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Problems of Mental Health
ANXIETY-RELATED DISORDERS
ANXIETY AND DISSOCIATIVE DISORDERSAnxiety disorders are the most common of all psychiatric
disorders. An individual with one of these disorders
experiences physiologic, cognitive, and behavioral
symptoms of anxiety. The physiologic manifestations are
related to the fight-or-flight response and result in
cardiovascular, respiratory, neuromuscular, and GI
stimulation. The cognitive symptoms include subjective
feelings of apprehension, uneasiness, uncertainty, or dread.Behavioral manifestations include irritability, restlessness,
pacing, crying and sighing, and complaints of tension and
nervousness. The common theme among anxiety disorders
is that the individual experiences a level of anxiety that
interferes with functioning in personal, occupational, and
social areas.
Anxiety experienced in response to a traumatic event mayinterrupt the formation of memories related to the event and
disrupt learning processes resulting in dissociation.
Disassociation can be initially viewed as an adaptive
defense against painful memories or feelings of
helplessness. When aspects of disassociation interfere with
the ability of the individual to function socially,
vocationally or interpersonally, then such dissociative
aspects may be considered a disorder.
In most situations of disassociation the response to a
traumatic event is not consciously connected to memories
of the event. Such dissociative disorders are characterized
by an alteration in conscious awareness, which includes
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forgetfulness and memory loss for past stressful events.
Other dissociate methods of withdrawing from anxiety
producing stimuli are depersonalization (a feeling of
disconnection from one's self) and derealization (a feelingof being disconnected from the surrounding environment).
The individual may also develop what appear to be
distinctly different personalities
Classification
Anxiety-related disorders, as defined by the Diagnostic and
Statistical Manual of Mental Disorders, Fourth Edition
Text Revision (DSM-IV-TR), include those listed here.
Anxiety Disorders Panic disorder without agoraphobia
Panic disorder with agoraphobia
Agoraphobia without history of panic disorder
Specific phobia
Social phobia
Obsessive-compulsive disorder (OCD)
Posttraumatic stress disorder (PTSD) Acute stress disorder
Generalized anxiety disorder
Anxiety disorder due to a general medical condition
Substance-induced anxiety disorder
Anxiety disorder not otherwise specified
Dissociative Disorders
Dissociative amnesia Dissociative fugue
Dissociative identity disorder
Depersonalization disorder
Dissociative disorder not otherwise specified
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Pathophysiology and Etiology
The underlying etiology of anxiety disorders as well as any
of the psychiatric disorders, is complex, having multiple
factors that interact. Therefore, it is essential to examine thebiochemical, genetic, psychosocial, and sociocultural
factors.
Biochemical Factors
The limbic system, which is called the emotional
brain, regulates emotional responses. Anxiety
disorders are associated with abnormalities within this
system (including thefrontal 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 psychiatricdisorders, 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,
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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 thedevelopment 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). People who have panic attacks have
also been reported to have higher levels of
norepinephrine.
Suppression of cortisol through administration ofdexamethasone 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 ofindividuals 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,
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and psychologically abused children found increased
EEG abnormalities in the frontal and temporal lobes.
Genetic Factors
First-degree relatives of individuals with panicdisorder 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
persons with agoraphobia also have agoraphobia.
Approximately 3% to 7% of persons with OCD havefirst-degree relatives with the same disorder.
Approximately 25% of first-degree relatives with
generalized anxiety disorder are also affected by
generalized anxiety disorder.
Dissociative disorders have not been identified as
being genetically transmitted.
Psychosocial Factors 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 andself-esteem. Individuals with poor self-concept and
decreased self-esteem have increased susceptibility to
anxiety-related disorders.
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Behavioral theory describes anxiety and associated
symptoms as a conditioned response to internal and
external stressors.
Cognitive theory describes faulty thinking patternsthat 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 thetrauma. Severe physical, sexual, and psychological
abuse in early childhood is associated with
dissociative identity disorder.
Sociocultural Factors
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.
Clinical ManifestationsSee Table below (Diagnostic Criteria for Anxiety
Disorders)
Diagnostic Evaluation
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Measurement tools for anxiety:
o Hamilton Rating Scale for Anxiety
o The State-Trait Anxiety Inventory
Measurement tools for OCDs:o Yale-Brown Obsessive-Compulsive Scale
o Florida Obsessive-Compulsive Inventory (FOCI)
Measurement tools for panic disorders:
o Acute Panic Inventory
o 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:
o Dissociation Impulsivity Scale (DIS)
o Dissociative Experiences Scale (DES)
o Dissociative Disorders Interview Schedule
(DDIS)
Diagnostic Criteria for Anxiety Disorders
ANXIETY DISORDERS
Acute stress disorder
Person has been exposed to a traumatic event either
witnessed or experienced
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Develops three or more of these dissociative
symptoms:
o Subjective sense of numbing
o
Absence of emotional responsivenesso Feeling dazed
o Derealization
o Depersonalization
o Dissociative amnesia
Duration of 2 days to 4 weeks
Generalized anxiety disorder
Persists for at least 6 months Symptoms present from three of the four categories:
o Motor tension (eg, trembling, restlessness,
inability to relax, and fatigue)
o Autonomic hyperactivity (eg, sweating,
palpitations, cold clammy hands, urinary
frequency, lump in throat, pallor or flushing,
increased pulse, and rapid respirations)o Apprehensiveness (eg, worry, dread, fear,
rumination, insomnia, and inability to
concentrate)
o Hypervigilance (eg, feeling edgy, scanning the
environment, and distractibility)
Obsessive-compulsive disorder
Preoccupation with persistent intrusive thoughts(obsessions), repeated performance of rituals designed
to prevent some event (compulsions), or both
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Anxiety occurs if obsessions or compulsions are
resisted and from feeling powerless to resist the
thoughts or rituals
Panic disorder
Recurrent unexpected anxiety attacks
Sudden onset with intense apprehension and dread
At least four of the following symptoms:
o Dyspnea
o Chest discomfort
o Dizziness
o Hot or cold flasheso Tingling of hands or feet
o Feelings of unreality
o Palpitations
o Syncope
o Diaphoresis
o Trembling
o
Fear of losing control, going crazy, or dyingPosttraumatic stress disorder
After experiencing a psychologically traumatic event
outside the range of usual experience (eg, rape,
combat, bombings, kidnapping), the person
reexperiences the event through recurrent dreams and
flashbacks.
Emotional numbness, detachment, and estrangementmay be used to defend against anxiety.
May experience sleep disturbance, hypervigilance,
guilt about surviving, poor concentration, and
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avoidance of activities that trigger memory of the
event.
