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CHAPTER 4
PROBLEM iDENTiFiCATiON,
NURSiNG DiAGNOSES,
AND PLANNiNG ACROSS
THE LiFE SPAN
This chapter reviews the most common problems (psychiatric diagnoses) that compromise optimal functioning across populations. Common psychiatric disorders and criteria are presented in the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM5; American Psychiatric Association [APA], 2013) and are presented for quick reference. In practice, the DSM5 is important for determining accurate diagnoses, which helps in determining appropriate medication and treatment regimens. The psychiatric and mental health nurse pursuing certification should have a good working knowledge and understanding of clinical presentations that help to substantiate particular diagnoses, serve as baseline indications at initial presentations, and provide targeted markers for determining effectiveness of interventions.
EUSTRESS AND DiSTRESS
It should be noted that experiences of stress undergird the expression of many medical or psychological pathologies. In fact, stress is linked to “turning on” pathophysiological expressions. As discussed in chapter 2, one of the theories linking to psychopathology is environmental stressors, which may take the form of infections, traumas, or abuses. As it stands, many medical conditions mimic psychiatric symptoms. And no wonder; we are talking about the condition as it presents in one organism, a person who is not separated into fragmented body components. Each system of the body may express dysfunction, which may or may not be rooted in our psychological and emotional selves. Table 4–1 considers particular medical conditions that may be comorbid with certain psychological problems.
102 PSYCHiATRiC–MENTAL HEALTH NURSiNG REViEW AND RESOURCE MANUAL, 5TH EDiTiON TABLE 4–1. PHYSICAL AND PSYCHOLOGICAL PRESENTATIONS: CHICKEN OR EGG? Cardiovascular P^ Migraine P (^) Essential hypertension P (^) Angina P (^) Tension headaches Musculoskeletal P^ Rheumatoid arthritis P (^) Low back pain P (^) Multiple sclerosis: anxiety, depression, euphoria, ataxia, muscle weakness, diffuse neurological signs with exacerbations and remissions Respiratory P^ Hyperventilation P (^) Asthma Endocrine P^ Hyperthyroidism P (^) Diabetes P (^) Impotence P (^) Frigidity P (^) Premenstrual syndrome P (^) Cushing’s syndrome: depression, insomnia, emotional lability, mania, psychosis P (^) Adrenocortical insufficiency: lethargy, depression, psychosis, delirium, anorexia, nausea, vomiting P (^) Hyperthyroidism: nervousness, irritability, insomnia, pressured speech, fear, impending death, anxiety disorders, psychosis, heat intolerance, diaphoresis, tremor P (^) Hypothyroidism: lethargy, depression, anxiety disorders, paranoia, psychosis, cold intolerance, dry skin, apathy P (^) Hyperglycemia: anxiety, agitation, delirium, acetone breath Neurological P^ Tumor: judgment, seizures, loss of speech, or smell P (^) Frontal lobe syndrome: mood or personality changes and irritability Integumentary P^ Neurodermatitis P (^) Eczema P (^) Psoriasis P (^) Pruritus Immunology P^ AIDS: depression, personality changes, impaired memory, mutism, progressive dementia, mania, delirium Gastrointestinal P^ Anorexia P (^) Peptic ulcer P (^) Irritable bowel syndrome P (^) Colitis P (^) Obesity P (^) Thiamine deficiency: confusion, confabulation, decreased concentration, neuropathy, Wernicke-Korsakoff’s psychosis P (^) Vitamin B12 deficiency: irritability, pallor, dizziness, ataxia, fatigue
104 PSYCHiATRiC–MENTAL HEALTH NURSiNG REViEW AND RESOURCE MANUAL, 5TH EDiTiON as the genetic predisposition of the patient-precipitant relationship are factors that will determine the patient’s ultimate coping resources. These strengths and coping resources are drawn from a person’s personal abilities, level of social support, material assets, and belief system. The nurse will explore these resources in planning care for the patient, as addressed later in this chapter. Criteria for diagnosing psychopathology are found in the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM5; APA, 2013).
