The limbic system, which is called the emotional brain, regulates emotional responses. Anxiety disorders are associated with abnormalities within this system (including the frontal cortex, hypothalamus, amygdala, hippocampus, brain stem, and the autonomic nervous system).
Neurotransmitters and their specific receptor sites function to transmit inhibiting or stimulating messages across the synapses between nerve cells in the brain. Abnormalities in the neurotransmitters or the receptor sites have been associated with multiple psychiatric disorders, including anxiety disorders.
Gamma-aminobutyric acid (GABA) is an inhibitory neurotransmitter that normally acts to decrease anxiety responses. An individual that genetically produces lower amounts of GABA may have an increased likelihood of developing anxiety or stress-related disorders (eg, PTSD).
Norepinephrine is a stimulating neurotransmitter, which is released as part of the fight-or-flight response and is associated with the cardiovascular and respiratory effects of anxiety. Serotonin is a neurotransmitter that regulates multiple responses, including sleep and alertness and sensations of hunger and satiation. Genetic variation resulting in a decrease in the number of select serotonin receptors (particularly 1A) may be associated with the development of panic disorder.
Panic disorders may be related to the reception of a false signal from the brain that there is a shortage of oxygen or an increase in carbon dioxide (suffocation alarm theory). Those who have panic attacks have also been reported to have higher levels of norepinephrine.
Suppression of cortisol through administration of dexamethasone has been associated with PTSD, suggesting heightened glucocorticoid feedback sensitivity.
Positron-emission tomography (PET) and computed tomography (CT) scanning have shown abnormalities in glucose metabolism in the frontal and prefrontal cortex and the basal ganglia of the brains of individuals with panic disorder. PET scans have also demonstrated increased blood flow and cerebral metabolism in the basal ganglia and frontal cortex of individuals with OCD.
OCD has been associated with increased serotonin responsiveness as well as striatum dysfunction. The striatum controls voluntary movement and it is hypothesized that individuals with OCD may be doing repetitive rituals to “self-medicate” for serotonin deficiencies.
Dissociative symptoms have been related to shrinkage of the hippocampus. Studies of physically, sexually, and psychologically abused children found increased electroencapholography (ECG) abnormalities in the frontal and temporal lobes.
First-degree relatives of individuals with panic disorder have a four to seven times greater chance of developing this disorder. Twin studies demonstrate a higher concordance rate for monozygotic than dizygotic twins.
Approximately 20% of first-degree relatives of people with agoraphobia also have agoraphobia.
Approximately 3% to 7% of people with OCD have firstdegree relatives with the same disorder.
Approximately 25% of first-degree relatives with generalized anxiety disorder are also affected by generalized anxiety disorder.
Environmental influences may interact with genetic predispositions in the pathogenesis of dissociative and other trauma-related disorders. Variations in regions of the serotonin transporter gene, among others, which regulates an enzyme that degrades several neurotransmitters (catechol-Omethyl transferase), have been found to be associated with adverse life events in individuals with dissociation. It has been speculated that the nature of this variation may be associated with development of anxiety or depression depending on the stressor.
Psychodynamic theory describes unconscious conflicts having early childhood origin and resulting from repressed wishes and drives. These conflicts cause guilt and shame, which lead to anxiety and associated symptoms.
Interpersonal theory implicates early relationships, which directly affect development of self-concept and self-esteem. Individuals with poor self-concept and decreased self-esteem have increased susceptibility to anxiety-related disorders.
Behavioral theory describes anxiety and associated symptoms as a conditioned response to internal and external stressors.
Cognitive theory describes faulty thinking patterns that lead to an individual’s misperceiving events affecting self, the future, and the world. These faulty thinking patterns contribute to the subjective experience of anxiety.
Dissociative disorders are generally associated with traumatic events. An individual responds to severe trauma (especially in early childhood) by “splitting off” or dissociating the self from the memory of the trauma. Severe physical, sexual, and psychological abuse in early childhood is associated with dissociative identity disorder.
Anxiety disorders and ritualistic behaviors are commonly seen in high-technology societies.
There is a higher incidence of anxiety disorders in urban communities than in rural communities.
Women are diagnosed more commonly with anxiety disorders except with OCD, which affects men and women equally. It is thought that this may represent a sociocultural rather than a genetic factor.
Acute and posttraumatic stress disorder share several symptoms, with the major difference between the two conditions being the time frame in which symptoms develop.
