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chapter 13 depressive disorders

Terms in this set (40)

Psychotic features
Indicates the presence of disorganized thinking, delusions (e.g., delusions of guilt or being punished for sins, somatic delusions of horrible disease or body rotting, delusions of poverty or going bankrupt), or hallucinations (usually auditory, voices berating person for sins).

Melancholic features
This outdated term indicates a severe form of endogenous depression (not attributable to environmental stressors) characterized by severe apathy, weight loss, profound guilt, symptoms that are worse in the morning, early morning awakening, and often suicidal ideation.

Atypical featuress*
Refers to people who have dominant vegetative symptoms (overeating and oversleeping). Onset is younger, psychomotor activities are slow, and anxiety is often an accompanying problem, which may cause misdiagnosis.

Catatonic features
Marked by nonresponsiveness, extreme psychomotor retardation (may seem paralyzed), withdrawal, and negativity.

Postpartum onset
Indicates onset within 4 weeks after childbirth. It is common for psychotic features to accompany this depression. Severe ruminations or delusional thoughts about the infant signify increased risk of harm to the infant.

Seasonal features - seasonal affective disorder (SAD)
Indicates that episodes mostly begin in fall or winter and remit in spring. These patients have reduced cerebral metabolic activity. SAD is characterized by anergia, hypersomnia, overeating, weight gain, and a craving for carbohydrates; it responds to light therapy.
Leading cause of disability in the United States
Depression is the leading cause of disability in the United States. The lifetime prevalence of a major depressive episode—or the total number of people in the United States who will experience the disorder within their lifetime—is 8.6% . Studies find that MDD is twice as common in women (11.2%) as in men (6.0%), although one may question the validity of these statistics, considering that men commit suicide at a far higher rate than women. The CMHS has determined that MDD and DD tend to have higher prevalence rates in lower-income groups; DD (chronic mild depression) occurs in about 3.4% of people during their lifetimes. About 40% of people with DD also meet the criteria for MDD or bipolar disorder (BD) in any given year.

Children and adolescents
Children as young as 3 years of age have been diagnosed with depression. MDD is said to occur in as many as 18% of preadolescents, which is perhaps a low estimate because depression in this age group is often underdiagnosed. Children and adolescents between 9 and 17 years of age have a 6% prevalence of depression, and 4.9% have MDD . Girls 15 years and older are twice as likely to experience a major depressive episode as boys. The dominant symptom of depression in children and adolescents tends to be irritability


Older adults
Although depression in older adults is common, it is not a normal result of aging. It is estimated that of the 35 million people over age 65, 2 million (almost 6%) suffer from severe depression, and another 5 million (around 14%) suffer from less severe forms of depression. Many older adults suffer from subsyndromal depression in which they experience many, but not all, the symptoms of a major depressive episode. These individuals have an increased risk of developing major depression and a disproportionate number of older adults with depression are likely to die by suicide. Unfortunately, the symptoms of depression often go unrecognized in this population, although older adults generally make frequent medical visits. Thus older individuals suffering from depression are at risk for being untreated.

Comorbidity
A depressive syndrome frequently accompanies other psychiatric disorders, such as anxiety disorders, schizophrenia, substance abuse, eating disorders, and schizoaffective disorder. People with anxiety disorders (e.g., panic disorder, generalized anxiety disorder, obsessive-compulsive disorder) commonly present with depression, as do people with personality disorders (particularly borderline personality disorder), adjustment disorder, and brief depressive reactions.

Mixed anxiety-depression is perhaps one of the most common psychiatric presentations. Symptoms of anxiety occur in an average of 70% of cases of major depression.