Phobias
Irrational fear of an object or situation that persists,although the person may recognize it as unreasonable
Types include:
o Agoraphobia: Fear of being alone in open or
public places where escape might be difficult;
may not leave home
o Social phobia: Fear of situations in which one
might be seen and embarrassed or criticized; fearof eating in public, public speaking, or
performing
o Specific phobia: Fear of a single object, activity,
or situation (eg, snakes, closed spaces, and
flying)
Anxiety severe if the object, situation, or activity
cannot be avoidedSubstance-induced anxiety disorder
Prominent anxiety, panic attacks, or obsessions or
compulsions predominate
Symptoms developed within 1 month of substance
intoxication or withdrawal
Drug use related to disturbance
Disturbance does not occur exclusively during thecourse of delirium
Significant distress or impairment in social and
occupational functioning results
DISSOCIATIVE DISORDERS
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Depersonalization disorder
Persistent or recurrent experience of feeling detached
from and outside one's mental processes or body
Reality testing intact Experience causes significant impairment in social or
occupational functioning or causes marked distress
Does not occur exclusively during course of another
mental disorder
Dissociative amnesia
One or more episodes of inability to recall important
information usually of a traumatic or stressfulnature
Other psychological (eg, multiple personality disorder)
and physical (eg, substance-induced) disorders ruled
out
Dissociative fugue
Sudden, unexpected travel away from home or one's
place of work with inability to remember past Confusion about personal identity or assumption of
new identity
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
Inability to recall important personal information tooextensive to be explained by ordinary forgetfulness
Other causes ruled out
Footnote
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Adapted from American Psychiatric Association (APA)
(2000). Diagnostic and statistical manual of mental
disorders (Fourth edition Text revision). Washington, D.C.:
APA.Management
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 acombination of drugs and psychotherapy, along with
education of the individual and family.
Psychoeducational strategies:
o Relaxation techniques
o Progressive muscle relaxationo Guided imagery or visualization exercises
o Stress management
o Assertiveness training
Psychotherapy:
o Psychodynamic assists persons in
understanding their experiences by identifying
unconscious conflicts and developing effectivecoping behaviors.
o Behavioral focuses on the individual
problematic behavior and works to modify or
extinguish the behavior. One form of behavioral
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therapy effective in management of phobic
disorders is systematic desensitization.
o Cognitive assists patient to question faulty
thought patterns (reframing) and examinealternatives. In PTSD and dissociative disorders,
the patient is assisted to view self as a survivor
rather than a victim.
o Hypnotherapy can be used as part of therapy
for those suffering dissociative disorders.
o Support group therapy useful in providing a
supportive and psychoeducational approach for
patients with anxiety or dissociative disorders. Somatic therapies:
o 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 brainwaves.
o Psychopharmacologic drugs used to treat
anxiety-related disorders are those that will
increase GABA (benzodiazepines), regulate
serotonin levels (antidepressants), or reduce
physiologic effects of anxiety by causing
peripheral beta-adrenergic blockade (beta-
adrenergic blockers).
o Narcotherapy sodium amobarbital or I.V.
sodium thiopental may assist the therapist in
gaining access to a patient's repressed memories
and buried conflicts. In a person experiencing
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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 theaccess of other personalities.
Complications
Undiagnosed medical reasons for anxiety could lead to
physical deterioration and a delay in obtaining
appropriate medical care. It is important to screen for
co-existing medical illness.
If panic and phobic disorders are left untreated, theycan 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 hand washing. 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.
Nursing Assessment
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Assess psychological, cognitive, and behavioral
symptoms.
o Defense mechanisms or coping measures used
o
Moodo Suicide potential
o Thought content and process
o Severity of subjective experience of anxiety
o Understanding of specific disorder
Explore social functioning.
o Ability to function in social and work situations
o Impact of symptoms on the patient's
relationships, especially work and familyrelationships
o Diversional and recreational behavior
o Identification of stressors related to self-concept,
role performance, life values, social status, and
support systems
o Benefits (primary and secondary gains) and risks
of the presenting symptoms
Nursing Diagnoses
Anxiety related to unexpected panic attacks or related
to re-experiencing traumatic events
Disturbed Thought Processes related to severe anxiety
Social Isolation 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 anxiety-related symptoms
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Disturbed Personal Identity related to a traumatic
event
Risk for Injury related to compulsive behaviors
Nursing Interventions
Reducing Symptoms of Anxiety
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 subjectivemanifestations of anxiety.
o Tachycardia, tachypnea
o 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.
DRUG ALERT
Benzodiazepines are associated with tolerance and
dependence and are appropriate for short-term use.
Withdrawal symptoms may occur when drug is abruptlydiscontinued. Gradual dosage reduction is necessary.
Overdose or taking benzodiazepines with alcohol or other
central nervous system (CNS) depressants can cause
respiratory depression requiring emergency intervention.
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Improving Concentration
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.
Increasing Social Interaction 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, bodyawareness, managing multiple role responsibilities,
and stress management.
Encouraging Independence
Identify secondary benefits, such as decreased
responsibility and increased dependency that inhibit
patient's move to independence.
Provide experiences in which patient can besuccessful.
Explore alternative methods of meeting dependency
needs.
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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.
Strengthening Identity 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 pastsuccesses in dealing with anxiety, focusing on slowing
of physiologic responses).
Reducing Harm from Behavior
Encourage limit setting on ritualistic behavior as part
of established treatment plan.
Assist patient in listing all objects and places that
trigger anxiety as part of exposure-responseprevention program.
Use cognitive strategies, such as reframing, to assist
patient in placing thoughts and feelings in a different
perspective.
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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.Community and Home Care Considerations
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 assesseffectiveness 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 the patient with continued support. The patientmay also be able to learn further techniques for the
management of anxiety through participation in these
programs. Such programs may also provide the patient
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with an opportunity to practice previously learned
skills in a supportive environment.
Patient Education and Health Maintenance
Teach patient and family members about anxiety.o Define anxiety and differentiate it from fear.
o Explain causes of anxiety.
o Identity events that can trigger anxiety.
o 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
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 Anxiety Disorders Association of
America, http://www.adaa.org.
Many Web sites provide support for individuals and family
members. Some examples include Agoraphobics Building
Independent Lives: http://www.anxietysupport.org/(for
https://remote.smh.ca/,DanaInfo=www.adaa.org+https://remote.smh.ca/,DanaInfo=www.anxietysupport.org+https://remote.smh.ca/,DanaInfo=www.adaa.org+https://remote.smh.ca/,DanaInfo=www.anxietysupport.org+7/27/2019 Problems of Mental Health
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sufferers from anxiety disorders); and for panic and anxiety
disorders, http://www.anxietynetwork.com/pdhome.html.
