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    Psychiatry ppt Psychiatry ppt Presentation Transcript

    • Psychiatr y Step III
    • Hypochondriasis The following clues need to be considered in making this daignosis:  Appropriate medical evaluation failed to find evidence of serious disease  Patient's preoccupation persisted despite adequate reassurance  Preoccupation lasted for 6 months or more  Preoccupation caused marked distress or impairment in functioning  Voiced concerns that are unrealistic but not beyond reason; for example, the patient may believe headaches indicate a brain tumor ( If its beyond reason then you will have to call it a “Delusion”)  Failure of the patient to be reassured after appropriate work-ups causing him or her to seek further tests and consultations
    • Hypochondriasis  Hypochondriasis Associations:  Seen in 50% of all patients with panic disorder  major depressive disorder  In these patients, coexisting hypochondriasis will respond to treatment for the primary disorder.
    • D/D 1. Physical Disease  Conditions with diffuse symptomatology involving many organ systems may, when undiagnosed, mimic hypochondriasis  Occasionally occult malignancies or early stages of multisystem disease (e.g., lupus) explain what at first appears to be hypochondriasis. It is most important to first rule out physical disease 2. Major depressive episode  Depressed mood, sleep and appetite changes, loss of interest, low self-esteem  Depressed patients in primary care usually have unexplained somatic complaints and are worried about what is wrong with them but have typical symptoms and signs of depression 3.
    • D/D 3. Panic disorder  Recurrent panic attacks with persistent dread of future attacks  Panic patients in primary care usually have numerous somatic symptoms and anxiety about their health. However, they also have recurrent panic attacks and worry about future attacks 4. Obsessive-compulsive disorder  Repetitious unwanted thoughts (obsessions) and repetitious unwanted actions (compulsions)  Patients with hypochondriasis do not have other obsessions or compulsions. Obsessions often involve contamination or harming someone; compulsions often involve cleaning or checking
    • D/D 5. Specific phobia of illness Fear and avoidance of a specific illness (e.g., AIDS) Patients with hypochondriasis have a conviction that serious disease is already present, whereas patients with illness phobia fear contracting illnesses they do not have 6. Somatization disorder Multiple somatic symptoms involving many organ systems with onset <30 years Somatization disorder occurs predominantly in women and involves multiple unexplained symptoms. By contrast, hypochondriasis is characterized chiefly by abnormal attitudes (i.e., fear, worry)
    • D/D 7. Psychotic disorders (schizophrenia, delusional disorder, major depressive disorder with psychotic features)  Patients with hypochondriasis have overvalued ideas but not delusional beliefs. Overvalued ideas are strongly held, but delusional ideas are accompanied by unshakeable conviction and are often bizarre
    • Hypochondriasis Therapy 1. Adopt a systematic approach to patients with hypochondriasis.  Here, you should aim to continue to care not a cure  Arrange regularly scheduled follow-ups.  Provide an explaination  Develop and maintain a positive relationship using interviewing skills. 2. Cognitive behavioral therapy as a primary mode of therapy 3. In patients with hypochondriasis who have coexisting depressive or anxiety disorders, rx with an antidepressant.  Start treatment with a serotonin reuptake inhibitor at low dose; for example, start sertraline, 12.5 mg/d, and increase by 12.5 mg every 5 days as tolerated until a daily dose of 50 mg is achieved
    • Somatization Disorder  Diagnostic criteria for a Somatoform Disorder  Physical symptoms that cannot be explained by an organic cause  “Secondary Gain “ aiming conditions are ruled out (Malingering or Factitious Disorder)  Causes significant dysfunction  Specific criteria for Somatization Disorder    Symptoms longer than 2 years Unexplained physical symptom with onset prior to age 30. Symptoms are vague and involve multiple organ symptoms     At least 2 Gastrointestinal (nausea, vomiting, bloating) At least 4 Pain ( Headache, abdominal pain, chestpain, dyspareunia) At least 1 Neurologic ( deafness, blindness, diplopia, fainting, dysphagia) At least 1 Sexual / genitourinary ( erectile dysfunction, dyspareunia, menorrhagia, irregular menses)  Important clues in history that can help in diagnosis  Extensive work up in the past that has been non diagnostic  Patient tends to switch physicians often because of dissatisfaction with previous physicians
    • Somatization management Never tell the patient that its “all in her head” Avoid excess investigations. A single physician should try to establish a long term empathetic relationship with the patient.  Cognitive therapy  Group therapy   
    • Delirium
    • Deliriun         PREDISPOSING FACTORS Age Cognitive impairment Increased comorbidity Male gender Depression Alcohol abuse Sensory impairment              PRECIPITATING FACTORS >6 total medications >3 new inpatient medications Psychotropic medication Infection ICU admission Hip fracture Dehydration Environmental change Restraint use Malnutrition Catheter use Iatrogenic event
    • Screening - Delirium  Perform a short mental status assessment for delirium at least daily in all hospitalized patients aged 70 or older  Daily, Screen inpatients who are predisposed to delirium, including those with cognitive impairment or multiple comorbidities and those admitted to the ICU Use for assessment for delirium:  Confusion Assessment Method  Mini-Mental Status Examination  Remember Delirium can have various Psychomotor variants – hypoactive, hyperactive, mixed and normal psychomotor activity
    • Confusion Assessment Method  Confusion Assessment Method Instrument (CAM)   Acute Onset 1. Is there evidence of an acute change in mental status from the patient's baseline?_____YES _____NO _____UNCERTAIN _____NOT APPLICABLE   Inattention (The questions listed under this topic are repeated for each topic where applicable.) 2A. Did the patient have difficulty focusing attention (for example, being easily distractible or having difficulty keeping track of what was being said)? _____Not present at any time during interview _____Present at some time during interview, but in mild form _____Present at some time during interview, in marked form _____Uncertain  2B. (If present or abnormal) Did this behavior fluctuate during the interview (that is tend to come and go or increase and decrease in severity)? _____YES _____NO _____UNCERTAIN_____NOT APPLICABLE 2C. (If present or abnormal) Please describe this behaviour:   Disorganized Thinking 3. Was the patient's thinking disorganized or incoherent, such as rambling or irrelevant conversation, unclear or illogical flow of ideas, or unpredictable switching from subject to subject? _____YES _____NO _____UNCERTAIN _____NOT APPLICABLE Altered Level of Consciousness 4. Overall, how would you rate this patient's level of consciousness? _____Alert (normal) _____Vigilant (hyperalert, overly sensitive to environmental stimuli, startled very easily) _____Lethargic (drowsy, easily aroused) _____Stupor (difficult to arouse) _____Coma (unarousable) _____Uncertain
    • CAM - Scoring  To have a positive CAM result, the patient must display: 1. Presence of acute onset and fluctuating discource AND 2. Inattention AND EITHER 3. Disorganized thinking OR 4. Altered level of consciousness
    • Differential Diagnosis Differential diagnoses include:  Dementia  Depression  Partial syndrome of delirium  Bipolar disease  Note that any acute change in mental status should be considered delirium until proven otherwise because of reversibility and the consequences of missing the diagnosis.  In hospitalized patients with altered cognition, assess delirium first, followed by partial syndrome of delirium, depression, and then dementia.