The presence of comorbid anxiety disorder and depression has a negative impact on the disease course. Comorbidity has been shown to result in a higher rate of suicide, greater severity of depression, greater impairment in social and occupational functioning, and poorer response to treatment This is especially true in older adults with depression who have concurrent symptoms of anxiety or an anxiety disorder
The incidence of major depression greatly increases with the occurrence of a medical disorder, and people with chronic medical problems are at a higher risk for depression than those in the general population. Depression is often secondary to a medical condition and may also be secondary to use of substances such as alcohol, cocaine, marijuana, heroin, and even anxiolytics and other prescription medications. Depression can also be a sequela, or consequence, of bereavement and grief.
Counseling and communication
Nurses often have great difficulty communicating with patients without talking. However, some patients with depression are so withdrawn that they are unwilling or unable to speak, and just sitting with them in silence may seem like a waste of time or be uncomfortable. As your anxiety increases, you may start daydreaming, feel bored, remember something that "must be done now," and so on. It is important to be aware that this time can be meaningful, especially if you have a genuine interest in learning about the patient with depression.

It is difficult to say when a withdrawn patient will be able to respond. However, certain techniques are known to be useful in guiding effective nursing interventions

Health teaching and health promotion
One basic premise of the recovery model of mental illness is that each individual controls his or her treatment based on individual goals. Within this model, health teaching is paramount because it allows patients to make informed choices. Health teaching is also an avenue for providing hope to the patient and should include:

•Depression is an illness that is beyond a person's voluntary control.
•Although it is beyond voluntary control, depression can be managed through medication and lifestyle.


Promotion of self-care activities

Milieu therapy
When a person has acute and severe depression, admission to an inpatient setting may be indicated. The patient with depression needs protection from suicidal acts and a supervised environment for regulating treatments. Often, being removed from a stressful interpersonal situation increases therapeutic value. Hospitals have protocols regarding the care and protection of the suicidal patient
First-line therapy

Indications
have a broad base of clinical use. In addition to their use in treating depressive disorders, the SSRIs have been prescribed with success to treat some of the anxiety disorders—in particular, obsessive-compulsive disorder and panic disorder (see

Fluoxetine has been found to be effective in treating some women who suffer from late-luteal-phase dysphoric disorder and bulimia nervosa.

Adverse reactions
Agents that selectively enhance synaptic serotonin within the CNS may induce agitation, anxiety, sleep disturbance, tremor, sexual dysfunction (primarily anorgasmia), or tension headache. The effect of the SSRIs on sexual performance may be the most significant undesirable outcome reported by patients.

Autonomic reactions (e.g., dry mouth, sweating, weight change, mild nausea, and loose bowel movements) may also be experienced with the SSRIs.

Potential toxic effects
serotonin syndrome. This syndrome is thought to be related to overactivation of the central serotonin receptors, caused by either too high a dose or interaction with other drugs.

Symptoms include abdominal pain, diarrhea, sweating, fever, tachycardia, elevated blood pressure, altered mental state (delirium), myoclonus (muscle spasms), increased motor activity, irritability, hostility, and mood change.

Severe manifestations can induce hyperpyrexia (excessively high fever), cardiovascular shock, or death. The risk of this syndrome seems to be greatest when an SSRI is administered in combination with a second serotonin-enhancing agent, such as a monoamine oxidase inhibitor (MAOI). A patient should discontinue all SSRIs for 2 to 5 weeks before starting an MAOI.
Neurotransmitter effects
inhibit the reuptake of norepinephrine and serotonin by the presynaptic neurons in the CNS, increasing the amount of time norepinephrine and serotonin are available to the postsynaptic receptors. This increase in norepinephrine and serotonin in the brain is believed to be responsible for mood elevations.

Indications
The sedative effects of the TCAs are attributed to the blockade of histamine receptors. Patients must take therapeutic doses of TCAs for 10 to 14 days or longer before they begin to work; full effects may not be seen for 4 to 8 weeks. An effect on some symptoms of depression, such as insomnia and anorexia, may be noted earlier. Choosing a TCA for a patient is based on what has worked for the patient or a family member in the past and the drug's adverse effects.

A stimulating TCA, such as desipramine (Norpramin) or protriptyline (Vivactil) may be best for a patient who is lethargic and fatigued. If a more sedating effect is needed for agitation or restlessness, drugs such as amitriptyline (Elavil) and doxepin (Sinequan) may be more appropriate choices. Regardless of which TCA is given, the initial dose should always be low and increased gradually.

