Systems-based Family Medicine Course Objectives: Psychiatric/Behavioral Health PA 601

Alcohol: screening tool -CAGE: (more than 2+ is considered positive)

"Have you ever felt you should Cut down on your drinking?" "Have people Annoyed you by criticizing our drinking?" "Have you ever felt Guilty about your drinking?" "Have you ever taken a drink first thing in the morning (Eye-opener)to steady your nerves or get rid of a hangover?"

Anorexia Nervosa: DSM5 criteria

(DSM-5) requires for diagnosis of anorexia nervosa all of: •restricted energy intake, leading to significantly low body weight for the age, sex, developmental trajectory, and physical health of the patient •intense fear of weight gain or becoming fat and/or persistent behavior that interferes with weight gain even though weight is significantly low •disturbance in how body weight or shape is experienced, overvaluation of body weight or shape on self, or persistently not recognizing the seriousness of the current low body weight

Bipolar I May have psychotic symptoms

(paranoia, delusions, hallucinations)

Second Gen (atypical) antipsychotics

-Olanzapine (Zyprexa) -Risperidone (Risperdal) -Ziprasidone (Geodon) -Aripiprazole (Abilify) -Quetiapine (Seroquel) MOA: Dopamine antagonists and serotonin 5-HT2 antagonists. Lower risk of extrapyramidal effects but increased risk of metabolic effects. Clozapine is not first-line but is most effective ed for treatment-resistant psychosis. meds should be tried for 4 weeks to establish efficacy

Bipolar I: Definition -Major Depressive Episode (not required for diagnosis) Five or more of the following symptoms have been present during the same 2-week-period and represent a change from previous functioning; at least one of the symptoms is either (1)depressed mood or (2) loss of interest or pleasure

1. Depressed mood most of the day, nearly every day, as indicated by either subjective report (feels sad, empty, or hopeless) or observation made by others 2. Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day (as indicated by either subjective account or observation) 3. Significant weight loss when not dieting or weight gain or decrease or increase in appetite nearly every day. 4. Insomnia or hypersomnia nearly every day 5. Psychomotor agitation or retardation nearly every day 6. Fatigue or loss of energy every day 7. Feelings of worthlessness or excessive or inappropriate guilt 8. Diminished ability to think or concentrate, or indecisiveness, nearly every day 9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide.

Bipolar I -During the period of mood disturbance and increased energy or activity, 3 or more of the following symptoms (4 if the mood is only irritable) are present to a significant degree and represent a noticeable change from usual behavior

1. Inflated self-esteem or grandiosity2. Decreased need for sleep (feels rested after only 3 hours)3. More talkative than usual or pressure to keep talking4. Flight of ideas or subjective experience that thoughts are racing5. Distractibility6. Increase in goal-directed activity (either socially, at work or school, or sexually) or psychomotor agitation7. Excessive involvement in activities that have a high potential for painful consequences (engaging in unrestrained buying sprees, sexual indiscretions or foolish business investments)

Depression (CURRENT)

1. Major depressive disorder A major depressive disorder consists of a syndrome of mood, physical and cognitive symptoms that occurs at any time of life. Many consider a physiologic or metabolic aberration to be causative. Complaints vary widely but frequently include a loss of interest and pleasure (anhedonia), withdrawal from activities, and feelings of guilt. Also included are inability to concentrate, some cognitive dysfunction, anxiety, chronic fatigue, feelings of worthlessness, somatic complaints (unexplained somatic complaints frequently indicate depression), loss of sexual drive, and thoughts of death. Unemployment has been associated with increase in depression risk. Diurnal variation with improvement as the day progresses is common. Vegetative signs that frequently occur are insomnia, anorexia with weight loss, and constipation. Occasionally, severe agitation and psychotic ideation are present. Psychotic major depression occurs up to 14% of all patients with major depression and 25% of patients who are hospitalized with depression. Psychotic symptoms (delusions, paranoia) are more common in depressed persons who are older than 50 years. Paranoid symptoms may range from general suspiciousness to ideas of reference with delusions. The somatic delusions frequently revolve around feelings of impending annihilation or somatic concerns (eg, that the body is rotting away with cancer). Hallucinations are less common than unusual beliefs and tend not to occur independent of delusions. In addition to psychotic major depression, other subcategories include major depression with atypical features that is characterized by hypersomnia, overeating, lethargy, and mood reactivity in which the mood brightens in response to positive events or news. Melancholic major depression is characterized by a lack of mood reactivity seen in atypical depression, the presence of a prominent anhedonia, and more severe vegetative symptoms. Major depression with a seasonal onset (seasonal affective disorder) is a dysfunction of circadian rhythms that occurs more commonly in the fall and winter months and is believed to be due to decreased exposure to full-spectrum light. Common symptoms include carbohydrate craving, lethargy, hyperphagia, and hypersomnia. Major depression with peripartum onset occurs during pregnancy or starts up to 4 weeks after delivery. Half of depressions associated with the peripartum period start during pregnancy. Most women (up to 80%) experience some mild letdown of mood in the postpartum period. For some of these (10-15%), the symptoms are more severe and similar to those usually seen in serious depression, with an increased emphasis on concerns related to the baby (obsessive thoughts about harming it or inability to care for it). When psychotic symptoms occur, there is frequently associated sleep deprivation, volatility of behavior, and manic-like symptoms. Postpartum psychosis is much less common (less than 2%), often occurs within the first 2 weeks, and requires early and aggressive management. Biologic vulnerability with hormonal changes and psychosocial stressors all play a role. The chances of a second episode are about 25% and may be reduced with prophylactic treatment. 2. Persistent depressive disorder (dysthymia) Dysthymia is a chronic depressive disturbance. Sadness, loss of interest, and withdrawal from activities over a period of two or more years with a relatively persistent course are necessary for this diagnosis. Generally, the symptoms are milder but longer-lasting than those in a major depressive episode. 3. Premenstrual dysphoric disorder Depressive symptoms occur during the late luteal phase (last 2 weeks) of the menstrual cycle. (See also Chapter 18.) Drug-induced depression has occurred with a number of medications. Corticosteroids are commonly associated with mood changes such as depression and hypomania or psychosis. Older antihypertensive medications such as reserpine, methyldopa, guanethidine, and clonidine have been associated with the development of depressive syndromes, as have digitalis, antiparkinsonian medications (eg, levodopa), retinoids, interferon, disulfiram, and anticholinesterase medications. Stimulant use results in a depressive syndrome when the drug is withdrawn. Alcohol, sedatives, and opioids are depressants but, paradoxically, are often used by patients in self-treatment of depression. Complications The most important complication is suicide, which often includes some elements of aggression. Suicide rates in the general population vary from 9 per 100,000 in Spain to 15 per 100,000 in the United States to 31 per 100,000 in Russia. In individuals hospitalized for depression, the lifetime risk rises to 4-6%. In patients with bipolar I disorder, the risk is higher. Men over the age of 50 are more likely to complete a suicide because of their tendency to use more violent means, particularly guns. On the other hand, women make more attempts but are less likely to complete a suicide. The suicide rate in the younger population, aged 15-35, continues to rise. Patients with cancer, respiratory illnesses, AIDS, and those being maintained on hemodialysis have higher suicide rates. Alcohol use is a significant factor in many suicide attempts. There are several groups of people who make suicide attempts. One group includes those individuals with acute situational problems. These individuals may be acutely distressed by a recent breakup in a relationship or another type of disappointment or overwhelmed by a stressful situation often with an aspect of public humiliation (eg, victims of cyber-bullying). A suicide attempt in such cases may be an impulsive or aggressive act not associated with significant depression. Another high-risk group includes individuals with severe depression. Severe depression may be due to conditions such as medical illness (eg, people with AIDS have a suicide rate over 20 times that of the general population) or comorbid psychiatric disorders (eg, panic disorders). Anxiety, panic, and fear are major findings in suicidal behavior. A patient may seem to make a dramatic improvement, but the lifting of depression may be due to the patient's decision to commit suicide. Another high-risk group are individuals with psychotic illness who tend not to verbalize their concerns and are often successful in their suicide attempt, although they make up only a small percentage of the total. Suicide is 10 times more prevalent in patients with schizophrenia than in the general population, with an increased frequency of jumping from bridges. In one study of 100 people who jumped from bridges, 47% had schizophrenia. The immediate goal of psychiatric evaluation is to assess the current suicidal risk and determine the need for hospitalization versus outpatient management. A useful question is to ask the person how many hours per day he or she thinks about suicide. If it is more than 1 hour, the individual is at high risk. Further assessing the risk by inquiring about intent, plans, means, and suicide-inhibiting factors (eg, strong ties to children or the church) is essential. Alcohol, hopelessness, delusional thoughts, and complete or nearly complete loss of interest in life or ability to experience pleasure are all positively correlated with suicide attempts. Other risk factors are previous attempts, a family history of suicide, medical or psychiatric illness (eg, anxiety, depression, psychosis), male sex, older age, contemplation of violent methods, a humiliating social stressor, and drug use (including long-term sedative or alcohol use), which contributes to impulsiveness or mood swings. Successful treatment of the patient at risk for suicide cannot be achieved if the patient continues to abuse drugs. An attempt is less likely to be suicidal if small amounts of poison or medication were ingested or scratching of wrists was superficial, if the act was performed near others or with early notification of others, or if the attempt was arranged so that early detection would be anticipated. The patient's current mood status is best evaluated by direct evaluation of plans and concerns about the future, personal reactions to the attempt, and thoughts about the reactions of others. Measurement of mood is often facilitated by using a standardized instrument such as the Hamilton or Montgomery-Asberg clinician-administered rating scales or the self-administered Quick Inventory of Depressive Symptomatology (QIDS-SR 16). Scales allow for initial assessment as well as ongoing treatment tracking. Suicide risk can be specifically assessed using an instrument such as the Columbia-Suicide Severity Risk Scale, https://cssrs.columbia.edu/wp-content/uploads/C-SSRS_Pediatric-SLC_11.14.16.pdf. The patient's immediate resources should also be assessed—people who can be significantly involved (most important), family support, job situation, financial resources, etc. If hospitalization is not indicated after a suicide attempt, the clinician must formulate and institute a treatment plan or make an adequate referral. (The National Suicide Prevention Lifeline, 1-800-273-8255, may be of assistance.) Medication should be dispensed in small amounts to at-risk patients. Although TCAs and SSRIs are associated with an equal incidence of suicide attempts, the risk of a completed suicide is much higher with TCA overdose. Guns and medications should be removed from the patient's household. Driving should be cautioned against until the patient improves. The problem is often worsened by the long-term complications of the suicide attempt, eg, brain damage due to hypoxia, peripheral neuropathies caused by staying for long periods in one position causing nerve compressions, and medical or surgical problems such as esophageal strictures and tendon dysfunctions. The reasons for self-mutilation, most commonly wrist cutting (but also autocastration, autoamputation, and autoenucleation, which are associated with psychoses), may be different from the reasons for a suicide attempt. The initial treatment plan, however, should presume suicidal ideation, and conservative treatment should be initiated.

Cannabis Use Disorder

9% of individuals who use cannabis Definition: continued problematic use despite negative consequences that causes significant distress or impairment in functioning •25%-50% of individuals who use cannabis daily are reported to develop cannabis use disorder (CUD) •cannabis use during adolescence may be associated with increased likelihood of cannabis use disorder

Caffeine Intoxication

>500mg •Anxiety •Agitation •Restlessness •Insomnia •Feeling of being "wired" >1gm •Tinnitus •Severe agitation •Cardiac arrhythmia

Psychological therapy for depression (CIRRENT)

B. Psychological It is often challenging to engage an individual in psychotherapeutic endeavors during the acute stage of a severe depression. While medications may be taking effect, a supportive and behavioral approach to strengthen existing coping mechanisms and appropriate consideration of the patient's continuing need to function at work, to engage in recreational activities, etc, are necessary as the severity of the depression lessens. Therapy during or just after the acute stage may focus on coping techniques, with some practice of alternative choices. Depression-specific psychotherapies help improve self-esteem, increase assertiveness, and lessen dependency. Interpersonal psychotherapy for depression has shown efficacy in the treatment of acute depression, helping patients master interpersonal stresses and develop new coping strategies. Cognitive behavioral therapy for depression addresses patients' patterns of negative thoughts, called cognitive distortions, which lead to feelings of depression and anxiety. Treatment usually includes homework assignments such as keeping a journal of cognitive distortions and of positive responses to them. The combination of medication therapy plus interpersonal psychotherapy or cognitive behavioral therapy is generally more effective than either modality alone. It is sometimes helpful to involve the spouse or other significant family members early in treatment. Mindfulness-based cognitive therapy has reduced relapse rates in several randomized controlled trials. In two studies, it was as effective as maintenance medication in preventing relapse. This therapy incorporates meditation and teaches patients to distance themselves from depressive thinking. C. Social Flexible use of appropriate social services can be of major importance in the treatment of depression. Since alcohol abuse is often associated with depression, early involvement in alcohol treatment programs such as Alcoholics Anonymous can be important to future success (see Alcohol Use Disorder [Alcoholism]). The structuring of daily activities during severe depression is often quite difficult for the patient, and loneliness is often a major factor. The help of family, employer, or friends is often necessary to mobilize the patient who experiences no joy in daily activities and tends to remain uninvolved and to deteriorate. Insistence on sharing activities will help involve the patient in simple but important daily functions. In some severe cases, the use of day treatment centers or support groups of a specific type (eg, mastectomy groups) is indicated. It is not unusual for a patient to have multiple legal, financial, and vocational problems requiring legal and vocational assistance. D. Behavioral When depression is a function of self-defeating coping techniques such as passivity, the role-playing approach can be useful. Behavioral techniques, including desensitization, may be used in problems such as phobias where depression is a by-product. When depression is a regularly used interpersonal style, behavioral counseling to family members or others can help in extinguishing the behavior in the patient. Behavioral activation, a technique of motivating depressed patients to begin engaging in pleasurable activities, has been shown to be a useful depression-specific psychotherapy. Exercise, especially aerobic and supervised by exercise professionals, has evidence in improving depressive symptoms.

Bipolar I: Definition -Hypomanic episode

A distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased activity or energy, lasting at least 4 consecutive days and present most of the day, nearly every day. •The episode is associated with an unequivocal change in functioning that is uncharacteristic of the individual when not symptomatic •The disturbance in mood and the change in functioning are observable by others •The episode is not severe enough to cause marked impairment in social or occupational functioning or to necessitate hospitalization, •If there are psychotic features, the episode is by definition: MANIC*********

1. Mania

A manic episode is a mood state characterized by elation with hyperactivity, overinvolvement in life activities, increased irritability, flight of ideas, easy distractibility, and little need for sleep. The overenthusiastic quality of the mood and the expansive behavior initially attract others, but the irritability, mood lability with swings into depression, aggressive behavior, and grandiosity usually lead to marked interpersonal difficulties. Activities may occur that are later regretted, eg, excessive spending, resignation from a job, a hasty marriage, sexual acting-out, and exhibitionistic behavior, with alienation of friends and family. Atypical manic episodes can include gross delusions, paranoid ideation of severe proportions, and auditory hallucinations usually related to some grandiose perception. The episodes begin abruptly (sometimes precipitated by life stresses) and may last from several days to months. Generally, the manic episodes are of shorter duration than the depressive episodes. In almost all cases, the manic episode is part of a broader bipolar disorder. Patients with four or more discrete episodes of a mood disturbance in 1 year have "rapid cycling." Substance abuse, particularly cocaine, can mimic rapid cycling.

Adverse effects of antipsychotics

increased prolactin (dopamine blockade in tuberoinfundibular pathway) Metabolic: hyperlipidemia, weight gain, hyperglycemia, increased abdominal fat. more common with 2nd gen

Clozapine

increased risk of agranulocytosis and myocarditis best drug for refractory Schizophrenia

HYPERSOMNIAS (DISORDERS OF EXCESSIVE SLEEPINESS)

A. Breathing-Related Sleep Disorders Obstructive sleep apnea is by far the most common of the breathing-related sleep disorders that include central sleep apnea and sleep-related hypoventilation. Obstructive sleep apnea hypopnea is characterized by snoring, gasping, or breathing pauses during sleep and five or more apneas or hypopneas per hour or evidence by polysomnography. B. Narcolepsy Syndrome Narcolepsy consists of a tetrad of symptoms: (1) sudden, brief (about 15 minutes) sleep attacks that may occur during any type of activity; (2) cataplexy—sudden loss of muscle tone involving specific small muscle groups or generalized muscle weakness that may cause the person to slump to the floor, unable to move, often associated with emotional reactions and sometimes confused with seizure disorder; (3) sleep paralysis—a generalized flaccidity of muscles with full consciousness in the transition zone between sleep and waking; and (4) hypnagogic hallucinations, visual or auditory, which may precede sleep or occur during the sleep attack. The attacks are characterized by an abrupt transition into REM sleep—a necessary criterion for diagnosis. The disorder begins in early adult life, affects both sexes equally, and usually levels off in severity at about 30 years of age. C. Kleine-Levin Syndrome This syndrome, which occurs mostly in young men, is characterized by hypersomnic attacks three or four times a year lasting up to 2 days, with hyperphagia, hypersexuality, irritability, and confusion on awakening. It has often been associated with antecedent neurologic insults. It usually remits after age 40. D. Periodic Limb Movement Disorder Periodic lower leg movements occur only during sleep with subsequent daytime sleepiness, anxiety, depression, and cognitive impairment. Restless leg syndrome includes movements while awake as well. E. Shift Work Sleep Disorder Shift work sleep disorder occurs when there is excessive fatigue as a consequence of work occurring during the normal sleep period. Treatment Narcolepsy can be managed by daily administration of a stimulant such as dextroamphetamine sulfate, 10 mg orally in the morning, with increased dosage as necessary. Modafinil and its enantiomer armodafinil are schedule IV medications FDA-approved for treating the excessive daytime fatigue of narcolepsy, sleepiness associated with obstructive sleep apnea, as well as for shift work sleep disorder. Usual dosing is 200-400 mg orally each morning for modafinil and 150-250 mg orally in the morning for armodafinil. The exact mechanism of action of modafinil and armodafil is unknown, yet they are thought to be less of an abuse risk than stimulants that are primarily dopaminergic. Common side effects include headache and anxiety; however, modafinil appears to be generally well tolerated. Modafinil may reduce the efficacy of cyclosporine, oral contraceptives, and other medications by inducing their hepatic metabolism. Imipramine, 75-100 mg orally daily, has been effective in treatment of cataplexy but not narcolepsy. Periodic limb movement disorder and REM sleep behavior disorder can be treated with clonazepam with variable results. There is no treatment for Kleine-Levin syndrome, although lithium can prevent recurrences in some.