PSYCHiATRiC–MENTAL HEALTH PRACTiCE
STANDARD 2: NURSiNG DiAGNOSiS
Several diagnostic classification systems exist for identifying problems and specific directions of care for mental disorders. The resource for developing nursing diagnoses was developed by the NANDA International (NANDA-I). The NANDA-I classification system (NANDA International, n.d. a) was developed by nurses to identify problems treatable by nurses. NANDA-I nursing diagnoses, unlike DSM5 (APA, 2013) diagnoses, identify the patient’s response to health problems, not the medical diagnosis. They are based upon the conceptualization of the human response to actual or potential health problems from the unique nursing perspective. The diagnosis is based upon an analysis and synthesis of collected data and the recognition of functional patterns and trends. Nursing diagnoses allow for recognition of emergent and urgent problems, patterns, and trends in comparison with normal standards. Diagnoses provide for prioritization; highest priorities are addressed first. An accurate diagnosis guides the direction of treatment and evaluation of care outcomes (NANDA International, n.d. a, n.d. b). A partial list of NANDA-I–approved diagnoses that might apply to patients with mental disorders are listed in Box 4.1. Once problems have been identified and nursing diagnoses made, the psychiatric–mental health nurse plans and implements nursing care addressing priorities for treatment. The highest priority is given to conditions that, if untreated, could result in harm. These would include conditions that involve basic survival needs or safety needs related to suicidal or homicidal ideation (SI or HI) or threat of harm from others (e.g., domestic violence, child or elder abuse). Intermediate priority is given to nonemergent, non–life-threatening, but distressing, painful, or dysfunctional symptoms (e.g., hallucinations, agitation). Lower priority is given to issues that are not specifically related to the illness or prognosis (e.g., occupational, social stressors). Maslow’s hierarchy of needs can be used to conceptualize the priorities for care planning. The nursing care plan specifies, by priority, the diagnoses, short-term and long-term goals and expected outcomes, and interventions, including the what, when, where, how, and who. When available, current, evidence-based practice guidelines, clinical pathways, or clinical algorithms can be used. When new or unusual care needs arise, the nurse is advised to use current research to identify evidence-based approaches. In planning for safe and effective quality care, the Joint Commission (2015) establishes annual Behavioral Health Care National Patient Safety Goals:
PROBLEM iDENTiFiCATiON, NURSiNG DiAGNOSES, AND PLANNiNG ACROSS THE LiFE SPAN 105
P Identify persons served correctly. Use at least two ways to identify individuals served.
for example, use the individual’s name and date of birth. This is done to make sure that each individual served gets the correct medicine and treatment.
P Use medications safely. Record and pass along correct information about a patient’s
medicines. Find out what medicines the patient is taking. Compare those medicines to new medicines given to the patient. Make sure the patient knows which medicines to take when they are at home. Tell the patient it is important to bring their up-to-date list of medicines every time he or she visits a doctor. Prevent infection. Use the goals to improve hand cleaning.
