Depression is a very common affective disorder involving feelings of sadness that are much more severe and longer lasting than the suspected precipitating event, and the mood of affected individuals is much more intense. The depression may not even be traceable to a specific event or stressor (i.e., there are no external causes). Patients who are depressed may have little energy, sleep disturbances, a lack of appetite, limited libido, and inability to perform activities of daily living. They may describe overwhelming feelings of sadness, despair, hopelessness, and disorganization.
In many cases, the depression is never diagnosed, and the patient is treated for physical manifestations of the underlying disease, such as fatigue, malaise, obesity, anorexia, or alcoholism and drug dependence. Clinical depression is a disorder that can interfere with a person’s family life, job, and social interactions. Left untreated, it can produce multiple physical problems that can lead to further depression or, in extreme cases, even suicide.
Research on the development of the drugs known to be effective in relieving depression led to formulation of the current hypothesis regarding the cause of depression. Scientists have theorized that depression results from a deficiency of biogenic amines in key areas of the brain; these biogenic amines include norepinephrine (NE), dopamine, and serotonin (5HT). Both NE and 5HT are released throughout the brain by neurons that react with multiple receptors to regulate arousal, alertness, attention, moods, appetite, and sensory processing.
The use of agents that alter the concentration of neurotransmitters in the brain is the most effective means of treating depression with drugs. The antidepressant drugs used today counteract the effects of neurotransmitter deficiencies in three ways. First, they may inhibit the effects of MAO, leading to increased NE or 5HT in the synaptic cleft. Second, they may block reuptake by the releasing nerve, leading to increased neurotransmitter levels in the synaptic cleft. Third, they may regulate receptor sites and the breakdown of neurotransmitters, leading to an accumulation of neurotransmitter in the synaptic cleft.
Antidepressants may be classified into three groups: the tricyclic antidepressants (TCAs), the MAOIs, and the selective serotonin reuptake inhibitors (SSRIs). Other drugs that are used as antidepressants similarly increase the synaptic cleft concentrations of these neurotransmitters.
1. A client with a history of abusing barbiturates abruptly stops taking the medication. The nurse should give priority to assessing the client for:
A. Depression and suicidal ideation
B. Tachycardia and diarrhea
C. Muscle cramping and abdominal pain
D. Tachycardia and euphoric mood 2. The client is having electroconvulsive therapy for treatment of severe depression. Prior to the ECT, the nurse should:
A. Apply a tourniquet to the client’s arm.
B. Administer an anticonvulsant medication.
C. Ask the client if he is allergic to shellfish.
D. Apply a blood pressure cuff to the arm.
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答案 Answers
1. B. Tachycardia and diarrhea Rationale: Barbiturates create a sedative effect. When the client stops taking barbiturates, he will experience tachycardia, diarrhea, and tachypnea. Answer A is incorrect even though depression and suicidal ideation go along with barbiturate use; it is not the priority. Muscle cramps and abdominal pain are vague symptoms that could be associated with other problems. Tachycardia is associated with stopping barbiturates, but euphoria is not. 2. D: Apply a blood pressure cuff to the arm Rationale: The client that is having ECT is given a sedative. When the blood pressure cuff is inflated the fingers twitch when he has a grand mal seizure. A, B, and C are incorrect because there is no need for the nurse to take these interventions prior to ECT.
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