    • Evaluating differential diagnosis 1. Dementia Insidious onset, slow progression, level of consciousness is usually normal, attention is preserved until late in the course  Any acute mental status change in a demented patient is likely to be superimposed delirium. Dementia (or cognitive impairment) is a strong risk factor for delirium; the two disorders commonly co-exist 2. Depression  Depressed mood is present. Psychomotor retardation or agitation also may be present. Level of consciousness and attention is usually normal  A study showed that one third of consults for “depression” in the hospital were hypoactive delirium 3. Bipolar disease, especially acute mania  Acute mania may be confused with hyperactive delirium, but is less common in the elderly. Usually the changes and fluctuations are less acute than delirium. Inattention, disorganized thinking, and psychomotor agitation may be present  Bipolar disease rarely presents in old age. Patients with this disease usually have a history of psychiatric illness or are taking medications that suggest the diagnosis. If in doubt, perform the full delirium work-up 4. Partial syndrome of delirium  Patients show some of the characteristics of delirium, but not enough to fulfill all criteria. Sometimes progresses to full-blown delirium  Associated with poor outcome and should be evaluated and treated similar to “full-blown” delirium
    • Ways to Prevent Hospital Delirium – high yield Prevent delirium in hospitalized patients by ensuring:  Assessment of multiple risk factors  Cognitive impairment , Sleep deprivation , Immobility, Visual impairment, Hearing impairment & Dehydration  Targeted treatment to correct or reduce the impact of risk factors  Avoidance of medications deemed inappropriate for older patients  Geriatrics consultation  Nursing-based interventions  Consider proactive, preoperative geriatric consultation to reduce postoperative delirium in hip fracture patients
    • Managing Delirium 1. Remove contributing factors, such as:  Offending medications , Fluid and electrolyte abnormalities , Severe pain , Hypoxemia , Severe anemia , Infections , Sensory deprivation 2. Maintain behavior control through behavioral or social measures rather than pharmacologic or physical restraints.  Note that a family member or caregiver will often ameliorate mild to moderate agitation; hiring a “sitter” or keeping the patient near the nursing station may be adequate.  Be aware that treatment with sedating medications may be necessary for severe or life-threatening agitation. There is no rationale for treating hypoactive delirium with sedating medications.  Avoid use of physical restraints unless no safer alternative is feasible and the patient is physically endangering self or others.
    • Managing Delirium Recognize that patients with delirium are vulnerable and require attentive supportive care to meet their needs and avoid iatrogenic complications.  Minimize indwelling catheters and other “tethers” such as intravenous lines, EKG leads, and restraints; let the patient out of bed as soon as possible.  Monitor urinary and bowel output, and avoid urinary retention and fecal impaction which can contribute to delirium.  Pay careful attention to nutrition, including assistance with meals and possible hand feeding—delirious patients may have difficulty attending to food and are at risk for acute malnutrition.  Provide adequate sensory input, including use of glasses and hearing aids, provision of clocks, calendar, and adequate lighting, and appropriate interpersonal contact.  Be aware that frequent orientation and structured interpersonal contact may facilitate cognitive “reconditioning.”  Recognize that environmental modifications such as minimizing staff noise, use of vibrating (silent) pagers, eliminating waking for vital signs except if essential, and reduced lighting at the nursing station may improve sleep at night.
    • Managing Delirium Consider using drugs to manage agitation in delirium, but not at the risk of worsening or prolonging the delirium itself.  Note that haloperidol and risperidone should be considered as the “least of the evils” and should only be used in life-threatening circumstances (such as in the ICU) or when behavioral measures have been ineffective.  Use the lowest dose of the least toxic agent that successfully controls the agitation.  Note that haloperidol in low doses is equally efficacious as atypical antipsychotics and may be less likely to cause oversedation, hemodynamic compromise, or respiratory depression compared to benzodiazepines.