Evaluation: Expected Outcomes 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
SOMATOFORM DISORDERS
Somatoform disorders are characterized by complaints ofphysical symptoms that cannot be explained by known
physical mechanisms. These disorders have in common the
belief that physical symptoms are real despite evidence to
the contrary. The affected individual experiences changes
or loss in physical function. The physical symptoms are not
under the individual's voluntary control. Significant
impairment occurs in social or occupational functioning.
Classification
Somatization disorder
Undifferentiated somatoform disorder
Conversion disorder
https://remote.smh.ca/,DanaInfo=www.anxietynetwork.com+pdhome.htmlhttps://remote.smh.ca/,DanaInfo=www.anxietynetwork.com+pdhome.html7/27/2019 Problems of Mental Health
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Pain disorder
Hypochondriasis
Body dysmorphic disorder
Somatoform disorder not otherwise specifiedPathophysiology and Etiology
The underlying etiology of somatoform disorders is
difficult to define. The following factors may interact in the
individual with these disorders.
Biochemical Factors
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 whichthere is the tendency to experience somatic sensation
as intense, noxious, and disturbing, may be related to
the development of somatoform disorders.
Genetic Factors
Somatization disorder has been found to have a 10%
to 20% frequency in first-degree female biologicalrelatives of women with this disorder.
Twin studies have validated some increased risk in
conversion disorder in monozygotic twins.
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The genetic basis for other somatoform disorders is
not well established.
Psychosocial Factors
Psychodynamic theory: the psychological source ofego 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 gainsreinforce 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, theindividual may not see self as a separate and distinct
person; instead the person may view himself as an
extension of the family.
Sociocultural Factors
Incidence of somatoform disorders is highest in rural
populations and in low socioeconomic groups.
Somatic symptoms are more common in cultures thatview 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).
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Clinical Manifestations
See Diagnostic Criteria for Somatoform Disorders
Diagnostic Evaluation 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 noorganic basis for the symptoms is validated.
Management
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 the patient from seeking multiple
providers with multiple recommendations for testing,
treatments, and drugs.
Psychotherapy:o Psychodynamic: assist the individual to express
conflicts and emotions verbally rather than
displacing them onto physical symptoms.
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o Behavioral: establish a program whereby
adaptive behavior is reinforced and illness
behaviors do not receive secondary gains.
o
Cognitive: restructure belief system thatperpetuates illness-related behaviors.
o Family therapy: assist family members to define
appropriate boundaries and support patient in
increasing self-responsibility.
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
co-morbid problem in individuals with somatoform
disorders. Antidepressant drugs may be used to treat
the mood disorder.
Complications
The patient with a known history of a somatoformdisorder may also have a co-existing medical
condition that may go undiagnosed. Careful screening
is essential to rule out medical problems.
Increased risk of suicide and substance abuse and
dependence disorders is possible in the patient with an
untreated somatoform disorder.
Nursing Assessment Assess physical complaints.
o Current and past history as well as duration of
problems
o Diagnostic testing completed
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o Number of health care providers consulted
o Types and amounts of drugs as well as whether
self-medicating (over-the-counter) or prescribed
Assess psychological processes.o Perception of illness and current stressors
o Self-concept and body image
o Secondary gains from physical symptoms
o Mood
o Suicide potential
Explore social functioning.
Refer to section on Anxiety Disorders for assessment data.
Nursing Diagnoses
Anxiety related to multiple physical symptoms and
belief that serious disease exists
Ineffective Coping related to preoccupation with
physical symptoms
Other nursing diagnoses and nursing interventions under
Anxiety Disorders may apply.
Diagnostic Criteria for Somatoform Disorders
BODY DYSMORPHIC DISORDER
Preoccupation with some imagined defect in
appearance in a normal-appearing person (or excessive
concern, if the defect is present)
o Preoccupation causes significant impairment in
social or occupational functioning or causes
marked distress
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CONVERSION DISORDER
Development of a symptom or deficit suggesting:
o Neurologic disorder (blindness, deafness, loss of
touch, or pain sensation)o Involuntary motor function (aphonia, impaired
coordination, paralysis, or seizures)
Not due to malingering or factitious disorder and not
culturally sanctioned
Causes impairment in social or occupational
functioning, causes marked distress, or requires
medical attention
HYPOCHONDRIASIS
Preoccupation with fears of having or the idea that one
has a serious disease
Preoccupation persists despite appropriate medical
tests and assurances to the contrary
Other disorders are ruled out; for example, somatic
delusional disorders Preoccupation causes significant impairment in social
or occupational functioning or causes marked distress
PAIN DISORDER
Pain in one or more anatomic sites is a major part of
the clinical picture
Causes significant impairment in social or
occupational functioning or causes marked distress Psychological factors are thought to cause onset,
severity, or exacerbation
If a medical condition present, it plays a minor role in
accounting for pain
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SOMATIZATION DISORDER
History of many physical complaints before age 30,
occurring over a period of years and resulting in
change of lifestyle Complaints must include all of the following:
o History of pain in at least four different sites or
functions
o History of at least two GI symptoms other than
pain
o History of at least one sexual or reproductive
symptom
o History of at least one symptom defined as orsuggesting a neurologic disorder
UNDIFFERENTIATED SOMATOFORM DISORDER
One or more physical complaints:
o Fatigue
o Loss of appetite
o
GI symptomso Urinary symptoms
No physiologic explanation revealed by investigation
Symptoms cause clinically significant distress or
impairment in social or occupational functioning
Duration of the disturbance at least 6 months
Footnote
Adapted from American Psychiatric Association (APA)(2000). Diagnostic and statistical manual of mental
disorders (Fourth edition Text revision). Washington, D.C.:
APA.
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Nursing Interventions
Encouraging Recognition of Anxiety
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.
Improving Coping 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.
Community and Home Care Considerations
Encourage patient to cooperate with referrals for
psychiatric or psychotherapy treatments. Promote patient attendance and participation at
community support groups.
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Teach patient and family importance of remaining
with one health care provider to ensure continuity of
care.
Nurses who encounter patients with somatoformdisorders in the community should maintain a matter-
of-fact attitude in order to decrease emphasis on
dramatic symptoms. Any approach to the patient
should include a focus on patient's strengths and
capabilities rather than on disability
Patient Education and Health Maintenance
Teach patient and family about the relationshipbetween 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, andexpectations.
Evaluation: Expected Outcomes
Verbalizes anxiety about specific problems rather than
expressing anxiety with physical symptoms
Makes decisions on own: demonstrates less
dependence on family and friends.
MOOD DISTURBANCES
DEPRESSIVE DISORDERS
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Depressive disorders are considered mood disorders. A
mood is a sustained emotion that, when extreme, colors the
person's view of the world. Mood disorders are
characterized by disturbances in feelings, thinking, andbehavior. These disorders may occur on a continuum
ranging from severe depression to severe mania
(hyperactivity). A depressive illness is painful and can be
psychophysiologically debilitating. Depression is much
more than just sadness; it affects the way one feels about
the future and can alter basic attitudes about the self. A
depressed person can become so despairing as to express
hopelessness. When moods become severe or prolonged orinterfere with a person's interpersonal or occupational
functioning, this may signal a mood disorder.