For acute stress, symptoms develop within 1 month of the traumatic event, and last for 2 days to 3 weeks whereas for posttraumatic stress disorder, the symptoms are more enduring and have lasted for a least 1 month at the time of diagnosis.
During the initial traumatic event, the individual needs to have displayed an initial response of horror, accompanied by intense feelings of helplessness in order to meet criteria for each of these disorders.
Both disorders share a cluster of dissociative symptoms with attempts to avoid stimuli associated with the original trauma while also reexperiencing intrusive memories and recollections of the traumatic event.
An examination and history would elicit findings that would include three or more of the following: a sense of numbness, a lack of emotional responses, feelings of depersonalization or derealization, a feeling of confusion, and a loss of memory for aspects of the original event.
There will also be increased sympathetic activation, hypervigilance and a pattern of reexperiencing the event through intrusive dreams, flashbacks or increased anxiety when presented with stimuli associated with the traumatic event. Increased sympathetic activation associated with anxiety is demonstrated through insomnia, difficulty concentrating, feelings of restlessness, and hypervigilance.
A pattern of worrying or anxiety that results in increased autonomic activity persisting for a period of at least 6 months.
An examination and history would reveal symptoms from three of four categories:
Motor (eg, trembling, restlessness, inability to relax, and fatigue).
Autonomic hyperactivity (eg, sweating, palpitations, cold clammy hands, urinary frequency, lump in throat, pallor or flushing, increased pulse, and rapid respirations).
Apprehensiveness (eg, worry, dread, fear, rumination, insomnia, and inability to concentrate).
Hypervigilance (eg, feeling edgy, scanning the environment, and distractibility).
A preoccupation with persistent intrusive thoughts (obsessions), repeated performance of rituals designed to prevent some event (compulsions), or both.
Anxiety occurs if obsessions or compulsions are resisted and from feeling powerless to resist the thoughts or rituals.
The presence of recurrent unexpected anxiety attacks for at least 1 month with a sudden onset of feelings of intense apprehension and dread.
These feelings result in sympathetic activation that manifests through the appearance of at least four of the following symptoms: chest discomfort or pain, dyspnea, palpitations, syncope, diaphoresis, trembling, hot or cold flashes, and dizziness.
A phobia is a persistent irrational fear of an object or situation that the person may recognize as being unreasonable.
Exposure to the feared object or situation may result in a panic attack.
An example is agoraphobia, which is a fear of being alone in open or public places where escape might be difficult.
Depersonalization disorder—a persistent or recurrent experience of feeling detached from oneself. A common sensation is of being an outside observer of one’s body. This experience can cause significant impairment in daily function.
Dissociative amnesia—one or more episodes of inability to recall important information, usually of a traumatic or stressful nature
Dissociative fugue—state manifested by sudden, unexpected travel away from home or one’s place of work with inability to remember the past. There may be confusion about personal identity or the assumption of a new identity.
Dissociative identity disorder—previously known as multiple personality disorder, this disorder is evidenced by the presence of two or more distinct identities, each with its own patterns of relating, perceiving, and thinking. At least two of these identities take control of the person’s behavior.
Measurement tools for anxiety:
Hamilton Rating Scale for Anxiety
State-Trait Anxiety Inventory
Measurement tools for OCDs:
Yale-Brown Obsessive-Compulsive Scale
Florida Obsessive-Compulsive Inventory (FOCI)
Measurement tools for panic disorders:
Acute Panic Inventory
Sheehan Client-Rated Anxiety Scale
Sodium lactate infusion or carbon dioxide inhalation will likely produce a panic attack in a person with panic disorder.
Increased arousal may be measured through studies of autonomic functioning (ie, heart rate, electromyography, sweat gland activity) in a person with PTSD.
Dexamethasone suppression test (DST) may be used to demonstrate heightened glucocorticoid feedback in individuals with PTSD.
Measurement tools for dissociation:
Dissociation Impulsivity Scale (DIS)
Dissociative Experiences Scale (DES)
Dissociative Disorders Interview Schedule (DDIS)
Various levels and sites of care can be provided: psychiatric inpatient, outpatient, or home care. Most care is provided on an outpatient basis. Site of care is based on many factors, including degree of disability of affected individual, community services available, and insurance and managed care considerations. Generally, the recommended treatment is a combination of drugs and psychotherapy, along with education of the individual and family.