    • Drug Rx for agitation associated with Delirium 1. Haloperidol : Usually agent of choice  Advantages: Relatively non-sedating. Few hemodynamic effects. May prevent delirium following hip surgery  Side effects : Extrapyramidal symptoms, especially if >2 mg/d, Neuroleptic malignant syndrome  Evidence: In a randomized trial comparing haloperidol, chlorpromazine, and lorazepam in the treatment of agitated delirium in young patients with AIDS, haloperidol had fewer side effects or adverse sequelae . Haloperidol may prevent delirium following hip surgery 2. Olanzapine :  Advantages : Increased sedation  Side effects : Hyperglycemia, May have fewer extrapyramidal side effects 3. Risperidone: Benefits : Similar to haloperidol, Relatively nonsedating, Few hemodynamic effects May have fewer extrapyramidal symptoms 4. Lorazepam :  Benefits : Second line agent. However, first line in cases of Use in delirium due to alcohol withdrawal, patients with Parkinson's disease, patients with history of neuroleptic malignant syndrome  Disadvantages : More paradoxical excitation, respiratory depression than haldol
    • Ser otonin Syndr ome - Occurs in a setting of a serotinergic drug ( refer the list)  can occur at therapeutic doses, over dosage or as an inadvertant interaction between the drugs. -Be aware of differentiating NMS from Serotonin Syndrome as patients may be on both types of drugs at same time ( eg: pts with bipolar disorder may be may be on an antimanic drug/antipsychotic + SSRI) - Be aware that classic features such as muscular hypertonicity and hyperthermia occur only in life threatening cases. Recognize that it has a spectrum of clinical features. - Recognize that Clonus and Hyperreflexia are highly suggestive of serotonin syndrome in mild to moderate cases. - Remember that if there is severe muscle rigidity ( hypertonicity ), it can mask the diagnostic features of serotonin syndrome such as clonus and hyperreflexia
    • A Case That Shook Medicine How One Man's Rage Over His Daughter's Death Sped Reform of Doctor Training By Barron H. Lerner Special to The Washington Post Tuesday, November 28, 2006; Page HE01 Many people have vowed to avenge the untimely death of a relative. Lawyer and journalist Sidney Zion actually did so -- to the benefit of patients and doctors-in-training nationwide. “ Libby Zion (18) dies in 1984 of an interaction between Meperidine and Phenelzine”
    • Physical Exam  Physical examination should include a focused assessment of deep-tendon reflexes, clonus, and muscle rigidity, in addition to an evaluation of the size and reactivity of the pupils, the dryness of the oral mucosa, the intensity of bowel sounds, skin color, and the presence or absence of diaphoresis.
    • Spectrum of Clinical Features
    • Drugs and Drug Interactions Associated with the Serotonin Syndrome
    • Caution!  Remember  Administration of serotonergic agents within five weeks after the discontinuation of fluoxetine therapy has produced a drug interaction culminating in the serotonin syndrome, presumably the result of the demethylation of fluoxetine to norfluoxetine, a serotonergic metabolite with a longer serum half-life than its parent compound  Remember Serotonin is metabolized by MAO-A to 5HIAA  Specific drugs, such as MAOIs that are irreversible or nonselective or that inhibit monoamine oxidase subtype A, are strongly associated with severe cases of the syndrome, especially when these agents are used in combination with meperidine, dextromethorphan, SSRIs, or methylenedioxymethamphetamine (MDMA, or "ecstasy) eg: Interaction b/w Phenelzine ( MAO – A inhibitor) and Meperidine has lead to death of a patient
    • Findings in Patient with Moderately Severe SerotoniSyndrome   Hyperkinetic neuromuscular findings of tremor or clonus and hyperreflexia should lead the clinician to consider the diagnosis of the serotonin syndrome. Remember “MYDRIASIS” is the KEY. Where as in Neuroleptic Malignant Sydrome  you will usually see Normal sized pupils
    • Algorithm for Diagnosis  The neuromuscular features of clonus and hyperreflexia are highly diagnostic for the serotonin syndrome, and their occurrence in the setting of serotonergic drug use establishes the diagnosis. Clinicians should be aware that muscle rigidity can overwhelm other neuromuscular findings and mask the diagnosis
    • Lab Anomalies  Laboratory abnormalities that occur in severe cases include metabolic acidosis, rhabdomyolysis, elevated levels of serum aminotransferases and creatinine, seizures, renal failure, and disseminated intravascular coagulopathy.  Many of these abnormalities arise, however, as a consequence of poorly treated hyperthermia.
    • Management  Discontinue the precipitant drug.  Mild cases ( hyperreflexia and tremor but no fever)  supportive care ( IV Fluids, vitals), Benzodiazepenes ( to control agitation and provide sedation)  Moderate cases  address cardiorespiratory and thermal abnormalities, give 5HT2a Antagonists ( Cyproheptadine is first choice or Chlorpromozine as alternative)  Hyperthermic pts with temp > 41C  give above therapies + sedation + neuromuscular paralysis ( vecuronium) + orotracheal Intubation. Control of hyperthermia needs eliminating excessive muscle activity  hence induce neuromuscular paralysis with Vecuronium followed by orotracheal intubation and ventilation  There is no role for antipyretic agents in the management of the serotonin syndrome; the increase in body temperature is due to muscular activity, not an alteration in the hypothalamic temperature set point.  Dantrolene, a centrally acting muscle relaxant is not useful here  Bromocriptine which is used in NMS, has no role here  in fact, it may worsen serotinergic signs.