P Identify patient safety risks. Find out which individuals served are most likely to try to
commit suicide. BOX 4.1. SELECT LISTING OF NANDA-I NURSING DIAGNOSES P (^) Anxiety (mild, moderate, severe, panic) P (^) Adjustment, impaired P (^) Confusion (acute, chronic) P (^) Coping (ineffective, readiness for enhanced, compromised family, defensive) P (^) Denial, ineffective P (^) Decisional conflict P (^) Family processes (dysfunctional, interrupted, readiness for enhanced) P (^) Fatigue P (^) Fear P (^) Grieving (anticipatory, dysfunctional) P (^) Health maintenance, ineffective P (^) Health-seeking behavior P (^) Hopelessness P (^) Identity, disturbed personal P (^) Loneliness, risk for P (^) Memory, impaired P (^) Noncompliance; nonadherence P (^) Nutrition, altered; more or less than body requirements P (^) Pain (acute, chronic) P (^) Parenting (enhanced readiness, impaired, risk for impaired) P (^) Posttraumatic syndrome or risk P (^) Rape trauma syndrome P (^) Relocation stress syndrome or risk P (^) Role performance, ineffective P (^) Self-care deficit (bathing, dressing, feeding, etc.) P (^) Self-esteem (chronic low, situational low, risk for low) P (^) Self-mutilation or risk for P (^) Sensory perception, disturbed or altered P (^) Sexual dysfunction P (^) Sexuality pattern, disturbed P (^) Sleep pattern, disturbed P (^) Social interaction, impaired P (^) Social isolation P (^) Sorrow, chronic P (^) Spiritual distress, risk; readiness for P (^) Suicide risk P (^) Thought process disturbed or altered P (^) Trauma, actual or risk P (^) Violence, risk for other- or self-directed P (^) Wandering
PROBLEM iDENTiFiCATiON, NURSiNG DiAGNOSES, AND PLANNiNG ACROSS THE LiFE SPAN 107
MAJOR PSYCHiATRiC MENTAL HEALTH PROBLEMS
Psychotic (Thought) Disorders
Pathogenesis: Theories Scientific research has determined that subtle prodromal symptoms of schizophrenia may be present from early childhood. They can include delayed language development and asymmetrical use of major muscles of the body. These early findings have led researchers to the hypothesis that schizophrenia is a neurodevelopmental condition. In other words, the brains of persons who develop schizophrenia may not develop normally. It has been hypothesized that the early migration of neurons in brain development may be faulty, resulting in abnormal connections (migrational defects), or excessive, inadequate, or improper pruning of synapses or neurons. It is also hypothesized that maternal flu infection or iron deficiency, as well as substance use by the person, increase the risk for development of psychotic-inducing disorders. Neurodegeneration theories describe the process of pruning away unnecessary connections in the brain going awry, resulting in destruction of too many neurons and their connections. A process called excitotoxicity (Stahl, 2008) has been used to describe the potential self-destruction of neurons resulting from too much glutamate and excitatory neuronal activity. Support for a neurodegenerative mechanism in schizophrenia comes from monozygotic twin studies showing that affected twins tend to have enlarged ventricles of the brain in comparison to their healthy twin siblings. Ventricular enlargement is due to atrophy of the brain tissues, creating more space for fluid in the ventricles. The pathophysiology of schizophrenia is also characterized by abnormal neurotransmission. Abnormally elevated levels of dopamine in the limbic system are thought to be responsible for positive symptoms (hallucinations, delusions, abnormal speech, and abnormal behavior). Because dopamine is essential for learning, memory, and motivation, the negative symptoms (amotivation, apathy, and anhedonia) and cognitive impairment may reflect lower-than-normal levels of dopamine in the prefrontal cortex. Although dopamine is the neurotransmitter most associated with schizophrenia, researchers are learning that other neurotransmitters, such as glutamate, may also have important roles.
