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INTRODUCTION Although much remains unknown about what causes mental illness, science in the past 30 years has made great strides in helping us understand how the brain works and in presenting possible causes of why some brains work differently from others. Such advances in neurobiologic research ar...

INTRODUCTION Although much remains unknown about what causes mental illness, science in the past 30 years has made great strides in helping us understand how the brain works and in presenting possible causes of why some brains work differently from others. Such advances in neurobiologic research are continually expanding the knowledge base in the field of psychiatry and are greatly influencing clinical practice. The psychiatric-mental health nurse must have a basic understanding of how the brain functions and of the current theories regarding mental illness. This chapter includes an overview of the major anatomic structures of the nervous system and how they work the neurotransmission process. It presents the major current neurobiologic theories regarding what causes mental illness, including genetics and heredity, stress and the immune system, arat mental siness. The use of medications to treat mental illness (psychopharmacology) is related to these neurobiologic theories. These medications directly affect the central nervous system (CNS) and subsequently behavior, perceptions, Thinking, and emotions. This chapter discusses five categories of drugs used to treat mental illness, including their mechanisms of action, their side effects, and the roles of the nurses in administration and client teaching. Although pharmacologic interventions are the most effective treatment for many psychiatric disorders, adjunctive therapies, such as cognitive and behavioral therapies, family therapy, and psychotherapy, can greatly enhance the success of treatment and the client\'s outcome. Chapter 3 discusses these psychosocial modalities. THE NERVOUS SYSTEM AND HOW IT WORKS Central Nervous System The CNS comprises the brain, the spinal cord, and associated nerves that control voluntary acts. Structurally, the brain consists of the cerebrum, cerebellum, brain stem, and limbic system. Figures 2.1 and 2.2 show the locations of brain structures.between the hemispheres. The pineal body is an endocrine gland that influences the activities of the pituitary gland, islets of Langerhans, parathyroids, adrenals, and gonads. The corpus callosum is a pathway connecting the two hemispheres and coordinating their functions. The left hemisphere controls the right side of the body and is the center for logical reasoning and analytic functions such as reading, writing, and mathematical lasks. The cigh hemisphere controls the left side of the body and is the center for creative thinking, intuition, and artistic abilities. Cerebrum The cerebral hemispheres are divided into four lobes: frontal, parietal, temporal, and occipital. Some functions of the lobes are distinct; others are integrated. The frontal lobes control the organization of thought, body movement, memories, emotions, and moral behavior. The integration of all this information regulates arousal, focuses attention, and enables problem solving and decision making. Abnormalities in the frontal lobes are associated with schizophrenia, ADHD, and dementia. The parietal lobes interpret sensations of taste and touch and assist in spatial orientation. The temporal lobes are centers for the senses of smell and hearing and for memory and emotional expression. The occipital lobes assist in coordinating language generation and visual interpretation such as depth perception Cerebellum The cerebellum is located below the cerebrum and is the center for coordination of movements and postural adjustments. It receives and integrates information from all areas of the body, such as the muscles, joints, organs, and other components of the CNS. Research has shown that inhibited transmission of dopamine, a neurotransmitter, in this area is associated with the lack of smooth coordinated movements in diseases such as Parkinson disease and dementia. Brain Stem The brain stem includes the midbrain, pons, and medulla oblongata and the nuclei for cranial nerves III through XII. The medulla, located at the top of the spinal cord, contains vital centers for respiration and cardiovascular functions. Above the medulla and in front of the cerebrum, the pons bridges the gap both structurally and functionally, serving as a primary motor pathway. The midbrain connects the pons and cerebellum with the cerebrum. It measures only 0.8 in (2 cm) length and includes most of the reticular activating system and the extrapyramidal system. The reticular activating system influences motor activity, sleep, consciousness, and awareness. The extrapyramidal system relays information about movement and coordination from the brain to the spinal nerves. The locus coeruleus, a small group of norepinephrine-producing neurons in the brain stem, is associated with stress, anxiety, and impulsive behavior. Limbic System The limbic system is an area of the brain located above the brain stem that ncludes the thalamus, hypothalamus, hippocampus, and amygdala (although ome sources differ regarding the structures this system includes). The halamus regulates activity, sepsation, and emotion. The hypothalamus is involved in temperature regulation, appetite control, endocrine function, sexual drive, and impulsive behavior associated with feelings of anger, rage, or excitement. The hippocampus and amygdala are involved in emotional arousal and memory. Disturbances in the limbic system have been implicated in a variety of mental illnesses, such as the memory loss that accompanies dementia and the poorly controlled emotions and impulses seen with psychotic or manic behavior. Neurotransmitters\* Approximately 100 billion brain cells form groups of neurons, or nerve cells, that are arranged in networks. These neurons communicate information with one another by sending electrochemical messages from neuron to neuron, a process called neurotransmission. These electrochemical messages pass from the dendrites (projections from the cell body), through the soma or cell body, down the axon (long extended structures), and across the synapses (gaps between cells) to the dendrites of the next neuron. In the nervous system, the electrochemical messages cross the synapses between neural cells by way of special chemical messengers called neurotransmitters. Neurotransmitters are the chemical substances manufactured in the neuron that aid in the transmission of information throughout the body. They either excite or stimulate an action in the cells (excitatory) or inhibit or stop an action (inhibitory). These neurotransmitters fit into specific receptor cells embedded in the membrane of the dendrite, just like a certain key shape fits into a lock. After neurotransmitters are released into the synapse and relay the message to the receptor cells, they are either transported back from the synapse to the axon to be stored for later use (reuptake) or metabolized and inactivated by enzymes, primarily monoamine oxidase (MAO) (Fig. 2.3).binding of transmitter to postsynaptic receptor; termination of transmitter action by (3a) reuptake of transmitter into the presynaptic terminal, (3b) enzymatic degradation, or (3c) diffusion away from the synapse; and (4) binding of transmitter to presynaptic receptors for feedback regulation of transmitter release. These neurotransmitters are necessary in just the right proportions to relay messages across the synapses. Studies are beginning to show differences in the amount of some neurotransmitters available in the brains of people with certain mental disorders compared with those who have no signs of mental illness (Fig. 2.4).Neurotransmission Neuroansmitters fit into specific receptor cells embedded in the membrane of the dendrite, similar to a lock and key mechanism. After neurotransmitters ate released into the synapse and relay the message to the receptor cells, they are either transported back from the synapse to the axon to be stored for later use (reuptake) or metabolized and mactivated by enzymes, primarily monoamine oxidase (MAO).Major neurotransmitters have been found to play a role in psychiatric illnesses as well as in the actions and side effects of psychotropic drugs. Table 2.1 lists the major neurotransmitters and their actions and effects. Dopamine and serotonin have received the most attention in terms of the study and treatment of psychiatric disorders. The following sections discuss the major neurotransmitters associated with mental disorders. Dopamine, a neurotransmitter located primarily in the brain stem, has been found to be involved in the control