Adverse effects
anticholinergic actions are similar (e.g., dry mouth, blurred vision, tachycardia, constipation, urinary retention, and esophageal reflux). These side effects are more common and more severe in patients taking antidepressants. They usually are not serious and are often transitory, but urinary retention and severe constipation warrant immediate medical attention. Weight gain is also a common complaint among people taking TCAs.

The α-adrenergic blockade of the TCAs can produce postural-orthostatic hypotension and tachycardia*. Postural hypotension can lead to dizziness and increase the risk of falls.

Administering the total daily dose of TCA at night is beneficial for two reasons. First, most TCAs have sedative effects and thereby aid sleep. Second, the minor side effects occur while the individual is sleeping, which increases compliance with drug therapy.

most serious effects are cardiovascular: dysrhythmias, tachycardia, myocardial infarction, and heart block have been reported. Because the cardiac side effects are so serious, TCA use is considered a risk in older adults and patients with cardiac disease. Patients should have a thorough cardiac workup before beginning TCA therapy.

Contraindications
people who have recently had a myocardial infarction (or other cardiovascular problems), those with narrow-angle glaucoma or a history of seizures, and women who are pregnant should not be treated with TCAs, except with extreme caution and careful monitoring.
Neurotransmitter effects

Indications
re particularly effective for people with atypical depression (characterized by mood reactivity, oversleeping, and overeating), as well as panic disorder, social phobia, generalized anxiety disorder, obsessive-compulsive disorder, posttraumatic stress disorder, and bulimia. The MAOIs commonly used in the United States at present are phenelzine (Nardil) and tranylcypromine sulfate (Parnate). Selegiline (Emsam), a newer MAOI delivered transdermally in a patch, does not seem to affect tyramine sensitivity.

Adverse/toxic effects
orthostatic hypotension, weight gain, edema, change in cardiac rate and rhythm, constipation, urinary hesitancy, sexual dysfunction, vertigo, overactivity, muscle twitching, hypomanic and manic behavior, insomnia, weakness, and fatigue.

The most serious reaction to the MAOIs is an increase in blood pressure, with the possible development of intracranial hemorrhage, hyperpyrexia, convulsions, coma, and death. Therefore, routine monitoring of blood pressure, especially during the first 6 weeks of treatment, is necessary.

Interactions


Drug
• Over-the-counter medications for colds, allergies, or congestion (any product containing ephedrine, phenylephrine hydrochloride, or phenylpropanolamine)
• Tricyclic antidepressants (imipramine, amitriptyline)
• Narcotics
• Antihypertensives (methyldopa, guanethidine, reserpine)
• Amine precursors (levodopa, l-tryptophan)
• Sedatives (alcohol, barbiturates, benzodiazepines)
• General anesthetics
• Stimulants (amphetamines, cocaine)

Food

Contraindications
•Cerebrovascular disease
•Hypertension and congestive heart failure
•Liver disease
•Consumption of foods containing tyramine, tryptophan, and dopamine
•Use of certain medications
•Recurrent or severe headaches
•Surgery in the previous 10 to 14 days
•Age younger than 16 years
-Biochemical
The brain is a highly complex organ that contains billions of neurons. There is much evidence to support the concept that many CNS neurotransmitter abnormalities may cause clinical depression. These neurotransmitter abnormalities may be the result of genetic or environmental factors or even of other medical conditions, such as cerebral infarction, hypothyroidism, acquired immunodeficiency syndrome (AIDS), or drug use.

Specific neurotransmitters in the brain are believed to be related to altered mood states. Two of the main neurotransmitters involved are serotonin (5-hydroxytryptamine [5-HT]) and norepinephrine. Serotonin is an important regulator of sleep, appetite, and libido; therefore, serotonin-circuit dysfunction can result in sleep disturbances, decreased appetite, low sex drive, poor impulse control, and irritability. Norepinephrine modulates attention and behavior. It is stimulated by stressful situations, which may result in overuse and a deficiency of norepinephrine. A deficiency, an imbalance as compared to other neurotransmitters, or an impaired ability to use available norepinephrine can result in apathy, reduced responsiveness, and slowed psychomotor activity

Stressful life events, especially losses, seem to be a significant factor in the development of depression. Norepinephrine, serotonin, and acetylcholine play a role in stress regulation. When these neurotransmitters become overtaxed through stressful events, neurotransmitter depletion may occur.