108 PSYCHiATRiC–MENTAL HEALTH NURSiNG REViEW AND RESOURCE MANUAL, 5TH EDiTiON Schizophrenia Syndrome The experience of psychosis is evident in many subtypes of schizophrenia, pointing to a clearer understanding of what is now referred to as schizophrenia syndrome. Nasrallal and Weiden (2014) posit the following occurrences that precipitate increased risk for the development of schizophrenia syndrome:
P Childhood traumas
P Paternal age older than 45
P Migration from another country
P Pregnancy and delivery complications
P Urbanicity
P Winter birth (vitamin D deficiency)
P Antibodies to one’s own N-nitrosodimethylamine (NDMA)
P Glutamate toxicity
Readers should view the Nasrallal & Weiden (2014) webinar listed in the references for details pertaining to these recent developments. The average age of onset for schizophrenia, a major psychotic disorder, usually start between ages 16 and 30 with men experiencing symptoms a little earlier than women. Although it is rare, children can develop the disorder, and most of the time, people do not get schizophrenia after age 45 (National Institute of Mental Health, 2015). Support for the neurodevelopmental theory comes from the observation that during the late adolescence, when most people develop full access to the frontal executive functions of the brain, persons with schizophrenia start to demonstrate disordered thinking. The date of onset is defined by a 6-month period of positive symptoms; however, the prodrome period leading up to the first acute episode may last days to years before the diagnosis. Family members often can look back after the diagnosis of schizophrenia and identify a period of altered behavior leading up to the first major episode of psychosis. During this time, an adolescent may withdraw from family or friends, use drugs, and exhibit changes in motivation and school performance. Subtle delays in language and motor skills may even have been present early in life. The three major symptom categories of schizophrenia that reflect brain abnormalities are the positive symptoms, negative symptoms, and cognitive dysfunction (diminished executive functioning and working memory). Evidence of delusions, hallucinations, and disorganized behaviors are the hallmarks that define “positive” symptoms, whereas “negative” symptoms include tendencies to withdraw from others, lack of motivation or concern about appearance,
110 PSYCHiATRiC–MENTAL HEALTH NURSiNG REViEW AND RESOURCE MANUAL, 5TH EDiTiON
Mood Disorders
Pathogenesis: Theories Monoamine Dysregulation Theory Monoamines are the neurotransmitters that include serotonin (5HT), norepinephrine (NE), and dopamine (DA). The hypothesis that depression is caused by a reduction or deficit in one or more of the monoamines forms the basis for treating with the traditional antidepressants. Cerebral blood flow is diminished and hippocampal volume is decreased (Rosedale et al., 2013). The actual mechanism of depression is probably more complicated, involving the monoamine receptors and other cellular events, including the regulation of gene expression (Stahl, 2008). Dysregulation of the HPA Axis Theory A second hypothesis about the pathophysiology of depression involves the stress response systems, in particular, the hypothalamic-pituitary-adrenal-axis (HPA axis). The HPA axis appears to be the main site where genetic, hormonal, and environmental influences converge in mood disorder etiology. In the autonomic and complex interplay between thoughts, emotions, and behaviors, when a person perceives stress, a circular biofeedback loop activates that stimulates the hypothalamus to secrete corticotropin-releasing hormone (CRH). This hormone stimulates the pituitary gland to release arenocorticotropic hormone (ACTH). This systemically circulating hormone activates the adrenal glands (atop the kidneys) to release the hormone cortisol. Circulating cortisol results in activation of the “fight-or-flight” response. All senses become hyperalert, blood is physiologically shunted from the digestive system out to skeletal muscles, pupils become dilated, respiration deepens and becomes more rapid, and cardiac output increases. These neurophysiological responses can be represented as the physiological resistance stage, outlined by Hans Selye (1956), when the person is taxing multiple organ systems while simultaneously evoking homeostatic balance. When stressors remain high for long periods of time (such as a state of homelessness, being in a combat zone, living in terrorizing or traumatizing environments) with concomitantly high cortisol levels, major biochemical, physiological, anatomical, and psychological damages may ensue. Early life stressors, such as the loss of a parent, trauma, or neglect, have been shown to produce lasting effects on the HPA axis, leading to chronic difficulty in managing stress and chronically elevated levels of cortisol. The support for this hypothesis of depression is that persons with major depressive disorder often present with hypercortisolemia, resistance of cortisol to suppression by dexamethasone, blunted ACTH responses to corticotrophin-releasing hormone (CRH) challenge, and elevated CRH concentrations in the cerebrospinal fluid (CSF).
