse. Athletes are at a special risk, especially female gymnasts, figure skaters, swimmers and distance runners. Among males it is seen in wrestlers and body builders
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S&S of Anorexia nervosa
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Refusal to maintain a minimum body weight. Fear or obsessions about being fat. Amenorrhea of three consecutive cycles. Feelings of lack of control. Inappropriate exercise. Complain of feeling full even when there is little intake of food. Lethargy, osteoporosis |
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Treatment of anorexia nervosa
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Nonpharmacological treatments have the greatest likelihood of causing a positive response. Behavioral management. CBT, interpersonal therapy (IP) and nutritional counseling. Total parenteral nutrition is reserved for severely malnourished patients when oral re-feeding fails. Also reserved for cases where there is electrolyte imbalance and cardiovascular crisis Many physical symptoms disappear after normal weight is restored |
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Bulimia nervosa, Binge eating disorder (BED)
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This emerged as a distinct disorder in 1979 on the DMS IV. Patients take large amounts of high caloric food (usually CHO) over a short period of time. Secretive behaviors of fasting, self-induced vomiting or abuse of laxatives and diuretics
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Etiology of BED
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Abnormal HPA-axis. Dysfunction in 5HT, NE, and DA. Probably a genetic factor since there is a 30% concordance in monozygotic twins. Usually women in their late teens through mid 30s. Like AN, athletes and wrestlers/body builders are at risk
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S&S of BED
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Concern about body image, but without a drive to thinness. Do not eat regular meals. Have guilt and depression after binges. Social isolation, troubled personal relationships. Physical indications are salivary gland inflammation, erosion of dental enamel, fluid and electrolyte imbalance, gastric reflux, esophageal tear, aspiration pneumonia |
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Treatment of BED
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BN patients have a better prognosis patients than ANUse of CBT, IP, and family counseling have the best success ratesThere is a newly developed 12 step program (the efficacy is yet to be evaluated)Antidepressants may be used in the acute early stage of treatment. SSRIs as an adjunct to CBT and IP
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