of complex movements, motivation, cognition, and regulation of emotional responses. It is generally excitatory and is synthesized from tyrosine, a dietary amino acid. Dopamine is implicated in schizophrenia and other psychoses as well as in movement disorders such as Parkinson disease. Antipsychotic medications work by blocking dopamine receptors and reducing dopamine activity Serotonin is derived from tryptophan, a dietary amino acid. The function of serotonin is mostly inhibitory, and it is involved in the control of food intake, sleep and wakefulness, temperature regulation, pain control, sexual behavior, and regulation of emotions. Serotonin plays an important role in anxiety, mood disorders, and schizophrenia. It has been found to contribute to the delusions, hallucinations, and withdrawn behavior seen in schizophrenia. Some antidepressants block serotonin reuptake, thus leaving it available longer in the synapse, which results in improved mood. Histamine The role of histamine in mental illness is under investigation. It is involved in peripheral allergic responses, control of gastric secretions, cardiac stimulation, and alertness. Some psychotropic drugs block histamine, resulting in weight gain, sedation, and hypotension. Acetylcholine s Acetylcholine is a neurotransmitter found in the brain, spinal cord, and peripheral nervous system, particularly at the neuromuscular junction of skeletal muscle. It can be excitatory or inhibitory. It is synthesized from dietary choline found in red meat and vegetables and has been found to affect the sleep-wake cycle and to signal muscles to become active. Studies have shown that people with Alzheimer disease have decreased acetylcholine-secreting neurons, and people with myasthenia gravis (a muscular disorder ir which impulses fail to pass the myoneural junction, which causes muscl weakness) have reduced acetylcholine receptors.Glutamate Glutamate is an excitatory amino acid that can have major neurotoxic effects at high levels. It has been implicated in the brain damage caused by stroke, hypoglycemia, sustained hypoxia or ischemia, and some degenerative diseases such as Huntington or Alzheimer.Gamma-Aminobutyric Acid mo Gamma-aminobutyric acid (y-aminobutyric acid, or GABA), an amino acid, is the major inhibitory neurotransmitter in the brain and has been found to modulate other neurotransmitter systems rather than to provide a directstimulus. Drugs that increase GABA function, such as benzodiazepines, used to treat anxiety and to induce sleep.BRAIN IMAGING TECHNIQUES At one time, the brain could be studied only, through surgery or autop During the past 25 years, however, several brain imaging techniques han been developed that now allow visualization of the brain\'s structure an function. These techniques are useful for diagnosing some disorders of th brain and have helped correlate certain areas of the brain with specifi functions. Brain imaging techniques are also useful in research to find the causes of mental disorders. Table 2:2 describes and compares several of these diagnostic techniques.Types of Brain Imaging Techniques Computed tomography (CT), also called computed axial tomography, is a tom procedure in which a precise x-ray beam takes cross-sectional images (slices) (SP layer by layer. A computer reconstructs the images on a monitor and also sub stores the images on magnetic tape or film. CT can visualize the brain\'s soft bra tissues, so it is used to diagnose primary tumors, metastases, and effusions the and to determine the size of the ventricles of the brain. Some people with schizophrenia have been shown to have enlarged ventricles; this finding is associated with a poorer prognosis and marked negative symptoms (Fig. 2.5; see Chapter 16). The person undergoing CT must lie motionless on dstretcher-like table for about 20 to 40 minutes as the stretcher passes through a tunnel-like \"ring\" while the serial x-rays are taken.In magnetic resonance imaging (MRI), a type of body scan, an energy field is created with a huge magnet and radio waves. The energy field is converted to a visual image or scan. MRI produces more tissue detail and contrast than CT and can show blood flow patterns and tissue changes such as edema. It can also be used to measure the size and thickness of brain structures; persons with schizophrenia can have as much as 7% reduction in cortical thickness. The person undergoing an MRI must lie in a small, closed chamber and remain motionless during the procedure, which takes about 45 minutes. Those who feel claustrophobic or have increased anxiety may require sedation before the procedure. Clients with pacemakers or metal implants, such as heart valves or orthopedic devices, cannot undergo MRI. More advanced imaging techniques, such as positron emission tomography (PET) and single-photon emission computed tomography (SPECT), are used to examine the function of the brain. Radioactive substances are injected into the blood; the flow of those substances in the brain is monitored as the client performs cognitive activities as instructed by the operator. PET uses two photons simultaneously; SPECT uses a single photon. PET provides better resolution with sharper and clearer pictures and s about 2 to 3 hours; SPECT takes 1 to 2 hours, PET and SPECients with ally for research, not for the diagnosis and treatment of clients with al disorders (Gur & Gur, 2017) (PIg. 2.5. A recent breakthrough is the i the chemical marker FDDP with PET to identify the amyloid plaques angles of Alzheimer disease in living clients; these conditions previously be diagnosed only through autopsy. These scans have shown that clients Alzheimer disease have decreased glucose metabolism in the brain and sed cerebral blood flow. Some persons with schizophrenia also demonstrate decreased cerebral blood flow. FIGURE 2.6. Example of axial (horizontal) positron emission tomography of a male patient with Alzheimer disease, showing defects (arrowheads) in metabolism in the regions of the cerebral cortex of brain. Some ae wen Aithough imaging techniques such as PET and SPECT have helped bring about tremendous advances in the study of brain diseases, they have somelimitations: The use of radioactive substances in PET and SPECT limits the number of times a person can undergo these tests. There is the risk that the client will have an allergic reaction to the substances. Some clients may find receiving intravenous doses of radioactive material frightening or unacceptable. Imaging equipment is expensive to purchase and maintain, so availability can be limited. A PET camera costs about \$2.5 million; a PET scanning facility may take up to \$6 million to establish. Some persons cannot tolerate these procedures because of fear or Researchers are finding that many of the changes in disorders such as schizophrenia are at the molecular and chemical levels and cannot be detected with current imaging techniques (Gur & Gur, 2017) NEUROBIOLOGIC CAUSES OF MENTAL ILLNESS Genetics and Heredity Unlike many physical illnesses that have been found to be hereditary, such as cystic fibrosis, Huntington disease, and Duchenne muscular dystrophy, the origins of mental disorders do not seem to be simple. Current theories and studies indicate that several mental disorders may be linked to a specific gene or combination of genes but that the source is not solely genetic; nongenetic factors also play important roles. To date, one of the most promising discoveries is the identification in 2007 of variations in the gene SORLI that may be a factor in late-onset Alzheimer disease. Research is continuing in an attempt to find genetic links to other diseases such as schizophrenia and mood disorders. This is the focus of the ongoing research of the National Human Genome Research Institute, funded by the National Institutes of Health and the U.S. Department of Energy. This international research project, started in 1988, is the largest of its kind. It has identified all human DNA and continues with research to discover the human characteristics and diseases to which each gene is related (encoding). In addition, the project also addresses the ethical, legal, and social implications of human genetics research. This program (known as Ethical, Legal, and Social Implications, or ELSI) focuses on privacy and fairness in the use and interpretation of genetic information, clinical integration of new genetic technologies, issues surrounding genetics research, and professional and public education.Three types of studies are commonly conducted to investigate the genetic basis of mental illness: 1\. Twin studies are used to compare the rates of certain mental illnesses or traits in monozygotic (identical) twins, who have an identical genetic makeup, and dizygotic (fraternal) twins, who have a different genetic makeup. Fraternal twins have the same genetic similarities and differences as nontwin siblings. 