PROBLEM iDENTiFiCATiON, NURSiNG DiAGNOSES, AND PLANNiNG ACROSS THE LiFE SPAN 111 Vitamin D Deficiency Theory Recent evidence suggests that vitamin D, which exerts neurological benefits on cognition, memory, and mood, may be deficient among persons who develop mood disorders (Farrington, 2013). Classifications of Mood Disorders Disorders of mood can include depression (unipolar disorder) or bipolar disorder, or the less acute but long-lasting dysthymic and cyclothymic variations. The distinction between unipolar depression and bipolar depression is important because the two disorders require different treatments. Bipolar depression is more likely to have a heritable (genetic) component than unipolar depression, and a person with bipolar disorder is more likely to have had previous symptoms, treatments, or hospitalizations. Depression can occur at any age, including the first and last years of life. Failure-to-thrive (FTT) in infants, a clinical condition often requiring pediatric hospitalization, may be indicative of infantile depression. Geriatric failure-to-thrive (GFTT), seen among some older adults, may also have roots in mood disorders. The average ages of onset for the development of mood disorders are listed below.
P Disruptive mood disorder dysregulation
P (^) Can occur at any age (infantile failure-to-thrive; geriatric failure-to-thrive) P (^) Generally between 20 and 50 years P (^) Mean age of onset: 40 years
P Bipolar disorder
P (^) Childhood (5 to 6 years) to age 50 P (^) Mean age of onset: 21 to 30 years Mood dysregulation can co-occur with other medical illnesses, such as cardiovascular disease, Parkinson’s disease, neurodegenerative and neurocognitive disorders, traumatic brain injuries, hypothyroidism, and cancer, as well as with life stressors. Although the average age for diagnosing bipolar disorder is in the late 20s or early 30s, many of the symptoms, including impulsivity and difficulty controlling emotions, can be present as early as age 4 or 5. These early BOX 4–3. MOOD DISORDERS P (^) Disruptive mood dysregulation disorder P (^) Dysthymia P (^) Seasonal affective disorder (SAD) P (^) Postpartum depression P (^) Adjustment disorder P (^) Bipolar I P (^) Bipolar II
PROBLEM iDENTiFiCATiON, NURSiNG DiAGNOSES, AND PLANNiNG ACROSS THE LiFE SPAN 113
P Physical
P (^) Body slowdown P (^) Sleep disturbances P (^) Weight loss or weight gain P (^) Insomnia or hypersomnia P (^) Fatigue or loss of energy Dysthymic Disorder As opposed to persistent, or chronic depression, in dysthymic disorder, people experience a depressed mood for most of the day more days than not, for at least 2 years. This describes people said to be in a “blue funk,” akin to Oscar the Grouch on Sesame Street. Persons with this mood dysregulation rarely present for psychiatric intervention. Adjustment Disorder Life changes can precipitate mood dysregulation, which may also be referred to as situational depression, or a primary stress response syndrome. Acknowledgement of some precipitant (e.g., recent divorce, change in school, off to military) that has occurred in the last 3 months or so may lead to this diagnosis. Seasonal Affective Disorder Some people experience depression during fall and winter, returning to normal moods in spring and summer. The fall-winter experience may be related to reduced natural light from sunshine that is evident in some parts of the world. Light inhibits the production of melatonin, a hormone that affects mood and induces sleep. Postpartum Depression Postpartum depression (“baby blues”) within the first 10 days postpartum that lasts at least 2 weeks is experienced by upwards of 70% of new mothers. The phenomenon is thought to be related to rapid fluctuations in hormones that occur around the perinatal period (before and after birth). Early recognition is critical for the health of both mother and infant. Untreated episodes may progress to an emergency situation of postpartum psychosis that could lead to infanticide.