At this time, no single mechanism of depressant action has been found. The relationships among the serotonin, norepinephrine, dopamine, acetylcholine, and GABA systems are complex and need further assessment and study. However, treatment with medication that helps regulate these neurotransmitters has proved empirically successful in the treatment of many patients.

-Alterations in hormonal regulation
Although neuroendocrine findings are as yet inconclusive, the neuroendocrine characteristic most widely studied in relation to depression has been hyperactivity of the hypothalamic-pituitary-adrenal cortical axis. People with major depression have increased urine cortisol levels and elevated corticotrophin-releasing hormone .

Dexamethasone, an exogenous steroid that suppresses cortisol, is used in the dexamethasone suppression test for depression. Results of this test are abnormal in about 50% of people with depression, which indicates hyperactivity of the hypothalamic-pituitary-adrenal cortical axis. However, the findings may also be abnormal in people with obsessive-compulsive disorder (OCD) and other medical conditions. Significantly, patients with MDD with psychotic features are among those with the highest rates of nonsuppression of cortisol on the dexamethasone suppression test.

-Diathesis-stress model
takes into account the interplay of biology and life events in the development of depressive disorders. It is believed that psychosocial stressors and interpersonal events trigger neurophysical and neurochemical changes in the brain. Early life trauma may result in long-term hyperactivity of the CNS corticotropin-releasing factor (CRF) and norepinephrine systems, with a consequent neurotoxic effect on the hippocampus, which leads to overall neuronal loss. These changes could cause sensitization of the CRF circuits to even mild stress in adulthood, leading to an exaggerated stress response
According to the stress-diathesis model, depression results from a dynamic interplay of biology and environment. Some people may be born with a predisposition toward depression which is triggered by experiencing a stressful life event. The experience of depression further alters the neurological connections in the brain, increasing the predisposition toward depression. The result is a vicious cycle of recurrent depressive disorder. Early, effective treatment is needed to break the cycle.
•Psychological factors
-Cognitive theory
the underlying assumption is that a person's thoughts will result in emotions. If a person looks at a life in a positive way, the person will experience positive emotions, but negative interpretation of life events can result in sorrow, anger, and hopelessness. Cognitive theorists believe that people may acquire a psychological predisposition to depression due to early life experiences. These experiences contribute to negative, illogical, and irrational thought processes that may remain dormant until they are activated during times of stress. Beck found that persons with depression process information in negative ways, even in the midst of positive factors. He believed that automatic, negative, repetitive, unintended, and not-readily-controllable thoughts perpetuate depression. Three thoughts constitute Beck's cognitive triad:

1. A negative, self-deprecating view of self
2. A pessimistic view of the world
3. The belief that negative reinforcement (or no validation for the self) will continue in the future

Coming to realize that one has an ability to interpret life events in positive ways helps a person recognize that he or she has an element of control over emotions and therefore depression.


-Learned helplessness
An older but still plausible theory of depression is that of learned helplessness. Seligman (1973) stated that although anxiety is the initial response to a stressful situation, it is replaced by depression if the person feels no control over the outcome of a situation. A person who believes that an undesired event is his or her fault and that nothing can be done to change it is prone to depression. The theory of learned helplessness has been used to explain the development of depression in certain social groups, such as older adults, people living in impoverished areas, and women.
Guilt is a common accompaniment to depression. A person may ruminate over present or past failings. Extreme guilt can assume psychotic proportions (e.g., "I have committed terrible sins, and God is punishing me for my evil ways").