Treatment of alcoholic hallucinosis and withdrawal

A. Hallucinosis Alcoholic hallucinosis, which can occur either during or on cessation of a prolonged drinking period, is not a typical withdrawal syndrome and is handled differently. Since the symptoms are primarily those of a psychosis in the presence of a clear sensorium, they are handled like any other psychosis: hospitalization (when indicated) and adequate amounts of antipsychotic medications. Haloperidol, 5 mg orally twice a day for the first day or so, usually ameliorates symptoms quickly, and the medication can be decreased and discontinued over several days as the patient improves. It then becomes necessary to deal with the chronic alcohol abuse, which has been discussed. B. Withdrawal The onset of withdrawal symptoms is usually 6-36 hours, and the peak intensity of symptoms is 48-72 hours after alcohol consumption is stopped. Providing adequate CNS depressants (eg, benzodiazepines) is important to counteract the excitability resulting from sudden cessation of alcohol intake. The choice of a specific sedative is less important than using adequate doses to bring the patient to a level of moderate sedation, and this will vary from person to person. All patients should be evaluated for their risk of alcohol withdrawal. Mild dependency requires "drying out." For outpatients, in some instances, a short course of tapering long-acting benzodiazepines—eg, diazepam, 20 mg/day orally initially, decreasing by 5 mg daily—may be a useful adjunct. When the history or presentation suggests that patients are actively in withdrawal or at significant risk for withdrawal, they should be hospitalized. Risk factors include a recent drinking history, frequent alcohol consumption, a past history of withdrawal, seizures, hallucinosis, or DTs, a past history of needing medication for detoxification, or a history of benzodiazepine or barbiturate use, abuse, or dependency. For all hospitalized patients, general management includes ensuring adequate hydration, correction of electrolyte imbalances (particularly magnesium, calcium, and potassium), and administering the vitamins thiamine (100 mg intravenously daily for 3 days then orally daily), folic acid (1 mg orally daily), and a multivitamin orally daily. Thiamine should be given prior to any glucose-containing solutions to decrease the risk of precipitating Wernicke encephalopathy or Korsakoff syndrome. Alcohol withdrawal is treated with benzodiazepines. Continual assessment is recommended to determine the severity of withdrawal, and symptom-driven medication regimens, which have been shown to prevent undersedation as well as oversedation and to reduce total benzodiazepine usage over fixed-dose schedules, should be used. The severity of withdrawal will determine a patient's level of care. For those at risk for withdrawal and with mild withdrawal symptoms, admission to a medical unit is adequate. For those with moderate withdrawal, a higher acuity hospital environment is recommended. Those with severe withdrawal should be admitted to the ICU. 1. Assessing alcohol withdrawal symptom severity The Clinical Institute Withdrawal Assessment for Alcohol, Revised (CIWA-Ar) is a validated tool that is widely used to determine severity of alcohol withdrawal. This survey assesses symptoms in 10 areas and can be administered relatively quickly (Figure 25-3). One caveat is that the patient must be able to communicate his or her symptoms to the provider. The maximum attainable score is 67. Clinical judgment should be used to determine final dosing of medications to patients who are in alcohol withdrawal because dosing will vary between patients and degrees of withdrawal. 2. Treating alcohol withdrawal symptoms based on CIWA-Ar score A. MINIMAL WITHDRAWAL SYMPTOMS (CIWA-AR SCORE LESS THAN 8) Patients who have a history suggestive of alcohol withdrawal risk with minimal withdrawal symptoms are suitable for withdrawal prophylaxis. The recommended benzodiazepine options include chlordiazepoxide or lorazepam orally, tapered over 3 days. The protocol calls for nursing assessment of sedation and withdrawal symptoms (CIWA-Ar) every 6 hours. If prophylactic medication is indicated, a sample tapering regimen may include lorazepam, 1 mg orally every 6 hours for 1 day, then 1 mg orally every 8 hours for 1 day, then 1 mg orally every 12 hours for 1 day, then discontinue; or chlordiazepoxide, 50 mg orally every 6 hours for 1 day, 25 mg orally every 6 hours for 2 days, then discontinue. Avoid chlordiazepoxide in the older patients or in patients with liver disease. Lorazepam is preferred in patients with liver disease. Sedation is assessed 30-60 minutes after each medication dose. The benzodiazepine dose is held for oversedation or if the respiratory rate is less than 10 breaths per minute. For CIWA-Ar score greater than 8, the provider must be notified, because this is suggestive of active withdrawal, and escalation of treatment must occur. B. MILD WITHDRAWAL SYMPTOMS (CIWA-AR SCORE 8-15) For patients in mild withdrawal, either chlordiazepoxide orally or lorazepam orally or intravenously can be used. Initially, chlordiazepoxide 50 mg orally or lorazepam 1 or 2 mg orally or intravenously is given hourly for 2 hours. Patients must be assessed for level of sedation and withdrawal symptoms (CIWA-Ar) every 4 hours. Dosing is adjusted as necessary to control symptoms without excessive sedation. After the first 2 hours, chlordiazepoxide or lorazepam is given every 4 hours and as needed. Typical dosing may include chlordiazepoxide 25-50 mg orally or lorazepam 0.5-1 mg orally or intravenously every 4 hours as needed. Additional doses of benzodiazepines should be given if the CIWA-Ar score remains between 8 and 15. C. MODERATE WITHDRAWAL (CIWA-AR SCORE 16-20) For patients in moderate withdrawal, chlordiazepoxide 100 mg orally or lorazepam 3 or 4 mg orally or intravenously is given every hour for the first 2 hours. CIWA-Ar monitoring should occur every 2 hours. Dosing is adjusted to control symptoms without excessive sedation. After initial dosing, continued treatment could include chlordiazepoxide 50 mg orally or lorazepam 1-2 mg orally or intravenously every 2 hours as needed for CIWA-Ar score between 16 and 20, and chlordiazepoxide 25 mg orally or lorazepam 0.5-1 mg orally or intravenously every 2 hours for CIWA-Ar score between 8 and 15. The maximum dose of chlordiazepoxide is 600 mg in 24 hours. Continuous pulse oximetry and cardiac monitoring should be considered. The degree of sedation should be monitored 30-60 minutes after each oral dose of medication and for 15 minutes after each parenteral dose. D. SEVERE WITHDRAWAL (CIWA-AR SCORE GREATER THAN 20) Patients with severe withdrawal are at risk for the development of DTs and should be transferred or admitted to the ICU. Intravenous lorazepam can be used to treat severe withdrawal. A potential treatment protocol is to administer lorazepam 1-2 mg intravenously every 15 minutes until the patient is calm and sedated but awake. Initial CIWA-Ar monitoring should occur every 30 minutes. The patient can then receive lorazepam 2 mg orally or intravenously every hour as needed when the CIWA-Ar score is between 16 and 20, and lorazepam 1-2 mg orally or intravenously every hour as needed when the CIWA-Ar score is between 8 and 15. If the patient requires more than 8 mg/hour of lorazepam as an initial dose or continues to demonstrate observable agitation, tremors, tachycardia, or hypertension despite high doses of lorazepam, consider adding dexmedetomidine. Dexmedetomidine, an alpha-2-agonist, produces sedation with minimal effect on respiratory drive. It is not recommended as a sole agent for the treatment of alcohol withdrawal but as adjunctive therapy along with benzodiazepines to decrease the hyperadrenergic output in patients with severe alcohol withdrawal not controlled by benzodiazepines or in patients at risk for respiratory depression from high-dose benzodiazepine administration. The recommended dosing of dexmedetomidine is 0.2-0.7 mcg/kg/hour, with lorazepam 1-2 mg intravenously every 8 hours plus lorazepam 1-2 mg intravenously every hour as needed for agitation. In limited cases of severe withdrawal requiring frequent lorazepam boluses for at least 6 hours, continuous intravenous lorazepam infusion can be considered, but the patient must be monitored extremely carefully for signs of respiratory depression. Continuous pulse oximetry and close observance of the patient's respiratory status are required. Sedation is assessed 15 minutes after each intravenous dose. If withdrawal symptoms are refractory to escalating benzodiazepine usage, despite the addition of dexmedetomidine, escalation to propofol should be considered. Patients receiving large doses of benzodiazepines often require intubation for airway protection, at which time initiation of propofol infusion for sedation, in addition to treatment of refractory alcohol withdrawal, is recommended. Phenobarbital monotherapy for alcohol withdrawal is used at some institutions, but randomized controlled trials comparing the efficacy of phenobarbital over benzodiazepines are needed to inform adoption of new treatment regimens. In all cases, benzodiazepines should be held if the patient is too sedated or has a respiratory rate less than 10 breaths per minute. Do not bolus lorazepam in doses greater than 4 mg intravenously. Mixing benzodiazepines, eg, chlordiazepoxide orally every 8 hours with lorazepam, is not recommended. Instead, select a single agent and titrate as needed. Once a patient has been stable for 24 hours, the benzodiazepine dose can be reduced by 20% daily until withdrawal is complete. 3. Managing other withdrawal-associated conditions Meticulous examination for other medical problems is necessary. Alcoholic hypoglycemia can occur with low blood alcohol levels (see Chapter 27). Patients with severe alcohol use disorder commonly have liver disease with associated clotting disorders and are also prone to injury—and the combination all too frequently leads to undiagnosed subdural hematoma. Phenytoin does not appear to be useful in managing alcohol withdrawal seizures per se. Sedating doses of benzodiazepines are effective in treating alcohol withdrawal seizures. Thus, other anticonvulsants are not usually needed unless there is a preexisting seizure disorder. Chronic brain syndromes secondary to a long history of alcohol intake are not clearly responsive to thiamine and vitamin replenishment. Attention to the social and environmental care of this type of patient is paramount. 4. Initiating psychological and social measures The psychological and behavioral treatment methods outlined under Treatment of At-Risk Drinking become the primary considerations after successful treatment of alcoholic hallucinosis or withdrawal. Psychological and social measures should be initiated in the hospital prior to discharge. This increases the possibility of continued posthospitalization treatment.

Treatment of at-risk drinking

A. Psychological The most important consideration for the clinician is to suspect the problem early and take a nonjudgmental attitude, although this does not mean a passive one. The problem of denial must be faced, preferably with significant family members at the first meeting. This means dealing from the beginning with any enabling behavior of the spouse or other significant people. Enabling behavior allows the patient with an alcohol use disorder to avoid facing the consequences of his or her behavior. There must be an emphasis on the things that can be done. This approach emphasizes the fact that the clinician cares and strikes a positive and hopeful note early in treatment. Valuable time should not be wasted trying to find out why the patient drinks. The immediate problem to be addressed is how to stop the drinking. Although total abstinence should be the ultimate goal, a harm reduction model indicates that gradual progress toward abstinence can be a useful treatment strategy. Motivational interviewing, a model of counseling that addresses both the patient's ambivalence and motivation for change, may contribute to reduced consumption over time. B. Social Encourage the patient to attend Alcoholics Anonymous meetings and the spouse to attend Al-Anon meetings. Success is usually proportionate to the utilization of Alcoholics Anonymous, religious counseling, and other resources. The patient should be seen frequently for short periods. Do not underestimate the importance of religion, particularly since the patient with alcohol use disorder is often a dependent person who needs a great deal of support. Early enlistment of the help of a concerned religious adviser can often provide the turning point for a personal conversion to sobriety. One of the most important considerations is the patient's job—fear of losing a job is one of the most powerful motivations for giving up alcohol. The business community is aware of the problem; about 70% of the Fortune 500 companies offer programs to their employees to help with the problem of alcoholism. Some specific recommendations that can be offered to employers include (1) avoid placement in jobs where the alcoholic patient must be alone, eg, as a traveling buyer or sales executive, (2) use supervision but not surveillance, (3) keep competition with others to a minimum, and (4) avoid positions that require quick decision making on important matters (high-stress situations). In general, commitment to abstinence and avoidance of situations that might be conducive to drinking are most predictive of a good outcome. C. Medical Hospitalization is not usually necessary but may be warranted if there are concomitant medical indications. Furthermore, if patients with heavy alcohol use are hospitalized for any other reason, providers must be vigilant for signs and symptoms of alcohol withdrawal. Because of the many medical complications of alcoholism, a complete physical examination with appropriate laboratory tests is mandatory, with special attention to the liver and nervous system. Use of sedatives as a replacement for alcohol is not desirable. The usual result is concomitant use of sedatives and alcohol and worsening of the problem. Lithium is not helpful in the treatment of alcoholism. Disulfiram (250-500 mg/day orally) has been used for many years as an aversive medication to discourage alcohol use. Disulfiram inhibits aldehyde dehydrogenase, causing toxic reactions when alcohol is consumed. The results have generally been of limited effectiveness and depend on the motivation of the individual to be compliant. Naltrexone, an opiate antagonist, in a dosage of 50 mg orally daily, lowers relapse rates over the 3-6 months after cessation of drinking, apparently by lessening the pleasurable effects of alcohol. One study suggests that naltrexone is most effective when given during periods of drinking in combination with therapy that supports abstinence but accepts the fact that relapses occur. Naltrexone is FDA-approved for maintenance therapy. Studies indicate that it reduces alcohol craving when used as part of a comprehensive treatment program. Acamprosate (333-666 mg orally three times daily) helps reduce craving and maintain abstinence and can be continued even during periods of relapse. Both acamprosate and oral naltrexone have been associated with reduction in return to drinking. D. Behavioral Conditioning approaches historically have been used in some settings in the treatment of alcoholism, most commonly as a type of aversion therapy. For example, the patient is given a drink of whiskey and then a shot of apomorphine, and proceeds to vomit. In this way a strong association is built up between the drinking and vomiting. Although this kind of treatment has been successful in some cases, after appropriate informed consent, many people do not sustain the learned aversive response.

AMPHETAMINES/COCAINE Withdrawal

•Depression with symptoms of hyperphagia and hypersomnia***** •People who have used stimulants chronically occasionally become sensitized ("kindling") to future use of stimulants. •In these individuals, even small amounts of mild stimulants such as caffeine can cause symptoms of paranoia and auditory hallucinations.

3. PARASOMNIAS (ABNORMAL BEHAVIORS DURING SLEEP)

A. Sleep Terror Sleep terror (pavor nocturnus) is an abrupt, terrifying arousal from sleep, usually in preadolescent boys although it may occur in adults as well. It is distinct from sleep panic attacks. Symptoms are fear, sweating, tachycardia, and confusion for several minutes, with amnesia for the event. B. Nightmares Nightmares occur during REM sleep; sleep terrors in stage 3 or stage 4 sleep. C. Sleepwalking Sleepwalking (somnambulism) includes ambulation or other intricate behaviors while still asleep, with amnesia for the event. It affects mostly children aged 6-12 years, and episodes occur during stage 3 or stage 4 sleep in the first third of the night and in REM sleep in the later sleep hours. Sleepwalking in older adults may be a feature of dementia. Idiosyncratic reactions to drugs (eg, marijuana, alcohol) and medical conditions (eg, partial complex seizures) may be causative factors in adults. D. Enuresis Enuresis is involuntary micturition during sleep in a person who usually has voluntary control. Like other parasomnias, it is more common in children, usually in the 3-4 hours after bedtime, but is not limited to a specific stage of sleep. Confusion during the episode and amnesia for the event are common. Treatment Treatment for sleep terrors is with benzodiazepines (eg, diazepam, 5-20 orally mg at bedtime), since it will suppress stage 3 and stage 4 sleep. Somnambulism responds to the same treatment for the same reason, but simple safety measures should not be neglected. Enuresis may respond to imipramine, 50-100 mg orally at bedtime, although desmopressin nasal spray (an ADH preparation) is likely the treatment of choice for nocturnal enuresis. Behavioral approaches (eg, bells that ring when the pad gets wet) have also been successful.

Neuroleptic malignant syndrome

AMS "lead pipe" muscle rigidity autonomic instability (tachycardia, tachypnea, fever, BP changes, hypersalivation, diaphoresis), incontinence, leukocytosis and rhabdomyolysis (increased CPK, LDH, LFTs) Management: discontinue meds. Supportive care (blankets, IV fluids). Bromocriptine, Amantadine. Dantrolene for rigidity and fever

Cocaine Intoxication -Overview

AVOID BETA BLOCKERS GIVE BENZOS

Psychadelics

About 6000 species of plants have psychoactive properties. Substance use disorder with psychedelics is not common. All of the common psychedelics (LSD, mescaline, psilocybin, dimethyltryptamine, and other derivatives of phenylalanine and tryptophan) can produce similar behavioral and physiologic effects. An initial feeling of tension is followed by emotional release such as crying or laughing (1-2 hours). Later and at higher doses, perceptual distortions occur, with visual illusions and hallucinations, and occasionally there is fear of ego disintegration (2-3 hours). Major changes in time sense and mood lability then occur (3-4 hours). A feeling of detachment and a sense of destiny and control occur (4-6 hours). Of course, reactions vary among individuals, and some of the drugs produce markedly different time frames. Occasionally, the acute episode is terrifying (a "bad trip"), which may include panic, depression, confusion, or psychotic symptoms. Preexisting emotional problems, the attitude of the user, and the setting where the drug is used affect the experience. Treatment of the acute episode primarily involves protection of the individual from erratic behavior that may lead to injury or death. A structured environment is usually sufficient until the drug is metabolized. In severe cases, antipsychotic medications with minimal side effects (eg, haloperidol, 5 mg intramuscularly) may be given every several hours until the individual has regained control. In cases where "flashbacks" occur (mental imagery from a "bad trip" that is later triggered by mild stimuli such as marijuana, alcohol, or psychic trauma), a short course of an antipsychotic medication—eg, olanzapine, 5-10 mg/day orally, or risperidone, 2 mg/day orally, initially, and up to 20 mg/day and 6 mg/day, respectively—is usually sufficient. Lorazepam or clonazepam, 1-2 mg orally every 2 hours as needed for acute agitation, may be a useful adjunct. An occasional patient may have "flashbacks" for much longer periods and may require small doses of antipsychotic medications over the longer term.

Alcohol use (ROSH)

According to the National Institute on Alcohol Abuse and Alcoholism, men age < 65 years who consume four or more standard drinks per day meet the threshold for alcohol-related health risks. Standard drinks are defined as a 12-ounce beer, a 5-ounce glass of wine, or 1.5 ounces of 80-proof liquor. Risky alcohol use puts an individual at risk for alcohol-related health issues. Alcohol-related health issues include hypertension, anxiety, depression, gastrointestinal symptoms, electrolyte disturbance, abnormal liver enzymes, macrocytosis, and comorbid substance use disorders. This behavior also places an individual at risk for developing alcohol use disorder.

Benzodiazepine Withdrawal Treatment

•Slow taper -sudden withdrawal may be associated with seizures •Loperamide for diarrhea •Anti-emetics •Tylenol and ibuprofen for headaches, body aches •Serious complications such as high blood pressure, seizures, delirium, and even death may occur during withdrawal especially if withdrawal is left untreated

TCAs (tricyclic antidepressants)

Amitriptyline, Clomipramine, Imipramine, Doxepin -Desipramine, Nortriptyline (secondary) MOA: inhibits reuptake of serotonin and NE IND: Depression, insomnia, neuropathies (post-herpetic neuralgia, diabetic neuropathy) -Used less often due to adverse effect profile and severe toxicity with overdose Adverse effects: Anticholinergic effects (dry mouth, constipation, urinary retention, tachycardia, orthostatic hypotension - confusion and hallucinations with elderly -Weight gain, prolonged QT (indicator of overdose) -Sedation (antihistamine), lowers seizure threshold, SIADH Overdose: 3 C's Cardiotoxicity or wide complex tachycardia (Na+ channel blocker effects), Convulsions (seizures), respiratory depression, Coma Sodium bicarb used for toxicity Contraindications: MAOI use, recent MI, seizure history

What are the most common somatic symptoms associated with generalized anxiety disorder?

Answer: Headaches and pain in the neck, shoulders, or back.

What is the first-line treatment for bipolar disorder in pregnant patients?

Answer: Lamotrigine.

Anti-HAM effects with first gen antipsychotics

Anticholinergic: dry mouth and eyes, blurred vision, urinary retention, constipation, hyperthermia Antihistamine: sedation, weight gain Anti-alpha 1 adrenergic: orthostatic hypotension, sexual dysfunction, cardiac abnormalities

AMPHETAMINES/COCAINE: Overdose Treatment

Antihypertensives for any hypertension Avoid beta blockers Concerns of coronary artery vasoconstriction and systemic hypertension, which can result from unopposed alpha- adrenergic stimulation. Obtain an ECG and monitor the patient constantly

D. Mood Disorders Secondary to Illness and Medications

Any illness, severe or mild, can cause significant depression. Conditions such as rheumatoid arthritis, multiple sclerosis, stroke, and chronic heart disease are likely to be associated with depression, as are other chronic illnesses. Depression is common in cancer, as well, with a particularly high degree of comorbidity in pancreatic cancer. Hormonal variations clearly play a role in some depressions. Varying degrees of depression occur at various times in schizophrenic disorders, CNS disease, and organic mental states. Alcohol dependency frequently coexists with serious depression. Drug-induced depression has occurred with a number of medications. Corticosteroids are commonly associated with mood changes such as depression and hypomania or psychosis. Older antihypertensive medications such as reserpine, methyldopa, guanethidine, and clonidine have been associated with the development of depressive syndromes, as have digitalis, antiparkinsonian medications (eg, levodopa), retinoids, interferon, disulfiram, and anticholinesterase medications. Stimulant use results in a depressive syndrome when the drug is withdrawn. Alcohol, sedatives, and opioids are depressants but, paradoxically, are often used by patients in self-treatment of depression.

Panic Attack: Management -First line

Benzodiazepines ("pam"s: alprazolam, lorazepam, diazepam) -calms nerves One must rule out MI, thyrotoxicosis

Bipolar I (ROSH)

Bipolar I disorder is a psychiatric disorder characterized by manic episodes, hypomanic episodes, and major depressive episodes. Bipolar II disorder is characterized by depressive episodes and at least one episode of hypomania. First-line treatment for bipolar major depression (a major depressive episode in either bipolar I disorder or bipolar II disorder) includes the FDA-approved medications quetiapine or lurasidone as monotherapy. If this treatment is ineffective, second-line treatment options include olanzapine plus fluoxetine (also FDA approved), valproate, or combination therapy with a first-line agent plus lithium or valproate. Third-line treatment regimens include monotherapy with lamotrigine, lithium, olanzapine, or carbamazepine. Third-line combination therapy regimens include olanzapine plus lithium or valproate, lithium plus a selective serotonin reuptake inhibitor, or a second-generation antipsychotic (i.e., quetiapine or olanzapine) plus an antidepressant. Patients who are refractory to drug therapy may be referred for electroconvulsive therapy. Medications are chosen based on the patient profile and the side effect profile.

Anorexia Nervosa (ROSH)

Bradycardia is commonly observed in patients with anorexia nervosa. Anorexia nervosa is a life-threatening eating disorder that is most commonly observed in adolescent girls. Comorbid psychiatric disorders such as depression are common. Patients with anorexia have an intense fear of gaining weight or becoming fat and have a disturbance of their body image, despite being underweight. It is this particular fear that causes patients to develop persistent behaviors to prevent weight gain, such as restricting food intake (restricting type) or developing purging behaviors, such as self-induced vomiting or misusing laxatives or diuretics (purging type). Individuals close to the patient may notice the patient wearing baggy clothes or extra layers of clothes to hide their body shape and also to address issues with thermoregulatory dysfunction due to loss of body fat. Mealtime rituals may be noted, such as cutting food into tiny pieces. Patients with anorexia nervosa can develop amenorrhea, which was previously required for the diagnosis in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), bradycardia, brittle hair and nails, hypotension, hypothermia, and lanugo. Osteopenia and eventual osteoporosis can also develop secondary to malnutrition. Fatal dysrhythmias can develop secondary to electrolyte disturbances. Seizures can occur due to hypoglycemia. Rare neurologic manifestations include Wernicke encephalopathy and Korsakoff syndrome. The diagnosis of anorexia nervosa is made based on DSM-5 criteria, in which a patient must be restricting their energy intake, have an intense fear of gaining weight, and have a distorted perception of their body weight or body shape. The diagnosis should be specified based on whether the patient restricts or purges and whether the patient is in any type of remission. Additionally, the severity should be specified. Severity of anorexia nervosa is based on body mass index. Evaluation of a patient with anorexia nervosa should include accurate weight assessment, orthostatic vital signs, electrocardiogram, urinalysis with specific gravity (to assess hydration status), complete blood count, complete metabolic panel, and thyroid function tests. Low creatinine, hyponatremia, hypokalemia, hypomagnesemia, and hypophosphatemia may be observed. An echocardiogram should be obtained in patients with syncope, dyspnea, and orthopnea, as mitral valve prolapse and myocardial fibrosis can occur. Depending on severity of weight loss, comorbid conditions, electrolyte abnormalities, dysrhythmias, and presence of suicidal ideation, inpatient treatment may be warranted. Treatment is focused on weight restoration and psychotherapy. A feeding tube may be needed. Patients should be closely monitored for refeeding syndrome.