Psychoeducational strategies:
Relaxation techniques.
Progressive muscle relaxation.
Guided imagery or visualization exercises.
Stress management.
Assertiveness training.
Psychotherapy:
Psychodynamic—assists people in understanding their experiences by identifying unconscious conflicts and developing effective coping behaviors.
Behavioral—focuses on the individual problematic behavior and works to modify or extinguish the behavior. One form of behavioral therapy effective in management of phobic disorders is systematic desensitization.
Cognitive—assists patient to question faulty thought patterns (reframing) and examine alternatives. In treatment of PTSD and dissociative disorders, reframing is used to help the patient view self as a survivor rather than a victim.
Hypnotherapy—can be used as part of therapy for those suffering dissociative disorders.
Support group therapy—useful in providing a supportive and psychoeducational approach for patients with anxiety or dissociative disorders.
Somatic therapies:
Biofeedback—relaxation through biofeedback is achieved when a person learns to control physiologic mechanisms that are not ordinarily within one’s awareness. Awareness and control are accomplished by monitoring body processes, including muscle tone, heart rate, and brain waves.
Psychopharmacologic—traditionally, drugs used to treat anxiety-related disorders were those that would increase GABA (benzodiazepines), regulate serotonin levels (antidepressants), or reduce physiologic effects of anxiety by causing peripheral beta-adrenergic blockade (beta-adrenergic blockers). Currently, selective serotonin reuptake inhibitors are prescribed as first-line treatment for managing several anxiety-related disorders due to their safety and tolerability. See Table 57-1, page 1814.
Narcotherapy—sodium amobarbital or IV sodium thiopental may assist the therapist in gaining access to a patient’s repressed memories and buried conflicts. In a person experiencing dissociative amnesia or dissociative fugue, the therapist may explore dissociated events. If the person is diagnosed with dissociative identity disorder, this type of interview may facilitate the access of other personalities.
Undiagnosed medical reasons for anxiety could lead to physical deterioration and a delay in obtaining appropriate medical care. It is important to screen for coexisting medical illness.
If panic and phobic disorders are left untreated, they can lead to increasing social withdrawal and isolation, which may severely impair the person’s social and work life.
Untreated OCD can lead to aggressive behavior toward self or others as well as depression. It can also lead to injuries from compulsive behavior such as skin breakdown from repeated handwashing.
Undiagnosed or untreated PTSD or acute stress disorder can lead to substance abuse or dependence, aggressive or violent behavior and, possibly, suicide.
If a person with a dissociative disorder goes untreated, aggressive behavior may develop toward self or others. Such behaviors may include assaults, depression, PTSD, psychoactive substance abuse disorder, rape, self-mutilation, and suicide attempts.
Assess psychological, cognitive, and behavioral symptoms.
Defense mechanisms or coping measures used.
Mood.
Suicide potential.
Thought content and process.
Severity of subjective experience of anxiety.
Understanding of specific disorder.
Explore social functioning.
Ability to function in social and work situations.
Impact of symptoms on patient’s relationships, especially work and family relationships.
Diversional and recreational behavior.
Identification of stressors related to self-concept, role performance, life values, social status, and support systems.
Benefits (primary and secondary gains) and risks of the presenting symptoms.
Anxiety related to unexpected panic attacks or related to reexperiencing traumatic events.
Acute Confusion related to severe anxiety.
Impaired Social Interaction related to avoidance behavior or related to embarrassment and shame associated with symptoms.
Ineffective Role Performance related to inability to function in usual social and occupational situations secondary to anxietyrelated symptoms.
Disturbed Personal Identity related to a traumatic event.
Risk for Injury related to compulsive behaviors.
Table 57-1 Dosage and Adverse Reactions of Anti-Anxiety Drugs | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
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Help patient identify anxiety-producing situations and plan for such events.
Assist patient to develop assertiveness and communication skills.
Practice stress-reduction techniques with patient.
Teach patient to monitor for objective and subjective manifestations of anxiety.
Tachycardia, tachypnea.
Signs and symptoms associated with autonomic stimulation—perspiration, difficulty concentrating, insomnia.
Promote use of stress-reduction techniques in managing symptoms of anxiety.
Encourage patient to verbalize feelings of anxiety.
Administer prescribed anxiolytics to decrease anxiety level.
Use short, simple sentences when communicating with patient.
Maintain a calm, serene manner.