Pathophysiology and Etiology
The exact causes for depressive disorders have not been
established. These disorders are thought to result from
complex interactions among various factors.
Biochemical Factors
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
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that was established in the brain from the initial
episode.
Neuroendocrine dysfunction:
o
Hypothalamic-pituitary-adrenal axis dysfunctionmay 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.
o Subclinical hypothyroidism has been associated
with depression, especially in women.o 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.
Genetic Factors
Risk of developing a mood disorder is 1 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 andperipheral 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).
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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 depressive 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-derivedneurotrophic growth factor, and the monoamine
oxidase A gene.
Medical Factors
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.
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Psychosocial Factors
Psychodynamic theory describes the occurrence of a
significant loss (object loss) that is associated with
anger and aggression, which is turned inward andleads 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 thoughtpatterns, 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
own fault and that nothing can be done to avoid or
change it is prone to developing depression.
Clinical Manifestations
See Characteristics of Depressive Disorders
Diagnostic Evaluation
Rating scales of depression to determine presence
and severity of the problem:
o Zung Depression Scaleo Raskin Depression Rating Scale
o Hamilton Rating Scale for Depression
o Beck Depression Inventory
Laboratory studies:
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o Thyroid function tests and thyrotropin-releasing
hormone stimulation test to detect underlying
hypothyroidism, which may cause depression.
o
DST to evaluate depression that may beresponsive to antidepressant or electroconvulsive
therapy (ECT).
o 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 andshortened 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 B12and folate levels, and toxicology studies.
Management
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 the patient's
illness, with primary concern being the risk of self-harm (suicide) as well as the presence of symptoms
that are severely disabling.
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Inpatient treatment is directed toward drug
management and supportive psychotherapy using
milieu management.
Somatic therapies:o Psychopharmacologic: drugs used to treat
depression are those that will increase serotonin
and norepinephrine
Pharmacology of Antidepressant Dru
DRUG:
CLASS/GENERIC/TRADE
NAME
ADULT
THERAPEUTIC
DOSAGERANGE
(MG/DAY)
ADVER
Tricyclic Agents For all tr
tetracycl
trigg
epispati
effe
cons
visio
effe
effe
hypo
palp
incr
Amitriptyline (Elavil, Endep)50-300 mg
Clomipramine (Anafranil) 25-250 mg
Desipramine (Norpramin,
Pertofrane)
75-300 mg
Doxepin (Adapin, Sinequan) 75-300 mg
Imipramine (Tofranil,
Tofranil-PM, Janimine, SK-
pyramine)
75-300 mg
Nortriptyline (Aventyl,
Pamelor)
25-150 mg
Protriptyline (Vivactil) 15-60 mg
Trimipramine (Surmontil) 75-200 mg
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effe
wav
prolTetracyclic Agent See Tricy
incr
weigcons
Mirtazapine (Remeron) 15-45 mg
Bicyclic Agent
weig
hype
Venlafaxine (Effexor) 75-375 mg
Selective Serotonin Reuptake Inhibitors
(SSRIs)
mou
drowdela
ejac
imp
orga
nerv
anxidizz
diar
mou
Citalopram (Celexa) 20-60 mgEscitalopram (Lexapro) 10-20 mg
Fluoxetine (Prozac) 20-80 mg
Paroxetine (Paxil) 10-50 mg
Sertraline (Zoloft) 50-150 mg
Fluvoxamine (Luvox) 50-300 mg
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mou
som
diar
trem
diarMonoamine Oxidase Inhibitors (MAOIs) For all M
hypo
gain
sexu
myo
painanti
beve
tyra
with
com
drug
caus
Isocarboxazid (Marplan) 30-50 mg
Phenelzine (Nardil) 45-90 mg
Tranylcypromine (Parnate) 20-60 mg
Pargyline (Eutonyl) 150 mg
Selegiline (Eldepryl,
Deprenyl)
10 mg
Dibenzoxazepine Agent
Amoxapine (Asendin) 100-600 mg
orth
refle
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extr
mov
Unicyclic Agent
Bupropion (Wellbutrin) 225-450 mg
cons
inso
agit
irreg
seiz
Triazolopyridine Agent
Trazodone (Desyrel) 150-600 mg
orthdizz
naus
Phenylpiperazine Agent
Nefazodone (Serzone) 200-600 hypo
nerv
o ECT may be used to treat severe depression thatis unresponsive to antidepressant drugs.
o Ultraviolet light therapy may be recommended
for depression that occurs during fall and winter
months (seasonal affective disorder).
The patient may select complementary and alternative
treatments. The use of herbal supplements, especially
St. John's wort, is a popular alternative for
antidepressant drugs .Use of nutritional or herbal
supplements should be discussed with the health care
provider due to the potential for drug interactions.
Psychotherapy:
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o Psychodynamic therapy assists the patient to
become aware of unconscious anger directed
toward object loss and work through these
feelings to alleviate depression.o Cognitive therapy is the recommended
psychotherapeutic approach for depression. This
approach includes identifying and challenging the
accuracy of the patient's negative thought
patterns and encouraging behaviors designed to
counteract depressive symptoms.
o Family therapy assists the patient and family
members in developing a sense of self that isseparate from that of the family as a whole. The
patient is then encouraged to take responsibility
for his own actions.
Characteristics of Depressive Disorders
Major Depressive Disorder
Occurs over a 2-week period Represents a change in previous functions
Impairs social and occupational functioning
Five or more of the following occur nearly every day
for most waking hours:
o Depressed mood
o Anhedonia (inability to experience pleasure)
o Significant weight loss or gain (more than 5% of
body weight per month)o Insomnia or hypersomnia
o Increased or decreased motor activity
o Anergy (fatigue or loss of energy)
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o Feelings of worthlessness or inappropriate guilt
(may be delusional)
o Decreased concentration or indecisiveness
o
Recurrent thought of death or suicidal ideation(with or without plan)
Specifiers
Severity
Psychotic features
Remission chronic
Seasonal affective disorder related to either winter or
summer Catatonic features
Melancholic features
Atypical features
Postpartum onset
Dysthymic Disorder
Occurs over a 2-year period (1 year for children and
adolescents), presence of depressed mood Still able to function in social and occupational
spheres
Presence of some of the following:
o Decreased or increased appetite
o Insomnia or hypersomnia
o Anergy or chronic fatigue
o Anhedoniao Decreased self-esteem
o Poor concentration or difficulty making decisions
o Perceived inability to cope with routine
responsibilities
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o Feelings of hopelessness or despair
o Pessimistic about the future, brooding over the
past, or feeling sorry for self
o
Recurrent thoughts of death or suicideFootnote
Adapted from American Psychiatric Association (APA)
(2000). Diagnostic and statistical manual of mental
disorders (Fourth edition Text revision). Washington, D.C.:
APA.