    • Differential Diagnosis  Anticholinergic Poisoning Patients with the anticholinergic syndrome have normal reflexes and show the "toxidrome" of mydriasis; agitated delirium; dry oral mucosa; hot, dry, erythematous skin; urinary retention; and an absence of bowel sounds. Hyperactive bowel sounds - along with neuromuscular abnormalities (clonus/hyperreflexia/rigidity), diaphoresis, and normal skin color — distinguish the serotonin syndrome from the anticholinergic toxidrome
    • Differential Diagnosis  Neuroleptic Malignant Syndrome  Neuroleptic malignant syndrome is an idiopathic ( idiosyncratic) reaction to dopamine antagonists, a condition that is defined by a slow onset, bradykinesia or akinesia, "lead pipe" muscular rigidity, hyperthermia, fluctuating consciousness, and autonomic instability (HYPER/HYPOTENSION).  Remember that Hyperthermia in response to neuroleptic administration is an idiopathic response; the normal outcome is hypothermia.  Signs and symptoms of the neuroleptic malignant syndrome typically evolve during several days, in contrast to the rapid onset and hyperkinesia of the serotonin syndrome. ( In NMS, you have rigidity but no Hyperkinesia. However, as discussed earlier in severe cases of serotonin syndrome, severe rigidity can mask these hyperkinetic neuromuscular findings ( clonus/ hypereflexia etc)  so, look at pupillary size as next step in differentiation. In Serotonin Syndrome, you have Mydriasis.  Knowledge of the precipitating drug also helps in distinguishing between syndromes: dopamine antagonists produce bradykinesia, whereas serotonin agonists produce hyperkinesia ( Clonus and Hyperreflexia)
    • Differential Diagnosis  Malignant Hyperthermia  Malignant hyperthermia is a pharmacogenetic disorder characterized by increasing concentrations of end-tidal carbon dioxide, hypertonicity (rigidity) , hyperthermia, and metabolic acidosis.  The disorder occurs within minutes after exposure to inhalational anesthetic agents. Also, seen with Succinylcholine.  On physical examination, the skin is often mottled, with cyanotic areas contrasting with patches of bright red flushing. The rigor mortis–like rigidity of skeletal muscles and “hyporeflexia” that are seen in malignant hyperthermia further distinguish this condition from the serotonin syndrome  Rx – Dantrolene, Supportive care
    • Dementia Check Neurology Slides
    • Depression
    • Depression - Prevention  Offer counseling to patients who have experienced stressful events, trauma, or losses.  Inquire about previous episodes of depression in patients currently without symptoms of depression, and stress the importance of early intervention.  Screen for symptoms of depression in women during the 4 to 6 weeks after giving birth, particularly in women with psychosocial stress during pregnancy and history of psychiatric disorder.  Consider antepartum counseling for women with risk factors for postpartum depression
    • DSM IV Criteria for Depression  A) 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 self-reported or observed by others.  2) 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; 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 nearly every day.  7) Feelings of worthlessness or excessive or inappropriate guilt nearly every day.  8) Diminished ability to think or concentrate nearly every day.  9) Recurrent thoughts of death, recurrent suicidal ideation without a specific plan.  B) The symptoms do not meet criteria for a mixed episode  C) The symptoms cause clinically significant distress or impairment in social, occupational, or other areas of functioning.  D) The symptoms are not due to the direct physiological effects of a substance (drug or medication) or a general medical condition (hypothyroidism).  E) The symptoms are not better accounted for by bereavement, i.e., after the loss of a loved one, the symptoms persist for longer than 2 months or are characterized by marked functional impairment, morbid preoccupation with worthlessness, suicidal ideation, psychotic symptoms, or psychomotor retardation.
    • D/D Medical Disorders  Recognize that there is an increased prevalence of depression in the following conditions:  Medical conditions:               Prescription drug effects:     Hypothyroidism Cushing's disease Dementia Parkinson's disease Stroke Multiple sclerosis Cancer Diabetes Coronary heart disease Fibromyalgia and other chronic pain states Chronic fatigue syndrome Vitamin B12 deficiency Infectious disease such as TB, viral hepatitis Glucocorticoids Interferon Reserpine and other centrally acting antihypertensives Substance abuse:    Anabolic steroids Ethyl alcohol Cocaine or amphetamine withdrawal
    • D/D MOOD DISORDERS : Differentiate major depression from other mood syndromes using DSM-IV criteria including:  Dysthymic disorder  Bipolar disorder  Minor depression  Situational adjustment reaction with depressed mood  Grief  Seasonal affective disorder
    • D/D  Dysthymia : Dysthymia is a chronic mood disorder characterized by depressed mood or anhedonia at least half the time for at least 2 years accompanied by two or more vegetative or psychological symptoms and functional impairment. Rx : Antidepressants  Situational adjustment reaction with depressed mood : Subsyndromal depression with clear precipitant. Usually resolves with resolution of acute stressor without medication . Supportive counselling and identification of stressor is required.  Seasonal Affective disorder : A subtype of major depression, occurring with seasonal change, typically fall or winter onset and seasonal remission, rarely onset is in the spring with remission in the fall or winter. It should have occurred in the two previous years, without nonseasonal depression. More common in northern latitudes  Responds to bright-light therapy and adjuvant therapy with SSRIs
    • D/D  Premenstrual Dysphoric disorder: Characterized by depressed mood, anxiety, and irritability during the week before menses, resolving with menses  May respond to SSRI treatment; intermittent treatment during part of the menstrual cycle may be effective  Grief Reaction : The syndrome of major depression may be transiently present in normal grief, however sadness without the complete syndrome is more common. Duration, intensity of symptoms, and associated change in function is variable and commonly affected by cultural and societal factors  Pervasive and generalized guilt and persistent vegetative signs and symptoms that are not consistent with the patient's or family's expectations for normal grief should arouse concern  Bereavement is often a precipitant of true mood disorder, and patients in this state should be carefully assessed and followed.  do supportive counseling . Remember Loss of self-esteem and Anhedonia is a symptom of depression rather than grief  Dementia : Characterized by impaired memory, judgement and other higher cortical functions  see DEMENTIA Slides   Anxiety disorder Psychotic disorders ( thought disorders) : Major depression may be accompanied by mood congruent hallucinations/ delusions ( where as mood incongruent delusions/ hallucinations may suggest a primary psychotic disorder. )