Use adjuncts to verbal communication, such as visual aids and role-playing, to stimulate memory and retention of information.
Teach relaxation techniques to diminish distress that interferes with concentration ability.
Encourage discussion of reasons for and feelings about social isolation.
Help patient identify specific causes and situations that produce anxiety that inhibits social interaction.
Recommend participation in programs directed at specific conflict areas or skill deficiencies. Such programs may focus on assertiveness skills, body awareness, managing multiple role responsibilities, and stress management.
Identify secondary benefits, such as decreased responsibility and increased dependency, that inhibit patient’s move to independence.
Provide experiences in which patient can be successful.
Explore alternative methods of meeting dependency needs.
Explore beliefs that support a helpless or dependent mode of behavior.
Teach and role-play assertive behaviors in specific situations.
Provide instruction in decision-making skills, allowing opportunities for practice and rehearsal of techniques in role-play situations.
Assist patient to improve skills based on performance.
Encourage family members to avoid fostering dependency.
Develop an honest, nonjudgmental relationship with patient.
Try to establish open communication.
Do not overwhelm patient.
Teach patient containment techniques to assist in coping with the painful memories becoming conscious (eg, visualizing a safe environment, recall of past successes in dealing with anxiety, focusing on slowing of physiologic responses).
Encourage patient to set limits on ritualistic behavior as part of established treatment plan.
Assist patient in listing all objects and places that trigger anxiety as part of exposure-response prevention program.
Use cognitive strategies, such as reframing, to assist patient in placing thoughts and feelings in a different perspective.
Participate as member of treatment team in establishing program for systematic desensitization.
Intervene as needed and obtain emergency assistance when patient is in immediate danger.
Patients with anxiety-related disorders are generally treated in an outpatient setting. Many of these patients may not see a mental health professional but will be treated by their family health care provider, utilizing pharmacologic therapy. Nurses who encounter patients taking prescribed drugs for anxiety should assess effectiveness and patient knowledge base regarding safe use of these drugs. Patients should be encouraged to utilize anxiety-reduction techniques.
Because anxiety disorders will affect family functioning, the nurse should provide support for the family, including teaching family members about the disorder and treatment measures.
Patients may elect to utilize alternative and complementary therapies in order to obtain relief from symptoms. Advise patients not to use nutritional supplement or “natural” remedy, such as St. John’s wort or kava kava, without discussing it with a health care provider; many drug interactions exist.
Several community support groups are available to provide patient with continued support. Patient may also be able to learn further techniques for the management of anxiety through participation in these programs. Such programs may also provide patient with an opportunity to practice previously learned skills in a supportive environment.
Teach patient and family members about anxiety.
Define anxiety and differentiate it from fear.
Explain causes of anxiety.
Identify events that can trigger anxiety.
Identify relevant signs and symptoms of anxiety.
Describe the drug regimen, including significant action, adverse effects, dosage considerations, and any food or drug interactions.
Identify, describe, and practice deep-muscle relaxation techniques, relaxation breathing, imagery, and other relaxation therapies (see page 30).
Teach family to give positive reinforcement for use of healthy behaviors.
Teach family not to assume responsibilities or roles normally assigned to patient.
Teach family to give attention to patient, not patient’s symptoms.
Teach alternative ways to perform activities of daily living (ADLs) if physical or emotional disability inhibits function and performance.
For additional information and support, refer to such agencies as the Anxiety Disorders Association of America (www.adaa.org).
Many websites provide support for individuals and family members. Some examples include Agoraphobics Building Independent Lives, www.anxietysupport.org (for sufferers from anxiety disorders), and for panic and anxiety disorders, www.anxietynetwork.com/pdhome.html.
Identifies stressors and demonstrates normal heart rate, respirations, sleep pattern, and subjective feelings of anxiety.
Demonstrates improved concentration and thought processes through improved ability to focus, think, and solve problems.
Reports increased participation and enjoyment in family- and community-related events
Reports going to work, keeps appointments.
Uses coping strategies in situations that are anxiety provoking.
Does not injure self or others.
Somatization disorder.
Undifferentiated somatoform disorder.
Conversion disorder.
Pain disorder.
Hypochondriasis.
Body dysmorphic disorder.
Somatoform disorder not otherwise specified.
An individual with a somatoform disorder may experience high levels of physiologic arousal (increased awareness of somatic sensations).