DRUG ALERT
Antidepressant therapy takes 2 to 4 weeks before beneficialeffects occur. Antidepressant drugs cannot be combined
due to additive serotonergic effects leading to serotonin
syndrome, a state of excessive serotonin in the synaptic
cleft. Symptoms include insomnia, confusion, agitation,
hyperreflexia, involuntary movements, and hypotension.
Hypertensive crisis can occur if patients take a monoamine
oxidase inhibitor antidepressant in combination with asympathomimetic drug or eat foods high in tyramine.
Complications
An undiagnosed medical condition causing depressive
symptoms could lead to physical deterioration and
delay in obtaining appropriate treatment.
Untreated depressive illness can lead to suicide.
Use of alcohol or drugs to feel better or numbdysphoric feelings.
Nursing Assessment
Assess posture and affect for:
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o Poor or slumped posture.
o Appearance of being older than stated age.
o Facial expression of sadness, dejection.
o
Episodes of weeping.o Anhedonia inability to experience pleasure.
Assess thought processes:
o Identify the presence of suicidal thoughts.
o Poor judgment, indecisiveness.
o Impaired problem solving, poor concentration.
o Negative thoughts.
Explore feelings for:
o Anger and irritability.o Anxiety, guilt.
o Worthlessness.
o Helplessness, hopelessness.
Assess physical behavior for:
o Psychomotor agitation or retardation.
o Vegetative signs of depression.
Change in eating patterns Change in sleeping patterns
Change in elimination patterns
Change in level of interest in sex
Change in personal hygiene
Assess for evidence of masked depression:
o Hypochondriasis.
o Psychosomatic disorders.
o Compulsive gambling.
o Compulsive overwork.
o Accident proneness.
o Eating disorders.
o Addictive illnesses.
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Assess for risk of suicide
NURSING ALERT
All mentally ill individuals, especially those who are
depressed, should be assessed for suicide risk and referredfor crisis intervention if they are deemed at risk.
Nursing Diagnoses
Hopelessness related to depressive thoughts
Risk for Injury related to hopelessness and impaired
problem solving
Bathing or Hygiene Self-Care Deficit related to lack ofmotivation and poor concentration
Disturbed Sleep Pattern related to insomnia
Nursing Interventions
Strengthening Coping and Sense of Hope
Initiate interaction with patient at a regularly
scheduled time.
Be clear and honest about your own feelings related topatient's behavior.
Encourage verbal expression of feelings.
Validate feelings that are appropriate to the situation.
Explore with patient what is producing and
maintaining the feeling of depression.
Encourage patient to identify events that cause
unpleasant emotional responses. Assess significant losses patient has experienced.
Identify cultural and social factors that may contribute
to how patient copes with loss and feelings.
Assess patient's support network.
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Maintaining Safety
Assess current suicide risk.
Implement appropriate level of observation based on a
focused suicide assessment (eg, constant observationor 15-minute checks).
Explain observation precautions to patient.
Remove harmful objects from patient's possession,
and assess environmental safety of patient's room and
unit.
Encourage patient to negotiate a no-self-harm and
no-suicide agreement with the staff.
Monitor need to revise level of observation. Provide additional structure by keeping patient
involved in therapeutic and psychorehabilitative
activities.
Encouraging Participation in ADLs
Collaborate with occupational and physical therapists
to determine patient's functional capacity toaccomplish ADLs.
If patient cannot accomplish ADLs independently,
provide hygiene activities in collaboration with
patient.
Acknowledge and reinforce patient's efforts to
maintain appearance; do not rush patient when self-
care is slow.
Reinforce what patient can do rather than what patientcannot do without assistance.
Remain with patient during mealtime to determine the
level of need for assistance or cueing in the ability to
eat.
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Facilitating Sleep
Determine patient's past and current sleep patterns and
sleep hygiene.
Ask what strategies patient has already used toimprove sleep, and elicit which ones have been
successful.
Consider decreasing the amount of daytime sleep by
encouraging participation in an activity.
Discuss alternative methods for facilitating sleep:
o Avoid caffeine and nicotine.
o Avoid emotionally charged or upsetting
discussions before bedtime.o Avoid exercise 30 minutes to 1 hour before bed.
o Increase physical activity within functional
limits.
o Use relaxation techniques.
o Try a warm bath or warm milk.
Administer prescribed drugs that cause sleepiness at
bedtime; avoid giving drugs that cause insomnia atnight.
Community and Home Care Considerations
Mood disorders tend to be chronic, with acute
episodes that may require inpatient treatment. The
patient in the home or community setting will require
ongoing monitoring regarding the use of drugs as well
as support and education in terms of the disorder. Community health care providers, including nurses,
must be aware of the need for primary and secondary
prevention programs directed at education as well as
early case finding and prompt treatment.
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Patient Education and Health Maintenance
Instruct patient and family members about symptoms
of depression.
Instruct patient and family members about purpose ofantidepressant drugs, effects, adverse effects and their
management, and how to recognize early signs and
symptoms of relapse.
Instruct patient and family members about the effect
of a depressive disorder on the family system.
Provide patient and family members with written
material on coping with depression.
Provide patient and family members with informationabout appropriate community-based programs and
support groups. Contact the National Foundation for
Depressive Illness, http://www.depression.org.
Evaluation: Expected Outcomes
Reports improvement in mood and increased interest
in daily living Remains free from self-harm
Accomplishes ADLs in an independent manner
Obtains a minimum of 5 hours of uninterrupted sleep
BIPOLAR DISORDERS
Bipolar disorders, also considered mood disorders, include
the occurrence of depressive episodes and one or more
elated mood episodes. An elated mood can include a rangeof affect, from normal mood to hypomania to mania. In the
most intense presentation, the person with bipolar disorder
experiences altered thought processes, which can produce
bizarre delusions.
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Pathophysiology and Etiology
Genetic Basis
Twin studies reveal a concordance rate of 65% inmonozygotic twins for bipolar disorder.
Risk for developing bipolar disorder is increased 4%
to 24% in first-degree relatives of people with bipolar
disorder.
Current research indicates that defective genes located
within chromosomes 18 and 21 may be related to
bipolar disorder.
Biochemical Factors
Patients with bipolar disorders may have lower plasma
norepinephrine, urinary MHPG, and platelet serotonin
uptake and higher red blood cell/plasma lithium rates
than do unipolar populations.
Pathology of the limbic system, basal ganglia, and
hypothalamus is proposed to contribute to thedevelopment of mood disorders.