Bulimia Nervosa (ROSH)

Bulimia nervosa is characterized by episodes of binge eating followed by inappropriate compensatory behavior that occurs at least once per week for at least 3 months. This behavior is secondary to an unhealthy perception of body image. During the periods of binge eating, individuals often feel they have no control over the amount of food they are consuming. Caloric restriction is a type of compensatory behavior that typically propagates the cycle of binge eating and vomiting. Compensatory behavior is most often demonstrated by self-induced vomiting but can include the inappropriate use of laxatives or emetics. Typically, bulimia nervosa is associated with other psychiatric disorders. These disorders include anxiety disorders, body dysmorphic disorder, depressive disorder, post-traumatic stress disorder, and substance use disorders. Unipolar depression and specific phobia disorder are the most common comorbid psychiatric disorders found with bulimia nervosa. Tobacco use and alcohol use disorder are more common in this patient population as well. Personality disorders, including borderline, avoidant, dependent, paranoid, histrionic, and obsessive-compulsive disorders, are also commonly present with bulimia nervosa.

Caffeine

Caffeine, along with nicotine and alcohol, is one of the most commonly used drugs worldwide although a caffeine use disorder is not described. About 10 billion pounds of coffee (the richest source of caffeine) are consumed yearly throughout the world. Tea, cocoa, and cola drinks also contribute to an intake of caffeine that is often astoundingly high in a large number of people. Low to moderate doses (30-200 mg/day) tend to improve some aspects of performance (eg, vigilance). The approximate content of caffeine in a (180-mL) cup of beverage is as follows: brewed coffee, 80-140 mg; instant coffee, 60-100 mg; decaffeinated coffee, 1-6 mg; black leaf tea, 30-80 mg; tea bags, 25-75 mg; instant tea, 30-60 mg; cocoa, 10-50 mg; and 12-oz cola drinks, 30-65 mg. A 2-oz chocolate candy bar has about 20 mg. Some herbal teas (eg, "morning thunder") contain caffeine. Caffeine-containing analgesics usually contain approximately 30 mg per unit. Symptoms of caffeinism (usually associated with ingestion of over 500 mg/day) include anxiety, agitation, restlessness, insomnia, a feeling of being "wired," and somatic symptoms referable to the heart and GI tract. It is common for a case of caffeinism to present as an anxiety disorder. It is also common for caffeine and other stimulants to precipitate severe symptoms in compensated schizophrenic and manic-depressive patients. Chronically depressed patients often use caffeine drinks as self-medication. This diagnostic clue may help distinguish some major affective disorders. Discontinuation of caffeine (greater than 250 mg/day) can produce withdrawal symptoms, such as headaches, irritability, lethargy, and occasional nausea.

Marijuana

Cannabis sativa, a hemp plant, is the source of marijuana. The parts of the plant vary in potency. The resinous exudate of the flowering tops of the female plant (hashish, charas) is the most potent, followed by the dried leaves and flowering shoots of the female plant (bhang) and the resinous mass from small leaves of inflorescence (ganja). The least potent parts are the lower branches and the leaves of the female plant and all parts of the male plant. The drug is usually inhaled by smoking but vaporizing is popular. There is a clinically distinct syndrome associated with "vaping" THC—vaping-associated lung injury—that may result in devastating pulmonary effects and a pathologically distinct pathophysiology. Effects occur in 10-20 minutes and last 2-3 hours. "Joints" of good quality contain about 500 mg of marijuana (which contains approximately 5-15 mg of tetrahydrocannabinol with a half-life of 7 days). Marijuana soaked in formaldehyde and dried ("AMP") has produced unusual effects, including autonomic discharge and severe, though transient, cognitive impairment. With moderate dosage, recreational marijuana (higher in the THC versus CBD component) produces two phases: mild euphoria followed by sleepiness. In the acute state, the user has an altered time perception, less inhibited emotions, psychomotor problems, impaired immediate memory, and conjunctival injection. High doses produce transient psychotomimetic effects. No specific treatment is necessary except in the case of the occasional "bad trip," in which case the person is treated in the same way as for psychedelic usage. Marijuana frequently aggravates existing mental illness and adversely affects motor performance. Studies of long-term effects have conclusively shown abnormalities in the pulmonary tree. Laryngitis and rhinitis are related to prolonged use, along with chronic obstructive pulmonary disease. Electrocardiographic abnormalities are common, but no chronic cardiac disease has been linked to marijuana use. Long-term usage has resulted in depression of plasma testosterone levels and reduced sperm counts. Abnormal menstruation and failure to ovulate have occurred in some women. Cognitive impairments are common. Health care utilization for a variety of health problems is increased in long-term marijuana smokers. Sudden withdrawal produces insomnia, nausea, myalgia, and irritability. Psychological effects of long-term marijuana usage are still unclear. Urine testing is reliable if samples are carefully collected and tested. Detection periods span 4-6 days in short-term users and 20-50 days in long-term users. At the beginning of 2021, in the United States, marijuana is legal for medical use, recreational use, or both, or decriminalized, in all but six states.

Wernicke encephalopathy

Caused by thiamine deficiency (vit B1) Consists of the triad of: •Confusion (AMS) •Ataxia •Ophthalmoplegia (typically sixth nerve palsy) and nystagmus The classic triad is often not present and it is not required for diagnosis. Early recognition and treatment with thiamine (IV) can prevent Korsakoff syndrome

Insomnia (ROSH)

Chronic insomnia is diagnosed if a patient experiences symptoms at least three times per week for at least 3 months. These symptoms include difficulty falling asleep and may include difficulty staying asleep. Other patients report waking at least 30 minutes prior to the desired waking time. Patients with insomnia typically take longer than 30 minutes to fall asleep and spend more than 30 minutes of wakefulness during the night. This causes daytime sleepiness, poor attention, mood disturbance, reduced energy, and ongoing worry about sleep. The preferred first-line treatment for insomnia is cognitive behavioral therapy (CBT). This therapy aids in identifying thoughts and behaviors that may prohibit falling asleep and staying asleep. Therapy usually includes establishing a bedtime routine and eliminating time in bed that is not spent sleeping. Avoiding the use of substances that interfere with sleep and discontinuing daytime sleep habits are included in the treatment plan. Reducing anxious thoughts associated with bedtime and teaching relaxation techniques are cognitive approaches used with CBT.

SSRIs

Citalopram, Escitalopram, Paroxetine, Fluoxetine, Sertraline, Fluvoxamine MOA: selectively inhibits CNS uptake of serotonin, leading to increased serotonin activity in the CNS IND: first line medical therapy for depression, Ptsd, panic disorder, PMS, and anxiety disorder. - effective, mild adverse effects and less toxic in overdose compared to other antidepressants (don't affect NE, Act, histamine, or dopamine) -Fluoxetine: only antidepressant approved for treatment of bulimia. long half-life 2-4days compared to other SSRIs (1 day). Longer washout period for switching to MAOI (5 weeks) compared to other SSRIs (2 weeks) -Antidepressants take 4-6 weeks to reach maximum efficiency Adverse effects: -GI (nausea and diarrhea), HA, fatigue and restlessness -Sexual dysfunction (decreased libido) -anxiety, insomnia, weight changes, SIADH and serotonin syndrome -Increased suicidality in children and young adults (BBW) -Avoid citalopram in patients with long QT syndrome

Insomnia

Classification & Clinical Findings Patients may complain of difficulty getting to sleep or staying asleep, intermittent wakefulness during the night, early morning awakening, or combinations of any of these. Transient episodes are usually of little significance. Stress, caffeine, physical discomfort, daytime napping, and early bedtimes are common factors. Psychiatric disorders are often associated with persistent insomnia. Depression is usually associated with fragmented sleep, decreased total sleep time, earlier onset of REM sleep, a shift of REM activity to the first half of the night, and a loss of slow wave sleep—all of which are nonspecific findings. In manic disorders, a reduced total sleep time and a decreased need for sleep are cardinal features and important early sign of impending mania. In addition to a decreased amount of sleep, manic episodes are characterized by a shortened REM latency and increased REM activity. Sleep-related panic attacks occur in the transition from stage 2 to stage 3 sleep in some patients with a longer REM latency in the sleep pattern preceding the attacks. Abuse of alcohol may cause or be secondary to the sleep disturbance. There is a tendency to use alcohol as a means of getting to sleep without realizing that it disrupts the normal sleep cycle. Acute alcohol intake produces a decreased sleep latency with reduced REM sleep during the first half of the night. REM sleep is increased in the second half of the night, with an increase in total amount of slow wave sleep (stages 3 and 4). Vivid dreams and frequent awakenings are common. Chronic alcohol abuse increases stage 1 and decreases REM sleep (most medications delay or block REM sleep), with symptoms persisting for many months after the individual has stopped drinking. Acute alcohol or other sedative withdrawal causes delayed onset of sleep and REM rebound with intermittent awakening during the night Heavy smoking (more than a pack a day) causes difficulty falling asleep—often independently associated with an increase in coffee drinking. Excess intake of caffeine, cocaine, and other stimulants (eg, over-the-counter cold remedies) near bedtime causes decreased total sleep time—mostly NREM sleep—with some increased sleep latency. Sedative-hypnotics—specifically, the benzodiazepines, which are the most commonly prescribed medications to promote sleep—tend to increase total sleep time, decrease sleep latency, and decrease nocturnal awakening, with variable effects on NREM sleep. Nonbenzodiazepine hypnotics have similar effects on sleep as do the benzodiazepines, though some evidence shows improved slow wave sleep and less residual next-morning somnolence with non-benzodiazepines, such as zolpidem. Withdrawal causes just the opposite effects and results in continued use of the medication for the purpose of preventing withdrawal symptoms. Antidepressants decrease REM sleep (with marked rebound on withdrawal in the form of nightmares) and have varying effects on NREM sleep. The effect on REM sleep correlates with reports that REM sleep deprivation produces improvement in some depressions. Persistent insomnias are also related to a wide variety of medical conditions, particularly delirium, pain, respiratory distress syndromes, uremia, asthma, thyroid disorders, and nocturia due to benign prostatic hyperplasia. Sleep apnea and restless leg movement are described below. Adequate analgesia and proper treatment of medical disorders will reduce symptoms and decrease the need for sedatives. Treatment In general, there are two broad classes of treatment for insomnia, and the two may be combined: psychological (cognitive behavioral) and pharmacologic. In situations of acute distress, such as a grief reaction, pharmacologic measures may be most appropriate. With primary insomnia, however, initial efforts should be psychologically based. This is true in older adults to avoid the potential adverse reactions of medications. The older population is at risk for complaints of insomnia because sleep becomes lighter and more easily disrupted with aging. Medical disorders that become more common with age may also predispose to insomnia. A. Psychological Psychological strategies should include educating the patient regarding good sleep hygiene: (1) Go to bed only when sleepy. (2) Use the bed and bedroom only for sleeping and sex. (3) If still awake after 20 minutes, leave the bedroom, pursue a restful activity (such as a bath or meditation), and only return when sleepy. (4) Get up at the same time every morning regardless of the amount of sleep during the night. (5) Discontinue caffeine and nicotine, at least in the evening if not completely. (6) Establish a daily exercise regimen. (7) Avoid alcohol as it may disrupt continuity of sleep. (8) Limit fluids in the evening. (9) Learn and practice relaxation techniques. (10) Establish a bedtime ritual and a routine time for going to sleep. Research suggests that cognitive behavioral therapy for insomnia is as effective as zolpidem with benefits sustained 1 year after treatment. B. Pharmacologic When the above measures are insufficient, medications may be useful. Lorazepam (0.5 mg orally nightly), temazepam (7.5-15 mg orally nightly), and the nonbenzodiazepine hypnotics zolpidem (5-10 mg orally nightly, with a limit of 5 mg indicated for women) and zaleplon (5-10 mg orally nightly) are often effective for the older population and can be given in larger doses—twice what is prescribed for older patients—in younger patients. Zaleplon is often used to treat insomnia characterized by middle-of-the-night awakening with difficulty falling back to sleep. Eszopiclone (2-3 mg orally) is similar in action to zolpidem and zaleplon and has a longer duration of action. A lower dose of 1 mg is indicated in older adults or those with hepatic impairment. It is important to note that short-acting agents like triazolam or zolpidem may lead to amnestic episodes if used on a daily ongoing basis. Longer-acting agents such as flurazepam (half-life of more than 48 hours) may accumulate in older adults and lead to cognitive slowing, ataxia, falls, and somnolence. In general, it is appropriate to use medications for short courses of 1-2 weeks. The medications described above have largely replaced barbiturates as hypnotic agents because of their greater safety in overdose and their lesser hepatic enzyme induction effects. Antihistamines such as diphenhydramine (25 mg orally nightly) or hydroxyzine (25 mg orally nightly) may also be useful for sleep, as they produce no pharmacologic dependency; their anticholinergic effects may, however, produce confusion or urinary symptoms in older adults. Trazodone, an atypical antidepressant, is a non-habit-forming, effective sleep medication in lower than antidepressant doses (25-150 mg orally at bedtime). Priapism is a rare side effect requiring emergent treatment. Doxepin, 3-6 mg per night, is a TCA that is also effective for insomnia. Ramelteon, 8 mg orally at bedtime, is a melatonin receptor agonist that helps with sleep onset and does not appear to have abuse potential. It appears to be safe for ongoing use without the development of tolerance. Melatonin is used in doses of 3-6 mg. While melatonin is effective in reducing sleep latency, it is not usually effective in maintaining sleep. Thus, other strategies or medications are often required for sleep maintenance. Triazolam was popular as a hypnotic medication because of its short duration of action. However, because it has been associated with dependency, transient psychotic reactions, anterograde amnesia, and rebound anxiety, it has been removed from the market in several European countries. If used, it should be prescribed only for short periods of time. The dual orexin receptor antagonists (DORAs) class of hypnotics are approved to help initiate and maintain sleep. DORAs such as suvorexant and lemborexant may be more effective than other hypnotics for some patients. However, the role of DORAs have not been established relative to other hypnotics and DORAs are more expensive since they are not generically available. DORAs have shown a significant increase in depressive symptoms in a subset of patients, so other hypnotics may be a better choice in depressed patients. The dose of suvorexant is 10-20 mg orally given about 30 minutes before bedtime, while lemborexant is typically given in dosages of 5-10 mg daily.

Bulimia Nervosa rapid review

DSM-5: recurrent episodes of binge eating followed by inappropriate compensatory behavior via self-induced vomiting, laxative misuse, excessive exercise, or caloric restriction (occurring at least once per week for 3 months) Sense of lack of control during eating episodes Self-evaluation is unduly influenced by body shape or weight PE: body weight usually within or above normal range, dental erosions, parotid gland swelling, callused knuckles Tx options: cognitive behavioral therapy, fluoxetine or other SSRIs, or combined CBT/pharmacotherapy

Cyclothymic Disorder

Definition -For at least 2 years (1 in child/adolescent) there have been numerous periods with hypomanic symptoms that do not meet criteria for a hypomanic episode and numerous periods with depressive symptoms that no not meet criteria for a major depressive episode Criteria During the 2 year period the hypomanic and depressive periods have been present for at least half the time and the individual has not been without the symptoms for more than 2 months at a time •Criteria for major depressive, manic or hypomanic episode have never been met •Symptoms cause clinically significant distress or impairment Treatment •Mood stabilizers (lithium) •Second generation antipsychotics

Bipolar I disorder

Definition For a diagnosis of bipolar I disorder, it is necessary to meet the following criteria for a manic episode** The manic episode may have been preceded by and may be followed by hypomanic or major depressive episodes. The mood disturbance is sufficiently severe to cause marked impairment in social or occupational functioning or to necessitate hospitalization to prevent harm to self or others, or there are psychotic features. MANIC episode A distinct period of abnormally and persistently elevated, expansive or irritable mood and abnormally and persistently increased activity or energy, lasting at least 1 week and present most of the the day, nearly every day (or any duration if hospitalization is necessary) Epidemiology •Age 20-30 years in mean age of onset (rare onset after 50) •Similar prevalence in males and females •Prevalence about 1% •The earlier the onset, the more likelihood of psychotic features and the poorer the prognosis

PANIC ATTACKS

Definition •an episode of intense fear along with cardiorespiratory, gastrointestinal, or neurologic changes that can persist up to several hours •This is not a mental disorder •They are discrete periods of heightened anxiety that affect much of the general population Symptoms An abrupt surge of intense fear or intense discomfort that reaches a peak within 10 minutes and during which time four or more of the following symptoms occur: These symptoms are all considered sympathetic system overdrive •Palpitations, pounding heart or tachycardia •Sweating •Trembling or shaking •Sensation of sob or smothering •Feelings of choking •Chest pain or discomfort •Nausea or abdominal distress •Feeling dizzy, light-headed or faint •Chills or heat sensations •Paresthesias •Derealization or depersonalization •Fear of losing control or "going crazy" •Fear of dying

Major depressive disorder

Diagnostic Criteria -Five or more of the following symptoms have been present during the same 2-week period and represent a change from previous functioning -At least one of the symptoms is either (1) depressed mood or (2) loss of interest or pleasure -Symptoms cause significant distress or impairment and not associated with another substance or medical condition 1. Depressed mood most of the day, nearly every day, as indicated by either subjective report (feels sad, hopeless, empty) or observation made by others (tearful). 2. Markedly diminished interest or pleasure in all, or almost all activities most of the day, nearly every day 3. Significant weight loss when not dieting or weight gain in a month (or increase/decrease in appetite nearly every day) 4. Insomnia or hypersomnia nearly every day 5. Psychomotor agitation or retardation nearly every day (observable by others, not just subjective feelings) 6. Fatigue or loss of energy nearly every day 7. Feelings of worthlessness or excessive or inappropriate guilt nearly every day 8. Diminished ability to think or concentrate, or indecisiveness, nearly every day 9. Recurrent thoughts of death, recurrent suicidal ideation Pathophysiology •Alteration in neurotransmitters: serotonin, epinephrine, norepinephrine, dopamine, acetylcholine and histamine. ->"chemical imbalance hypothesis" •Inflammatory and oxidative stress hypothesis diagnosis •The diagnostic validity of the 9-item PHQ-9 was established in studies involving 8 primary care and 7 obstetrical clinics. •PHQ-9 scores > 10 had a sensitivity of 88% and a specificity of 88% for Major Depressive Disorder. •Reliability and validity of the tool have indicated it has sound psychometric properties. Internal consistency of the PHQ-9 has been shown to be high. Management -CBT, interpersonal therapy -SSRIs first line medical management. with no effect after 4 weeks, switch to another SSRI -SNRIs second line (Duloxetine, Venlafaxine) -TCAs -ECT therapy: rapid response if unresponsive to therapy

Panic disorder

Diagnostic Criteria -Recurrent unexpected panic attacks (at least 2) and At least one of the attacks has been followed by 1 month or more of one or both of the following 1. Persistent concern or worry about additional panic attacks or their consequences 2. A significant maladaptive change in behavior related to the attacks The disturbance is not attributable to the physiological effects of a substance The disturbance is not better explained by another mental disorder experience of panic attacks accompanied by persistent fear of having additional attacks******* Epidemiology and risk factors •Most common age of onset is 20-29 •Twice as common in women •Increased risk if first degree relative with panic disorder •Incidence ranges from 1.5-5% over lifetime •>60% also have major depression •Risk factors: panic related symptoms in childhood and adolescence Etiology Etiology not well understood May have gene-environment interaction Symptoms likely due to dysfunction in corticolimbic interactions during emotional processing Management 1.Pharmacologic •SSRI first line (sertraline, citalopram, fluoxetine) •SNRI (venlafaxine) •TCA if SSRI is ineffective 2. Cognitive Behavioral Therapy (BHT)

Posttraumatic stress disorder

Diagnostic Criteria Exposure to actual or threatened death, serious injury, or sexual violence in one or more of the following ways: (known trigger) 1. Directly experiencing the traumatic event 2. Witnessing, in person, the event(s) as it occurred to others 3. Learning that the event(s) occurred to a close family member or close friend (violent or accidental) 4. Experiencing repeated or extreme exposure to aversive details of the traumatic event(s) (does not include exposure through social media, television, etc) Presence of nine or more of the following symptoms from any of the 5 categories that begin or worsen after the traumatic event occurred. 1. Intrusion 2. Negative mood 3. Dissociation 4. Avoidance 5. Arousal •Recurrent, involuntary and intrusive distressing memories of the traumatic event •Recurrent distressing dreams in which the content and/or affect of the dream are related to the event •Dissociative reactions (flashbacks) in which the individual feels or acts as if the traumatic event(s) were recurring. •Intense or prolonged psychological distress or marked physiological reactions in response to internal or external cues that symbolize or resemble an aspect of the traumatic events (EX: fireworks) •Persistent inability to experience positive emotions (happiness, satisfaction, love) An altered sense of the reality of one's surroundings or oneself •(seeing oneself from another's perspective, being in a daze, time slowing) Inability to remember an important aspect of the traumatic events •Efforts to avoid distressing memories, thoughts or feelings about or closely associated with the traumatic event •Efforts to avoid external reminders (people, places, conversations, activities, objects, situations) that arouse distressing memories, thoughts or feelings about the traumatic event •Sleep disturbance •Irritable behavior and angry outbursts (typically expressed as verbal or physical aggression toward people or objects •Hypervigilance (multiple checking) •Problems with concentration •Exaggerated startle response Similar to Acute Stress Disorder, but symptoms last longer than 1 month and event happened sometime in the past Exposure to actual or threatened death, serious injury, or sexual violence in one or more of the following ways: Age >6*********** •One or more intrusion symptoms •Persistent avoidance of stimuli •Two or more negative mood symptoms •Two or more arousal symptoms Management •SSRI: first line medical treatment •Trazadone for insomnia •Cognitive behavioral therapy: •Prazosin may be used for nightmares

Bipolar II

Diagnostic criteria -At least 1 major depressive episode + at least 1 hypomanic episode •Mania episode makes it Bipolar I Disorder