The phenomenon of alexithymia, or deficient communication between brain hemispheres, may result in difficulty expressing emotions directly, and therefore distress may be expressed as physical symptoms.
The concept of somatosensory amplification, in which there is the tendency to experience somatic sensation as intense, noxious, and disturbing, may be related to the development of somatoform disorders.
Somatization disorder has been found to have a 10% to 20% frequency in first-degree female biological relatives of women with this disorder.
Twin studies have validated some increased risk in conversion disorder in monozygotic twins.
The genetic basis for other somatoform disorders is not well established.
Psychodynamic theory—the psychological source of ego conflict is denied and finds expression through displacement of anxiety onto physical symptoms. Both primary gain (anxiety relief) and secondary gains (increased dependence and relief from normal responsibilities) are common to these disorders.
Behavioral theory—the child learns from parent to express anxiety through somatization; secondary gains reinforce symptoms.
Cognitive theory—the individual has cognitive distortions in which benign symptoms are magnified and interpreted as serious disease.
Family theory—a family system that is overly enmeshed may utilize dysfunction in one person as a means to handle anxiety. In such families, the individual may not see self as a separate and distinct person; instead, the person may view him- or herself as an extension of the family.
Incidence of somatoform disorders is highest in rural populations and in low socioeconomic groups.
Somatic symptoms are more common in cultures that view direct expression of emotions as unacceptable.
Women may experience certain chronic pain conditions more commonly than men (this may have more of a cultural than a genetic basis).
This disorder is characterized by a preoccupation with some imagined defect in appearance in an otherwise normal-appearing person (or excessive concern, if the defect is present).
The preoccupation causes significant impairment in social or occupational functioning or cause marked distress.
With this condition, the individual develops symptoms compatible with a neurological disorder.
Examples include loss of vision, deafness, peripheral neuropathy, or bladder and bowel dysfunction. Some patients may exhibit paralysis or seizure activity.
These symptoms cannot be associated with a physical illness for the diagnosis of this disorder.
A fixed preoccupation the individual has a serious medical condition.
This belief often persists in spite of medical tests or procedures that do not find any physical condition.
This preoccupation often leads to significant problems with daily function.
Characterized by the presence of acute or chronic pain, which may be associated with a physical injury or have a psychological cause.
When associated with a physical cause, the pain appears to be more intense or disabling than expected.
Pain is generally found in more than one place on the body.
A chronic condition characterized by the presence of numerous physical complaints prior to age 30, with at least 6 months’ duration at time of diagnosis.
Physical examination and history elicits reports of pain in at least four bodily locations, gastrointestinal dysfunction, reproductive concerns or dysfunction, and at least one symptom reflecting a neurologic disorder.
An undifferentiated form of the disorder exists, with fewer presenting symptoms primarily consisting of fatigue, gastrointestinal symptoms, and pain.
Individuals with somatoform disorders will present in the medical rather than the psychiatric setting because of their belief that the problems are medical.
The individual should receive a thorough medical evaluation (if possible, avoiding repeating tests that have already had negative results).
The diagnosis of somatoform disorder will be made after a thorough medical evaluation in which no organic basis for the symptoms is found.
Level and setting of care to be provided is determined. In general, the individual will be treated on an outpatient basis, unless underlying mood disorder is present leading to risk for self-harm.
Referral to psychiatric treatment is generally rejected by the individual with a somatoform disorder; therefore, the goal of management is to maintain a long-term relationship with a specific health care provider to prevent patient from seeking multiple providers with multiple recommendations for testing, treatments, and drugs.
Psychotherapy:
Psychodynamic—assist the individual to express conflicts and emotions verbally rather than displacing them onto physical symptoms.
Behavioral—establish a program whereby adaptive behavior is reinforced and illness behaviors do not receive secondary gains.
Cognitive—restructure belief system that perpetuates illness-related behaviors.
Family therapy—assist family members to define appropriate boundaries and support patient in increasing selfresponsibility.
Somatic therapies: somatoform disorders are usually not treated with psychopharmacologic drugs because these patients are susceptible to dependency on drugs used.
Mood disorders, especially depression, are a common comorbid problem in individuals with somatoform disorders. Antidepressant drugs may be used to treat the mood disorder.
A patient with a known history of a somatoform disorder may have a coexisting medical condition that could go undiagnosed. Careful screening is essential to rule out medical problems.