Psychosocial Factors
Psychosocial stressors appear to have an important
role early in the illness, in concert with the electrical
kindling and behavioral sensitization models.
Mania and hypomania have been viewed by
psychoanalytic theorists as a defense againstdepression.
Clinical Manifestations
See Characteristics of Bipolar Disorders
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Diagnostic Evaluation
Rating scale assessment tools:
o Young Mania Rating Scale
o
Manic State Rating Scale There appear to be no laboratory features that
distinguish major depressive episodes found in major
depressive disorder from those in bipolar I or bipolar
II disorder.
Complete psychophysiologic examination.
Complete assessment to rule out medical conditions.
Management Patients may receive treatment in acute inpatient
psychiatric hospitals or in the community in an
outpatient program. The decision about treatment
setting is made according to severity of patient's
illness, including degree of mania or depression as
well as risk of self-harm or harm to others.
Inpatient treatment is directed toward drugmanagement as well as supportive psychotherapy in
order to alleviate the acute manic symptoms.
Pharmacologic treatment for acute mania consists of
the following:
o Lithium (Lithobid)
o Anticonvulsants, such as carbamazepine
(Tegretol) and valproate (Depakene), for mood-
stabilizing propertieso Neuroleptic agents, such as risperidone
(Risperdal), for acute psychotic thinking
o Benzodiazepines, such as clonazepam (Klonopin)
or lorazepam (Ativan), for acute agitation
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Psychotherapy is used as described above in the
section related to depression.
Psychiatric home care nursing to facilitate compliance
with drugs and therapeutic interventions. Community-based support group participation.
DRUG ALERT
Patients taking lithium can develop toxicity related to
elevated levels in the blood; therefore, lithium blood levels
must be monitored periodically. Initial therapy requires
daily monitoring until a safe, therapeutic level is attained;
weekly and then monthly monitoring is then recommended.Lithium toxicity is related to decreased serum sodium
levels and inadequate hydration. Therefore, patients taking
lithium must have normal sodium intake and drink at least
2 to 3 qt (2 to 3 L) of water daily.
Complications
Untreated bipolar disorder can lead to physicalexhaustion.
Poor judgment and risk-taking behavior can lead to
financial problems.
Alcohol and drug abuse problems can develop and
cause disruption in the family.
Concurrent medical conditions may be exacerbated.
Nursing Assessment Assess mood for stability; range of affect, from elation
to irritability to severe agitation; laughing, joking, and
talking continuously; uninhibited familiarity with
interviewer.
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Assess behavior for constant activity, starting many
projects but finishing few, mild to severe
hyperactivity, spending large sums of money,
increased appetite, indiscriminate sex, minimal to nosleeping, outlandish or bizarre dress, poor
concentration.
Assess thought processes for flight of ideas; pressured
speech, usually with content that is sexually explicit;
clang associations (sound of word, rather than its
meaning, directs subsequent associations); delusions;
hallucinations.
Characteristics of Bipolar Disorders
BIPOLAR I DISORDER
Presence of only one manic episode
No past major depressive episodes
Manic episode not accounted for by schizoaffective
disorder
Manic episode not superimposed on schizophrenia,schizophreniform disorder, delusional disorder, or
psychotic disorder
Specifiers
Mixed symptoms
Severity/psychotic
Remission specifiers
Catatonic features Postpartum onset
BIPOLAR II DISORDER
Presence or history of one or more major depressive
episodes
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Presence or history of at least one hypomanic episode
No manic or mixed episodes
Symptoms cause clinically significant distress or
impairment in social or occupational functioningSpecifiers
Hypomanic
Depressed
CYCLOTHYMIC DISORDER
Over a 2-year period, there are numerous periods
without hypomanic symptoms and numerous periodswith depressive symptoms that do not meet criteria for
a major depressive episode
During the 2-year period, the patient has not been
without these symptoms for more than 2 months at a
time
No major depressive episode, manic episode, or mixed
episode during the first 2 years of the disturbance
Symptoms are not due to physiologic aspects Symptoms cause clinically significant distress or
impairment in all aspects of functioning
Footnote
Adapted from American Psychiatric Association (APA)
(2000). Diagnostic and statistical manual of mental
disorders (Fourth edition Text revision). Washington, D.C.:
APA.
Nursing Diagnoses
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Disturbed Thought Processes related to biological
changes as demonstrated by agitation, hyperactivity,
and inability to concentrate
Disturbed Sleep Pattern related to hyperactivity andperceived lack of need for sleep
Compromised Family Processes related to role
changes, economic strain, and lack of knowledge
about the patient's illness
Imbalanced Nutrition: Less Than Body Requirements
related to hyperactivity
Nursing InterventionsImproving Thought Processes and Decreasing Sensory
Overload
Assess patient's degree of distorted thinking.
Redirect patient when you are unable to follow
thought processes.
Use brief explanations.
Remain consistent in approach and expectations. Frequently orient patient to reality; speak in a clear,
simple manner.
Provide patient with a relaxing area with decreased
environmental stimulation.
Assist patient with a gradual and progressive
integration into the social environment while
observing for behavioral changes that indicate
readiness for participation in further activities.
Improving Sleep Pattern
Establish a distraction-free environment at bedtime.
Help patient avoid the intake of caffeine and nicotine.
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Administer prescribed drugs as ordered, and monitor
patient's response.
Improving the Effect of Bipolar Illness on Family
Assess family's external support network, andencourage participation in family therapy and support
groups.
Assess communication and boundaries within family.
Observe and assess interaction patterns within family,
and discuss their influence on patient and family
functioning.
Provide patient and family with information aboutbipolar disorder and the treatment plan, prognosis, and
aftercare plan.
Ensuring Adequate Nutrition
Maintain accurate documentation of food and fluid
intake.
Offer small, frequent meals of high-calorie foods.
Include foods that the patient likes and that can beeaten on the move.
Serve patient meals in a low-stimulus environment.
Monitor patient's serum electrolyte and albumin levels
and weigh patient every other day.
Monitor patient's vital signs.
Patient Education and Health Maintenance
Instruct patient and family about bipolar illness,
including symptoms of relapse.
Instruct patient and family members about
psychopharmacologic treatment, including its purpose,
effects, adverse effects, and management.
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Advise patient and family members about community-
based support groups or health care agencies that are
relevant to his care.
For additional information, refer them to suchorganizations as the National Association of Mental
Illness, http://www.nami.org.