2\. Adoption studies are used to determine a trait among biologic versus adoptive family members. Family studies are used to compare whether a trait is more common among first-degree relatives (parents, siblings, and children) than among more distant relatives or the general population. Although some genetic links have been found in certain mental disorders, studies have not shown that these illnesses are solely genetically linked. Investigation continues about the influence of inherited traits versus the influence of the environment-the \"nature versus nurture\" debate. The influence of environmental or psychosocial factors is discussed in Chapter 3. Stress and the Immune System (Psychoimmunology) Researchers are following many avenues to discover possible causes of mental illness. Psychoimmunology, a relatively new field of study, examines the effect of psychosocial stressors on the body\'s immune system. A compromised immune system could contribute to the development of a variety of illnesses, particularly in populations already genetically at risk. So far, efforts to link a specific stressor with a specific disease have been unsuccessful. However, the immune system and the brain can influence neurotransmitters. When the inflammatory response is critically involved in illnesses such as multiple sclerosis or lupus erythematosus, mood dysregulation and even depression are common (Raison & Miller, 2017).Infection as a Possible Cause Some researchers are focusing on infection as a cause of mental illness. Most studies involving viral theories have focused on schizophrenia, but so far, none has provided specific or conclusive evidence. Theories that are being de veloped and tested include the existence of a virus that has an affinity fortissues of the CNS, the possibility that a virus may actually alter human genes, and maternal exposure to a virus during critical fetal development of the nervous system. Prenatal infections may impact the developing brain of the fetus, giving rise to a proposed theory that inflammation may causally contribute to the pathology of schizophrenia (DeBost et al., 2017).Thou is THE NURSE'S ROLE RESEARCH AND EDUCATION Amid all the reports of research in these areas of neurobiology, genetics, and heredity, the implications for clients and their families are still not clear or specific. Often, reports in the media regarding new research and studies are confusing, contradictory, or difficult for clients and their families to understand. The nurse must ensure that clients and families are well informed about progress in these areas and must also help them to distinguish between facts and hypotheses. The nurse can explain if or how new research may affect a client\'s treatment or prognosis. The hurse is a good resource for providing information and answering questions. PSYCHOPHARMACOLOGY Medication management is a crucial issue that greatly influences the outcomes of treatment for many clients with mental disorders. The following sections discuss several categories of drugs used to treat mental disorders (psychotropic drugs): antipsychotics, antidepressants, mood stabilizers, anxiolytics, and stimulants. Nurses should understand how these drugs work; their side effects, contraindications, and interactions; and the nursing interventions required to help clients manage medication regimens. Several terms used in discussions of drugs and drug therapy are important for nurses to know. Efficacy refers to the maximal therapeutic effect that a drug can achieve. Potency describes the amount of the drug needed to achieve that maximum effect; low-potency drugs require higher dosages to achieve efficacy, while high-potency drugs achieve efficacy at lower dosages. Half-life is the time it takes for half of the drug to be removed from the bloodstream. Drugs with a shorter half-life may need to be given three or four times a day, but drugs with a longer half-life may be given once a day. The time that a drug needs to leave the body completely after it has been discontinued is about five times its half-life.Keeping clients informed The U.S. Food and Drug Administration (FDA) is responsible for supervising the testing and marketing of medications for public safety. These activities include clinical drug trials for new drugs and monitoring the effectiveness and side effects of medications. The FDA approves each drug for use in a particular population and for specific diseases. At times, a drug will prove effective for a disease that differs from the one involved in original testing and FDA approval. This is called off-label use. An example is some anticonvulsam drugs (approved to prevent seizures) that are prescribed for their effects biliine il moaof elients with bipolar disorder (off-labelsuch side effects are rare, the FDA may issue a black box warning. This means that package inserts must have a highlighted box, separate from the text, which contains a warning about the serious or life-threatening side effects. Several psychotropic medications discussed later in this chapter carry black box warnings. Principles that Guide Pharmacologic Treatment The following are several principles that guide the use of medications to treat psychiatric disorders: such ag de electiveness is evaluated largely by its abilty to diminish or Many psychotropic drugs must be given in adequate dosages for some time before their full effects are realized. For example, tricyclic antidepressants can require 4 to 6 weeks before the client experiences optimal therapeutic benefit. The dosage of medication is often adjusted to the lowest effective dosage for the client. Sometimes a client may need higher dosages to stabilize his or her target symptoms, while lower dosages can be used to sustain those effects over time. As a rule, older adults require lower dosages of medications than do younger clients to experience therapeutic effects. It may also take longer for a drug to achieve its full therapeutic effect in older adults. Psychotropic medications are often decreased gradually (tapering) rather than abruptly. This is because of potential problems with rebound (temporary return of symptoms), recurrence (of the original symptoms), or withdrawal (new symptoms resulting from discontinuation of the drug). Follow-up care is essential to ensure compliance with the medication regimen, to make needed adjustments in dosage, and to manage side effects. Compliance with the medication regimen is often enhanced when the regimen is as simple as possible in terms of both the number of medications prescribed and number of daily doses Antipsychotic DrugsAntipsychotic drugs, formerly known as neuroleptics, are used to treat the symptoms of psychosis, such as the delusions and hallucinations seen in schizophrenia, schizoaffective disorder, and the manic phase of bipolar disorder. Off-label uses of antipsychotics include treatment of anxiety and insomnia; aggressive behavior; and delusions, hallucinations, and other disruptive behaviors that sometimes accompany Alzheimer disease. Antipsychotic drugs work by blocking receptors of the neurotransmitter dopamine. They have been in clinical use since the 1950s. They are the primary medical treatment for schizophrenia and are also used in psychotic episodes of acute mania, psychotic depression, and drug-induced psychosis. Clients with dementia who have psychotic symptoms sometimes respond to low dosages of conventional antipsychotics. Second-generation antipsychotics can increase mortality rates in elderly clients with dementia-related psychosis. Short-term therapy with antipsychotics may be useful for transient psychotic symptoms such as those seen in some clients with borderline personality disorder. Table 2.3 lists available dosage forms, usual daily oral dosages, and extreme dosage ranges for conventional and atypical antipsychotic drugs. The low end of the extreme range is typically used with older adults or children with psychoses, aggression, or extreme behavior management problems.Mechanism of Action The major action of all antipsychotics in the nervous system is to block receptors for the neurotransmitter dopamine; however, the therapeutic mechanism of action is only partially understood. Dopamine receptors are classified into subcategories (D,, D2, D3, Da, and Ds), and D2, D3, and Da have been associated with mental illness. The conventional, or first-generation, antipsychotic drugs are potent antagonists (blockers) of D2, Dz, and Da. This not only makes them effective in treating target symptoms but also produces many extrapyramidal side effects (discussion to follow) because of the blocking of the D2 receptors. Newer, atypical or second-generation antipsychotic drugs, such