Anorexia nervosa (CURRENT)

ESSENTIALS OF DIAGNOSIS -Restriction of calorie intake leading to underweight BMI (BMI < 18.5). -Intense fear of gaining weight or behavior that prevents weight gain. -Distorted perception of body image, with undue influence of weight on self-worth. -Denial of the medical seriousness of underweight status. GENERAL CONSIDERATIONS Anorexia nervosa is characterized by underweight BMI, intense fear of gaining weight, and distorted perception of body image. Anorexia nervosa typically begins in the years between adolescence and young adulthood. Ninety percent of patients are female, most of middle and upper socioeconomic status. The prevalence of anorexia nervosa is greater than previously suggested since prior diagnostic criteria were more restrictive and individuals with anorexia often conceal their illness. Many adolescents have mild versions of the disorder without severe weight loss. The American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5) classifies the severity of anorexia according to BMI: mild, BMI 17-18.49; moderate, BMI 16-16.99; severe, BMI 15-15.99; extreme, BMI less than 15. There are two subtypes of anorexia nervosa: binge-eating/purging type and restricting type. The binge-eating/purging subtype is characterized by recurrent episodes of binge-eating or purging (ie, self-induced vomiting and/or abuse of diuretics, laxatives, enemas, cathartics). The restricting subtype is characterized by dieting, fasting, or excessive exercising without associated binge-eating or purging. The cause of anorexia nervosa is not known. Although multiple endocrinologic abnormalities exist in patients with anorexia nervosa, most authorities believe they are secondary to malnutrition and not the primary disorder. Most experts favor a primary psychiatric origin, but no hypothesis explains all cases. Comorbidity with depression, anxiety, or obsessive-compulsive disorder is not uncommon and can be pernicious. The patient characteristically comes from a family whose members are highly goal-oriented. One theory holds that the patient's refusal to eat is an attempt to regain control of one's body in defiance of parental control. The patient's unwillingness to inhabit an "adult body" may also represent a rejection of adult responsibilities and the implications of adult interpersonal relationships. Patients are often perfectionistic in behavior and exhibit obsessional personality characteristics. Obsessional preoccupation with food is also common. A. Symptoms and Signs Patients with anorexia nervosa may exhibit severe emaciation and frequently complain of cold intolerance or constipation. Bradycardia, hypotension, and hypothermia may be present in severe cases. Examination demonstrates loss of body fat, dry and scaly skin, and increased lanugo body hair. Parotid enlargement and edema may also occur. In females of reproductive age, cessation of menstruation is common. B. Laboratory Findings Laboratory findings are variable but may include anemia, leukopenia, electrolyte abnormalities, and elevations of BUN and serum creatinine. Serum cholesterol levels are often increased. Endocrine abnormalities include depressed levels of LH and FSH and impaired response of LH to gonadotropin-releasing hormone. DIAGNOSIS AND DIFFERENTIAL The diagnosis is based on weight loss to a BMI less than 18.5, distorted body image, and fear of weight gain or of loss of control over food intake. Other medical or psychiatric illnesses that can account for anorexia and weight loss must be excluded. Behavioral features required for the diagnosis include intense fear of gaining weight, disturbance of body image, and refusal to exceed a minimal normal weight. The differential diagnosis includes bulimia nervosa, binge-eating disorder, endocrine and metabolic disorders (eg, panhypopituitarism, Addison disease, hyperthyroidism, and diabetes mellitus), GI disorders (eg, Crohn disease and gluten enteropathy), chronic infections (eg, tuberculosis), cancers (eg, lymphoma), and rare CNS disorders (eg, hypothalamic tumor). TREATMENT The goal of treatment is restoration of normal body weight and improvement in psychological comorbidities. Hospitalization may be necessary. Treatment programs conducted by experienced teams successfully restore normal weight in approximately two-thirds of cases. The remainder continue to experience difficulties with underweight, eating behaviors, and associated psychiatric conditions. Two to 6% of patients die of the complications of the disorder or commit suicide. Various treatment methods have been used without clear evidence of superiority of one over another. Supportive care by clinicians and family is the most important feature of any therapy. Cognitive-behavioral therapy, intensive psychotherapy, and family therapy may be tried. A variety of medications including tricyclic antidepressants, SSRIs, and lithium carbonate are effective in some cases; however, clinical trial results have been disappointing. Patients with severe malnutrition must be hemodynamically stabilized and may require enteral or parenteral feeding. Forced feedings should be reserved for life-threatening situations, since the goal of treatment is to reestablish normal eating behavior. WHEN TO REFER Adolescents and young adults with otherwise unexplained profound weight loss should be evaluated by a psychiatrist or eating disorders specialist. All patients with diagnosed anorexia nervosa should be co-managed with a psychiatrist or eating disorders specialist. WHEN TO ADMIT Signs of hypovolemia, major electrolyte disorders, and severe protein-energy malnutrition. Failure to improve with outpatient management.

Anxiety disorders (CURRENT)

ESSENTIALS OF DIAGNOSIS Persistent excessive anxiety or chronic fear and associated behavioral disturbances. Somatic symptoms referable to the autonomic nervous system or to a specific organ system (eg, dyspnea, palpitations, paresthesias). Not limited to an adjustment disorder. Not a result of physical disorders, other psychiatric conditions (eg, schizophrenia), or drug abuse (eg, cocaine). Stress, fear, and anxiety all tend to be interactive. The principal components of anxiety are psychological (tension, fears, difficulty in concentration, apprehension) and somatic (tachycardia, hyperventilation, shortness of breath, palpitations, tremor, sweating). Other organ systems (eg, GI) may be involved in multiple-system complaints. Fatigue and sleep disturbances are common. Sympathomimetic symptoms of anxiety are both a response to a CNS state and a reinforcement of further anxiety. Anxiety can become self-generating, since the symptoms reinforce the reaction, causing it to spiral. Additionally, avoidance of triggers of anxiety leads to reinforcement of the anxiety. The person continues to associate the trigger with anxiety and never relearns through experience that the trigger need not always result in fear, or that anxiety will naturally improve with prolonged exposure to an objectively neutral stressor. Anxiety may be free-floating, resulting in acute anxiety attacks, occasionally becoming chronic. Lack of structure is frequently a contributing factor, as noted in those people who have "Sunday neuroses." They do well during the week with a planned work schedule but cannot tolerate the unstructured weekend. Planned-time activities tend to bind anxiety, and many people have increased difficulties when this is lost, as in retirement. B. Panic Disorder Panic attacks are recurrent, unpredictable episodes of intense surges of anxiety accompanied by marked physiologic manifestations. Agoraphobia, fear of being in places where escape is difficult, such as open spaces or public places where one cannot easily hide, may be present and may lead the individual to confine his or her life to home. Distressing symptoms and signs such as dyspnea, tachycardia, palpitations, dizziness, paresthesia, choking, smothering feelings, and nausea are associated with feelings of impending doom (alarm response). Although these symptoms may lead to overlap with some of the same bodily complaints found in the somatic symptom disorders, the key to the diagnosis of panic disorder is the psychic pain and suffering the individual expresses. Panic disorder is diagnosed when panic attacks are accompanied by a chronic fear of the recurrence of an attack or a maladaptive change in behavior to try to avoid potential triggers of the panic attack. Recurrent sleep panic attacks (not nightmares) occur in about 30% of panic disorders. Anticipatory anxiety develops in all these patients and further constricts their daily lives. Panic disorder tends to be familial, with onset usually under age 25; it affects 3-5% of the population, and the female-to-male ratio is 2:1. The premenstrual period is one of heightened vulnerability. Patients frequently undergo evaluations for emergent medical conditions (eg, heart attack or hypoglycemia), which are then ruled out before the correct diagnosis is made. GI symptoms (eg, stomach pain, heartburn, diarrhea, constipation, nausea and vomiting) are common, occurring in about one-third of cases. MI, pheochromocytoma, hyperthyroidism, and various recreational drug reactions can mimic panic disorder and should be considered in the differential diagnosis. Patients who have panic disorder can become demoralized, hypochondriacal, agoraphobic, and depressed. These individuals are at increased risk for major depression and suicide. Alcohol abuse (in about 20%) results from self-treatment and is frequently combined with dependence on sedatives. Some patients have atypical panic attacks associated with seizure-like symptoms that often include psychosensory phenomena (a history of stimulant abuse often emerges). About 25% of panic disorder patients also have obsessive-compulsive disorder (OCD) Treatment Antidepressants are the first-line pharmacotherapy for panic disorder. Several SSRIs, including fluoxetine, paroxetine, and sertraline, are approved for the treatment of panic disorder. The SNRI venlafaxine is FDA-approved for treatment of panic disorder. As with GAD, panic disorder is often a chronic condition; the long-term use of benzodiazepines can result in tolerance or even benzodiazepine dependence. While panic disorder often responds to high-potency benzodiazepines such as clonazepam and alprazolam, the best use of these agents is generally early in the course of treatment concurrently with an antidepressant. Once the antidepressant has begun working after 4 or more weeks, the benzodiazepine may be tapered. Whether the indications for benzodiazepines are anxiety or insomnia, the medications should be used judiciously. The longer-acting benzodiazepines are used for the treatment of alcohol withdrawal and anxiety symptoms; the intermediate medications are useful as sedatives for insomnia (eg, lorazepam), while short-acting agents (eg, midazolam) are used for medical procedures such as endoscopy. In psychiatric disorders, the benzodiazepines are usually given orally; in controlled medical environments (eg, the ICU), where the rapid onset of respiratory depression can be assessed, they often are given intravenously. Because lorazepam does not produce active metabolites and has a half-life of 10-20 hours, it is useful in treating older adult patients or those with liver dysfunction. Ultra-short-acting agents, such as triazolam, have half-lives of 1-3 hours and may lead to rebound withdrawal anxiety. Longer-acting benzodiazepines, such as flurazepam, diazepam, and clonazepam, produce active metabolites, have half-lives of 20-120 hours, and should be avoided in older adults; however, some clinicians prefer clonazepam because of its long half-life and thus ease of dosing to once or twice a day. Medication dosage must be individualized as patients vary widely in their response and effects can be long-lasting. An adequate and scheduled dose early in the course of symptom development will obviate the need for "pill popping," which can contribute to dependency problems. The side effects of all the benzodiazepine antianxiety agents are patient- and dose-dependent. As the dosage exceeds the levels necessary for sedation, the side effects include disinhibition, ataxia, dysarthria, nystagmus, and delirium. (The patient should be told not to operate machinery and drive with caution until he or she is well stabilized without side effects.) Paradoxical agitation, anxiety, psychosis, confusion, mood lability, and anterograde amnesia have been reported, particularly with the shorter-acting benzodiazepines. These agents produce cumulative clinical effects with repeated dosage (especially if the patient has not had time to metabolize the previous dose), additive effects when given with other classes of sedatives or alcohol, and residual effects after termination of treatment (particularly in the case of medications that undergo slow biotransformation). Overdosage results in respiratory depression, hypotension, shock syndrome, coma, and death. Flumazenil, a benzodiazepine antagonist, is effective in overdosage. Overdosage (see Chapter 38) and withdrawal states are medical emergencies. Serious side effects of chronic excessive dosage are development of tolerance, resulting in increasing dose requirements, and physiologic dependence, resulting in withdrawal symptoms similar in appearance to alcohol and barbiturate withdrawal (withdrawal effects must be distinguished from reemergent anxiety). Abrupt withdrawal of sedative medications may cause serious and even fatal convulsive seizures. Psychosis, delirium, and autonomic dysfunction have also been described. Both duration of action and duration of exposure are major factors related to likelihood of withdrawal. Common withdrawal symptoms after low to moderate daily use of benzodiazepines are classified as somatic (disturbed sleep, tremor, nausea, muscle aches), psychological (anxiety, poor concentration, irritability, mild depression), or perceptual (poor coordination, mild paranoia, mild confusion). The presentation of symptoms will vary depending on the half-life of the medication. The potential for interactions with benzodiazepines and other medications must be considered B. Behavioral Behavioral approaches are widely used in various anxiety disorders, often in conjunction with medication. Any of the behavioral techniques can be used beneficially in altering the contingencies (precipitating factors or rewards) supporting any anxiety-provoking behavior. Relaxation techniques can sometimes be helpful in reducing anxiety. Desensitization, by exposing the patient to graded doses of a phobic object or situation, is an effective technique and one that the patient can practice outside the therapy session. Emotive imagery, wherein the patient imagines the anxiety-provoking situation while at the same time learning to relax, helps decrease the anxiety when the patient faces the real-life situation. Physiologic symptoms in panic attacks respond well to relaxation training. Both GAD and panic disorder appear to respond as well to cognitive behavioral therapy as they do to medications. Exercise, both aerobic and resistance training, has demonstrated effects in reducing anxiety symptoms across many anxiety disorders as well. C. Psychological Cognitive behavioral therapy is the first-line psychotherapy in treatment of anxiety disorders. For anxiety disorders it includes a cognitive component of examining the thoughts associated with the fear and a behavioral technique of exposing the individual to the feared object or situation. The combination of medication and cognitive behavioral therapy is more effective than either alone. Mindfulness meditation can also be effective in decreasing symptoms of anxiety. Group therapy is the treatment of choice when the anxiety is clearly a function of the patient's difficulties in dealing with social settings. Acceptance and commitment therapy have been used with some success in anxiety disorders. It encourages individuals to keep focused on life goals while they "accept" the presence of anxiety in their lives. D. Social Peer support groups for panic disorder and agoraphobia have been helpful. Social modification may require measures such as family counseling to aid acceptance of the patient's symptoms and avoid counterproductive behavior in behavioral training. Any help in maintaining the social structure is anxiety-alleviating, and work, school, and social activities should be maintained. School and vocational counseling may be provided by professionals, who often need help from the clinician in defining the patient's limitations.

Alcohol Use Disorder

ESSENTIALS OF DIAGNOSIS Physiologic dependence as manifested by evidence of withdrawal when intake is interrupted. Tolerance to the effects of alcohol. Evidence of alcohol-associated illnesses, such as alcoholic liver disease, cerebellar degeneration. Continued drinking despite strong medical and social contraindications and life disruptions. Impairment in social and occupational functioning. Depression. Blackouts. Other signs: Alcohol stigmata: alcohol odor on breath, alcoholic facies, flushed face, scleral injection, tremor, ecchymoses, peripheral neuropathy. Surreptitious drinking. Unexplained work absences. Frequent accidents, falls, or injuries of vague origin; in smokers, cigarette burns on hands or chest. Laboratory tests: elevated values of mean corpuscular volume, serum liver biochemical tests, uric acid, and triglycerides. Alcohol use disorder is a syndrome consisting of two phases: at-risk drinking and moderate to severe alcohol misuse. At-risk drinking is the repetitive use of alcohol, often to alleviate anxiety or solve other emotional problems. A moderate to severe alcohol use disorder is similar to that which occurs following the repeated use of other sedative-hypnotics and is characterized by recurrent use of alcohol despite disruption in social roles (family and work), alcohol-related legal problems, and taking safety risks by oneself and with others. The National Institute on Alcohol Abuse and Alcoholism formally defines at-risk drinking as more than four drinks per day or 14 drinks per week for men or more than three drinks per day or seven drinks per week for women. A drink is defined by the CDC as 12 oz of beer, 8 oz of malt liquor, 5 oz of wine, or 1.3 oz or a "shot" of 80-proof distilled spirits or liquor. Individuals with at-risk drinking are at an increased risk for developing or are developing an alcohol use disorder. Alcohol and other drug abuse patients have a much higher prevalence of lifetime psychiatric disorders. While male-to-female ratios in alcoholic treatment agencies remain at 4:1, there is evidence that the rates are converging. Women delay seeking help, and when they do, they tend to seek it in medical or mental health settings. Adoption and twin studies indicate some genetic influence. Ethnic distinctions are important—eg, 40% of Japanese have aldehyde dehydrogenase deficiency and are more susceptible to the effects of alcohol. Depression is often present and should be evaluated carefully. The majority of suicides and intrafamily homicides involve alcohol. Alcohol is a major factor in rapes and other assaults. There are several screening instruments that may help identify an alcohol use disorder. One of the most useful is the Alcohol Use Disorder Identification Test (AUDIT) A. Acute Intoxication The signs of alcoholic intoxication are the same as those of overdosage with any other CNS depressant: drowsiness, errors of commission, psychomotor dysfunction, disinhibition, dysarthria, ataxia, and nystagmus. For a 70-kg person, an ounce of whiskey, a 4- to 6-oz glass of wine, or a 12-oz bottle of beer (roughly 15, 11, and 13 grams of alcohol, respectively) may raise the level of alcohol in the blood by 25 mg/dL. For a 50-kg person, the blood alcohol level would rise even higher (35 mg/dL) with the same consumption. Blood alcohol levels below 50 mg/dL rarely cause significant motor dysfunction (the legal limit for driving under the influence is commonly 80 mg/dL). Intoxication as manifested by ataxia, dysarthria, and nausea and vomiting indicates a blood level greater than 150 mg/dL, and lethal blood levels range from 350 mg/dL to 900 mg/dL. In severe cases, overdosage is marked by respiratory depression, stupor, seizures, shock syndrome, coma, and death. Serious overdoses are frequently due to a combination of alcohol with other sedatives. B. Withdrawal There is a wide spectrum of manifestations of alcohol withdrawal, ranging from anxiety, decreased cognition, and tremulousness, through increasing irritability and hyperreactivity to full-blown delirium tremens (DTs). Alcohol withdrawal syndrome can be categorized as mild, moderate, or severe withdrawal, withdrawal seizures, and DTs. Symptoms of mild withdrawal, including tremor, anxiety, tachycardia, nausea, vomiting, and insomnia, begin within 6 hours after the last drink, often before the blood alcohol levels drop to zero, and usually have passed by day two. Severe or major withdrawal occurs 48-96 hours after the last drink and is usually preceded by prolonged heavy alcohol use. Symptoms include disorientation, agitation, diaphoresis, whole body tremor, vomiting, hypertension, and hallucinations (visual > tactile > auditory). Moderate withdrawal symptoms and signs fall between those of minor and major withdrawal. Withdrawal seizures can occur as early as 8 hours after the last drink but usually do not manifest more than 48 hours after alcohol cessation. Seizures are more prevalent in persons who have a history of withdrawal syndromes. These seizures are generalized tonic-clonic seizures, are brief in duration, and resolve spontaneously. If withdrawal is untreated, these seizures can recur in about 60% of patients. DTs will develop in approximately half of these patients. If seizures are focal, associated with trauma or fever, or have an onset more than 48 hours after the last drink, another etiology for seizures must be considered. DT is the most severe form of alcohol withdrawal. It is an acute organic psychosis that usually manifests 48-72 hours after the last drink but may occur up to 7-10 days later. It is characterized by extreme mental confusion, agitation, tremor, diaphoresis, sensory hyperacuity, visual hallucinations (often of snakes, bugs, etc), and autonomic hyperactivity (tachycardia and hypertension). Complications of DTs include (1) dehydration, (2) electrolyte disturbances (hypokalemia, hypomagnesemia), (3) arrhythmias and seizures, and (4) cardiovascular collapse and death. The acute withdrawal syndrome is often unexpected, occurring when the patient has been hospitalized for an unrelated problem, thus presenting as a diagnostic dilemma. Suspect alcohol withdrawal in every unexplained delirium. The mortality rate from DTs, which was upward of 35%, has steadily decreased with early diagnosis and improved treatment. In addition to the immediate withdrawal symptoms, there is evidence of persistent longer-term ones, including sleep disturbances, anxiety, depression, excitability, fatigue, and emotional volatility. These symptoms may persist for 3-12 months, and in some cases, they become chronic. C. Alcoholic (Organic) Hallucinosis This syndrome occurs either during heavy drinking or on withdrawal and is characterized by a paranoid psychosis without the tremulousness, confusion, and clouded sensorium seen in withdrawal syndromes. The patient appears normal except for the auditory hallucinations, which are frequently persecutory and may cause the patient to behave aggressively and in a paranoid fashion. D. Chronic Alcoholic Brain Syndromes These encephalopathies are characterized by increasing erratic behavior, memory and recall problems, and emotional instability—the usual signs of organic brain injury due to any cause. Wernicke-Korsakoff syndrome due to thiamine deficiency may develop with a series of episodes. Wernicke encephalopathy consists of the triad of confusion, ataxia, and ophthalmoplegia (typically sixth nerve palsy). Early recognition and treatment with thiamine can minimize damage. One of the possible sequelae is Korsakoff psychosis, characterized by both anterograde and retrograde amnesia, with confabulation early in the course. Early recognition and treatment with intravenous thiamine and B complex vitamins can minimize damage. Excessive alcohol consumption in men has been associated with faster cognitive decline compared with light to moderate alcohol consumption. E. Laboratory Findings Ethanol may contribute to the presence of an otherwise unexplained osmolar gap. There may also be increased serum liver biochemical tests, uric acid, and triglycerides and decreased serum potassium and magnesium. The most definitive biologic marker for chronic alcoholism is carbohydrate deficient transferrin, which can detect heavy use (60 mg/day over 7-10 days) with high specificity. Other useful tests for diagnosing alcohol use disorder are gamma-glutamyl transpeptidase (GGT) measurement (levels greater than 30 units/L are suggestive of heavy drinking) and mean corpuscular volume (MCV) (more than 95 fL in men and more than 100 fL in women). If both are elevated, a serious alcohol problem is likely. Use of other recreational drugs with alcohol skews and negates the significance of these tests. differential The differential diagnosis of alcoholism is essentially between primary alcohol use disorder (when no other major psychiatric diagnosis exists) and secondary alcohol use disorder (when alcohol is used as self-medication for major underlying psychiatric problems such as schizophrenia or affective disorder). The differentiation is important, since the latter group requires treatment for the specific psychiatric problem. In primary and secondary alcoholism, at-risk drinking can be distinguished from alcohol addiction by taking a careful psychiatric history and evaluating the degree to which recurrent drinking impacts the social role functioning and physical safety of the individual. The differential diagnosis of alcohol withdrawal includes other sedative withdrawals and other causes of delirium. Acute alcoholic hallucinosis must be differentiated from other acute paranoid states such as amphetamine psychosis or paranoid schizophrenia. The history and laboratory test results are the most important features in differentiating chronic organic brain syndromes due to alcohol from those due to other causes. The medical, economic, and psychosocial problems of alcoholism are staggering. The central and peripheral nervous system complications include chronic brain syndromes, cerebellar degeneration, cardiomyopathy, and peripheral neuropathies. Direct effects on the liver include cirrhosis, esophageal varices, and eventual hepatic failure. Indirect effects include protein abnormalities, coagulation defects, hormone deficiencies, and an increased incidence of liver neoplasms. Fetal alcohol syndrome includes one or more of the following developmental defects in the offspring of alcoholic women: (1) low birth weight and small size with failure to catch up in size or weight, (2) mental retardation, with an average IQ in the 60s, and (3) a variety of birth defects, with a large percentage of facial and cardiac abnormalities. The fetuses are quiet in utero, and there is an increased frequency of breech presentations. There is a higher incidence of delayed postnatal growth and behavior development. The risk is appreciably higher with the more alcohol ingested by the mother each day.