    • Depression – Indications for hospitalization Hospitalize patients:  With significant suicidal ideation or intent who do not have adequate safeguards in their family environment  With intent to hurt others  To assess their ability to care for themselves and adhere to their treatment in light of the supports available in their home environment  Who are in need of detoxification or substance abuse treatment  Who are candidates for ECT  With comorbid dysfunctional family systems that exacerbate their depressive disorder or interfere with treatment
    • Depression – Drug therapy A. Treat first episodes of depression to achieve complete remission, and continue treatment for 4 to 9 months thereafter.   Aim for complete remission of symptoms and return to normal functioning.  If remission is not achieved with the initial antidepressant, switch to another agent or consider adding or switching to cognitive therapy.  In first episodes, continue treatment with antidepressant medication at the same dosage required to achieve remission for an additional 4 to 9 months.  Consider long-term maintenance therapy in patients over age 70 and in those with diabetes mellitus. B. Treat recurrences of major depression with long-term maintenance therapy
    • Depression – Drug therapy     Treat patients who are suffering a first recurrence of major depression for longer than the initial episode. For first recurrence, consider maintenance treatment for one to two times the interepisode interval, e.g., if the second episode occurs 18 months after the first episode, the treatment should be 18 to 36 months. For older patients (>70 years) with major depression who respond to an SSRI, consider treating for 2 years to prevent recurrence. Consider lifetime maintenance therapy for patients with three or more recurrences or patients with a first recurrence and risk factors for further recurrences including: 1.Family history of bipolar disorder 2. Recurrence within 1 year of successful treatment of previous episode 3.Young age of onset (adolescent) 4.Severe (debilitating or suicidal attempt) and sudden onset of symptoms
    • Depression – Drug Therapy  Counsel patients to improve medication adherence, emphasizing:  The importance of taking the medication daily  That symptomatic improvement may be noticed within 1 week but often takes 2 to 4 weeks  That they must continue to take medicine even if feeling better  That they must not stop taking the antidepressant without checking with their physician  Potential side effects  Offer St. John's wort as a potential treatment for patients with mild to moderate depression or subsyndromal depression
    • Anti-Depressant Drugs A. SSRI : Fluoxetine, Duloxetine, Paroxetine, Citalopram, Fluvoxamine  Side effects : Nausea and diarrhea, anxiety, nervousness, somnolence, impaired sexual function  All SSRIs are contraindicated with MAOIs in view of possible SEROTONIN SYNDROME B. SNRI : Venlafaxine (Effexor), Mirtazepine Side effects : Gastrointestinal complaints (nausea, dry mouth, anorexia, constipation, and flatulence), CNS complaints (dizziness, somnolence, insomnia, nervousness, abnormal dreams, and tremor), sweating, abnormalities of sexual function (abnormal ejaculation and impotence in men, anorgasmia in women, and decreased libido), problems of special senses (abnormal vision), cardiovascular effects (hypertension and vasodilatation), and yawning C. Bupropion : Dopamine reuptake inhibitor, Advantage : very less weight gain. Adverse effects : lowers seizure threshold, Anorexia, dry mouth, rash, sweating, tinnitus, tremor, abdominal pain, agitation, anxiety, dizziness, insomnia, myalgia, nausea, palpitation, pharyngitis, and urinary frequency D. TCAs : Amitryptiline, Nortryptiline, Amoxapine, Imipramine, Clomipramine, Side Effects : mainly anticholinergic  Dry mouth, dizziness, constipation, nausea. Sedation, Anticholinergic hypotension, Orthostatic hypotension , Prolongs QT interval and can lead to Torsades depointes For pts with Torsades due to Tricyclic overdose , Admit to ICU and treat with bicarbonate. If Torsades give magnesium and lidocaine. D/C all QT prolonging drugs. E. Weight gain is a significant side effect, except with Bupropion F. Mirtazipine can cause Agranulocytosis – monitor blood counts, report to ER if sorethroat, fever, chills etc appears
    • ST.Johns Wort  Definitive method of action unclear. Animal studies suggest St. John's wort may work by inhibition of serotonin uptake. Hypericum extract also has been shown to decrease cell surface 5-HT receptors  Attractive to patients with moderate depression who are unwilling or unable to take conventional treatment. Adverse effects are generally mild  GI symptoms, dizziness or confusion, sedation, dry mouth, photosensitivity  St. John's wort activates cytochrome P450 and may reduce the concentration of medications such as digoxin, theophylline, simvastatin, and warfarin.  St. John's wort interferes with antiretroviral therapy by activating 3A4 isoform of cytochrome P450. This effect may result in decreased concentrations of protease inhibitors and nonnucleoside reverse transcriptase inhibitors. St. John's wort should not be used in conjunction with SSRIs, especially in the elderly, as it may cause symptoms of serotonin excess (hyperthermia, tachycardia, diaphoresis, rigidity)
    • Depression – Non drug therapy  Consider psychotherapeutic options including:    Cognitive therapy Interpersonal therapy Problem-solving therapy  Offer patients with mild to moderate depression psychotherapeutic options or drug therapy. Offer patients with severe depression combination therapy with psychotherapy and antidepressants  Consider combined drug therapy and psychotherapy in patients with mild to moderate depression, but recognize that there is limited available evidence showing added benefit.  Treat patients with dysthymia with antidepressant medication, but note that psychotherapy may play a role in treating residual symptoms.  Treat patients with a history of major depression with current subsyndromal depression using drug therapy to achieve complete remission and offer psychotherapy to treat residual symptoms.
    • Pregnancy & Mood disorders  Understand peri-partum mood disorders  Differentiate post partum blues from post partum depression  Managing post partum blues and post partum psychosis  Which drugs are safe in treating mania in pregnancy?