114 PSYCHiATRiC–MENTAL HEALTH NURSiNG REViEW AND RESOURCE MANUAL, 5TH EDiTiON NANDA-I: Mood Disorders
P Risk for suicide related to:
P (^) Feelings of hopelessness, helplessness, or worthlessness P (^) Anger turned inwards P (^) Reality distortions
P Low self-esteem related to:
P (^) Learned helplessness P (^) Significant losses P (^) Cognitive distortions leading to negative self-image
P Dysfunctional grieving related to:
P (^) Real or perceived loss P (^) Bereavement overload (not adequately dealing with losses)
P Social isolation related to:
P (^) Negative self-perception P (^) Egocentric behaviors Bipolar I and II Pathogenesis: Monoamine Dysregulation Theory Bipolar manic episodes may involve the same neurotransmitter systems as depression, with problems related to overactivity rather than underactivity. Elevated levels of serotonin (5HT), norepinephrine (NE), and dopamine (DA) in areas of the brain regulating mood and behavior could explain symptoms such as irritable or expansive mood, pressured speech, flight of ideas, decreased sleep, and increased goal-directed activity. Sensitivity and kindling are two terms that have been used to describe neuronal activity in bipolar disorder. Early in the course of the illness, mood episodes may be triggered by significant stressors. Over time, the brain appears to become sensitized to stress and much less stress is necessary to trigger an episode. The neurons respond to slight provocations like kindling wood for fire: a small spark and the kindling catches fire immediately. Bipolar I disorder is characterized by episodes of severe mood swings, from mania to depression. Bipolar II disorder is a milder form, characterized by milder episodes of hypomania that alternate with depression. Both mood disorders can occur in children and adolescents. Mixed featured types may include the presence of psychosis or rapid cycling (cyclothymia—four or more episodes with a 12-month period). Observable symptoms that may be noted by the nurse include
116 PSYCHiATRiC–MENTAL HEALTH NURSiNG REViEW AND RESOURCE MANUAL, 5TH EDiTiON NANDA-I for Suicide, Homicide, Aggression, Abuse, Assault
P Risk for suicide, homicide, aggression, abuse, or assault
P Hopelessness
P Ineffective coping related to negative role-modeling
P Risk for violence to others related to childhood environment of violence
Psychiatric–Mental Health Practice Standard 4: Planning Improvement outcomes for all patients with mood disorders:
P The patient will experience no harm or injury.
P The patient does not display physical agitation toward self or others.
P The patient eats well-balanced meals and gets adequate rest and sleep.
P The patient interacts appropriately.
P The patient maintains reality orientation.
P The patient discusses losses with staff and family or significant others.
P The patient sets realistic goals for him- or herself.
P The patient identifies aspects of self-control over his or her life situation.
P The patient can concentrate and make decisions.
Improvement outcomes for patients with suicidal (SI) or homicidal (HI) ideation or aggressive behaviors:
P The patient will seek help through the mental health system.
P The patient will state that he or she is no longer having SI, HI, or aggressive feelings.
P The patient will be able to recognize anger and seek staff to talk about feelings.
P The patient will exert internal control over anger.
P The patient will not cause harm to self or others.
P The patient will use problem-solving to seek solutions.
PROBLEM iDENTiFiCATiON, NURSiNG DiAGNOSES, AND PLANNiNG ACROSS THE LiFE SPAN 117
Anxiety Disorders
Pathogenesis: Anxiety The anxiety disorders are characterized by fear and worry that can be polarizing. Polarization leads to dysfunction by interfering with the ability to make a decision. The neurobiology of fear is thought to involve brain circuits that are regulated by the amygdala—the small, almond- shaped brain structure that is responsible for detecting threat and initiating the stress response. Conditions of worrying may involve a different brain circuit that passes through the basal ganglia. The connection with the basal ganglia is especially important in obsessive-compulsive disorder (OCD), where we see overlap with other disorders linked to basal ganglia dysfunction, such as ADHD and tics. Anxiety disorders and depression often share symptoms that are associated with a chronic stress response. Is anxiety a symptom, a syndrome, or a disorder? Symptoms associated with chronic stress include tension headaches, migraine headaches, and musculoskeletal pain. In addition, a chronic response to stress by way of the HPA axis (Chapter 2, Figure 2–1), with increased circulating levels of cortisol, has been linked to increased abdominal fat, impaired immune function, disrupted glucose metabolism, cardiovascular symptoms (e.g., hypertension), gastric ulcers, and hippocampal atrophy with learning and memory impairments. As noted previously, sympathetic nervous system activation of the autonomic nervous system activates the fight-or-flight mechanism with its automation of increased heart and respiratory rates, dilation of pupils, and sweating responses due to noradrenergic norepinephrine release. HPA activation is elicited when anxious. Do anxiety disorders, therefore, suggest alteration of norepinephrine (NE), gamma-amino-butyric acid (GABA), epinephrine (E)? The brain’s GABA receptors can be modulated by central nervous system depressants such as alcohol and benzodiazepines. When people drink alcohol or take benzodiazepines, anxiety levels tend to subside. During withdrawal from those same substances, anxiety increases. These findings support the hypothesis that the neurotransmitter GABA and its receptors are important in the symptoms of anxiety, with too little GABA associated with symptoms of anxiety. On the other hand, too much arousal from NE or glutamate may also lead to symptoms of anxiety. Anxiety can be a normal emotion in threatening circumstances. It is the emotional component of the “fight or flight” stress response and has important survival functions. Anxiety can also be part of a syndrome or symptom complex associated with certain medical or substance-related conditions. Examples include hyperthyroidism, attention-deficit hyperactivity disorder (ADHD), and alcohol or benzodiazepine withdrawal. Finally, anxiety can be the primary component of a disorder.