Bulimia Nervosa

Eating disorder characterized by frequent binge eating combined with compensatory behaviors to prevent weight gain Maintain a normal weight (or maybe overweight) and compensatory behaviors are ego-dystonic (troublesome for the patient) More common in females onset in late teens early adulthood PE -teeth pitting or enamel erosion (from vomiting) -Russell's sign: calluses on the dorsum of the hand from self-induced vomiting -Parotid gland hypertrophy Lab findings: -Hypokalemia, hypomagnesemia (cardiac arrhythmias) -Increased amylase (parotid gland hypertrophy + vomiting) and metabolic alkalosis from vomiting Diagnostic Criteria -Recurrent episodes of binge eating - eating within a 2 hour period more than people would in a similar period with lack of control during an overeating syndrome. Occurs at least weekly for 3 months. may be triggered by stress or mood changes -Compensatory behaviors ->Purging type: self-induced vomiting, diuretic, laxative, or enema abuse ->Non-purging type: reduced calorie intake, dieting, fasting, excessive exercise, diet pills Management: -Psychotherapy: CBT, group and interpersonal therapy -Pharmacotherapy: Fluoxetine is the only FDA approved med for Bulimia Nervosa - reduces binge-purge cycle. CVD events possible with electrolyte problems

SEDATIVES (ANXIOLYTICS) -Overdosage Treatment

Flumazenil, a benzodiazepine antagonist, is effective in overdosage. •Overdosage and withdrawal states are medical emergencies •Serious side effects of chronic excessive dosage are development of tolerance, resulting in increasing dose requirements, and physiologic dependence, resulting in withdrawal symptoms •Withdraw is treated with a long acting benzodiazepine such as clonazepam (Klonopin)

Anorexia Nervosa (PPP)

Failure to maintain normal body weight. fear and preoccupation with body weight, body image, and being thin MC in teenage girls ages 14-18. 90% are women Seen mainly in athletes, dancers 60% incidence with depression HIGHEST MORTALITY RATE OF ALL PSYCHIATRIC CONDITIONS (due to arrhythmias) 5-18% Presentation -Exhibits behaviors targeted at maintaining a low weight (excess water intake, food-related obsessions, hoarding. Ego-syntonic (behaviors are acceptable to them and in harmony with self-image goals) -Restrictive: reduced caloric intake, dieting, fasting, excessive exercise, diet pills -Binging/purging type: self-induced vomiting and diuretic, laxative, or enema use PE: -Emaciation, hypotension, bradycardia, lanugo, dry skin, salivary gland hypertrophy, amenorrhea, arrhythmias, osteopenia -Russel's sign: calluses on dorsum of hand from self-induced vomiting -BMI 17.5kg/m2 or less OR Body weight <85% of ideal weight Diagnostic criteria -restriction of caloric intake leading to significantly low body weight -Intense morbid fear of gaining weight or behaviors to prevent weight gain -Distorted body image - self perception of being overweight LABS: -Hypokalemia (GI loss from laxative/vomiting), increased BUN (dehydration), hypochloremic metabolic alkalosis (from vomiting), hypogonadism (low estrogen), hypothyroidism Management: -Medical stabilization: hospitalize for <75% body weight, dehydration, or cardiac arrhythmias -Nutritional rehabilitation: refeeding syndrome: increased insulin leads to hypophosphatemia, cardiac complication -CBT, supervised meals, weight monitoring -SSRIs and atypical antipsychotics

Alcohol MOA

GABA receptor are inhibitory, and thus alcohol has a sedating effect

Opioid Withdrawal Symptom overview

GI symptoms very common

GAD (ROSH)

Generalized anxiety disorder is characterized by the lack of ability to control worrisome thoughts and stress, causing an impact on daily activities and significantly distressing the patient. To be diagnosed, these symptoms have to occur on more days than not for a period of at least 6 months. Patients often present with somatic symptoms that accompany the anxiety, such as muscle tension and fatigue. Comorbid conditions, including social phobia, specific phobia, and panic disorder, are commonly associated with generalized anxiety disorder. Pathogenesis of the disorder includes genetic predisposition, neuropsychological factors, childhood trauma, and neuroticism. People with chronic physical illness, chronic mental illness, and parental loss or separation are at greater risk of developing generalized anxiety disorder later in life. The generalized anxiety disorder seven-item scale (GAD-7) is typically used in primary care to identify patients who may have the disorder and is used as a screening tool. The diagnosis is made when an individual finds it difficult to control worry and when the worry is associated with three of the following: restlessness, easy fatigue, difficulty concentrating, irritability, muscle tension, and sleep disturbance.

Risperidone

Greater incidence of movement disorders

First Gen (typical) antipsychotics

Haloperidol, Droperidol, Fluphenazine, Chlorpromazine, Perphenazine, Thioridazine Most effective for positive symptoms increased risk of extrapyramidal Sx, Tardive dyskinesia, and neuroleptic malignant syndrome

Caffeine Withdrawal

Headaches •Irritability •Nausea •Lethargy •Depression

COCAINE -IV use and ethanol

Intravenous use of cocaine hydrochloride or CRACK is effective in 30 seconds and produces a short-lasting, fairly intense high of about 15 minutes duration. The combined use of cocaine and ethanol results in the metabolic production of cocaethylene by the liver. ->This substance produces more intense and long-lasting cocaine-like effects. Smoking (volatilized cocaine because of the lower boiling point) acts in seconds and results in an intense high lasting several minutes. ->The intensity of the reaction is related to the marked lipid solubility of the freebase form and produces by far the most severe medical and psychiatric symptoms.

Bipolar Risk Factors -Increased rapid cycling

Increased rapid cycling •Female •Earlier age at onset •Use of cannabis •First degree relative with bipolar disorder (highest risk factor for bipolar)

Cocaine MOA

Increases dopamine

Aripiprazole

Less potential for weight gain

Quetiapine

Lower incidence of extrapyramidal symptoms

Bupropion

MOA: inhibits neuronal presynaptic uptake of dopamine and NE IND: MDD and SDD -Less GI, weight gain, and sexual adverse effects compared to SSRIs -Smoking cessation Adverse effects: Seizures -dry mouth, nausea, insomnia, agitation, anxiety, weight loss, HTN, HA -increased risk of psychosis at high doses -avoid abrupt withdrawal Contraindications: Epilepsy or increased seizure risk (eating disorders, bulimia and anorexia) or patients with abrupt discontinuation of alcohol, benzos, barbiturate, or antiepileptic meds) -Avoid with MAOI use in past 2 weeks

MDD (ROSH)

Major depressive disorder is characterized by depressed mood, loss of interest in daily activities, sleep disturbance, weight changes, psychomotor symptoms, fatigue, thoughts of worthlessness, difficulty concentrating, and recurrent thoughts of death. At least five of these symptoms must be present for at least 2 weeks to diagnose major depressive disorder. The pathogenesis of major depressive disorder is multifactorial. Studies have shown a genetic predisposition toward depression, and women are more frequently affected. Childhood trauma or early-onset anxiety may contribute to the development of depression. Other historical factors include low self-esteem, substance misuse, parental loss, low parental warmth, marital issues, and low education status. Screening exams should include questions pertinent to suicide risk. Assessment may also include laboratory testing to rule out other causes of depression, including a pregnancy test for women and thyroid testing. Treatment goals should focus on restoring baseline function and the ability to participate in activities of daily living without impairment.

Bipolar overview

Manic = impaired behavior, psychosis, or days period (over 7)

MARIJUANA CLINICAL FINDINGS

Marijuana produces two phases: •Mild euphoria followed by sleepiness. •In the acute state, the user has an altered time perception, less inhibited emotions, psychomotor problems, impaired immediate memory, and conjunctival injection High doses produce transient psychotomimetic effects. •Mimics the symptoms of psychosis, including delusions and/or delirium, as opposed to just hallucinations

Treatment of Depression (CURRENT)

Milder forms of depression usually do not require medication therapy and can be managed by psychotherapy and the passage of time. In severe cases—particularly when vegetative signs are significant and symptoms have persisted for more than a few weeks—antidepressant medication therapy is often effective. Medication therapy is also suggested by a family history of major depression in first-degree relatives or a past history of prior episodes. The antidepressant medications may be classified into four groups: (1) the newer antidepressants, including the SSRIs, SNRIs, and bupropion, vilazodone, vortioxetine, and mirtazapine, (2) the TCAs and clinically similar medications, (3) the MAO inhibitors (Table 25-6), and (4) stimulants. ECT and repetitive transcranial magnetic stimulation are procedural treatments for depression. These modalities are described in greater detail below. Medication selection is influenced by the history of previous response or lack thereof if that information is available. There is mixed and inconclusive evidence about the utility and cost-effectiveness of genetic testing to choose an antidepressant treatment strategy. A positive family history of response to a particular medication may suggest that the patient will respond similarly. If no background information is available, a medication such as sertraline, 25 mg orally daily and increasing gradually up to 200 mg depending on response and side effects, or venlafaxine at 37.5 mg/day and titrated gradually as indicated to a maximum dose of 225 mg/day can be selected and a full trial instituted. During the medication trial, patients should be monitored for worsening mood or suicidal ideation every 1-2 weeks until week 6. The STAR*D trial suggests that if there is no response to the first medication, the best alternatives are to switch to a second agent that may be from the same or different class of antidepressant; if there is partial response to the first agent, another approach is to try augmenting it with a second agent, such as bupropion (150-450 mg/day), lithium (eg, 300-900 mg/day orally), thyroid medication (eg, liothyronine, 25-50 mcg/day orally), or a second-generation antipsychotic (eg, aripiprazole [5-15 mg/day]). The Agency for Health Care Policy and Research has produced clinical practice guidelines that outline one algorithm of treatment decisions (Figure 25-2). Cognitive issues such as concentration and memory problems are common to depression; the evidence shows that these issues sometimes persist even after depression has remitted, with a higher risk in those individuals who have had more depressive episodes. Psychotic depression should be treated with a combination of an antipsychotic and an antidepressant such as an SSRI at their usual doses. Mifepristone may have specific and early activity against psychotic depression. ECT is generally regarded as the single most effective treatment for psychotic depression, with remission rates between 60% and 90%. Major depression with atypical features or seasonal onset can be treated with bupropion or an SSRI with good results. MAO inhibitors appear more effective than TCAs, and an MAO inhibitor may be used if more benign antidepressant strategies prove unsuccessful. Melancholic depression may respond to ECT, TCAs, and SNRIs, which are preferable to SSRIs. However, SSRIs are often used in the treatment of melancholic depression and are effective in many cases. Caution: Depressed patients often have suicidal thoughts, and the amount of medication dispensed should be appropriately controlled particularly if prescribing an MAO inhibitor, TCA, and to a lesser extent, venlafaxine. At the same time, adults with untreated depression are at higher risk for suicide than those who are treated sufficiently to reduce symptoms. It has been thought that in children and adolescent populations, antidepressants may be associated with some slightly increased risk of suicidality. One meta-analysis indicates that suicidality persists even after symptoms of depression are treated, suggesting other causes such as increased impulsivity among younger patients. After age 25, antidepressants may have neutral or possibly protective effects until age 65 years or older. The older TCAs have a narrow therapeutic index. One advantage of the newer medications is their wider margin of safety. Nonetheless, even with newer agents, because of the possibility of suicidality early in antidepressant treatment, close follow-up is indicated. In all cases of pharmacologic management of depressed states, caution is indicated until the risk of suicide is considered minimal.

Tetracyclic Antidepressants

Mirtazapine (Remeron) -MOA: increases release of NE and serotonin via central presynaptic alpha-2 adrenergic receptor antagonism. High affinity for histamine H1 receptors (sedative properties). -Postsynaptic serotonin 5-HT2 and 5HT3 receptor antagonist, increasing neurotransmission mediated by 5HT1 receptors IND: Depression, especially in patient with insomnia or significant weight loss (appetite stimulating and sedating properties). Fewer sexual adverse effects compared to SSRIs -anxiety disorders: anxiolytic properties with Trazodone ADV effects: sedation, weight gain (appetite stimulant) -Dry mouth, constipation, tremor, dizziness, agranulocytosis -increased suicidality in children, adolescents, young adults Contraindications: use with MAOI (serotonin syndrome)

Possible symptoms in mania

Mood ranging from euphoria to irritability. Sleep disruption. Hyperactivity. Racing thoughts. Grandiosity or extreme overconfidence. Variable psychotic symptoms.

Bipolar I management

Mood stabilizers: Lithium first line (acute mania and long-term) Lithium also decreases suicide risk •Valproic acid or carbamazepine useful for rapid cycling or mixed features (also for seizures) 2nd gen atypical antipsychotics: risperidone, Quetiapine, Olanzapine, Ziprasidone are effective monotherapy or adjunctive therapy to mood stabilizers (combo is faster and more effective) Psychotherapy: CBT, interpersonal, sleep hygiene Bipolar depression: Lithium, Questipine, Lurasidone, Lamotrigine Antidepressant monotherapy may precipitate mania or hypomania Acute mania management -Antipsychotics (Risperidone or Olanzapine > Haloperidol) or mood stabilizers (Lithium, valproic acid) -Antipsychotics or benzos for acute psychosis or agitation -ECT if refractory of life threatening presentation

Bipolar II: Treatment

Mood stabilizers: Lithium first line (decreases suicide risk) or second gen (atypical) antipsychotics (Risperidone, Quetiapine, Olanzapine, Ziprasidone) Valproic acid or Carbamazepine for rapid cycling CBT, sleep hygiene, interpersonal therapy

Suicide (ROSH)

Most patients who die by suicide have an interaction with a primary care provider or another clinician within the previous year. This is an opportunity for clinicians to identify patients at risk and plan interventions to reduce the risk of suicide. Higher mortality rates from suicide are seen in men than in women. In the United States, suicide rates are greatest in young adults 18 to 25 years of age. Risk factors for suicide include a history of previous suicide attempts and psychiatric disorders, including depression, bipolar disorder, alcohol use disorder, schizophrenia, panic disorder, and post-traumatic stress disorder. Patients who identify as LGBTQ are at greater risk of suicide. Military personnel and those with unskilled occupations have greater rates of suicide as well. A history of chronic pain or general medical illness increases the risk of suicide. Other risk factors include childhood adversity or trauma, family history of suicide, or a history of traumatic brain injury. Clinicians should ask about risk factors and suicidal thoughts or behavior at routine visits. Management of suicidal thoughts or behavior in patients includes reducing immediate risk and medically stabilizing the patient.

Alcohol Use Disorder Treatments -Medications

Naltrexone -1st line •Opiate antagonist •Lowers relapse rates over the 3-6 months after cessation of drinking, apparently by lessening the pleasurable effects of alcohol •Associated with hepatotoxicity; not indicated if patient on opioids Disulfuram •Aversive medication (causing toxic reactions when alcohol is consumed) •high rates of non-adherence

Opioid Use Treatment

Narcan (Naloxone) used for overdose •May precipitate withdrawal •Begin 0.4 mg IV and repeat every few minutes PRN Medical Detox MEDS •Buprenorphine/Naloxone (Suboxone)*** -Long acting opiate effect without euphoria or "high" prevents withdrawal -Slowly tapered •Methadone

Substance Use Disorders -Characterized by the triad of

PSYCHOLOGICAL DEPENDENCE •Craving and the behavior involved in procurement of the drug PHYSIOLOGICAL DEPENDENCE •Withdrawal symptom on discontinuance of the drug TOLERANCE •The need to increase the dose to obtain the desired effects

Panic Disorder (ROSH)

Panic disorder is an uncommon psychiatric disorder characterized by recurrent, unexpected panic attacks followed by a month or more of either persistent worry about additional panic attacks or significant maladaptive behaviors of avoidance. The disorder cannot be attributed to the effects of another medical condition or to substance use. The disorder also cannot be attributed to another mental disorder. Panic attacks involve episodes of intense fear or discomfort that typically last a few minutes. Symptoms include palpitations, sweating, shaking, feeling of choking or smothering, chest pain or pressure, nausea, dizziness, chills or heat sensation, fear of dying, or numbness and tingling. Other etiologies that could cause these types of symptoms, such as angina, thyroid disorders, or pheochromocytoma, should be ruled out as part of the evaluation. Serotonin reuptake inhibitors, serotonin and norepinephrine reuptake inhibitors, monoamine oxidase inhibitors, and benzodiazepines have all been used to treat panic disorder and are chosen based on the patient profile while considering potential side effects.

PCP

Phencyclidine (PCP, angel dust, peace pill, hog) is simple to produce and mimics to some degree the traditional psychedelic drugs. PCP is a common deceptive substitute for LSD, tetrahydrocannabinol, and mescaline. It is available in crystals, capsules, and tablets to be inhaled, injected, swallowed, or smoked (it is commonly sprinkled on marijuana). Absorption after smoking is rapid, with onset of symptoms in several minutes and peak symptoms in 15-30 minutes. Mild intoxication produces euphoria accompanied by a feeling of numbness. Moderate intoxication (5-10 mg) results in disorientation, detachment from surroundings, distortion of body image, combativeness, unusual feats of strength (partly due to its anesthetic activity), and loss of ability to integrate sensory input, especially touch and proprioception. Physical symptoms include dizziness, ataxia, dysarthria, nystagmus, retracted upper eyelid with blank stare, hyperreflexia, and tachycardia. There are increases in blood pressure, respiration, muscle tone, and urine production. Usage in the first trimester of pregnancy is associated with an increase in spontaneous abortion and congenital defects. Severe intoxication (20 mg or more) produces an increase in degree of moderate symptoms, with the addition of seizures, deepening coma, hypertensive crisis, and severe psychotic ideation. The drug is long-lasting (several days to several weeks) owing to high lipid solubility, gastroenteric recycling, and the production of active metabolites. Overdosage may be fatal, with the major causes of death being hypertensive crisis, respiratory arrest, and convulsions. Acute rhabdomyolysis has been reported and can result in myoglobinuric kidney failure. Differential diagnosis involves the whole spectrum of street drugs, since in some ways phencyclidine mimics sedatives, psychedelics, and marijuana in its effects. Blood and urine testing can detect the acute problem.

Nonselective MAOIs

Phenelzine, Isocarboxazid, Tranylcypromine MOA: increased levels of NE, serotonin IND: refractory depression Adverse effects: -Orthostatic hypotension most common, insomnia, weight gain, anxiety, sexual dysfunction -Hypertensive crisis after ingesting foods high in tyramine (aged cheese, smoked, pickled or cured meats/poultry/fish/red wine, beer and chocolate) MAOI prevents breakdown of tyramine, leading to HTN Drug interactions: increased risk for serotonin syndrome if MAOI used with SSRIs, SNRIs, St. John's Wart, MDMA, cocaine, Tramadol, Dextromethorphan -Wait 2 weeks before switching from MAOI to SSRIs (5 weeks for Fluoxetine due to its longer half life)

Depression ESSENTIALS of DIAGNOSIS

Present in most depressions Mood varies from mild sadness to intense despondency and feelings of guilt, worthlessness, and hopelessness. Difficulty in thinking, including inability to concentrate, ruminations, and lack of decisiveness. Loss of interest, with diminished involvement in work and recreation. Somatic complaints such as disrupted, lessened, or excessive sleep; loss of energy; change in appetite; decreased sexual drive. Present in some severe depressions Psychomotor retardation or agitation. Delusions of a somatic or persecutory nature. Withdrawal from activities. Physical symptoms of major severity, eg, anorexia, insomnia, reduced sexual drive, weight loss, and various somatic complaints. Suicidal ideation.