as clozapine (Clozaril), are relatively weak blockers of De, which may account for the lower incidence of extrapyramidal side effects. In addition, second-generation antipsychotics inhibit the reuptake of serotonin, as do some of the antidepressants, increasing their effectiveness in treating the depressive aspects of schizophrenia. Paliperidone (Invega),iloperidone (Fanapt), asenapine (Saphris), and lurasidone (Latuda) are the newest second-generation agents. Paliperidone (Invega) is chemically similar to risperidone (Risperdal); however, it is an extended-release preparation. This means the client can take one daily dose in most cases, which may be a factor in increased compliance. Asenapine (Saphris) is a sublingual tablet, so clients must avoid food or drink for 10 to 15 minutes after the medication dissolves. The third generation of antipsychotics, called dopamine system stabilizers, is being developed. These drugs are thought to stabilize dopamine output; that is, they preserve or enhance dopaminergic transmission when it is too low and reduce it when it is too high. This results in control of symptoms without some of the side effects of other antipsychotic medications. Aripiprazole (Abilify), the first drug of this type, was approved for use in 2002. Cariprazine (Vraylar) and brexpiprazole (Rexulti) are newer third-generation antipsychotics. These drugs are used for schizophrenia, manic episodes, and as adjunct medication in both bipolar disorder and depression. The most common side effects are sedation, weight gain, akathisia, headache, anxiety, and nausea (Stahl, 2017). Six antipsychotics are available in depot injection, a time-release form of intramuscular medication for maintenance therapy. Two first-generation antipsychotics use sesame oil as the vehicle for these injections, so the medication is absorbed slowly over time; thus, less frequent administration is needed to maintain the desired therapeutic effects. Decanoate fluphenazine (Prolixin) has a duration of 7 to 28 days, and decanoate haloperidol (Haldol) has a duration of 4 weeks. After the client\'s condition is stabilized with oral these medications, administration by depot iniection is ra weeks to maintain Six antipsychotics com Insan asian medication for maintenacicle for these injections, so ta antipsychotics use sesame oil as the vehicle for these injections, so the medication is absorbed slowly over time; thus, less frequent administration is needed to maintain the desired therapeutic effects. Decanoate fluphenazine (Prolixin) has a duration of 7 to 28 days, and decanoate haloperidol (Haldo) has a duration of 4 weeks. After the client\'s condition is stabilized with oral doses of these medications, administration by depot injection is required every 2 to 4 weeks to maintain the therapeutic effect. Risperidone (Risperdal Consta), paliperidone (Invega Sustenna), and olanzapine pamoate (Zyprexa Relprevv), second-generation antipsychotics, encapsulate active medication into polymer-based microspheres that degrade slowly in the body, gradually releasing the drug at a controlled rate. Risperdal Consta, 25 mg, is given every 2 weeks. Invega Sustenna, 117 mg, is given every 4 weeks. Zyprexa Relprevv can be given 210 mg every 2 weeks or 405 mg every 4 weeks. Zyprexa Relprevv has the potential to cause postinjection delirium/sedation syndrome, including sedation, confusion, disorientation, agitation, and cognitive impairment that can progress to ataxia, convulsions, weakness, and hypertension, which can lead to arrest. For that reason, the client must be directly observed by a health care professional for 3 hours after the injection and must be alert, oriented, and symptom-free before he or she can bereleased (Meyers et al., 2017). Aripiprazole (Abilify Maintena), a third-generation antipsychotic, is slowly absorbed into the bloodstream because of insolubility of aripiprazole particles (Otsuka America Pharmaceuticals, 2018). After initiation with oral medication, Abilify Maintena 400 mg is given monthly.Side Effects Extrapyramidal Side Effects. Extrapyramidal symptoms (EPSs), serious neurologic symptoms, are the major side effects of antipsychotic drugs. They include acute dystonia, pseudoparkinsonism, and akathisia. Although often collectively referred to as EPS, each of these reactions has distinct features. One client can experience all the reactions in the same course of therapy, which makes distinguishing among them difficult. Blockade of D, receptors in the midbrain region of the brain stem is responsible for the development of EPSs. First-generation antipsychotic drugs cause a greater incidence of EPSs than do second-generation antipsychotic drugs, with ziprasidone (Geodon) rarely causing EPSs (Virani, Bezchlibnyk-Butler, & Jeffries, 2017).Therapies for acute dystonia, pseudoparkinsonism, and akathisia are similar and include lowering the dosage of the antipsychotic, changing to a different antipsychotic, or administering anticholinergic medication (discussion to follow). While anticholinergic drugs also produce side effects, atypical antipsychotic medications are often prescribed because the incidence of EPSsassociated with them is decreased. Acute dystonia includes acute muscular rigidity and cramping, a stiff or thick tongue with difficulty swallowing, and, in severe cases, laryngospasm and respiratory difficulties. Dystonia is most likely to occur in the first week of treatment, in clients younger than 40 years, in males, and in those receiving high-potency drugs such as haloperidol and thiothixene. Spasms or stiffness in muscle groups can produce torticollis (twisted head and neck), opisthotonus (tightness in the entire body with the head back and an arched neck), or oculogyric crisis (eyes rolled back in a locked position). Acute dystonic reactions can be painful and frightening for the client. Immediate treatment with anticholinergic drugs, such as intramuscular benztropine mesylate (Cogentin) or intramuscular or intravenous diphenhydramine (Benadryl), usually brings rapid relief. Table 2.4 lists the drugs and their routes and dosages used to treat EPSs. The addition of a regularly scheduled oral anticholinergic, such as benztropine, may allow the client to continue taking the antipsychotic drug with no further dystonia. Recurrent dystonic reactions would necessitate a lower dosage or a change in the antipsychotic drug. Assessment of EPSs using the Simpson-Angus rating scale is discussed further in Chapter 16.by the generic label of EPS. Symptoms resemble those uf Parkinson disease and include a stiff, stooped posture; masklike facies; decreased arm swing; a shuffling, festinating gait (with small steps); cogwheel rigidity (ratchet-like movements of joints); drooling; tremor; bradycardia; and coarse pill-rolling movements of the thumb and fingers while at rest. Parkinsonism is treated by changing to an antipsychotic medication that has a lower incidence of EPS or by adding an oral anticholinergic agent or amantadine, which is a dopamine agonist that increases transmission of dopamine blocked by the antipsychotic drug. Akathisia is reported by the client as an intense need to move about. The dient appears restless or anxious and agitated, often with a rigid posture or git and a lack of spontaneous gestures. This feeling of internal restlessness and the inability to sit still or rest often leads clients to discontinue their antipsychotic medication. Akathisia can be treated by a change in antipsychotic medication or by the addition of an oral agent such as a beta-blocker, anticholinergic, or benzodiazepine.Neuroleptic Malignant Syndrome. Neuroleptic malignant syndrome (NMS) is a potentially fatal idiosyncratic reaction to an antipsychotic (or neuroleptic) drug. The major symptoms of NMS are rigidity; high fever; autonomic instability such as unstable blood pressure, diaphoresis, and pallor; delirium; and elevated levels of enzymes, particularly creatine phosphokinase.NMS, but high dosages of high-potency drugs increase the risk. NMS most often occurs in the first 2 weeks of therapy or after an increase in dosage, but it can occur at any time. Dehydration, poor nutrition, and concurrent medical illness all increase the risk for NMS. Treatment includes immediate discontinuance of all antipsychotic medications and the institution of supportive medical care to treat dehydration and hyperthermia until the client\'s physical condition stabilizes. After NMS, the decision to treat the client with other antipsychotic drugs requires full discussion between the client and the physician to weigh the relative risks against the potential benefits of therapy. Tardive Dyskinesia. Tardive dyskinesia (TD), a syndrome of permanent involuntary movements, is most commonly caused by the long-term use of conventional antipsychotic