Helplessness is evidenced by the inability to carry out the simplest tasks (e.g., grooming, doing housework, working, caring for children), because they seem too difficult to accomplish. With feelings of helplessness come feelings of hopelessness, which are particularly correlated with suicidality. Even though most depressive episodes are time limited, people experiencing them believe things will never change. This feeling of utter hopelessness can lead people to view suicide as a way out of constant mental pain. Hopelessness, one of the core characteristics of depression and risk factors for suicide, is a combined cognitive and emotional state that includes the following attributes:

•Negative expectations for the future
•Loss of control over future outcomes
•Passive acceptance of the futility of planning to achieve goals
•Emotional negativism, as expressed in despair, despondency, or depression

Anger and irritability are natural outcomes of profound feelings of helplessness. Anger in depression is often expressed inappropriately through destruction of property, hurtful verbal attacks, or physical aggression toward others. However, anger may be directed toward the self in the form of suicidal or subsuicidal behaviors (e.g., alcohol abuse, substance abuse, overeating, smoking, etc.). These behaviors often result in feelings of low self-esteem and worthlessness.
Lethargy and fatigue may result in psychomotor retardation, in which movements are extremely slow, facial expressions are decreased, and gaze is fixed. The continuum of psychomotor retardation may range from slowed and difficult movements to complete inactivity and incontinence. Psychomotor agitation, in which patients constantly pace, bite their nails, smoke, tap their fingers, or engage in some other tension-relieving activity, may also be observed. At these times, patients commonly feel fidgety and unable to relax.

Grooming, dress, and personal hygiene are markedly neglected. People who usually take pride in their appearance and dress may be poorly groomed and allow themselves to look shabby and unkempt.

Vegetative signs of depression are universal. Vegetative signs refer to alterations in those activities necessary to support physical life and growth (eating, sleeping, elimination, sex). For example, changes in eating patterns are common. About 60% to 70% of people with depression report having anorexia; overeating occurs more often in DD.

Change in sleep patterns is a cardinal sign of depression. Often, people experience insomnia, wake frequently, and have a total reduction in sleep, especially deep-stage sleep . One of the hallmark symptoms of depression is waking at 3 or 4 AM and then staying awake or sleeping for only short periods. The light sleep of a person with depression tends to prolong the agony of depression over a 24-hour period. For some, sleep is increased (hypersomnia) and provides an escape from painful feelings. In any event, sleep is rarely restful or refreshing.

Changes in bowel habits are common. Constipation is seen most frequently in patients with psychomotor retardation. Diarrhea occurs less frequently, often in conjunction with psychomotor agitation.

Interest in sex declines (loss of libido) during depression. Some men experience impotence, and a declining interest in sex often occurs among both men and women, which can further complicate marital and social relationships.q
is used most commonly for depression. While as many as 50% of people taking antidepressants fail to achieve full remission, clinical trials of ECT report a rate of 70% to 90% remission. Suicidal thoughts respond to ECT in 80% of cases. Psychotic illnesses are the second most common indication for ECT. For drug-resistant patients, a combination of ECT and antipsychotic medication has resulted in sustained improvement about 80% of the time

•When a patient is suicidal or homicidal, and there is a need for a rapid, definitive response
•If previous medication trials have failed
•When there is marked agitation, marked vegetative symptoms, or catatonia
•For major depression with psychotic features

is useful in treating patients with major depression, especially when psychotic symptoms are present.

Patients who have depression with marked psychomotor retardation and stupor also respond well.

is also indicated for manic patients whose conditions are resistant to treatment with lithium and antipsychotic drugs and for rapid cyclers.

A rapid cycler is a patient with bipolar disorder who has many episodes of mood swings close together (four or more in 1 year). People with schizophrenia (especially catatonic), those with schizoaffective syndromes, psychotic patients who are pregnant, and patients with Parkinson's disease can also benefit from ECT.

is not necessarily effective, however, in patients with DD, atypical depression, personality disorders, drug dependence, or depression secondary to situational or social difficulties.

The usual course of ECT for a patient with depression is 2 or 3 treatments per week to a total of 6 to 12 treatments.

Although no absolute contraindications to ECT exist, several conditions pose risks and require careful workup and management. Since the heart can be stressed at the onset of the seizure and for up to 10 minutes after, careful assessment and management in hypertension, congestive heart failure, cardiac arrhythmias, and other cardiac conditions is warranted. ECT also stresses the brain as a result of increased cerebral oxygen, blood flow, and intracranial pressure.

Conditions such as brain tumors and subdural hematomas may increase the risk of using ECT. Providers of care and patients need to weigh the risk of continued disability or potential suicide from depression against ECT treatment risks.