Evaluation: Expected Outcomes
Improved thought processes demonstrated by clear
sentences with no evidence of flight of ideas and
completion of simple tasks
Sleeps for at least 5 hours at night Family members verbalize realistic, goal-directed
thinking related to the patient's abilities, recovery, and
control of condition
No weight loss noted
THOUGHT DISTURBANCES (PSYCHOTIC
DISORDERS)
SCHIZOPHRENIA, SCHIZOPHRENIFORM, ANDDELUSIONAL DISORDERS
Schizophrenia, schizophreniform, and delusional disorders
included in this section have defining features of psychotic
symptoms. Psychotic symptoms are produced by a loss of
ego boundaries or a gross impairment in reality testing,
which includes prominent hallucinations and delusions,
disorganized speech, and grossly disorganized or catatonicbehavior. Schizophrenia can be classified as positive or
negative type, although most patients have a mixture of
these symptoms. The positive symptoms include
hallucinations, delusions, loose associations, and bizarre or
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disorganized behavior. The negative symptoms include
restricted emotion (flat affect), anhedonia (lack of interest
in pleasurable activities), avolition (lack of motivation or
initiative), alogia (lack of speech, or poverty of content),and social withdrawal.
Pathophysiology and Etiology
The exact cause of these disorders remains unclear. The
current consensus is that they result from complex
interactions among various factors.
Schizophrenia, Schizophreniform Disorder
Genetic factors:o Studies of monozygotic twins reveal a 50%
concordance rate with a 15% rate with dizygotic
twins.
o If one parent is affected with schizophrenia, a
12% rate is demonstrated in the children, while
having two parents with the disorder increases
the risk to 35% to 39%.o Research is focused on a number of different
genes that may be related to the development of
schizophrenia. An increased risk of schizophrenia
is seen in individuals with genetic variation in the
catechol-O-methyltransferase gene, which is
involved in the manufacture of an enzyme that
metabolizes neurotransmitters. Other current
candidate genes include GRM3, DISC1,
dysbindin, and neuregulin.
Biochemical and structural brain factors:
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o Dopamine hypothesis hyperactivity in the
dopaminergic system, possibly due to receptor
neurons that are functionally hyperactive.
o
Norepinephrine, serotonin, glutamate, and GABAmay also play a role in modulating the symptoms
of schizophrenia.
o Endogenous dysfunction of N-methyl-D-
aspartate receptor-mediated neurotransmission
could lead to the development of schizophrenia.
o Neuroanatomic studies cerebral ventricular
enlargement; sulcal enlargement; cerebellar
atrophy; decreased cranial, cerebral, and frontalsize; abnormalities in basal ganglia; structural
abnormalities at the cellular level, particularly in
the limbic and periventricular regions.
o Functional and metabolic studies regional
cerebral blood flow studies demonstrated
hypofrontality: schizophrenic patients were
unable to increase blood flow to their frontallobes during a task thought to increase frontal
lobe functions; PET studies also consistently
found evidence for a relative hypofrontality.
o Electrophysiologic studies EEG findings in
schizophrenic patients demonstrated decreased
alpha and increased delta activity; changes in
evoked potential studies and amplitude reduction
may occur in responses reflecting selective
attention and stimulus evaluation. P300 response
(reduced amplitude to unexpected stimuli using
auditory and visual parameters) is the most
pronounced and is prolonged. This defect leads to
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information or sensory overload and an inability
to screen out irrelevant stimuli.
o Research evidence supports speculation that
schizophrenia is a neurodevelopmental disorderthat may result from brain injury occurring early
in life and interfering with normal developmental
events.
Psychosocial factors:
o Psychodynamic theory proposes that the essential
feature of schizophrenia is a defect in
interpersonal relationships due to a withdrawal of
the libido into the self.o Interpersonal theory proposes that the lack of a
warm, nurturing relationship in the early years of
life contributes to the lack of self-identity, reality
misperception, and relationship withdrawal that is
apparent in the disorder.
o Family theory related to the role of the family in
the development of schizophrenia has not beenvalidated by research. An area of family
functioning that has been implicated is increased
relapse risks in families characterized by high
expressed emotion. This characteristic is
described as emotional overinvolvement along
with hostile and critical feedback.
Delusional Disorder Little has been established about the etiology of
delusional disorder.
There is no demonstrated genetic linkage.
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It is possible that psychosocial stressors have a role in
the etiology of delusional disorder in some persons.
This is illustrated in some of the rarer conditions such
as shared psychotic disorder.Clinical Manifestations
See Characteristics of Schizophrenia, Schizophreniform,
and Schizoaffective Disorders
Diagnostic Evaluation
Clinical diagnosis is developed on historical
information and thorough mental status examination. No laboratory findings have been identified that are
diagnostic of schizophrenia.
Routine battery of laboratory tests may be useful in
ruling out possible organic etiologies, including CBC,
urinalysis, liver function tests, thyroid function tests,
RPR, HIV test, serum ceruloplasmin (rules out an
inherited disease, Wilson's disease, in which the bodyretains excessive amounts of copper), PET scan, CT
scan, and MRI.
Rating scale assessment:
o Scale for the Assessment of Negative Symptoms
o Scale for the Assessment of Positive Symptoms
o Brief Psychiatric Rating Scale
ManagementSchizophrenia and Schizophreniform Disorder
Patients may receive treatment in inpatient settings or
in community-based outpatient programs or
psychiatric home care. The level of care depends on
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the severity of symptoms and the risk of harm to self
and others.
These disorders generally require long-term treatment;
therefore, a case management approach is important inorder to coordinate multiple services.
Pharmacologic therapy with either the typical or
atypical neuroleptics (antipsychotics) is the mainstay
of treatment.The typical neuroleptics have multiple
adverse effects that require careful management .The
atypical neuroleptics have fewer adverse effects and
may also be more effective in decreasing the negative
symptoms of schizophrenia. Pharmacologic therapywith both the typical and atypical neuroleptics can
include the use of long-lasting, or depot, injections.
Three drugs are currently available in depot
formulations, haloperidol (Haldol), fluphenazine
(Prolixin), and risperidone (Risperdal). The reader is
directed to a pharmacology source for further details
regarding the typical and atypical neuroleptics.
Pharmacology of Antipsychotic Drugs
DRUG:
CLASS/GENERIC/TRADE
NAME
ADULT
THERAPEUTIC
DOSAGE
RANGE
(MG/DAY)
ADVERSE
REACTIONS
ButyrophenoneHaloperidol (Haldol) 2-40 mg Extrapyramida
adverse effect
are common.