drugs. About 20% to 30% of patients on long-term treatment develop symptoms of TD, and the pathophysiology is still unclear. The symptoms of TD include involuntary movements of the tongue, facial and neck muscles, upper and lower extremities, and truncal musculature. Tongue thrusting and protruding, lip smacking, blinking, grimacing, and other excessive unnecessary facial movements are characteristic. After it has developed, TD is irreversible, although decreasing or discontinuing antipsychotic medications can arrest its progression. Unfortunately, antipsychotic medications can mask the beginning symptoms of TD; that is, increased dosages of the antipsychotic medication cause the initial symptoms to disappear temporarily. As the symptoms of TD worsen, however, they \"break through\" the effect of the antipsychotic drug.In 2017, the FDA approved vacate mor (Austedo, Teva) as the first drugs to treat TD. These drugs are vesicular monoamine transporter 2 (VMAT2) inhibitors. It is believed that these drugs decrease activity of monoamines, such as dopamine, serotonin, and norepinephrine, thereby decreasing the abnormal movements associated with Huntington chorea and TD. Valbenazine has a dosage range of 40 to 80 mg daily, and deutetrabenazine ranges from 12 to 48 mg daily. Both drugs cause somnolence, QT prolongation, akathisia, and restlessness. In addition, valbenazine can cause nausea, vomiting, headache, and balance disturbances. Deutetrabenazine can also cause NMS and increased depression and suicidality in patients with Huntington chorea (Kim, Baker, & Levien, 2018). Preventing TD is the primary goal when administering antipsychotics. This can be done by keeping maintenance dosages as low as possible, changing medications, and monitoring the client periodically for initial signs of TDusing a standardized assessment tool such as the Abnormal Involuntary Movement Scale (see Chapter 16). Clients who have already developed signs of TD but still need to take an antipsychotic medication are often given one of the atypical antipsychotic drugs that have not yet been found to cause or therefore worsen TD. Anticholinergic Side Effects. Anticholinergic side effects often occur with the use of antipsychotics and include orthostatic hypotension, dry mouth, constipation, urinary hesitance or retention, blurred near vision, dry eyes, photophobia, nasal congestion, and decreased memory. These side effects usually decrease within 3 to 4 weeks but do not entirely remit. The client taking anticholinergic agents for EPSs may have increased problems with anticholinergic side effects. Using calorie-free beverages or hard candy may alleviate dry mouth, and stool softeners, adequate fluid intake, and the inclusion of grains and fruit in the diet may prevent constipation. Other Side Effects. Antipsychotic drugs also increase blood prolactin levels. Elevated prolactin may cause breast enlargement and tenderness in men and women; diminished libido, erectile and orgasmic dysfunction, and menstrual irregularities; and increased risk for breast cancer. It can also contribute to weight gain. Weight gain can accompany most antipsychotic medications, but it is most likely with the second-generation antipsychotic drugs, with ziprasidone (Geodon) being the exception. Weight increases are most significant with clozapine (Clozaril) and olanzapine (Zyprexa). Since 2004, the FDA has made it mandatory for drug manufacturers that atypical antipsychotics carry a warning of the increased risk for hyperglycemia and diabetes. Though the exact mechanism of this weight gain is unknown, it is associated with increased appetite, binge eating, carbohydrate craving, food preferencewarning of the increased lisk for hyperglycemia and diabetes. Though the exact mechanism of this weight gain is unknown, it is associated with increased appetite, binge eating, carbohydrate craving, food preference changes, and decreased satiety in some clients. Prolactin elevation may stimulate feeding centers, histamine antagonism stimulates appetite, and there may be an as yet undetermined interplay of multiple neurotransmitter and receptor interactions with resultant changes in appetite, energy intake, and feeding behavior. Penninx and Lange (2018) found that genetics can also make clients more prone to weight gain and metabolic syndrome. Metabolic syndrome is a cluster of conditions that increase the risk for heart disease, diabetes, and stroke. The syndrome is diagnosed when three or more of the following are present: Obesity-excess weight, increased body mass index (BMI), and increased High cholesterol-with at least 150 mg/dL. of triglyceride; less than 40 mg/dL of high-density lipoprotein for women and 50 mg/dL for men Obesity is common in clients with schizophrenia, further increasing the risk for type 2 diabetes mellitus and cardiovascular disease. In addition, clients with severe, persistent mental illness are less likely to exercise or eat low-fat nutritionally balanced diets; this pattern decreases the likelihood that they can minimize potential weight gain or lose excess weight. The increased risk of heart disease results in a shorter life expectancy (Penninx & Lange, 2018).a difficult task. Gill, Zechner, Zambo, Swarbrick, and Murphy (2016) found that clients had greater success when staff provided information and practical for physical activity was modified to account for the client\'s cognitive difficulties where they existed. Community-based social support was providedtherapy. Initially, clients needed to have a weekly white blood cell (WBC) count above 3,500/mm\' to obtain the next week\'s supply of clozapine. Currently, all clients must have weekly WBCs drawn for the first 6 months. If the WBC is 3,500/mm\' and the absolute neutrophil count (ANC) is 2,000/mm\', the client may have these labs monitored every 2 weeks for 6 months and then every 4 weeks. This decreased monitoring is dependent on continuous therapy with clozapine. Any interruption in therapy requires a return to more frequent monitoring for a specified period of time. After clozapine has been discontinued, weekly monitoring of the WBC and ANC is required for 4 weeks.Client Teaching The nurse informs clients taking antipsychotic medication about the types of side effects that may occur and encourages clients to report such problems to the physician instead of discontinuing the medication. The nurse teaches the client methods of managing or avoiding unpleasant side effects and maintaining the medication regimen. Drinking sugar-free fluids and eating sugar-free hard candy ease dry mouth. The client should avoid calorie-laden beverages and candy because they promote dental caries, contribute to weight gain, and do little to relieve dry mouth. Methods to prevent or relieve constipation include exercising and increasing water and bulk-forming fonds in the diet. Stool softeners are permossible, but the client should avoidlaxatives. The use of sunscreen is recommended because photosensitivity can cause the client to sunburn easily. Ciens should monitor the amount of sleepiness or drowsiness they feel Il the client forgets a dose Af antipsychotic medication, he or she can take the missed dose if it is only 3 or 4 hours late. If the dose is more than 4 hours overdue or the next dose is due, the client can omit the forgotten dose. The nurse encourages clients who have difficulty remembering to take their medication to use a chart and to record doses when taken or to use a pillboxAntidepressant drugs are primarily used in the treatment illness, anxiety disorders, the depressed phase of bipolar disorder, and psychotic depression. Off-label uses of antidepressants include the treatment of chronic pain, migraine headaches, peripheral and diabetic neuropathies, sleep apnea, dermatologic disorders, panic disorder, and eating disorders. Although the mechanism of action is not completely understood, antidepressants somehow interact with the two neurotransmitters, norepinephrine and serotonin, that regulate mood, arousal, attention, sensory processing, and appetite.Antidepressants are divided into four groups: Tricyclic and the related cyclic antidepressants 1\. Selective serotonin reuptake inhibitors (SSRIs) 2\. MAO inhibitors (MAOIs) 3\. Other antidepressants such as desvenlafaxine (Pristiq), venlafaxine (Effexor), bupropion (Wellbutrin), duloxetine (Cymbalta), trazodone (Desyrel), and nefazodone (Serzone) Table 2.5 lists the dosage forms, usual daily dosages, and extreme dosa ranges. The cyclic compounds became available in the 1950s and for years were the first choice of drugs to treat depression even though they cause varying degrees of sedation, orthostatic hypotension (drop in blood pressure on rising), and anticholinergic side effects. It addition, cyclic antidepressants arepotentially