Increased risk of suicide and substance abuse and dependence disorders is possible in patient with an untreated somatoform disorder.
Assess physical complaints.
Current and past history as well as duration of problems.
Diagnostic testing completed.
Number of health care providers consulted.
Types and amounts of drugs as well as whether self-medicating (over-the-counter) or prescribed.
Assess psychological processes.
Perception of illness and current stressors.
Self-concept and body image.
Secondary gains from physical symptoms.
Mood.
Suicide potential.
Explore social functioning.
Anxiety related to multiple physical symptoms and belief that serious disease exists.
Ineffective Coping related to preoccupation with physical symptoms.
Discuss current life stressors in the areas of social, occupational, and family functioning.
Assist patient to identify anxiety-producing situations and plan coping strategies.
Avoid focus on physical symptoms (after appropriate screening to rule out physical etiology).
Maintain focus on feelings and emotional responses rather than on somatic symptoms.
Teach and reinforce problem-solving approach to stressors.
Practice use of stress-reduction techniques with patient.
Encourage use of support groups.
Set limits on manipulative behaviors in a matter-of-fact manner.
Decrease reinforcement of secondary gains for physical symptoms.
Help patient identify and use positive means to meet emotional needs.
Encourage patient to cooperate with referrals for psychiatric or psychotherapy treatments.
Promote patient attendance and participation at community support groups.
Teach patient and family the importance of remaining with one health care provider to ensure continuity of care.
Nurses who encounter patients with somatoform disorders in the community should maintain a matter-of-fact attitude in order to decrease emphasis on dramatic symptoms. Any approach to patient should include a focus on patient’s strengths and capabilities rather than on disability.
Teach patient and family about the relationship between stressors, anxiety, and physical symptoms.
Family should expect person to function despite physical symptoms; doing things and making decisions for patient will increase dependent behaviors.
Encourage family therapy, which may be helpful in order to clarify roles, communication, and expectations.
Verbalizes anxiety about specific problems rather than expressing anxiety with physical symptoms.
Makes decisions on own; demonstrates less dependence on family and friends.
Biogenic amine theory proposes that there is a norepinephrine and serotonin deficiency in individuals with a depressive disorder. Changes in quantity and sensitivity of receptor sites for these neurotransmitters may also be important.
Kindling theory describes a process whereby external environmental stressors activate internal physiologic stress responses, which trigger the first depressive episode. Subsequent episodes can occur with less stress in response to the electrophysiologic sensitivity that was established in the brain from the initial episode.
Neuroendocrine dysfunction:
Hypothalamic-pituitary-adrenal axis dysfunction may be present in some individuals. Abnormalities include increased cortisol levels, resistance of cortisol to suppression by dexamethasone, and blunted adrenocorticotropin hormone response to corticotropin-releasing factor.
Subclinical hypothyroidism has been associated with depression, especially in women.
Dysfunction of circadian rhythms has been theorized to be related to depression. Abnormal sleep EEGs have been demonstrated in many individuals. Increased early morning awakening is common, as are multiple nighttime awakenings.
Risk of developing a mood disorder is 11/2 to 3 times greater in individuals with a first-degree relative with a mood disorder.
Twin studies reveal a higher rate of concordance in monozygotic twins than in dizygotic twins.
Mood states are associated with activation of several neuroendocrine pathways within the central and peripheral nervous systems. These pathways involve a number of neurochemical processes that involve activation of a particular binding protein identified as cyclic amp response binding protein 1 (CREB-1). Genetic profiles of individuals with depression have found evidence that genes involved in the cellular signaling pathways utilizing CREB-1 are associated with major depression. There then may be alleles (coding genes) that are related to the development of mood disorder.
Genetic variation in a certain region of the serotonin transporter gene (5-HTT) has been found to interact with the perception of stressful events (possibly through neuroendocrine pathways) to produce higher levels of depression and suicidality than in individuals without this variation.
While genetic evidence has supported conceptualizations of neurochemical and biologic alteration in the development of mood and other psychiatric disorders, no one single gene or factor has appeared to emerge as the main culprit. Most likely, a number of different genes and disposing factors are involved. Possible genes include 5-HTT, brain-derived neurotrophic growth factor, and the monoamine oxidase A gene.
Many drugs have the adverse effect of depression, including hormones, cardiovascular drugs, psychotropic drugs, and anti-inflammatory and anti-ulcer drugs.