Ziprasidone

Prolonged QT Less likely to cause weight gain

Anorexia Nervosa

Psychological disorder marked by: -an intense fear of weight gain -a distorted body image that results in low body weight due to self-imposed severe dietary restriction or other weight loss behaviors, such as purging or excessive exercise •The affected individual's appetite and craving for food is usually preserved •Disordered thinking leads to self-imposed starvation Epidemiology •Prevalence in females: 1 in 100-200 •More than 90% of those affected are females Bimodal peak in incidence •Adolescence (Age 12-15 years) •Late adolescence and early adulthood (Age 17-21 years) •Rarely appears before puberty or after age 40 Etiology •Cultural pressures in industrial societies with an overemphasis on a slim female figure •Genetics- higher incidence in twins and first-degree relatives in studies Symptoms •Extremely limited diet with overall reduction in food intake and exclusion of high caloric foods •Extreme exercising to lose weight •Purging: self-induced vomiting or misuse of laxatives/diuretics (without binge eating) •Body image distortion: the individual feels they are globally overweight or that certain parts of the body are too big (abdomen, buttocks, thighs) •Self-esteem is overly dependent on body shape and weight •Obsession with body size, frequent weight measurement, and looking in the mirror for perceived fat •Denial in the serious medical implications of malnutrition Signs •Emaciation •Hypothermia •Significant hypotension (esp orthostatic) = due to dehydration •Bradycardia •Skin dryness/flaking •Lanugo (downy body hair on the trunk and extremities) •Peripheral edema •Petechia •Sallow complexion •Dental enamel erosion •Osteoporosis •Amenorrhea Laboratory findings & Imaging •Hypokalemia (GI loss from laxatives or vomiting) •Increased BUN (dehydration) •Hypochloremic metabolic alkalosis •Low estrogen •Hypothyroidism Treatment •Individuals usually seek evaluation because of persuasion or coercion by family members/friends •They are usually not concerned with the weight loss but may have concerns due to the somatic or psychological distress related to starvation/dehydration •The information about the degree of weight loss usually needs to come from a family member Multidisciplinary approach: •Psychiatrist •Psychologist •Social worker •Registered dietician •Dentist •Family medicine provider •Intensive medical intervention to correct fluid and electrolyte imbalance, cardiac problems, organ failure •Hospitalization and inpatient management may be necessary in the first stage of treatment •Weight gain goals: 2-3 lb/week as an inpatient and 0.5-1 lb/week in outpatient programs •Antidepressants •Second-gen antipsychotics •Lithium Prognosis •Psychotherapeutic treatment is indicated for 1 or more years following weight restoration •45% of patients have an overall good outcome •30% have an intermediate outcome •25% have a poor outcome and rarely achieve a normal weight •5-10% of patients die from complications

Panic Disorder rapid review

Recurrent unexpected panic attacks include Sxs such as -Palpitations -Shortness of breath -Chest pain -Dizziness -Depersonalization or derealization -Numbness or tingling -Fear of dying or losing control Worry about future attacks or maladaptive behavior related to panic attacks for at least 1 month Panic attacks do not only occur in response to particular stimulus Treat with SSRI, CBT, or both

1. SSRIs, SNRIs, and atypical antidepressants

SSRIs include fluoxetine, sertraline, paroxetine, fluvoxamine, and citalopram and its enantiomer escitalopram (Table 25-6). The chief advantages of these agents are that they are generally well tolerated, the starting dose is typically a therapeutic dose for most patients, and they have much lower lethality in overdose compared to TCAs or MAO inhibitors. (Notably, citalopram carries a warning regarding QT prolongation in doses above 40 mg, and 20 mg is considered the maximum dose for patients older than 60 years. There is no similar FDA warning for escitalopram.) The SNRIs include venlafaxine, desvenlafaxine, duloxetine, milnacipran, and levomilnacipran. In addition to possessing the strong serotonin reuptake blocking properties of the SSRIs, the SNRIs are also norepinephrine reuptake blockers. The combined serotonergic-noradrenergic properties of these medications may provide benefits in pain conditions such as neuropathy and fibromyalgia as well as conditions such as stress incontinence. The atypical antidepressants are bupropion, nefazodone, trazodone, vilazodone, vortioxetine, and mirtazapine (Table 25-6). All of these antidepressants are effective in the treatment of depression, both typical and atypical. The SSRI medications have been effective in the treatment of panic disorder, bulimia, GAD, OCD, and PTSD Most of the medications in this group tend to be activating and are given in the morning so as not to interfere with sleep. Some patients, however, may have sedation, requiring that the medication be given at bedtime. This reaction occurs most commonly with paroxetine, fluvoxamine, and mirtazapine. The SSRIs can be given in once-daily dosage. Nefazodone and trazodone are usually given twice daily. Bupropion and venlafaxine are available in extended-release formulations and can be given once daily. There is usually some delay in response; fluoxetine, for example, requires 2-6 weeks to act in depression, 4-8 weeks to be effective in panic disorder, and 6-12 weeks in treatment of OCD. The starting dose (10 mg) is given for 1 week before increasing to the average daily oral dose of 20 mg for depression, while OCD may require up to 80 mg daily. Some patients, particularly older adults, may tolerate and benefit from as little as 10 mg/day or every other day. The other SSRIs have shorter half-lives and a lesser effect on hepatic enzymes, which reduces their impact on the metabolism of other medications (thus not increasing significantly the serum concentrations of other medications as much as fluoxetine). The shorter half-lives also allow for more rapid clearing if adverse side effects appear. Venlafaxine appears to be more effective with doses greater than 200 mg/day orally, although some individuals respond to doses as low as 75 mg/day. The side effects common to these medications are headache, nausea, tinnitus, insomnia, and nervousness. Akathisia has been common with the SSRIs; other extrapyramidal symptoms (eg, dystonias) have occurred infrequently but particularly in withdrawal states. Because SSRIs affect platelet serotonin levels, abnormal bleeding can occur. Sertraline and citalopram appear to be the safest agents in this class when used with warfarin. Sexual side effects of erectile dysfunction, retrograde ejaculation, and dysorgasmia are very common with the SSRIs. Oral phosphodiesterase-5 inhibitors (such as sildenafil, 25-50 mg; tadalafil, 5-20 mg; or vardenafil, 10-20 mg taken 1 hour prior to sexual activity) can improve erectile dysfunction in some patients and have been shown to improve other SSRI-induced sexual dysfunction in both men and women. Adjunctive bupropion (75-150 mg orally daily) may also enhance sexual arousal. Cyproheptadine, 4 mg orally prior to sexual activity, may be helpful in countering drug-induced anorgasmia but also is quite sedating and may counter the therapeutic benefits of SSRIs as well. Taking a "drug holiday," ie, skipping a day of medication periodically when sexual activity is anticipated, can also decrease sexual side effects. The SSRIs are strong serotonin uptake blockers and may in high dosage or in combination with MAO inhibitors, including the antiparkinsonian drug selegiline, cause a "serotonin syndrome." This syndrome is manifested by rigidity, hyperthermia, autonomic instability, myoclonus, confusion, delirium, and coma. This syndrome can be troublesome in older adults. Research indicates that SSRIs are safer agents to use than TCAs in patients with cardiac disease; the SSRI sertraline is a safe and effective antidepressant treatment in patients with acute MI or unstable angina Withdrawal symptoms, including dizziness, paresthesias, dysphoric mood, agitation, and a flu-like state, have been reported for the shorter-acting SSRIs and SNRIs but may occur with other classes including the TCAs and MAO inhibitors. These medications should be discontinued gradually over a period of weeks or months to reduce the risk of withdrawal phenomena. Most studies show that SSRIs are not associated with birth defects. Paroxetine has some association with a fetal heart defect and should be avoided in favor of other SSRIs during pregnancy. Untreated depression in the mother can contribute substantially to deficits in the verbal, intellectual and motor development of a newborn. Peripartum effects may be a concern and are documented anecdotally in the literature. Maternal major mood disorder in pregnancy by itself carries its own risks to the mother and fetus and has been linked to low birth weight and preterm delivery. Postpartum effects of prenatal depression have not been studied. The decision to use SSRIs and other psychotropic agents during pregnancy and postpartum must be a collaborative decision based on a thorough risk-benefit analysis for each individual. Venlafaxine lacks significant anticholinergic side effects. Nausea, nervousness, and profuse sweating appear to be the major side effects. Venlafaxine appears to have few drug-drug interactions. It does require monitoring of blood pressure because dose-related hypertension may develop in some individuals. Venlafaxine prescribing in the United Kingdom has been restricted to psychiatrists. Venlafaxine appears to carry a greater risk of lethal arrhythmias in instances of overdose relative to the SSRIs, but less risk than with the TCAs. Desvenlafaxine, a newer form of the medication, is started at its target dose of 50 mg/day orally and does not require upward titration although higher doses have been well studied and some patients benefit from 100 mg/day. Duloxetine may also result in small increases in blood pressure. Common side effects include dry mouth, dizziness, and fatigue. Inhibitors of 1A2 and 2D6 may increase duloxetine levels with a risk of toxicity. Milnacipran, approved for the treatment of fibromyalgia, and levomilnacipran, approved for the treatment of major depression, carry many of the side effects common to other SNRIs including a mild tachycardia, hypertension, sexual side effects, mydriasis, urinary constriction, and occasional abnormal bleeding. Levomilnacipran is started at 20 mg/day orally then increased to 40 mg/day after 2-3 days. The target dose is 40-120 mg given once daily. Milnacipran is typically started at 12.5 mg/day orally, titrated to 12.5 mg twice daily after 2 days, and then to 25 mg twice daily after 7 days. The target dose is typically 100-200 mg/day given in in two divided doses. While not approved for the treatment of major depression, the evidence suggests that milnacipran, like levomilnacipran, is an effective antidepressant agent. Nefazodone appears to lack the anticholinergic effects of the TCAs and the agitation sometimes induced by SSRIs. Nefazodone should not be given with terfenadine, astemizole, or cisapride, which are not commercially available in the United States. Because nefazodone inhibits the liver's cytochrome P450 3A4 isoenzymes, concurrent use of these medications can lead to serious QT prolongation, ventricular tachycardia, or death. Through the same mechanism of enzyme inhibition, nefazodone can elevate cyclosporine levels sixfold to tenfold. Nefazodone carries an FDA warning given its association with liver failure in rare cases. Pretreatment and ongoing monitoring of liver biochemical enzymes is indicated. Mirtazapine is thought to enhance central noradrenergic and serotonergic activity with minimal sexual side effects compared with the SSRIs. Its action as a potent antagonist of histaminergic receptors may make it a useful agent for patients with depression and insomnia. It is also an effective antiemetic due to its antagonism of the 5-HT3 receptor. Its most common adverse side effects include somnolence, increased appetite, weight gain, lipid abnormalities, and dizziness. The labeling for mirtazapine indicated that agranulocytosis was seen in 2 of 2796 patients in premarketing studies. An association of agranulocytosis or a clinically significant neutropenia with the medication appears to be modest. Although it is metabolized by P450 isoenzymes, it is not an inhibitor of this system. It is given in a single oral dose at bedtime starting at 15 mg and titrated up to 45 mg with some evidence that 30 mg may be optimal for most people. Vortioxetine is an antidepressant that blocks serotonin reuptake, is a partial agonist of the 5-HT1A receptor, and affects a variety of other serotonin receptor sites. The side effects attributed to its serotonergic effects include GI upset and sexual dysfunction. Vortioxetine has demonstrated efficacy in improving some cognitive symptoms of depression and received regulatory approval for this indication in Europe and the United States. Vortioxetine is typically dosed at 10 mg/day orally and may be increased to 20 mg/day.

Mood disorders differential

Since depression may be a part of any illness—either reactively or as a secondary symptom—careful attention must be given to personal life adjustment problems and the role of medications. Schizophrenia, partial complex seizures, organic brain syndromes, panic disorders, and anxiety disorders must be differentiated. Thyroid dysfunction and other endocrinopathies should be ruled out. Malignancies are sometimes associated with depressive symptoms and may antecede the diagnosis of tumor. Strokes, particularly dominant hemisphere lesions, can occasionally present with a syndrome that looks like major depression.

Insomnia disorder -OVERVIEW

Sleep consists of two distinct states as shown by electroencephalographic studies: (1) REM (rapid eye movement) sleep, also called dream sleep, D state sleep, or paradoxic sleep, and (2) NREM (non-REM) sleep, also called S stage sleep, which is divided into stages 1, 2, 3, and 4 and is recognizable by different electroencephalographic patterns. Stages 3 and 4 are "delta" sleep. Dreaming occurs mostly in REM and to a lesser extent in NREM sleep. Sleep is a cyclic phenomenon, with four or five REM periods during the night accounting for about one-fourth of the total night's sleep (1.5-2 hours). The first REM period occurs about 80-120 minutes after onset of sleep and lasts about 10 minutes. Later REM periods are longer (15-40 minutes) and occur mostly in the last several hours of sleep. Most stage 4 (deepest) sleep occurs in the first several hours. Age-related changes in normal sleep include an unchanging percentage of REM sleep and a marked decrease in stage 3 and stage 4 sleep, with an increase in wakeful periods during the night. These normal changes, early bedtimes, and daytime naps play a role in the increased complaints of insomnia in older people. Variations in sleep patterns may be due to circumstances (eg, "jet lag") or to idiosyncratic patterns ("night owls") in persons who perhaps because of different "biologic rhythms" habitually go to bed late and sleep late in the morning. Creativity and rapidity of response to unfamiliar situations are impaired by loss of sleep. There are also rare individuals who have chronic difficulty in adapting to a 24-hour sleep-wake cycle (desynchronization sleep disorder), which can be resynchronized by altering exposure to light.

Suicide: Management

Social circle needed to send home

Specific Phobia (ROSH)

Specific phobia is characterized by anxiety surrounding a specific object or situation. This specific fear leads to maladaptive behavior changes, such as avoidance, and can impact social and professional interactions. Cognitive behavioral therapy, particularly therapy that includes exposure, has been shown to greatly reduce the symptoms of phobia disorders. The therapy consists of strategies to reduce fearful thoughts and resulting maladaptive behaviors. Repeated exposures to the specific phobia that are graded beginning with less anxiety-provoking stimulus help patients practice confronting and working through their fears. Patients gradually work up to the most anxiety-provoking situations and learn anxiety management and cognitive strategies to be able to work through the situation in a healthier manner.

Cocaine

Stimulant misuse is quite common, either alone or in combination with abuse of other drugs. The stimulants include illicit drugs such as methamphetamine ("speed")—one variant is a smokable form called "ice," which gives an intense and long-lasting high—and methylphenidate and dextroamphetamine, which are under prescription control. Moderate usage of any of the stimulants produces hyperactivity, a sense of enhanced physical and mental capacity, and sympathomimetic effects. The clinical picture of acute stimulant intoxication includes sweating, tachycardia, elevated blood pressure, mydriasis, hyperactivity, and an acute brain syndrome with confusion and disorientation. Tolerance develops quickly, and, as the dosage is increased, hypervigilance, paranoid ideation (with delusions of parasitosis), stereotypy, bruxism, tactile hallucinations of insect infestation, and full-blown psychoses occur, often with persecutory ideation and aggressive responses. Stimulant withdrawal is characterized by depression with symptoms of hyperphagia and hypersomnia. People who have used stimulants chronically (eg, anorexigenics) occasionally become sensitized ("kindling") to future use of stimulants. In these individuals, even small amounts of mild stimulants such as caffeine can cause symptoms of paranoia and auditory hallucinations. Cocaine is a stimulant. It is a product of the coca plant. The derivatives include seeds, leaves, coca paste, cocaine hydrochloride, and the free base of cocaine. Cocaine hydrochloride is the salt and the most commonly used form. Freebase, a purer (and stronger) derivative called "crack," is prepared by simple extraction from cocaine hydrochloride. There are various modes of use. Coca leaf chewing involves toasting the leaves and chewing with alkaline material (eg, the ash of other burned leaves) to enhance buccal absorption. One achieves a mild high, with onset in 5-10 minutes and lasting for about an hour. Intranasal use is simply snorting cocaine through a straw. Absorption is slowed somewhat by vasoconstriction (which may eventually cause tissue necrosis and septal perforation); the onset of action is in 2-3 minutes, with a moderate high (euphoria, excitement, increased energy) lasting about 30 minutes. The purity of the cocaine is a major determinant of the high. Intravenous use of cocaine hydrochloride or "freebase" is effective in 30 seconds and produces a short-lasting, intense high of about 15 minutes' duration. The combined use of cocaine and ethanol results in the metabolic production of cocaethylene by the liver. This substance produces more intense and long-lasting cocaine-like effects. Smoking freebase (volatilized cocaine because of the lower boiling point) acts in seconds and results in an intense high lasting several minutes. The intensity of the reaction is related to the marked lipid solubility of the freebase form and produces by far the most severe medical and psychiatric symptoms. Cardiovascular collapse, arrhythmias, MI, and transient ischemic attacks have been reported. Seizures, strokes, migraine symptoms, hyperthermia, and lung damage may occur, and there are several obstetric complications, including spontaneous abortion, abruptio placentae, teratogenic effects, delayed fetal growth, and prematurity. Cocaine can cause anxiety, mood swings, and delirium, and chronic use can cause the same problems as other stimulants. Clinicians should be alert to cocaine use in patients presenting with unexplained nasal bleeding or septal perforations, headaches, fatigue, insomnia, anxiety, depression, and chronic hoarseness. Sudden withdrawal of the drug is not life-threatening but usually produces craving, sleep disturbances, hyperphagia, lassitude, and severe depression (sometimes with suicidal ideation) lasting days to weeks. Treatment for acute intoxication is imprecise and difficult. Since the high is related to blockage of dopamine reuptake, the dopamine agonist bromocriptine, 1.5 mg orally three times a day, alleviates some of the symptoms of craving associated with acute cocaine withdrawal. Other dopamine agonists such as apomorphine, levodopa, and amantadine are under study for this purpose. Treatment of psychosis is the same as that of any psychosis: antipsychotic medications in dosages sufficient to alleviate the symptoms. Any medical symptoms (eg, hyperthermia, seizures, hypertension) are treated specifically. These approaches should be used in conjunction with a structured program for use disorder, most often based on the Alcoholics Anonymous model. Hospitalization may be required if self-harm or violence toward others is a perceived threat (usually indicated by paranoid delusions).

Amphetamines

Stimulants •Include illicit drugs such as methamphetamine (speed/meth) •Ice, Crank, Speed, Uppers, Bennies, Black Beauties •Lisdexamfetamine (Vyvanse) and dextroamphetamine (Adderal) which are prescription medications found in cold medications •Tolerance develops quickly •As the dosage is increased, hypervigilance, paranoid ideation (with delusions of parasitosis), stereotypy, bruxism, tactile hallucinations of insect infestation, and full-blown psychoses occur, often with persecutory ideation and aggressive responses.

Substance Use -Divisions

Substance use disorders Substance-induced disorders •Intoxication •Withdrawal •Other substance/medication induced mental disorders

AMPHETAMINES/COCAINE WITHDRAWAL

Sudden withdrawal of the drug is not life-threatening but usually produces craving, sleep disturbances, hyperphagia, a state of physical or mental weariness; lack of energy, and severe depression (sometimes with suicidal ideation) lasting days to weeks.

Post-Traumatic Stress Disorder (PTSD) raspid review

Sx duration > 1 month Persistently reexperiencing of event Persistently ↑ arousal Avoidance of stimuli ↑ risk for suicide, substance use

2. Tricyclic antidepressants (TCAs) and clinically similar medications

TCAs were the mainstay of medication therapy for depression for many years. They have also been effective in panic disorder, pain syndromes, and anxiety states. Specific ones have been studied and found to be effective in OCD (clomipramine), enuresis (imipramine), psychotic depression (amoxapine), and reduction of craving in cocaine withdrawal (desipramine). TCAs are characterized more by their similarities than by their differences. They tend to affect both serotonin and norepinephrine reuptake; some medications act mainly on the former and others principally on the latter neurotransmitter system. Individuals receiving the same dosages vary markedly in therapeutic drug levels achieved (older adult patients require smaller doses), and determination of plasma drug levels is helpful when clinical response has been disappointing. Nortriptyline is usually effective when plasma levels are between 50 and 150 ng/mL; imipramine at plasma levels of 200-250 ng/mL; and desipramine at plasma levels of 100-250 ng/mL. High blood levels are not more effective than moderate levels and may be counterproductive (eg, delirium, seizures). Patients with GI side effects benefit from plasma level monitoring to assess absorption of the drug. Most TCAs can be given in a single dose at bedtime, starting at low doses (eg, nortriptyline 25 mg orally) and increasing by 25 mg every several days as tolerated until the therapeutic response is achieved (eg, nortriptyline, 100-150 mg) or to maximum dose if necessary (eg, nortriptyline, 150 mg). The most common cause of treatment failure is an inadequate trial. A full trial consists of giving a therapeutic daily dosage for at least 6 weeks. Because of marked anticholinergic and sedating side effects, clomipramine is started at a low dose (25 mg/day orally) and increased slowly in divided doses up to 100 mg/day, held at that level for several days, and then gradually increased as necessary up to 250 mg/day. The TCAs have anticholinergic side effects to varying degrees (amitriptyline 100 mg is equivalent to atropine 5 mg). One must be particularly wary of the effect in older adult men with prostatic hyperplasia. The anticholinergic effects also predispose to other medical problems such as constipation, confusion, heat stroke, or dental problems from xerostomia. Orthostatic hypotension is common, is not dose-dependent, and may not remit with time on medication; this may predispose to falls and hip fractures in older adults. Cardiac effects of the TCAs are functions of the anticholinergic effect, direct myocardial depression, quinidine-like effect, and interference with adrenergic neurons. These factors may produce altered rate, rhythm, and contractility, particularly in patients with preexisting cardiac disease, such as bundle-branch or bifascicular block. Even relatively small overdoses (eg, 1500 mg of imipramine) have resulted in lethal arrhythmias. Electrocardiographic changes range from benign ST segment and T wave changes and sinus tachycardia to a variety of complex and serious arrhythmias, the latter requiring a change in medication. Because TCAs have class I antiarrhythmic effects, they should be used with caution in patients with ischemic heart disease, arrhythmias, or conduction disturbances. SSRIs or the atypical antidepressants are better initial choices for this population. TCAs lower the seizure threshold, so this is of particular concern in patients with a propensity for seizures. Loss of libido and erectile, ejaculatory, and orgasmic dysfunction are common and can compromise compliance. Trazodone rarely causes priapism (1 in 9000), but when it occurs, it requires treatment within 12 hours (epinephrine 1:1000 injected into the corpus cavernosum). Delirium, agitation, and mania are infrequent complications of the TCAs but can occur. Sudden discontinuation of some of these medications can produce "cholinergic rebound," manifested by headaches and nausea with abdominal cramps. Overdoses of TCAs are often serious because of the narrow therapeutic index and quinidine-like effects (see Chapter 38).