lethal if taken in an overdose. During that same period, the MAOIs were discovered to have a positive effect on people with depression. Although the MAOIs have a low incidence of sedation and anticholinergic effects, they must be used with extreme caution for several reasons: A life-threatening side effect, hypertensive crisis, may occur if the client ingests foods containing tyramine (an amino acid) while taking MAOIs. Because of the risk of potentially fatal drug interactions, MAOIs cannot be given in combination with other MAOIs, tricyclic antidepressants, meperidine (Demerol), CNS depressants, many antihypertensives, or general anesthetics. MAOIs are potentially lethal in overdose and pose a potential risk in clients with depression who may be considering suicide. The selective serotonin reuptake inhibitors (SSRIs), first available in 1987 with the release of fluoxetine (Prozac), have replaced the cyclic drugs as the fist choice in treating depression because they are equal in efficacy and produce fewer troublesome side effects. The SSRIs and clomipramine are effective in the treatment of obsessive-compulsive disorder (OCD) as well. Prozac Weekly is the first and only medication that can be given once a week as maintenance therapy for depression after the client has been stabilized on fluoxetine. It contains 90 mg of fluoxetine with an enteric coating that delays release into the bloodstream.Preferred Drugs for Clients at High Risk for Suicide Suicide is always a primary consideration when treating clients with. depression. SSRIs, venlafaxine, nefazodone, and bupropion are often better choices for those who are potentially suicidal or highly impulsive because they carry no risk of lethal overdose in contrast to the cyclic compounds and the MAOIs. However, SSRIs are effective only for mild and moderate depression. Evaluation of the risk for suicide must continue even after treatment with antidepressants is initiated. The client may feel more energized but still have suicidal thoughts, which increases the likelihood of a suicide attempt. Also, because it often takes weeks before the medications have a full therapeutic effect, clients may become discouraged and tired of waiting to feel better, which can result in suicidal behavior. There is an FDA-required warning for SSRIs and increased suicidal risk in children and adolescents. Mechanism of Action The precise mechanism by which antidepressa their rotice their therapes etes is not known, but much is known about their action on the CNS. The maor interaction is with the monoamine neurotransmitter systems in de particularly norepinephrine and serotonin. Both of neurotransmitters are released throughout the brain and help regulate arous! vigilance, attention, mood, sensory processing, and appetite. Norepinephie serotonin, and dopamine are removed from the synapses after release by reuptake into presynaptic neurons. After reuptake, neurotransmitters are reloaded for subsequent release or metabolized by tie enzyme MAO. The SRIs block the reuptake of serotonin, the gre antidepressants and venlafaxine block the reuptake of norepiphin: primarily and block serotonin to some degree, and the MAOIs interfere with enzyme metabolism. This is not the complete explanation, however; the blockade of serotonin and norepinephrine reuptake and the inhibition of MAO occur in a matter of hours, while antidepressants are rarely effective until taken for several weeks. The cyclic compounds may take 4 to 6 weeks to be effective, MAOIs need 2 to 4 weeks for effectiveness, and SSRIs may be effective in 2 to 3 weeks. Researchers believe that the actions of these drugs are an \"initiating event\" and that eventual therapeutic effectiveness resulls when neurons respond more slowly, making serotonin available at the synapses (Burchum & Rosenthal, 2018). Side Effects of Selective Serotonin Reuptake InhibitorsSide Effects of Selective Serotonin Reuptake Inhibitors SRIs have fewer side effects compared to the cyclic compounds. Enhance! lead to several common side effects such & anxiety, agitation, akathsia (motor restlessness, nausea, insomnia, and senat dysfunction, specifically diminished sexual drive or difficulty achieving a tachycardia, diaphore problem during antidepressant therapy, although SSRIs cause less weight gi cyclic compounds, derivatives such as m than other antidepressants. Taking medications with food usually car free diet; Box 2.1 list minimize nausea. Akathisia is usually treated with a beta-blacker, such a determine whether propranolol (Inderal) or a benzodiazepine. Insomnia may continue to be treating depression w problem even if the client takes the medication in the morning; a sedative MAOIs. hypnotic or low-dosage trazodone may be needed. Less common side effects include sedation (particularly with paroxetie (Paxill), sweating, diarrhea, hand tremor, and headaches. Diarrhea and headaches can usually be managed with symptomatic treatment. Sweating and continued sedation most likely indicate the need for, & change to another antidepressant Side Effects of Cyclic Antidepressants Cyclic compounds have more side effects than do SSRIs and the newer miscellaneous compounds. The individual medications in this category vary in terms of the intensity of side effects, but generally side effects fall into the same categories. The cyclic antidepressants block cholinergic receptors, resulting in anticholinergic effects such as dry mouth, constipation, urinary hesitancy or retention, dry nasal passages, and blurred near vision. More severe anticholinergic effects such as agitation, delirium, and ileus may occur, particularly in older adults. Other common side effects include orthostatic hypotension, sedation, weight gain, and tachycardia. Clients may develop tolerance to anticholinergic effects, but these side effects are common reasons that clients discontinue drug therapy. Clients taking cyclic compounds frequently report sexual dysfunction similar to problems experienced with SRis. Both weight gain and sexual dysfunction are cited as common reasons for noncompliance (Stahl, 2017).Side Effects of Monoamine Oxidase Inhibitors The most common side effects of MAOIs include daytime sedation, insomnia, weight gain, dry mouth, orthostatic hypotension, and sexual dysfunction. The sedation and insomnia are difficult to treat and may necessitate a change in medication. Of particular concern with MAOIs is the potential for a life-threatening hypertensive crisis if the client ingests food that contains tyramine or takes sympathomimetic drugs. Because the enzyme MAO is necessary to break down the tyramine in certain foods, its inhibition results in increased serum tyramine levels, causing severe hypertension, hyperpyrexia, tachycardia, diaphoresis, tremulousness, and cardiac dysrhythmias. Drugs that may cause potentially fatal interactions with MAOIs include SSRIs, certain cyclic compounds, buspirone (BuSpar), dextromethorphan, and opiate derivatives such as meperidine. The client must be able to follow a tyramine-free diet; Box 2.1 lists the foods to avoid. Studies are currently underway to determine whether a selegiline transdermal patch would be effective in treating depression without the risks of dietary tyramine and orally ingested MAOIS. Yogurt, sour cream, peanuts, brewer\'s yeast, and monosodium glutamate (MSG). Adapted from Ohio State University Wexner Medical Center, Columbus, OH (2018) Side Effects of Other Antidepressants Of the other or novel antidepressant medications, nefazodone, trazodone, and mirtazapine commonly cause sedation. Both nefazodone and trazodone commonly cause headaches: Nefazodone can also cause dry mouth and nausea. Bupropion, venlafaxine, and desvenlafaxine may cause loss of appetite, nausea, agitation, and insomnia. Venlafaxine may also cause dizziness, sweating, or sedation. Sexual dysfunction is much less common with the novel antidepressants, with one notable exception: Trazodone can cause priapism (a sustained and painful erection that necessitates immediate treatment and discontinuation of the drug). Priapism may also result in impotence.Drug Interactions An uncommon but potentially serious drug interaction called serotonin syndrome (Or scrotonergic syndrome) can result from taking an MAOI and an SSRI at the same time. It can also occur if the client takes one of these drugs 100 close to the end of therapy with the other. In other words, one drug must clear the person\'s system before initiation of therapy with the other. Symptoms include agitation, sweating, rigidity, hyperreflexia, and, in extreme reactions, even coma and death (Burchum & Rosenthal, 2018). These symptoms are similar to those seen with an SSRI overdose. Client Teaching Clients should take SSRIs first thing in the morning unless sedation is a