Clinically significant depressive symptoms are detected in approximately 12% to 36% of individuals with a nonpsychiatric general medical condition.
Psychodynamic theory describes the occurrence of a significant loss (object loss) that is associated with anger and aggression, which is turned inward and leads to negative feelings about self. The negative feelings about the self, including shame and guilt, then lead to depression.
Life events and environmental stress, such as loss of a family member through death, divorce, or separation; lack of social support; and significant health problems, have all been associated with the onset of depression.
Cognitive theory describes how faulty thought patterns, including negative distortions of life experiences, produce negative self-evaluation, pessimistic thinking, and hopelessness.
Learned helplessness theory posits that a person who internalizes the belief that an unwanted event is his or her own fault and that nothing can be done to avoid or change it is prone to developing depression.
A major depressive episode reflects a level of depression that persists over a 2-week period.
Certain qualifying terms can be used that indicate whether the depression is associated with a change in the seasons (seasonal affective disorder) or follows the birth of an infant (postpartum).
Should delusions or hallucinations exist, the depression would be said to have psychotic features.
Major depression results in a significant change in ability to work or participate in social activities.
Physical examination and history findings should reveal at least five or more symptoms that include:
Depressed mood, fatigue.
Insomnia or an increased need for sleep.
Lack of interest in pleasurable activities (anhedonia).
Recent gain or loss of weight that represents at least 5% of body weight.
Feelings of worthlessness.
Inability to concentrate or make a decision.
Suicidal ideation.
A chronic, less intense level of depressed mood characterized by the same symptoms as seen in major depression and that lasts for at least 2 years in adults, at least 1 year in children and adolescents.
A major distinguishing feature is that dysthymia does not alter the ability to participate in social or work-related functions to the extent of major depression.
Rating scales of depression—to determine presence and severity of the problem:
Zung Depression Scale
Raskin Depression Rating Scale
Hamilton Rating Scale for Depression
Beck Depression Inventory
Laboratory studies:
Thyroid function tests and thyrotropin-releasing hormone stimulation test—to detect underlying hypothyroidism, which may cause depression.
DST—to evaluate depression that may be responsive to antidepressant or electroconvulsive therapy (ECT).
Twenty-four-hour urinary 3-methoxy-4-hydroxyphenylglycol (MHPG)—may show slightly lower level in unipolar depression than in bipolar depression.
Polysomnography—an increase in the overall amount of rapid-eye-movement (REM) sleep and shortened REM latency period in patients with major depression.
Additional diagnostic tests to evaluate physical conditions, such as CT scan or magnetic resonance imaging (MRI), complete blood count (CBC), chemistry panel, rapid plasma reagin (RPR), human immunodeficiency virus (HIV) test, EEG, vitamin B12 and folate levels, and toxicology studies.
Patients may receive treatment in acute inpatient psychiatric hospitals or in the community in an outpatient program. Decision about treatment setting is made according to the severity of patient’s illness, with primary concern being the risk of self-harm (suicide) as well as the presence of symptoms that are severely disabling.
Inpatient treatment is directed toward drug management and supportive psychotherapy using milieu management.
Somatic therapies:
Psychopharmacologic: drugs used to treat depression are those that will increase serotonin and norepinephrine (see Table 57-2, pages 1820 to 1821). A selective norepinephrine reuptake inhibitor (reboxetine) has seen used in Europe, but is not yet approved for use in the United States.
ECT may be used to treat severe depression that is unresponsive to antidepressant drugs.
Ultraviolet light therapy may be recommended for depression that occurs during fall and winter months (seasonal affective disorder).
Patient may select complementary and alternative treatments. The use of herbal supplements, especially St. John’s wort, is a popular alternative for antidepressant drugs. However, use of nutritional or herbal supplements should be discussed with the health care provider because of the potential for drug interactions.
Psychotherapy:
Psychodynamic therapy helps patient to become aware of unconscious anger directed toward object loss and “work through” these feelings to alleviate depression.
Cognitive therapy is the recommended psychotherapeutic approach for depression. This approach includes identifying and challenging the accuracy of patient’s negative thought patterns and encouraging behaviors designed to counteract depressive symptoms.
Family therapy assists patient and family members in developing a sense of self that is separate from that of the family as a whole. Patient is then encouraged to take responsibility for his or her own actions.
Table 57-2 Dosage and Adverse Reactions of Antidepressant Drugs | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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