PROBLEM iDENTiFiCATiON, NURSiNG DiAGNOSES, AND PLANNiNG ACROSS THE LiFE SPAN 119 Generalized Anxiety Disorder (GAD)
P Excessive anxiety and worry; “worry warts” (worrying more days than not for at least
6 months, about a number of events or activities)
P Average age of onset is in 20s
P The anxiety and worry are associated with 3 or more of the following 6 symptoms:
P (^) Restlessness P (^) Being easily fatigued P (^) Difficulty concentrating P (^) Irritability P (^) Muscle tension P (^) Sleep disturbance Phobia: Specific, Social, or Agoraphobia
P Marked or persistent fear that is excessive or unreasonable, cued by the presence or
anticipation of a specific object or situation
P Exposure to the phobic stimulus almost invariably provokes an immediate anxiety
response, which may take the form of a panic attack.
P The person recognizes that the fear is excessive.
P (^) The phobic stimulus is avoided. Obsessive-Compulsive Disorder (OCD)
P Highly co-occurring with ADHD and tic disorders
P Can occur before age 9 (rule out PANDAS)
P Either obsessions or compulsions that cause marked distress, are time-consuming,
and interfere with functioning P (^) Obsessions: recurrent and persistent thoughts, impulses, or images that are intrusive and inappropriate P (^) Compulsions: repetitive behaviors that the person feels driven to perform; aimed at anxiety reduction Body Dysmorphic Disorder
P Physically normal appearance and body, but patient believes that parts of the body are
abnormal, misshapen, or ugly
P Impairs function
120 PSYCHiATRiC–MENTAL HEALTH NURSiNG REViEW AND RESOURCE MANUAL, 5TH EDiTiON Hoarding Disorder
P Tendency to collect and accumulate objects without apparent value, to the point of
functional impairment; functional paralysis Trichotillomania
P Hair-pulling disorder; hair may be pulled from various areas of body (head, eyelashes,
pubic area, armpits)
P Pulling is accompanied by tension release.
P (^) May result in development of a bezoar (hair ball in stomach) that may require surgical removal Excoriation (Skin Picking) Disorder
P New to DSM5 (APA, 2013)
P Usually begins in adolescence; mostly focuses on face or head
P (^) Picking at skin to the point of trauma, bleeding Separation Anxiety Disorder
P Normal developmental achievement at around 6 to 18 months of age
P Suggests significant functional impairment if continues in toddlers and older children.
Trauma-Related Anxiety Disorders Posttraumatic Stress Disorder (PTSD)
P Person has been exposed to a traumatic event
P Traumatic event is persistently re-experienced
P Persistent avoidance of stimuli associated with the trauma and numbing of general
responsiveness
P Persistent symptoms of increased arousal
P Duration is longer than 1 month
P (^) Can occur in children and adolescents Acute Stress Disorder
P Similar to PTSD except that onset follows during or immediately after a stressful event
P Lasts a month or less