problem; generally, paroxetine most often causes sedation. If the client forgets a dose of an SSRI, he or she can take it up to 8 hours after the missed dose. To minimize side effects, clients generally should take cyclic compounds at night in a single daily dose when possible. If the client forgets a dose of a cyclic compound, he or she should take it within 3 hours of the missed dose or omit the dose for that day. Clients should exercise caution when driving or performing activities requiring sharp, alert reflexes until sedative effects can be determined. Clients taking MAOIs need to be aware that a life-threatening hyperadrenergic crisis can occur if they do not observe certain dietary restrictions. They should receive a written list of foods to avoid while taking MAOIs. The nurse should make clients aware of the risk for serious or even fatal drug interactions when taking MAOIs and instruct them not to take any additional medication including OTC preparations, without checking with the physician or pharmacist Mood-Stabilizing Drugs Mood-stabilizing drugs are used to treat bipolar disorder by stabilizing the client\'s mood, preventing or minimizing the highs and lows that characterize bipolar illness, and treating acute episodes of mania. Lithium is the most established mood stabilizer; some anticonvulsant drugs, particularly carbamazepine (Tegretol) and valproic acid (Depakote, Depakene), are effective mood stabilizers. Other anticonvulsants, such as gabapentin (Neurontin), topiramate (Topamax), oxcarbazepine (Trileptal), and lamotrigine (Lamictal), are also used for mood stabilization. Occasionally, clonazepam (Klonopin) is also used to treat acute mania. Clonazepam is included in the discussion of antianxiety agents.Mechanism of Action Although lithium has many neurobiologic effects, its mechanism of action in bipolar illness is poorly understood. Lithium normalizes the reuptake of certain neurotransmitters such as serotonin, norepinephrine, acetylcholine, and dopamine. It also reduces the release of norepinephrine through competition with calcium and produces its effects intracellularly rather than within neuronal synapses; it acts directly on G-proteins and certain enzyme subsystems such as cyclic adenosine monophosphates and phosphatidylinositol. Lithium is considered a first-line agent in the treatment of bipolar disorder (Stahl, 2017). The mechanism of action for anticonvulsants is not clear because it relates to their off-label use as mood stabilizers. Valproic acid and topiramate are known to increase the levels of the inhibitory neurotransmitter GABA. Both valproic acid and carbamazepine are thought to stabilize mood by inhibiting the kindling process. This can be described as the snowball-like effect seenwhen minor seizure activity seems to build up into more frequent and severe seizures. In seizure management, anticonvulsants raise the level of the threshold to prevent these minor seizures. It is suspected that this same kindling process may also occur in the development of full-blown mania with stimulation by more frequent minor episodes. This may explain why anticonvulsants are effective in the treatment and prevention of mania as well.Dosage Lithium is available in tablet, capsule, liquid, and sustained-release forms; no parenteral forms are available. The effective dosage of lithium is determined by monitoring serum lithium levels and assessing the client\'s clinical response to the drug. Daily dosages generally range from 900 to 3,600 mg; more importantly, the serum lithium level should be about 1 mEq/L. Serum lithium levels of less than 0.5 mEq/L are rarely therapeutic, and levels of more than 1.5 mEq/L are usually considered toxic. The lithium level should be monitored every 2 to 3 days while the therapeutic dosage is being determined; then, it should be monitored weekly. When the client\'s condition is stable, the level may need to be checked once a month or less frequentlyDosages usually range from 800 to 1,200 mg/day; the extreme dosage range is 200 to 2,000 mg/day. Valproic acid is available in liquid, tablet, and capsule forms and as sprinkles with dosages ranging from 1,000 to 1,500 mg/day; the extreme dosage range is 750 to 3,000 mg/day. Serum drug levels, obtained 12 hours after the last dose of the medication, are monitored for therapeutic levels of both these anticonvulsants.Side Effects Common side effects of lithium therapy include mild nausea or diarrhea, anorexia, fine hand tremor, polydipsia, polyuria, a metallic taste in the mouth,and fatigue or lethargy. Weight gain and acne are side effects that occur later in lithium therapy; both are distressing for clients. Taking the medication with food may help with nausea, and the use of propranolol often improves the fine tremor. Lethargy and weight gain are difficult to manage or minimize and frequently lead to noncompliance. Toxic effects of lithium are severe diarrhea, vomiting, drowsiness, muscle weakness, and lack of coordination. Untreated, these symptoms worsen and can lead to renal failure, coma, and death. When toxic signs occur, the drug should be discontinued immediately. If lithium levels exceed 3 mEg/L, dialysis may be indicated. Side effects of carbamazepine and valproic acid include drowsiness, sedation, dry mouth, and blurred vision. In addition, carbamazepine may cause rashes and orthostatic hypotension, and valproic acid may cause weight gain, alopecia, and hand tremor. Topiramate causes dizziness, sedation, weight loss (rather than gain), and increased incidence of renal calculi (Burchum & Rosenthal, 2018).Client Teaching For clients taking lithium and the anticonvulsants, monitoring blood levels periodically is important. The time of the last dose must be accurate so that plasma levels can be checked 12 hours after the last dose has been taken671-1026 7 Taking these medications with meals minimizes nausea. The client should not attempt to drive until dizziness, lethargy, fatigue, or blurred vision has subsided.insomnia, obsessive-compulsive disorder (OCD), depression, postraumatic stress disorder, and alcohol withdrawal. Antianxiety drugs are among the most widely prescribed medications today. A wide variety of drugs from different classifications have been used in the treatment of anxiety and insomnia. Benzodiazepines have proved to be the most effective in relieving anxiety and are the drugs most frequently prescribed. Benzodiazepines may also be prescribed for their anticonvulsant and muscle relaxant effects. Buspirone is a nonbenzodiazepine often used for the relief of anxiety and therefore is included in this section. Other drugs such as propranolol, clonidine (Catapres), and hydroxyzine (Vistaril) that may be used to relieve anxiety are much less effective and are not included in this discussion.Mechanism of Action Benzodiazepines mediate the actions of the amino acid GABA, the major inhibitory neurotransmitter in the brain. Because GABA receptor channels selectively admit the anion chloride into neurons, activation of GABA receptors hyperpolarizes neurons and thus is inhibitory. Benzodiazepines produce their effects by binding to a specific site on the GABA receptor. Buspirone is believed to exert its anxiolytic effect by acting as a partial agonist at serotonin receptors, which decreases serotonin tumover (Stahl, 2017). The benzodipspines vary in terms of their hal\'-lives, the means by whichthey are metabolized, and their effectiveness in treating anxiety and insomnia. Table 2.6 lists dosages, half-lives, and speed of onset after a single dose. Drugs with a longer half-life require less frequent dosing and produce fewer rebound effects between doses; however, they can accumulate in the body and produce \"next-day sedation\" effects. Conversely, drugs with shorter half-lives do not accumulate in the body or cause next-day sedation, but they do have rebound effects and require more frequent dosing.Temazepam (Restoril), triazolam (Halcion), and flurazepam (Dalmane) are most often prescribed for sleep rather than for relief of anxiety. Diazepam (Valium), chlordiazepoxide (Librium), and clonazepam are often used to manage alcohol withdrawal as well as to relieve anxiety. Side Effects Although not a side effect in the true sense, one chief problem encountered with the use of benzodiazepines is their tendency to cause physical dependence. Significant discontinuation symptoms occur when the drug is stopped; these symptoms often resemble the original symptoms for which the client sought treatment. This is especially a problem for clients with long-term benzodiazepine use, such as those with panic disorder or generalized anxietydisorder. Psychological dependence on benzodiazepines is common; clients fear the return of anxiety symptoms or believe they are incapable of handling anxiety without the