    • Mania - Pregnancy  Lithium is teratogenic (Ebstein anomaly )  Valproic acid causes neural tube defects. First trimester: Haloperidol for psychosis, clonazepam for agitation; if mood stabilizer is necessary, lithium may be first choice ( category D drug, but risk may be acceptable given the problem of mania. ECT is an alternative ( but it as a monotherpay may not be sufficient for mood stabilization – ECT is safe in pregnancy, only issue might be fetal arrhythmias). Second/Third trimester/Postpartum: Lithium or anticonvulsants, haloperidol and/or clonazepam if truly needed. Continue treatment postpartum if no obstetric complications. Follow breast-fed infants closely
    • Eating Disor der s
    • Screen these pts Ask direct questions to screen for abnormal eating practices (calorie restriction, binging, purging etc) in these groups:  Adolescents participating in gymnastics, dance, wrestling, swimming, and other athletic programs  Adolescents with chronic diseases  Adolescents with a history of obsessivecompulsive personality traits or childhood anxiety disorders  Persons with a family history of eating disorders
    • Diagnosis Symptoms: 1. Ask about diagnostic criteria:  Eating and exercise patterns  Weight and patterns of weight loss  Attitudes about weight, body image, fear of weight gain  Amenorrhea or delayed menarche in females  Use of diuretics, laxatives, or purging behaviors 2. Ask about medical complications:  Abdominal pain  Bloating  Constipation  Cold intolerance  Dizziness, fatigue, and vague complaints  Loss of libido in both sexes  Changes in menstrual regularity, intensity, or duration in females
    • Diagnosis – Look on physical  Eroded tooth enamel from repeated forced vomiting  Hair and skin changes such as yellow skin and lanugo  Pitting edema or poor skin turgor  Brittle nails  Dry scaly skin  Parotid gland swelling  Russell's sign or abrasions on the dorsum of the hand  Muscle weakness and muscle wasting  Discomfort or avoidance of being weighed  Weight loss recent > 10%
    • Anorexia Nervosa Diagnose anorexia nervosa when all the following are present:     Intense fear of gaining weight Undue emphasis on body shape Body weight <85% of predicted Amenorrhea for 3 consecutive months
    • Bulimia Nervosa Diagnose bulimia nervosa when all the following are present:  Recurrent episodes of binge eating characterized by eating a larger amount of food than most people would eat in a discrete period and a sense of having no control over eating during the episode  Recurrent, inappropriate, compulsive behavior to prevent weight gain, such as self-induced vomiting; abuse of laxatives, diuretics, or other drugs; or excessive exercise   Binging and purging at least twice per week for 3 months  Self-evaluation unduly influenced by body shape and weight
    • Complications – Eating Disorders  Cardiac arrhythmias  Congestive Heart Failure  Electrolyte disturbances  Amenorrhea  Osteoporosis  Stress fractures  Endocrinopathies
    • Labs 1. Obtain the following lab values in all patients:  CBC, Electrolytes, BUN , Creatinine, Glucose, TSH 2. Obtain the following lab values in malnourished and symptomatic patients:  Calcium, Magnesium, Phosphorus, Albumin Liver function, ECG 3. Obtain FSH, LH, prolactin levels, and bone densitometry if amenorrhea is present.
    • Differential Diagnosis  Consider other medical causes of weight loss, progressive weight loss, and amenorrhea, such as:  Chronic infections  Intestinal disorders with malabsorption  Endocrinopathies  Malignancy  Other psychiatric illnesses  Consider differential diagnosis early in treatment, because patients may be in denial or may withhold information concerning their fear of fat.
    • Diagnosis  Some step3 questions might give you a pt with eating disorder and may ask you to figure out the next step by giving you clues through acidbase, electrolyte imbalances Hypokalemia, hypochloremic Alkalosis seen with Vomiting Hypokalemia, Non anion gap Acidosis seen with Laxative abuse  Stool Laxative screen Hypokalemia, Metabolic Alkalosis seen with Diuretic abuse  Urine Diuretic screen
    • Treatment – Eating Disorders Hospitalize patient for:  Severe malnutrition and associated complications:  Weight <75% of individually estimated healthy body  Metabolic abnormalities:  Potassium <3 mEq/L  Marked orthostatic hypotension, with one of the following:        An increase in pulse of >20 bpm Blood pressure <90/60 mm Hg A decrease in blood pressure of >20 mm Hg after standing Bradycardia (heart rate <40 bpm) and other cardiac arrhythmias Inability to sustain core body temperature (<97°F [36.1°C]) Signs of inadequate cerebral perfusion Signs of dehydration or hepatic, renal, or cardiovascular organ compromise requiring acute treatment  Comorbid psychiatric problems that heighten suicidal risk such as exacerbation of a mood disorder or severe alcohol abuse
    • Anorexia - Refeeding Undertake refeeding of hospitalized patients with anorexia nervosa with care:  Set a realistic weight gain target of 2 to 3 lbs per week  Start intake levels at 30 to 40 kcal/kg per day (approximately 1000 to 1600 kcal per day) and progressively increase to as high as 70 to 100 kcal/kg per day  Monitor serum potassium levels regularly in patients who are persistent vomiters, and treat hypokalemia with oral or intravenous potassium  When life-preserving nutrition must be provided to a patient who refuses to eat, choose nasogastric over intravenous feedings  Monitor patients for refeeding syndrome, especially those being aggressively refed orally, enterally, or parenterally  At the initiation of treatment, monitor vital signs, food and fluid intake, and output, and look for edema, rapid weight gain, signs of congestive heart failure, and gastrointestinal symptoms  Monitor serum phosphorus, magnesium, potassium, and calcium daily for 5 days after initiating refeeding and every other day for several weeks thereafter  Obtain ECGs as indicated  Provide phosphorus, magnesium, and/or potassium supplementation when indicated
    • Non-Drug therapy  Recommend psychotherapy for all patients with anorexia nervosa.  Consider cognitive behavioral therapy for patients with bulimia nervosa. Consider medication (either fluoxetine or imipramine) in conjunction with Cognitive Behavior therapy.  Recommend nutritional rehabilitation to all patients with anorexia nervosa and bulimia nervosa.