Decreased
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incidence of
orthostatic
hypotension a
compared withphenothiazine
Aliphatic Phenothiazines
Chlorpromazine (Thorazine) 30-800 mg Orthostatic
hypotension,
sedation, dry
mouth,
extrapyramida
adverse effectagranulocytos
ocular change
Piperidine Phenothiazines
Mesoridazine (Serentil) 100-400 mg Sedation,
orthostatic
hypotension,
fewerextrapyramida
symptoms tha
other
phenothiazine
Thioridazine (Mellaril) 200-800 mg
Piperazine Phenothiazines
Fluphenazine (Prolixin) 2.5-40 mg Extrapyramida
symptoms, an
lower incidenc
of orthostatic
hypotension
than with othe
phenothiazine
Perphenazine (Trilafon) 8-64 mg
Trifluoperazine (Stelazine) 15-40 mg
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Dibenzoxipine
Loxapine (Loxitane) 60-250 mg Extrapyramida
adverse effect
hypotension,dizziness
Thioxanthene
Thiothixene (Navane) 20-60 mg Extrapyramida
adverse effect
hypotension,
tachycardia,
insomnia
Atypical Antipsychotics Extrapyramidaadverse effect
can occur with
the use of any
of the atypical
antipsychotics
although the
incidence ofoccurrence
usually less
than that seen
with other
classes of
antipsychotic
medications
Aripiprazole (Abilify) 10-30 mg Headache,
anxiety,
insomnia,
nausea,
vomiting,
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dizziness, and
drowsiness
Clozapine (Clozaril) 150-600
mg(requirescareful titration)
Seizure,
agranulocytos(weekly white
blood cell
count),
hypotension,
tachycardia,
cardiac
dysrhythmia,
drowsiness,sedation,
increased
salivation
Olanzapine (Zyprexa) 5-20 mg Orthostatic
hypotension,
tachycardia,
drowsiness,agitation,
akathisia,
constipation
Pimozide (Orap) 1-10 mg Orthostatic
hypotension,
tachycardia,
drowsiness,
sedation,
akathisia,
akinesia
Quetiapine (Seroquel) 200-800 mg Orthostatic
hypotension,
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tachycardia,
drowsiness,
dizziness, dry
mouthRisperidone (Risperdal) 4-16 mg Orthostatic
hypotension,
tachycardia,
drowsiness,
dizziness, dry
mouth
Ziprasidone (Geodon) 20-80 mg Dysrhythmia,
drowsiness,dizziness,
nausea,
restlessness,
constipation
Management of Adverse Effects of Neuroleptic Drugs
SYMPTOM MANAGEMENT
Orthostatic Hypotension Assess for orthostatic bloodpressure changes and dizziness
and teach the patient:
o When rising from bed
chair, get up slowly.
o Sit at side of bed for a
few minutes, dangling legs.
o Do ankle pumps before
standing.
o Once standing, move
slowly.
o Do not twist or turn
quickly.
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o Use assistive devices,
hand rails, canes, walkers
when necessary for
functional deficits.o Do not drive or operate
machinery when dizzy.
Peripheral Anticholinergic Effects
Dry mouth and nose, blurred
vision, constipation, urine
retention
Dry mouth:
o Brush teeth after each
meal with a fluoridated
toothpaste.o Rinse mouth frequently
o Limit caffeinated or
alcoholic drinks because the
can be dehydrating.
o Stop smoking due to th
irritation of oral mucosa.
o
Suck on sugarless candor gum; avoid sugared cand
to decrease the risk of funga
infections and dental caries.
o Avoid dry or spicy
foods.
o Drink fluids between
meals unless you are on a
specific fluid restriction.o Avoid acidic beverage
due to potential irritation.
o Use dressing, juices, or
sauces (if allowed) to moist
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food.
Constipation:
o Drink fluids (within
prescribed limits set by healcare provider).
o Eat roughage: fruits,
vegetables (raw leafy types)
to increase bulk and help
soften stool.
o Eat dried fruits, such a
prunes or dates, for laxativeeffect.
o Maintain activity level
within functional limits.
o Consult with health car
provider to determine
appropriate use of over-the-
counter laxatives (MetamucCitrucel) or prescribed stool
softeners.
Urine retention:
o Void at regular interva
o Ensure privacy.
Extrapyramidal Adverse Effects
Short-TermAkathisia: restless legs,
jitters, nervous energy, motor
agitation
o Reassure patient.
o Differentiate between
agitation and akathisia.
o Consider reducing
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dosage.
o Consider switching
patient to another class of
antipsychotic.Akathisia: Weakness
(hypotonia), fatigue, painful
muscles, anergy (lack of
energy), absence of
movement
o Assess functional
ability.
o Dose reduction or
cessation should improve
movement if problems are
due to akinesia versus
psychotic symptoms.
Dystonias, dyskinesias:grimacing, torticollis,
intermittent spasms,
opisthotonos, oculogyric
crises, head-neck stiffness,
myoclonic twitches,
laryngeal-pharyngeal
dystonia
o Consider prophylaxiswith anticholinergic
medications.
o Treat with I.M. or I.V.
anticholinergics, as
prescribed.
Parkinsonian effects: muscle
stiffness, cog wheel rigidity,
shuffling gait, stooped
posture, drooling
o Treat with
anticholinergics, as
prescribed.
o Stop the antipsychotic,
as directed.
Long-Term
Tardive dyskinesia: a
delayed effect of neuroleptic
drugs usually occurring after
6 months of treatment
involving abnormal,
involuntary, irregular, and
o Complete regular
objective rating/assessment
of the movement disorder.
o Reduce or stop
neuroleptic as directed.
o Consider clozapine
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choreoathetoid movements
of the muscles of the head,
limbs, and trunk
(Clozaril) or risperidone
(Risperdal).
o Comprehensive medica
psychiatric assessmentnecessary with close
monitoring of movement
disorder.
Psychosocial treatments (social skills training, ADL
instruction).
Supportive therapy that is reality oriented and
pragmatic.
Family therapy. Psychoeducational individual, group, and family
support.
Support groups in the community.
Community-based partial hospitalization programs.
Psychiatric home care nursing.
Vocational and social skills education.
Characteristics of Schizophrenia, Schizophreniform,
and Schizoaffective Disorders
SCHIZOPHRENIA SUBTYPES
Paranoid
Dominant hallucinations and delusions
No disorganized speech, disorganized behavior, ordisorganized affect present
Disorganized
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Dominant disorganized speech and disorganized
behavior
Delusions and hallucinations if present are not
prominent or fragmentedResidual
No longer has positive symptoms, such as delusions,
hallucinations, or disorganized speech or behaviors
However, persistence of some symptoms is noted,
such as:
o Marked social isolation or withdrawal
o Marked impairment in role function (wageearner, student, or homemaker)
o Markedly peculiar behavior
o Marked impairment in personal hygiene
o Marked lack of initiative, interest, or energy
o Blunted or inappropriate affect
Catatonic
Motor immobility (waxy flexibility) Excessive purposeless motor activity (agitation)
Extreme negativism or mutism
Peculiar voluntary movement
o Posturing
o Stereotyped movements
o Prominent mannerisms
o Prominent grimaces Echolalia or echopraxia
Undifferentiated
Has positive symptoms (does have hallucinations,
delusions, and bizarre behaviors)
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