drugs. This can lead to overuse or abuse of these drugs. -Buspirone does not cause this type of physical dependence. The side effects most commonly reported with benzodiazepines are those associated with CNS depression, such as drowsiness, sedation, poor coordination, and impaired memory or clouded sensorium. When used for sleep, clients may complain of next-day sedation or a hangover effect. Clients often develop a tolerance to these symptoms, and they generally decrease in intensity. Common side effects from buspirone include dizziness, sedation, nausea, and headache (Stahl, 2017). Elderly clients may have more difficulty managing the effects of CNS depression. They may be more prone to falls from the effects on coordination and sedation. They may also have more pronounced memory deficits and may have problems with urinary incontinence, particularly at night.often develop a tolerance to these symptoms, and they generally decrease in intensity. Common side effects from buspirone include dizziness, sedation, nausea, and headache (Stahl, 2017). Elderly clients may have more difficulty managing the effects of CNS depression. They may be more prone to falls from the effects on coordination and sedation. They may also have more pronounced memory deficits and may have problems with urinary incontinence, particularly at night. Client Teaching Clients need to know that antianxiety agents are aimed at relieving symptoms such as anxiety or insomnia but do not treat the underlying problems that cause the anxiety. Benzodiazepines strongly potentiate the effects of alcohol; one drink while on a benzodiazepine may have the effect of three drinks. Therefore, clients should not drink alcohol while taking benzodiazepines. Clients should be aware of decreased response time, slower reflexes, and possible sedative effects of these drugs when attempting activities such as driving or going to work. Benzodiazepine withdrawal can be fatal. After the client has started a course of therapy, he or she should never discontinue benzodiazepines abruptly or without the supervision of the physicián (Burchum & Rosenthal, 2018).Stimulants Stimulant drugs, specifically amphetamines, were first used to treat psychiatric disorders in the 1930s for their pronounced effects on CNS stimulation. In the past, they were used to treat depression and obesity, but those uses are uncommon in current practice. Dextroamphetamine (Dexedrine) has been widely abused to produce a high or to remain awake for long periods. Today, the primary use of stimulants is for ADHD in childrenand adolescents, residual attention-deficit disorder in adults, and narcolepsy (attacks of unwanted but irresistible daytime sleepiness that disrupt the person\'s life).The primary stimulant drugs used to treat ADHD are methylphenidate (Ritalin), amphetamine (Adderall), and dextroamphetamine (Dexedrine). Pemoline (Cylert) is infrequently used for ADHD because of the potential for liver problems. Of these drugs, methylphenidate accounts for 90% of the stimulant medication given to children for ADHD (Stahl, 2017). About 10% to 30% of clients with ADHD who do not respond adequately to the stimulant medications have been treated with antidepressants. In 2003, atomoxetine (Strattera), a selective norepinephrine reuptake inhibitor, was approved for the treatment of ADHD, becoming the first nonstimulant medication specifically designed and tested for ADHD.Mechanism of Action Amphetamines and methylphenidate are often termed indirectly acting amines because they act by causing release of the neurotransmitters (norepinephrine, dopamine, and serotonin) from presynaptic nerve terminals as opposed to having direct agonist effects on the postsynaptic receptors. They also block the reuptake of these neurotransmitters. Methylphenidate produces milder CNS stimulation than amphetamines; pemoline primarily affects dopamine and therefore has less effect on the sympathetic nervous system. It was originally thought that the use of methylphenidate and pemoline to treat ADHD in children produced the reverse effect of most stimulants---a calming or slowing of activity in the brain. However, this is not the case; the inhibitory centers in the brain are stimulated, so the child has greater abilities to filter out distractions and manage his or her own behavior. Atomoxetine helps block thereuptake of norepinephrine into neurons, thereby leaving more of the neurotransmitter in the synapse to help convey electrical impulses in the brain.Dosage For the treatment of narcolepsy in adults, both dextroamphetamine and methylphenidate are given in divided doses totaling 20 to 200 mg/day. The higher dosages may be needed because adults with narcolepsy develop tolerance to the stimulants and so require more medication to sustain improvement. Stimulant medications are also available in sustained-release preparations so that once-a-day dosing is possible. Tolerance is not seen in persons with ADHD. The dosages used to treat ADHD in children vary widely depending on the physician; the age, weight, and behavior of the child; and the tolerance of the family for the child\'s behavior. Table 2.7 lists the usual dosage ranges for these stimulants. Arrangements must be made for the school nurse or another authorized adult to administer the stimulants to the child at school. Sustained-release preparations eliminate the need for additional dosing at school.The most common side effects of stimulants are anorexia, weight loss, nausea, and irritability. The client should avoid caffeine, sugar, and chocolate, which may worsen these symptoms. Less common side effects include dizziness, dry nouth, blurred vision, and palpitations. The most common long-term problem with stimulants is the growth and weight suppression that occurs in some hildren. This can usually be prevented by taking \"drug holidays\" on veekends and holidays or during summer vacation, which helps restore ormal eating and growth patterns. Atomoxetine can cause decreased appetite, ausea, vomiting, fatigue, or upset stomach. Client Teaching he potential for abuse exists with stimulants, but this is seldom a problem in hildren. Taking doses of stimulants after meals may minimize anorexia and ausea. Caffeine-free beverages are suggested; clients should avoid chocolate d excessive sugar. Most important is to keep the medication out of the ild\'s reach because as little as a 10-day supply can be fatal.with alcohol in the body. This agent\'s only use is as a deterrent to aninking alcohol in persons receiving treatment for alcoholism. It is useful for persons who are motivated to abstain from drinking and who are not impulsive. Five to 10 minutes after a person taking disulfiram ingests alcohol, symptoms begin to appear: facial and body flushing from vasodilation, a throbbing headache, sweating, dry mouth, nausea, vomiting, dizziness, and weakness. In severe cases, there may be chest pain, dyspnea, severe hypotension, confusion, and even death. Symptoms progress rapidly and last from 30 minutes to 2 hours. Because the liver metabolizes disulfiram, it is most effective in persons whose liver enzyme levels are within or close to normal range. Disulfiram inhibits the enzyme aldehyde dehydrogenase, which is involved in the metabolism of ethanol. Acetaldehyde levels are then increased from five to 10 times higher than normal, resulting in the disulfiram-alcohol reaction. This reaction is potentiated by decreased levels of epinephrine and norepinephrine in the sympathetic nervous system caused by inhibition ofdopamine B-hydroxylase (Virani et al., 2017). Education is extremely important for the client taking disulfiram. Many common products such as shaving cream, aftershave lotion, cologne, deodorant, and OTC medications such as cough preparations contain alcohol; when used by the client taking disulfiram, these products can produce the same reaction as drinking alcohol. The client must read product labels carefully and select items that are alcohol free.Other side effects reported by persons taking disulfiram include fatigue, drowsiness, halitosis, tremor, and impotence? Disulfiram can also interfere with the metabolism of other drugs the client is taking, such as phenytoin (Dilantin), isoniazid, warfarin (Coumadin), barbiturates, and long-acting benzodiazepines such as diazepam and chlordiazepoxide. Acamprosate (Campral) is sometimes prescribed for persons in recovery from alcohol abuse or dependence. It helps reduce the physical and emotional discomfort encountered during the first weeks or months of sobriety, such as sweating, anxiety, and sleep disturbances. The dosage is two tablets (333 mg each) three times a day. Persons with renal impairments cannot take this drug. Side effects are reported as mild and include diarrhea, nausea, flatulence, and pruritus.