    • Drug Therapy Consider the following therapy options:  Fluoxetine, 60 mg/d (one of the FDA-approved indications for fluoxetine), or sertraline, 100 mg/d (not FDA approved), to reduce the frequency of binge eating and purging (bulemia). However, Psychotropic drugs have a minimal role in Anorexia  Ondansetron, a 5-HT3 antagonist, to decrease binge eating and purging  Topiramate, a broad-spectrum anti-epileptic drug, to decrease binge eating and purging  Light therapy in patients with bulimia nervosa with seasonal exacerbation of symptoms  Note that bupropion is contraindicated in the treatment of eating disorders due to an elevated incidence of grand mal seizures.  Start estrogen and progesterone replacement with combined oral contraceptives in patients with anorexia who have been amenorrheic for more than 3 months to preserve bone mass
    • Exercise Induced Amenorrhea  Female Athlete Triad : Disordered eating , osteoporosis and amenorrhea that occurs in women engaged in regular strenuous exercise or sports activities  Weight loss in athletes  low body fat  low Leptin levels  disruption of GnRh pulsatility Reduced LH, FSH  Anovulation and Reduced estrogen  Amenorrhea. Low body fat means reduced peripheral (adipocyte) aromatization of androgen precursors to estrogen, further lowering total estrogen levels.  High Risk of Osteoporosis and Stress fractures ( get an x-ray if you suspect stress fracture)
    • Exercise Induced Amenorrhea Management  Get Dexa scan  Rule out other differentials  prolactinomas, hypothyroidism, PCOS  Decreasing intensity of training and improving nutritional status are crucial steps in reversing the pattern of menstrual irregularity.  Since oligomenorrhea is correlated with low bone density, calcium supplementation and adequate vitamin D intake are essential for bone health.  Start Estrogen replacement in the form of Low dose oral contraceptives.( for cycle regulation and to improve bone density)
    • Schizophrenia
    • Diagnosis - Schizophrenia 1. The presence of at least two of the following for most of time for at least 1 month:  Delusions  Hallucinations  Disorganized speech such as frequent derailment or incoherence  Grossly disorganized or catatonic behavior  Negative symptoms such as affective flattening, alogia, or avolition 2. Look for family history 3. There should be continuous signs of disturbance for at least 6 months. 4. R/o Organic brain disease, metabolic disorders, drug abuse, infectious diseases ( HIV, Sepsis, syphilis, brain abscess, septic emboli) and malignancies
    • Schizo-affective disorder At least two of the DSM IV criteria in the previous slide for at least 1 month + features of one of the following mood disorders A. Depression B. Mania 
    • Depression and Mania 1. Depression (at of Criterialeast fivetwo the following for a 2-week period, including at least one of the first items):          Depressed mood most of the day Markedly diminished interest or pleasure in almost all activities Significant weight change Insomnia or hypersomnia Psychomotor agitation or retardation Fatigue or loss of energy Feelings of worthlessness or excessive inappropriate guilt Diminished ability to think or concentrate Recurrent thoughts of death or suicide 2. Mania (four or more of the following at the same time, lasting at least 1 week or if hospitalization is needed; first item is required):        Elevated, expansive, or irritable mood lasting at least 1 week Inflated self-esteem or grandiosity Decreased need for sleep More talkative than usual or pressure to keep talking Flight of ideas or subjective experience that thoughts are racing Distractibility Increase in goal-directed activity, excessive involvement in pleasurable activities that have a high potential for painful consequences
    • Schizophrenia Management      Hospitalize patients whose behavior may cause harm to themselves or others Obtain psych consult Form an alliance with the patient's families in caring for the pt as it is an essential part of management. Cognitive therapy Psychoeducational family interventions
    • Schizophrenia - Drugs A. Second-generation agents (First- Line therapy)      Olanzapine Risperidone Clozapine Ziprasidone Quetiapine 6. Aripiprazole B. First-generation Agents      Trifluperazine Thiothixine Haloperidol Fluphenazine Chlorpromozine C. Mood-stabilizers : Carbamazepine, Lamotrigine, lithium, Divalproex sodium – use as adjuncts in schizoaffective disorder D. Anti-Depressants : use as adjunct in schizoaffective disorder E. ANXIOLYTICS: BZDs ( Alprozolam, lorazepam, clonazepam, diazepam, oxazepam), Buspirone.  All BZDs cause tolerance and may need up-titration of dose. Buspirone does
    • Drugs effect          - Benefits- Side Comparision All second generation agents have less extrapyramidal side effects ( Akathisia, Acute dystonia, tardive dyskinesia, parkinsonism). First generation agents are pure D2 antagonists where as second generatio are both D2 and serotinergic antagonists. Anticholinergic side effects ( drymouth, sedation, constipation) can occur with most schizophrenia drugs. Recognize presentation of anti-cholinergic delirium in geriatric pts using these drugs. Most agents – CPZ, Second generation agents – can cause orthostatic hypotension. More of a problem with CPZ due to its Alpha1 antagonizing properties. Recognize Hyperprolactinemia can occur with most of these drugs because they are dopamine (D2) antagonists. Less risk of hyperprolactinemia and sexual dysfunction with Queitapine and Aripiprazole. Weight-gain is a problem. Only drugs that do not cause much weight gain are Ziprasidone and Aripiprazole. Olanzapine, Queitapine and Risperidone cause significant weight gain Neuroleptic Malignant syndrome is more likely with first generation agents, however, can be possible with second generation agents. Photosensitivity is a unique side effect of CPZ.