3. Monoamine oxidase inhibitors

The MAO inhibitors are generally used as third-line medications for depression (after a failure of SSRIs, SNRIs, TCAs, or the atypical antidepressants) because of the dietary and other restrictions required (Table 25-7). They should be considered third-line medications for refractory panic disorder as well as depression; however, this hierarchy has become more flexible since MAO inhibitor skin patches (selegiline) have become available. They deliver the MAO inhibitor to the bloodstream bypassing the GI tract so that dietary restrictions are not necessary in the lowest dosage strength (6 mg/24 hours). Oral MAO inhibitors are administered in gradual stepwise dosage and may be given in the morning or evening, depending upon their effect on sleep. They tend to take effect in a low dosage range (Table 25-6). Blood levels are not congruent with therapeutic response. The MAO inhibitors commonly cause symptoms of orthostatic hypotension (which may persist) and sympathomimetic effects of tachycardia, sweating, and tremor. Nausea, insomnia (often associated with intense afternoon drowsiness), and sexual dysfunction are common. Zolpidem 5-10 mg orally at bedtime can ameliorate MAO-induced insomnia. CNS effects include agitation and toxic psychoses. Dietary limitations (see Table 25-7) and abstinence from medication products containing phenylpropanolamine, phenylephrine, meperidine, dextromethorphan, and pseudoephedrine are mandatory for MAO-A type inhibitors (those marketed for treatment of depression), since the reduction of available MAO leaves the patient vulnerable to exogenous amines (eg, tyramine in foodstuffs). Treatment for a resultant hypertensive crisis has been the same as for pheochromocytoma (see Chapter 26), but there have been reports of success with nifedipine, 10 mg chewed and placed under the tongue, normalizing blood pressure in 1-5 minutes. The restrictions on the proscribed foodstuffs and sympathomimetic medications are in effect during treatment and for 2-3 weeks after cessation of therapy. Termination of therapy with MAO inhibitors may be associated with anxiety, agitation, cognitive slowing, and headache. Very gradual withdrawal and short-term benzodiazepine therapy will ameliorate symptoms.

Opioids (CURRENT)

The group includes natural derivatives of opium (opiates), synthetic surrogates (opioids), and a number of polypeptides, some of which have been discovered to be natural neurotransmitters. The principal narcotic of abuse is heroin (metabolized to morphine), which is not used as a legitimate medication. Heroin has taken a more widespread geographic distribution, involving primarily White men and women in their late 20s living outside of large urban areas. The other common opioids are prescription medications that differ in milligram potency, duration of action, and agonist and antagonist capabilities (see Chapter 5). The opioid analgesics can be reversed by the opioid antagonist naloxone. The clinical symptoms and signs of mild narcotic intoxication include changes in mood, with feelings of euphoria; drowsiness; nausea with occasional emesis; needle tracks; and miosis. The incidence of snorting and inhaling ("smoking") heroin has risen, particularly among cocaine users. Overdosage causes respiratory depression, peripheral vasodilation, pinpoint pupils, pulmonary edema, coma, and death. Tolerance and withdrawal are major concerns when continued use of opioids occurs, although withdrawal causes only moderate morbidity (similar in severity to a bout of "flu"). Grades of withdrawal are categorized from 0 to 4: grade 0 includes craving and anxiety; grade 1, yawning, lacrimation, rhinorrhea, and perspiration; grade 2, previous symptoms plus mydriasis, piloerection, anorexia, tremors, and hot and cold flashes with generalized aching; grades 3 and 4, increased intensity of previous symptoms and signs, with increased temperature, blood pressure, pulse, and respiratory rate and depth. In withdrawal from the most severe addiction, vomiting, diarrhea, weight loss, hemoconcentration, and spontaneous ejaculation or orgasm commonly occur. Complications of heroin administration include infections (eg, pneumonia, septic emboli, hepatitis, and HIV infection from using nonsterile needles), traumatic insults (eg, arterial spasm due to drug injection, gangrene), and pulmonary edema. Treatment for overdosage (or suspected overdosage) is discussed in Chapter 38. Treatment for withdrawal begins if grade 2 signs develop. If a withdrawal program is necessary, use methadone, 10 mg orally (use parenteral administration if the patient is vomiting), and observe. If signs (piloerection, mydriasis, cardiovascular changes) persist for more than 4-6 hours, give another 10 mg; continue to administer methadone at 4- to 6-hour intervals until signs are not present (rarely greater than 40 mg of methadone in 24 hours). Divide the total amount of medication required over the first 24-hour period by two and give that amount every 12 hours. Each day, reduce the total 24-hour dose by 5-10 mg. Thus, a moderately addicted patient initially requiring 30-40 mg of methadone could be withdrawn over a 4- to 8-day period. Clonidine, 0.1 mg orally several times daily over a 10- to 14-day period, is both an alternative and an adjunct to methadone detoxification; it is not necessary to taper the dose. Clonidine is helpful in alleviating cardiovascular symptoms but does not significantly relieve anxiety, insomnia, or generalized aching. There is a protracted abstinence syndrome of metabolic, respiratory, and blood pressure changes over a period of 3-6 months. Alternative strategies for the treatment of opioid withdrawal have included rapid and ultrarapid detoxification techniques. However, data do not support the use of either method. Treatment of opioid use disorder is key given evidence of significant morbidity and mortality, including what has been called the "opioid epidemic" in the United States. Opioid use disorder may be treated with medications and psychosocial interventions such as Narcotics Anonymous (NA). Buprenorphine, a partial agonist, is a mainstay of office-based treatment of opiate dependency. Its use requires certified training along with a special license from the Drug Enforcement Agency. Buprenorphine is a mu partial agonist and kappa antagonist. Unlike conventional opioids, buprenorphine may have a role in the treatment of major depression. Recently, a long-acting injectable form demonstrated efficacy. Methadone maintenance programs are of some value in opioid use disorder. Under carefully controlled supervision, the person with opioid use disorder is maintained on high doses of methadone (40-120 mg daily) that satisfy craving and block the effects of heroin to a great degree. Opioid antagonists (eg, naltrexone) can also be used successfully for treatment of the patient who has been free of opioids for 7-10 days. Naltrexone blocks the narcotic "high" of heroin when 50 mg is given orally every 24 hours initially for several days and then 100 mg is given every 48-72 hours. A monthly injectable form of naltrexone is available and may enhance compliance. Liver disorders are a major contraindication

Mood disorders complications

The most important complication is suicide, which often includes some elements of aggression. Suicide rates in the general population vary from 9 per 100,000 in Spain to 15 per 100,000 in the United States to 31 per 100,000 in Russia. In individuals hospitalized for depression, the lifetime risk rises to 4-6%. In patients with bipolar I disorder, the risk is higher. Men over the age of 50 are more likely to complete a suicide because of their tendency to use more violent means, particularly guns. On the other hand, women make more attempts but are less likely to complete a suicide. The suicide rate in the younger population, aged 15-35, continues to rise. Patients with cancer, respiratory illnesses, AIDS, and those being maintained on hemodialysis have higher suicide rates. Alcohol use is a significant factor in many suicide attempts. There are several groups of people who make suicide attempts. One group includes those individuals with acute situational problems. These individuals may be acutely distressed by a recent breakup in a relationship or another type of disappointment or overwhelmed by a stressful situation often with an aspect of public humiliation (eg, victims of cyber-bullying). A suicide attempt in such cases may be an impulsive or aggressive act not associated with significant depression. Another high-risk group includes individuals with severe depression. Severe depression may be due to conditions such as medical illness (eg, people with AIDS have a suicide rate over 20 times that of the general population) or comorbid psychiatric disorders (eg, panic disorders). Anxiety, panic, and fear are major findings in suicidal behavior. A patient may seem to make a dramatic improvement, but the lifting of depression may be due to the patient's decision to commit suicide. Another high-risk group are individuals with psychotic illness who tend not to verbalize their concerns and are often successful in their suicide attempt, although they make up only a small percentage of the total. Suicide is 10 times more prevalent in patients with schizophrenia than in the general population, with an increased frequency of jumping from bridges. In one study of 100 people who jumped from bridges, 47% had schizophrenia. The immediate goal of psychiatric evaluation is to assess the current suicidal risk and determine the need for hospitalization versus outpatient management. A useful question is to ask the person how many hours per day he or she thinks about suicide. If it is more than 1 hour, the individual is at high risk. Further assessing the risk by inquiring about intent, plans, means, and suicide-inhibiting factors (eg, strong ties to children or the church) is essential. Alcohol, hopelessness, delusional thoughts, and complete or nearly complete loss of interest in life or ability to experience pleasure are all positively correlated with suicide attempts. Other risk factors are previous attempts, a family history of suicide, medical or psychiatric illness (eg, anxiety, depression, psychosis), male sex, older age, contemplation of violent methods, a humiliating social stressor, and drug use (including long-term sedative or alcohol use), which contributes to impulsiveness or mood swings. Successful treatment of the patient at risk for suicide cannot be achieved if the patient continues to abuse drugs. An attempt is less likely to be suicidal if small amounts of poison or medication were ingested or scratching of wrists was superficial, if the act was performed near others or with early notification of others, or if the attempt was arranged so that early detection would be anticipated. The patient's current mood status is best evaluated by direct evaluation of plans and concerns about the future, personal reactions to the attempt, and thoughts about the reactions of others. Measurement of mood is often facilitated by using a standardized instrument such as the Hamilton or Montgomery-Asberg clinician-administered rating scales or the self-administered Quick Inventory of Depressive Symptomatology (QIDS-SR 16). Scales allow for initial assessment as well as ongoing treatment tracking. Suicide risk can be specifically assessed using an instrument such as the Columbia-Suicide Severity Risk Scale, https://cssrs.columbia.edu/wp-content/uploads/C-SSRS_Pediatric-SLC_11.14.16.pdf. The patient's immediate resources should also be assessed—people who can be significantly involved (most important), family support, job situation, financial resources, etc. If hospitalization is not indicated after a suicide attempt, the clinician must formulate and institute a treatment plan or make an adequate referral. (The National Suicide Prevention Lifeline, 1-800-273-8255, may be of assistance.) Medication should be dispensed in small amounts to at-risk patients. Although TCAs and SSRIs are associated with an equal incidence of suicide attempts, the risk of a completed suicide is much higher with TCA overdose. Guns and medications should be removed from the patient's household. Driving should be cautioned against until the patient improves. The problem is often worsened by the long-term complications of the suicide attempt, eg, brain damage due to hypoxia, peripheral neuropathies caused by staying for long periods in one position causing nerve compressions, and medical or surgical problems such as esophageal strictures and tendon dysfunctions. The reasons for self-mutilation, most commonly wrist cutting (but also autocastration, autoamputation, and autoenucleation, which are associated with psychoses), may be different from the reasons for a suicide attempt. The initial treatment plan, however, should presume suicidal ideation, and conservative treatment should be initiated.

Serotonin receptor antagonists and agonists

Trazodone (Desyrel) Nefazodone (Serzone) MOA: postsynaptic serotonin 5-HT2A and 5-HT2C inhibition. Weakly inhibits presynaptic serotonin uptake -Alpha-1 adrenergic receptor antagonist (leads to sedation) IND: anxiolytic and hypnotic effects (used for insomnia) -sleep aid (low dose) -does not affect REM sleep or cause sexual adverse effects Adverse effects: Sedation most common, dizziness, dry mouth, nausea, orthostatic hypotension, HA -Priapism -increased suicidality in younger people. cardiac arrhythmias -BBW for fulminant hepatitis (nefazodone)

Ptsd (ROSH)

The patient in the vignette is most likely suffering from post-traumatic stress disorder (PTSD) secondary to her recent rape. Post-traumatic stress disorder is characterized by having flashbacks of a traumatic event, such as sexual assault, military combat, severe burns, physical abuse, childhood neglect, or witnessing death or an injury. Secondary to these flashbacks, the patient will have a decrease in responsiveness and avoidance toward similar events associated with the trauma. The most important factor for diagnosing patients with post-traumatic stress disorder is the patient's history. After the known trauma, the patient may experience symptoms such as intrusive thoughts, including flashbacks or nightmares; avoidance of similar situations, places, or people who were present at the time of the event; negative thoughts in cognition and in their mood; and increased arousal and reactivity, commonly shown as angry outbursts, irritable behavior, or exaggerated startle response. According to the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders, (DSM-5), these symptoms must last for a minimum of 1 month to be diagnosed as post-traumatic stress disorder. If the symptoms are present for less than 1 month, then the correct diagnosis is acute stress disorder. Treatment for post-traumatic stress disorder is twofold. It is important to initiate both cognitive behavior therapy and pharmacotherapy with a selective serotonin reuptake inhibitor (SSRI) such as sertraline or paroxetine. SSRIs are the only FDA-approved class of medications and considered the pharmacotherapy of choice for PTSD. For patients who are experiencing insomnia, the addition of trazodone nightly may be helpful. Overall, the sooner therapy is initiated in patients with post-traumatic stress disorder, the better the prognosis.

Substance use disorders

The term "dependency" was previously used to describe a severe form of substance abuse and drug addiction characterized by the triad of: (1) a psychological dependence or craving and the behavior involved in procurement of the drug; (2) physiologic dependence, with withdrawal symptoms on discontinuance of the drug; and (3) tolerance, ie, the need to increase the dose to obtain the desired effects. The terms "dependency" and "abuse" were dropped in DSM-5 in favor of the single term "substance use disorder," ranging from mild to severe. Many patients could have a severe and life-threatening abuse problem without ever being dependent on a drug. Substance use disorder is a treatable, chronic medical illness. Clinicians and health care systems must work against bias toward people with substance use disorder. Medication-assisted treatment is available for a number of substance use disorders and is a key element in their management. There is accumulating evidence that an impairment syndrome exists in many former (and current) drug users. It is believed that drug use produces damaged neurotransmitter receptor sites and that the consequent imbalance produces symptoms that may mimic other psychiatric illnesses. "Kindling"—repeated stimulation of the brain—renders the individual more susceptible to focal brain activity with minimal stimulation. Stimulants and depressants can produce kindling, leading to relatively spontaneous effects no longer dependent on the original stimulus. These effects may be manifested as mood swings, panic, psychosis, and occasionally overt seizure activity. The imbalance also results in frequent job changes, partner problems, and generally erratic behavior. Patients with PTSD frequently have treated themselves with a variety of drugs. Chronic abusers of a wide variety of drugs exhibit cerebral atrophy on CT scans, a finding that may relate to the above symptoms. Early recognition is important, mainly to establish realistic treatment programs that are chiefly symptom-directed. The clinician faces three problems with substance use disorders: (1) the prescribing of substances such as sedatives, stimulants, or opioids that might produce dependency; (2) the treatment of individuals who have already misused drugs, most commonly alcohol; and (3) the detection of illicit drug use in patients presenting with psychiatric symptoms. The usefulness of UA for detection of drugs varies markedly with different drugs and under different circumstances (pharmacokinetics is a major factor) (see also Chapter 5). Water-soluble drugs (eg, alcohol, stimulants, opioids) are eliminated in a day or so. Lipophilic substances (eg, barbiturates, tetrahydrocannabinol) appear in the urine over longer periods of time: several days in most cases, 1-2 months in chronic marijuana users. Sedative drug determinations are quite variable, amount of drug and duration of use being important determinants. False-positives can be a problem related to ingestion of some legitimate medications (eg, phenytoin for barbiturates, phenylpropanolamine for amphetamines, chlorpromazine for opioids) and some foods (eg, poppy seeds for opioids, coca leaf tea for cocaine). Manipulations can alter the legitimacy of the testing. Dilution, either in vivo or in vitro, can be detected by checking urine-specific gravity. Addition of ammonia, vinegar, or salt may invalidate the test, but odor and pH determinations are simple. Hair analysis can determine drug use over longer periods, particularly sequential drug-taking patterns. The sensitivity and reliability of such tests are considered good, and the method may be complementary to UA.

DSM5: Substance Use

The terms dependency and abuse were dropped and replaced with substance use disorder with modifiers of mild, moderate or severe.

Chronic Alcoholic Brain Syndromes: Clinical Findings

These encephalopathies are characterized by increasing erratic behavior, memory and recall problems, and emotional instability—the usual signs of organic brain injury due to any cause.

Anxiolytics -Indications

They are commonly prescribed as sedatives and to treat withdrawal symptoms such as from alcohol withdrawal; other indications include anxiety and panic disorders, insomnia, muscle spasms, epilepsy, and as pre- and perioperative medications.

2. Cyclothymic disorder

This is a chronic mood disturbance with episodes of subsyndromal depression and hypomania. The symptoms must have at least a 2-year duration and are milder than those that occur in depressive or manic episodes. Occasionally, the symptoms will escalate into a full-blown manic or depressive episode, in which case reclassification as bipolar I or II would be warranted.

Anorexia Nervosa rapid review

Three core features -Restriction of energy intake relative to requirements leads to significantly low body weight -Intense fear of gaining weight or persistent behavior interfering with weight gain -Disturbance in body image Two types -Restricting -Binge-eating and purging type Recommended interventions -Determination of setting -Medical stabilization -Nutritional rehabilitation -Psychotherapy -For youth, best evidence is for family-based therapy, including parental management of ongoing weight restoration

SUBSTANCE USE DISORDERS -Diagnostic Findings

Urinalysis for detection of drugs varies markedly with different drugs and under different circumstances (pharmacokinetics is a major factor). •Water-soluble drugs (eg, alcohol, stimulants, opioids) are eliminated in a day or so. •Lipophilic substances (eg, barbiturates, tetrahydrocannabinol) appear in the urine over longer periods of time: several days in most cases, 1-2 months in chronic marijuana users. Hair analysis can determine drug use over longer periods, particularly sequential drug-taking patterns. •The sensitivity and reliability of such tests are considered good, and the method may be complementary to urinalysis.

SNRIs

Venlafaxine, Duloxetine, Desvenlafaxine -MOA: inhibits neuronal reuptake of serotonin, NE, and dopamine -IND: Duloxetine may be used as a first line agent, in patient with fatigue or neuropathy pain syndromes in association with depression -venlafaxine is used for depression and anxiety disorder -ADV effects: hyponatremia -NE effects: Hypertension, sweating, dizziness, dry mouth, constipation -Contraindications: MAOI use, renal/hepatic impairment, seizures, avoid abrupt discontinuation, use in caution with HTN. SNRIs and St. John's Wart increases risk of serotonin syndrome

intimate partner violence (ROSH)

When intimate partner violence has been identified, supporting the patient is of utmost importance. Expressing empathy, acknowledging the patient's struggle, and thanking the patient for their trust are vital components to establishing a rapport that will allow them to make autonomous decisions. Comments about offering assistance such as "I'd like to offer any help that I'm able to" or "I want to give you resources that might help your situation" are necessary to open the topic of resources. Offering empathy and assistance will help patients know that they can move forward with any action plan when they are ready. Offering a referral to discuss safety and mental health services may raise awareness about services that are available. The danger of violence increases when victims attempt to leave the relationship, seek outside intervention, or become suicidal or homicidal. Asking patients whether they have a safety plan in place may help open the discussion to acts of preparing a place to go, establishing a signal to alert someone to call 911, or preparing a kit with essentials in case they need to leave suddenly.

ALCOHOL USE DISORDERS: ETIOLOGY

•Alcohol and other drug abuse patients have a much higher prevalence of lifetime psychiatric disorders. •While male-to-female ratios in alcoholic treatment agencies remain at 4:1, there is evidence that the rates are converging. ->Women delay seeking help, and when they do, they tend to seek it in medical or mental health settings. •Adoption and twin studies indicate some genetic influence. •Depression is often present and should be evaluated carefully. •The majority of suicides and intrafamily homicides involve alcohol •Alcohol is a major factor in rapes and other assaults.

SEDATIVES (ANXIOLYTICS) -BENZODIAZPINE most common

•All BZDs have anxiolytic, hypnotic, muscle relaxant, anticonvulsant, and amnesic effects mediated through central nervous system inhibition (specifically gamma-aminobutyric acid [GABA] system inhibition) •BZDs are known to be relatively safe for short-term use (2-4 weeks), but their safety profile is unestablished for duration of use ≥ 5 weeks and it is reported up to 50% of patients using BZDs for ≥ 1 month may develop signs of dependence

Substance Use: General

•All drugs that are taken in excess have in common direct activation of the brain reward system, which is involved in the reinforcement of behaviors and the production of memories. •They produce such an intense activation of the reward system that normal activities may be neglected

Persistent Depressive Disorder: Dysthymia

definition •Depressed mood for most of the day, for more days than not, as indicated by either subjective account or observation by others, for at least 2 years (in children or adolescent 1 year) •Not symptom free for >2 months at a time Criteria Presence, while depressed, of 2 or more of the following: 1. Poor appetite or overeating 2. Insomnia or hypersomnia 3. Low energy or fatigue 4. Low self-esteem 5. Poor concentration or difficulty making decisions 6. Feelings of hopelessness Criteria for a MDD may be continuously present for 2 years -> There has NEVER been a manic or hypomanic episode, and criteria for cyclothymic disorder have not been met Risk factors •More common in women •1% prevalence •Patient with history of traumatic brain injury (15-30% of patients with TBI with develop PDD) •Previous abuse •History of substance abuse (not current or they don't qualify for this diagnosis) •Acute loss or traumatic event •Racial/ethnic minority status, low socioeconomic status Treatment Combination treatment with psychotherapy and pharmacotherapy more efficacious than either alone Medical •SSRI •SNRI Psychotherapy •Interpersonal •Cognitive •Insight-orientated psychotherapies

extrapyramidal symptoms

dopamine blockade in nigrostriatal pathway

Akathisia

feeling of restlessness Management: reduce dose or switch med. Propranolol, Benzos

Olanzapine

higher incidence of weight gain and DM

Commonly used antidepressant medications (listed in alphabetical order within classes).

https://accessmedicine.mhmedical.com/ViewLarge.aspx?figid=269142449&gbosContainerID=0&gbosid=0&groupID=0&sectionId=269142399

Antidepressant drug interactions with other medications (listed in alphabetical order within classes).

https://accessmedicine.mhmedical.com/ViewLarge.aspx?figid=269142489&gbosContainerID=0&gbosid=0&groupID=0&sectionId=269142399

Serotonin syndrome

increased serotonergic activity in the CNS Etiologies: within 24 (especially 6) hours with initiation or change in serotonergic drugs (SSRIs, SNRIs, TCAs, MAOIs, Triptans, MDMA, cocaine, amphetamines) PE -Cognitive effects; AMS, confusion, agitation, hallucinations, hypomania -Autonomic instability; hyperthermia, tachycardia, diaphoresis, BP changes -GI effects; N/V/Diarrhea -Neuromuscular hyperactivity: spontaneous or inducible clonus, hypertonia (increased DTR), tremor, restlessness -Mydriasis (dilated pupils), dry mucous membranes, flushed skin Diagnosis -Hunter Criteria Mild Management -Discontinuation of offending drugs -Supportive care: mainstay, O2, IV fluids, Benzos for agitation and hyperthermia Moderate management -above + Cyproheptadine -Antipyretics should not be used

Spouse or Intimate partner violence

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Spouse or Intimate partner neglect

page 566 (PPP) Intimate partner violence is a pattern of abusive behavior by a current or former intimate partner. The abuse can be physical, sexual, or emotional and can include economic deprivation. Although anyone can experience intimate partner violence, women are more likely than men to be impacted by intimate partner violence; lesbian, gay, bisexual, transgender, and questioning persons experience higher rates of intimate partner violence than other groups. Regardless of the type of abuse, the goal of the abuser is to gain control over the victim. Intimate partner violence is common but is often not diagnosed. There is also concern for an increase in intimate partner violence during the isolation of the COVID-19 pandemic. The prevalence estimate of intimate partner violence varies depending on the setting. Rates are higher when measured in emergency departments than when measured in the general population. In a randomized controlled trial of intimate partner violence screening in emergency departments, the prevalence over 12 months ranged from 4% to 18%. While intimate partner violence occurs in all locations, cultural backgrounds, and socioeconomic groups, prevalence estimates can vary by certain demographic characteristics. Specific risk factors include being young (aged 18-24 years), pregnant, single, divorced, or separated; self-identifying as an indigenous person (eg, American Indian or Native Alaskan), multiracial, or non-Hispanic Black; or having coexisting mental illness. Since patients often do not voluntarily report abuse, clinicians must seek clues that suggest abuse, including an explanation of the injuries that does not fit with what is being seen; frequent visits to the emergency department; and somatic complaints such as chronic headache, abdominal pain, and fatigue. The patient may be vague about some of her symptoms and may avoid eye contact. If the abusing partner is present, he or she may answer all the questions or may decline to leave the room. It is critical that the patient has the opportunity to speak with the clinician alone. The patient's description of the events should be carefully detailed using nonjudgmental language in the event that there are subsequent legal issues. Physical examination often reveals injuries in the central area of the body. There may be injuries on the forearms as well if the patient tried to defend herself. As with any situation of expected abuse, bruises that are in various stages of healing may be an important clue. All physical examination findings should be well documented. In addition to the physical consequences, abuse can have psychological consequences. PTSD, depression, anxiety, and alcohol or other substance abuse can develop in those who experience intimate partner violence. Somatization is also common. Several instruments have been developed to screen for intimate partner violence. These include the HITS (Hurt, Insult, Threaten, Screamed at) tool, the Women Abuse Screening Tool (WAST), the Partner Violence Screen (PVS), the Abuse Assessment Screen (AAS), and the Women's Experience with Battering (WEB) scale. A systematic review of these screening tools showed that most tools only had been evaluated in a relatively small number of studies and the sensitivities and specificities varied widely within and between the tools. Many studies have addressed how the questions about intimate partner violence are asked. Inclusion of one question in the context of the medical history, "Have you ever been hit, kicked, punched, or otherwise hurt by someone within the past year? If so, by whom?" has been shown to increase identification of intimate partner violence. The SAFE questions are also useful. Stress/Safety: Do you feel safe in your relationship? Afraid/Abused: Have you ever been in a relationship where you were threatened, hurt, or afraid? Friend/Family: Are your friends aware you have been hurt? Emergency Plan: Do you have a safe place to go and the resources you need in an emergency? In one randomized trial, women preferred written questionnaires over face-to-face interviewing. The USPSTF recommends that clinicians screen women of childbearing age for intimate partner violence and provide or refer women who screen positive to intervention services. Interventions for intimate partner violence start with validating statements, such as "This is an unfortunately common problem, and there are resources that can help." The clinician may then assess immediate safety using a tool such as the Brief Danger Assessment, where positive responses to two or more questions signify increased risk of homicide or severe injury: Has the physical violence increased in frequency during the past year? Has your partner ever used a weapon against you or threatened you with a weapon? Do you believe your partner is capable of killing you? Does your partner ever try to choke you? Is your partner violently and constantly jealous of you? Engaging other health care professionals, such as social workers, and referring to local intimate partner violence organizations can facilitate the legal and practical steps to improve safety. In some practice settings where social workers or local resources are limited, provision of the National Hotline: 1-800-799-7233 and the use of a private location in the clinic with a phone can allow the woman to speak with hotline providers in a safe environment. It is important to ensure a plan for follow-up before the end of the visit. There is no evidence that treatment of the abuser changes abuser behavior. When to refer Persons experiencing intimate partner violence should be referred to social services so that they can provide information on local resources. A national domestic violence hotline (1-800-799-SAFE) can provide information on local resources. In general, mandatory reporting of intimate partner violence or suspicion of it in adult women who are competent is not required in most states. However, mandatory reporting by clinicians is required in several states. Clinicians should be familiar with their state guidelines.

Tardive dyskinesia

repetitive involuntary movement mostly involving the face (lip smacking, teeth grinding, rolling of the tongue) - long term use (first gen)

Acute Dystonia

spasms of neck and face (trismus, tongue protrusions, facial grimace, torticollis, difficulty speaking) Occurs hours - days after meds initiation Acute Management: Diphenhydramine, Benztropine

Parkinsonism

tremor, rigidity, bradykinesia

PSYCHEDELICS

•6000 species of plants have psychoactive properties. •All of the common psychedelics (LSD, mescaline, psilocybin, dimethyltryptamine, and other derivatives of phenylalanine and tryptophan) can produce similar behavioral and physiologic effects •Alter human perception and mood •Hallucinogenic •MESCALINE (PEYOTE CACTUS) •PSILOCYBIN (MUSHROOMS)

Bipolar II: Definition -Hypomanic episode

•A distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased activity or energy, lasting at least 4 consecutive days and present most of the day, nearly every day. 1. Inflated self-esteem or grandiosity 2. Decreased need for sleep (feels rested after only 3 hours) 3. More talkative than usual or pressure to keep talking 4. Flight of ideas or subjective experience that thoughts are racing 5. Distractibility 6. Increase in goal-directed activity (either socially, at work or school, or sexually) or psychomotor agitation 7. Excessive involvement in activities that have a high potential for painful consequences (engaging in unrestrained buying sprees, sexual indiscretions or foolish business investments) < 1 week, does not require hospitalization, not associated with marked impairment of social/occupational function and no psychotic features -3 symptoms affecting mood, thinking, or behavior

Alcohol Use Disorder (Definition)

•A problematic pattern of alcohol use leading to clinically significant impairment or distress as manifested by 2 or more occurring withing 12 month period

PSYCHEDELICS CLINICAL FINDINGS

•An initial feeling of tension is followed by emotional release such as crying or laughing (1-2 hours). •Later, perceptual distortions occur, with visual illusions and hallucinations, and occasionally there is fear of ego disintegration (2-3 hours). •Major changes in time sense and mood lability then occur (3-4 hours). •A feeling of detachment and a sense of destiny and control occur (4-6 hours). •Occasionally, the acute episode is terrifying (a "bad trip"), which may include panic, depression, confusion, or psychotic symptoms •Preexisting emotional problems, the attitude of the user, and the setting where the drug is used affect the experience. •Reactions vary among individuals, and some of the drugs produce markedly different time frames.

PSYCHEDELICS: DIMETHYLTRYPTAMINE

•An intense naturally-occurring psychedelic that's also found endogenously in the human body. •It's not as popular as LSD or psilocybin, though its use has grown over time. •The most popular route of administration is inhalation, but it's also frequently taken orally in ayahuasca-like preparations •It is used as a recreational psychedelic drug in US and UK, and prepared by various cultures for ritual purposes as an entheogen as part of a religious ceremony.

AMPHETAMINES/COCAINE Withdrawal Treatment

•Antipsychotics for any psychosis •Bromocriptine may help alleviate some of the cravings •Control agitation and hyperthermia with benzodiazepines

COCAINE

•Cocaine is a stimulant and a product of the coca plant. •Cocaine hydrochloride is the salt and the most commonly used form. •Freebase, a purer (and stronger) derivative called "crack," is prepared by simple extraction from cocaine hydrochloride. •Intranasal use is simply snorting cocaine through a straw. ->Absorption is slowed somewhat by vasoconstriction (which may eventually cause tissue necrosis and septal perforation) ->The onset of action is in 2-3 minutes, with a moderate high (euphoria, excitement, increased energy) lasting about 30 minutes. Heart attack and deterioration of nasal septum

Acute treatment of panic attack:

•Benzodiazepines (Alprazolam, Clonazepam): but have potential abuse

COCAINE: Complications

•Cardiovascular collapse, arrhythmias, myocardial infarction, and transient ischemic attacks have been reported. •Seizures, strokes, migraine symptoms, hyperthermia, and lung damage may occur, •Several obstetric complications, including spontaneous abortion, abruptio placentae, teratogenic effects, delayed fetal growth, and prematurity. •Cocaine can cause anxiety, mood swings, and delirium, and chronic use can cause the same problems as other stimulants.

Alcohol Withdrawal: Complicated-Clinical Manifestations

•Cessation of alcohol use that has been heavy and prolonged Withdrawal seizures •Onset 6-48 hours after last drink •Usually generalized tonic-clonic Alcoholic hallucinosis •Onset 12-48 hours after last drink •Visual/auditory/tactile hallucinations •Clear sensorium and normal vital signs Delirium tremens •Onset 2-5 days after last drink •Delirium (altered sensorium), hallucinations, agitation •Abnormal vital signs (tachycardia, HTN, fever)

Korsakoff psychosis

•Characterized by both anterograde and retrograde amnesia, with confabulation early in the course. •Early recognition and treatment with intravenous thiamine and B complex vitamins can minimize damage (banana bag)

OPIODS COMPLICATIONS

•Complications of heroin administration include infections (eg, pneumonia, septic emboli, hepatitis, and HIV infection from using nonsterile needles), traumatic insults (eg, arterial spasm due to drug injection, gangrene), and pulmonary edema SKIN POPPING -blindly aiming to hit vein (after all injection sites used) and hits tissue -> necrosis

Alcohol Use Disorder Treatment -Non-medication

•Counseling •AA has the highest rate of success

Signs of Anxiolytic Use

•Disinhibition, ataxia, dysarthria, nystagmus, and delirium ->(The patient should be told not to operate machinery and drive with caution until he or she is well stabilized without side effects) •Paradoxical agitation, anxiety, psychosis, confusion, mood lability, and anterograde amnesia have been reported, particularly with the shorter-acting benzodiazepines.

PHECYCLIDINE (PCP) -Physical Symptoms

•Dizziness, •Ataxia, •Dysarthria, •Nystagmus, •Retracted upper eyelid with blank stare, •Hyperreflexia •Tachycardia. •Increases in blood pressure, respiration, muscle tone, and urine production "tearing down a door"

Anxiolytic Use Disorder -Definition

•Encompasses a range of clinically significant problematic behaviors and functional difficulties resulting from anxiolytic use over a 12-month period. •Associated features may include dose increases, tolerance to and craving for drug effect, and failure to cut back on use.

Opioid Intoxication Symptoms

•Euphoria and sedation •Pupil constriction (PINPOINT) •Altered mental status •Respiratory depression •Bradycardia •Hypotension

Generalized Anxiety Disorder

•Excessive anxiety and worry occurring more days than not for at least 6 months, about a number of events or activities (such as school or work performance) •The individual finds it difficult to control the worry (EX: 1 mo hx is not diagnostic for GAD) Criteria -Then anxiety and worry are associated with 3 or more of the following 6 symptoms (with at least some symptoms having been present for more days than not for the past 6 months) 1. Restlessness or feeling keyed up or on edge 2. Being easily fatigued 3. Difficulty concentration or mind going blank 4. Irritability 5. Muscle tension 6. Sleep disturbance •The anxiety, worry or physical symptoms cause clinically significant distress or impairment in social, occupational or other important areas of functioning (EX: divorce due to symptoms) •Not a result of substance use •Not better explained by another disorder •Other key points: it is NOT episodic (panic disorder), situational (phobias) nor focal Epidemiology A. 10-14 year old child/adolescent B. Early adulthood (mean age 30) C. Peak in older adulthood (often with chronic medical illness) •More common in women •More common in older adults, especially widowed, separated or divorced Etiology •Not well understood •Emerging studies suggest possible environmental and genetic factors likely involved and result in development of dysfunctional neural processing of emotional stimuli •Thought to experience persistent activation of areas of the brain associated with mental activity and introspective thinking following worry-inducing stimuli, leading to dysregulation of worry Management •SSRIs are first line medication •SNRI •Buspirone (BuSpar) can be an adjunct (non-sedating) •Cognitive behavioral therapy •Psychotherapy •Can use benzos while awaiting the longer acting medication to take effect

MARIJUANA WITHDRAWAL symptoms

•Insomnia •Nausea •Myalgia •Irritability

MARIJUANA LONG TERM USE

•Laryngitis and rhinitis are related to prolonged use, along with chronic obstructive pulmonary disease. (SAME AS SMOKERS) •No chronic cardiac disease has been linked to marijuana use. •Depression of plasma testosterone levels and reduced sperm counts. •Abnormal menstruation and failure to ovulate have occurred in some women. •Cognitive impairments are common.

PHECYCLIDINE (PCP) TREATMENT Emergency and Supportive Measures

•Maintain a patent airway and assist respirations if necessary.•Treat coma, hyperthermia, hypertension, and seizures•For recent large ingestions, consider giving activated charcoal orally or by gastric tube.•Patients with delirium may benefit from a dose of physostigmine (reversible cholinesterase inhibitor)

Specific phobia

•Marked fear or anxiety about a specific object or situation (flying, heights, animals, shots, seeing blood, etc) •The phobic object or situation almost always provokes immediate fear or anxiety •The phobic object or situation is actively avoided or endured with intense fear or anxiety •The fear or anxiety is out of proportion to the actual danger posed •The fear, anxiety or avoidance is persistent 6 months or more •Causes clinically significant distress or impairment •Not explained by other mental illness or substance use Epidemiology •More common in women •Childhood onset is most common Etiology •Maladaptive activation of evolutionarily defined fear pathway is a possible cause Treatment •Exposure and desensitization therapy is treatment of choice •Can use SHORT term benzo or BB in some patients

Suicide -Protective factors:

•Marriage •Pregnancy

MARIJUANA TREATMENT

•No specific treatment is necessary except in the case of the occasional "bad trip," in which case the person is treated in the same way as for psychedelic usage. •Marijuana frequently aggravates existing mental illness and adversely affects motor performance.

Bipolar I Disorder -Criteria have been met for AT LEAST ONE MANIC episode***

•Only requirement for diagnosis = ONE MANIC EPISODE •The occurrence of the manic and major depressive episode(s) is not better explained by other schizophrenic or delusional disorders

Uncomplicated Alcohol Withdrawal-Clinical Manifestations

•Onset 6-36 hours after last drink •Autonomic hyperactivity (sweating or tachycardia) •Increased hand tremor •Insomnia •Irritability •Anxiety •N/V/D •HTN •NO: seizures, hallucinations or dt

PHENCYCLIDINE (PCP)

•Phencyclidine (PCP, angel dust) is simple to produce and mimics to some degree the traditional psychedelic drugs •PCP is a common deceptive substitute for LSD, tetrahydrocannabinol, and mescaline. •It is available in crystals, capsules, and tablets to be inhaled, injected, swallowed, or smoked (it is commonly sprinkled on marijuana).

Suicide -Risk Factors

•Plan: previous attempt strongest single predictive factor -(70% of people who committed suicide succeeded on their first try) -Organized plan is higher risk than no organized plan •Access to firearms •Gender: females attempt more than men, but men are more successful •Increases with age (elderly white men have the highest risk) •Race: white>blacks •Psychiatric disorders: majority who attempt or commit suicide have underlying psychiatric disorders •Substance abuse •Marital status: alone> never married> widowed > separated or divorced> married without children> married with children (marriage is protective)

PHECYCLIDINE (PCP) CLINICAL FINDINGS

•Rapid absorption with smoking. •Onset of symptoms in several minutes and peak symptoms in 15-30 minutes. •Mild intoxication produces euphoria accompanied by a feeling of numbness. •Moderate intoxication (5-10 mg) results in disorientation, detachment from surroundings, distortion of body image, combativeness, unusual feats of strength (partly due to its anesthetic activity), and loss of ability to integrate sensory input, especially touch and proprioception. •MIMICS SCHIZOPHRENIA

Alcohol Intoxication -Criteria

•Recent ingestion of alcohol •Clinically significant problematic behavioral or psychological changes that developed during or shortly after ingestion On or more of the following signs or symptoms: •Slurred speech •Incoordination •Unsteady gait •Nystagmus •Impairment in attention or memory •Stupor or coma

Hyperemesis Cannabis or Cannabinoid Hyperemesis Syndrome

•Severe recurrent nausea and vomiting also sweating high belly and cramping pain ->give antipsychotic for treatment

Suicide -Risk factors (SAD PERSONS = mnemonic)

•Sex (male) •Age (teenager or ≥ 45 years) •Depression •Previous attempt •Ethanol or drug use •Rational thinking loss •Separated, divorced, or widowed •Organized plan •No social support •Stated future attempt •Most completed suicides involve firearms •Most attempted suicides involve ingestions (antidepressants)

SUBSTANCE USE DISORDERS -KINDLING

•Repeated stimulation of the brain—renders the individual more susceptible to focal brain activity with minimal stimulation. •Stimulants and depressants can produce kindling, leading to relatively spontaneous effects no longer dependent on the original stimulus. •These effects may be manifested as mood swings, panic, psychosis, and occasionally overt seizure activity. •The imbalance also results in frequent job changes, partner problems, and generally erratic behavior.

SEDATIVES (ANXIOLYTICS) -Overdosage results in

•Respiratory depression •Hypotension •Shock syndrome •Coma •Death

AMPHETAMINES/COCAINE: CLINICAL FINDINGS

•Sweating •Tachycardia •Elevated blood pressure •Mydriasis •Hyperactivity •An acute brain syndrome with confusion and disorientation.

Benzodiazepine Withdrawal Syndrome

•Symptoms of withdrawal typically appear within 2-3 half-lives of the benzodiazepine being withdrawn and they last several weeks. -Short-acting drug withdrawal symptoms typically start 1-2 days after the drug withdrawal and last for about 2-4 weeks. -Long-acting drug withdrawal symptoms typically start 2-7 days after the drug withdrawal and last for about 2-8 weeks. •The symptoms and severity of withdrawal are highly variable for benzodiazepines with some chronic users able to withdraw from the drug without difficulty while others may experience protracted symptoms.

Substance use disorder impairment syndrome

•There is accumulating evidence that an impairment syndrome exists in many drug users. •It is believed that drug use produces damaged neurotransmitter receptor sites and the the consequent imbalance produces symptoms that may mimic other psychiatric illnesses.

Major Depressive Disorder with a Seasonal Onset

•This is MDD with a specifier •The specifier only applies to RECURRENT major depressive disorder •There has been a regular temporal relationship between the onset of major depressive episodes in major depressive disorder and a particular time of year (does not apply if depressed because they are unemployed during this time) •Full remissions also occur at a characteristic time of the year Criteria •In the last 2 years, two major depressive episodes have occurred that demonstrate the temporal seasonal relationship and no non-seasonal depressive episodes have occurred •And seasonal major depressive episodes substantially outnumber the nonseasonal major depressive episodes that may have occurred over the individual's lifetime. Treatment •SSRI •Light therapy •Buproprion (BuSpar)

PSYCHEDELICS TREATMENT

•Treatment of the acute episode primarily involves protection of the individual from erratic behavior that may lead to injury or death •A structured environment is usually sufficient until the drug is metabolized. •In severe cases, antipsychotic medications with minimal side effects (eg, haloperidol, 5 mg intramuscularly) may be given every several hours until the individual has regained control. •In cases where "flashbacks" occur (mental imagery from a "bad trip" that is later triggered by mild stimuli such as marijuana, alcohol, or psychic trauma), a short course of an antipsychotic drug—eg, olanzapine, 5-10 mg/day orally, or risperidone, 2 mg/day orally, initially. •Lorazepam or clonazepam, 1-2 mg orally every 2 hours as needed for acute agitation, may be a useful adjunct. •An occasional patient may have "flashbacks" for much longer periods and may require small doses of antipsychotic medications over the longer term.

PHECYCLIDINE (PCP) CLINICAL COMPLICATIONS

•Usage in the first trimester of pregnancy is associated with an increase in spontaneous abortion and congenital defects. •Severe intoxication (20 mg or more) produces an increase in degree of moderate symptoms, with the addition of seizures, deepening coma, hypertensive crisis, and severe psychotic ideation. •Overdosage may be fatal, with the major causes of death being hypertensive crisis, respiratory arrest, and convulsions. •Acute rhabdomyolysis has been reported and can result in myoglobinuric kidney failure.

Wernicke Encephalopathy -The diagnosis requires 2 of the following 4 features

•serum evidence of dietary deficiency •ocular signs •cerebellar dysfunction •altered mental state or mild memory impairment