    • Drugs effect - Benefits- Side Comparision  Weight gain that’s a common side effect of these drugs – lead to insulin resistance and dyslipidemia. Get lipid panel and FBS  Clozapine has a dreadful side effect – Agranulocytosis – hence monitor blood count. D/C the drug if signs of infection appears and then get a blood count stat.  Clozapine also has high risk of seizures. Haloperidol reduces seizure threshold.  Haloperidol, Ziprasidone can prolong QT interval. Caution : concomitant use with quinolones, anti-arrythmics, Tricyclics etc that also prolong QT – can lead to Torsades/ Vfib  Risperidone is usually first choice to treat Schizophrenia because it is least sedating. Use olanzapine if insomnia is an issue ( Anticholinergic – sedative effect). If positive symptoms are very predominant, use Haloperidol.
    • Schizophrenia Management  In Symptomatic schizophrenia, start antipsychotic      treatment ASAP. For Typical symptoms of schizophrenia or schizoaffective disorder, consider the newer, secondgeneration antipsychotics as first-line agents. Start lowest possible doses to minimize side effects. Improvements can be slow and may take 4 to 6 weeks to achieve a medication-steady blood state  SO, avoid increasing the dosage before an adequate period Continue antipsychotic medication for at least 1 year after a full remission of psychotic symptoms. After this a trial off medication may be considered except in suicidal or violent patients In chronic, relapsing illness, use antipsychotic medications for a minimum of 5 symptom-free years.
    • Schizophrenia management  In stable pts, reduce dose reduction to the lowest possible dose that controls symptoms  When tapering medications, reduce the dose very slowly (10% to 20% per month) and observe the patient every 2 weeks. Return to the previously effective dose if there is an exacerbation of symptoms.  Use clozapine in treatment-refractory patients ( and for those with predominant negative symptoms) in whom adequate trials of at least two agents from dissimilar chemical groups have failed and when adherence is not an issue. ( Caution: Agranulocytosis)  Use lowest possible doses in the elderly.  Use long-acting injectable (risperidone) or depot (haloperidol or fluphenazine) medication in patients nonadherent to oral therapy or those who are forgetful about using Rx.
    • Schizophrenia management      Be sure to monitor weight monthly and test for blood glucose and lipid abnormalities at least every 12 weeks in patients on second-generation agents. Recognize that side effects of some second-generation antipsychotics may lead to health problems such as obesity and diabetes Consider prophylactic use of anti-Parkinson agents such as benztropine to reduce extrapyramidal side effects on a case-by-case basis when using antipsychotic agents. Consider clozapine in people who are judged to be at risk for suicidal behavior In patients with concurrent mood symptoms use adjuncts to Antipsychotic therapy – 1. For Depression use SSRIs 2. For Mania – use mood stabilizers 3. For anxiety, use anxiolyitics
    • Addressing Extrapyramidal Side effects  Akathisia : An acute side effect. Can also be Tardive. Acute means onset within 6 weeks of initiation of the drug. Tardive akathisia is the one that appears after a minimum of 3 months’ exposure to an antipsychotic agent. Akathisia can also appear as a withdrawal from antipsychotics.  Common with first-generation antipsychotics (neuroleptics)  Defined as subjective (feeling of inner restlessness and the urge to move) as well as objective components (rocking while standing or sitting, lifting feet as if marching on the spot and crossing and uncrossing the legs while sitting)  Treatment is Beta blockers. If b-blocker fails, consider BZDs. If everything failed, use clonidine/ amantidine.
    • Addressing Extrapyramidal Side  effects Akathisia and Restless Legs Syndrome Distinguishing Position Myoclonic jerks Akathisia Sub-diaphragmatic Restless Legs Syndrome Usually from ankle to knee Rare Very common: especially at night Subjective distress Almost invariable Common and is due to disturbed sleep Relieved by movement Rarely Almost always Motor component Almost always Rarely Sensory component Usually present Always present; dysesthesia Worsening on lying Rare Very common Sleep disturbance Rare Almost always present Movements if able to sleep Stop Continue almost unabated Help from behavioral tricks e.g. walking, stretching, massage, cold compresses Rare Almost always
    • Addressing Extrapyramidal Side effects  Acute Dystonia : Dystonia is a brief or sustained muscle spasm, often with Acute Dystonia : Dystonia is a brief or sustained muscle spasm, often with     slow abnormal movements. Although any muscle group may be involved, it most commonly affects facial muscles (eyes, jaw, tongue). In differentiating from Tardive dyskinesia  consider the onset. Onset here is acute ( within 24 hrs after administering the agent) Acute dystonia – causes 1. Toxic causes : Metoclopromide, Antipsychotics (Haloperidol, phenothiazines), Lithium, chloroquine, levodopa, cocaine 2. Non toxic : Spinocerebellar degeneration, Thyrotoxicosis, Wilsons disease, Tumor, A-V malformation, CVA Differential : Catatonic states, Dyskinesias, Seizures Treatment : Dystonias may increase in severity after initial presentation and therefore all patients should be treated. Initial treatment is usually provided with a parenteral formulation, followed by oral medication for 2 to 3 days to prevent recurrence. Milder forms can be treated with oral medication alone. Choices: ( physiology involves cholinergic excess. So use, anticholinergic Rx) 1. Benztropine : 1mg IM/IV followed by 1mg orally daily 2. Diphenhydram 1MG/KG IM/IV followed by oral 3. Diazepam 4. Trihehiphenydyl.
    • Types of Acute Dystonia Various types of dystonia, involving particular muscle groups have been described:  Laryngeal dystonia - spasm of pharyngeal and laryngeal muscles resulting in stridor.  Oculogyric crisis - spasm of extra-ocular muscles, forcing the eyes into upward or lateral gaze.  Opisthotonus - spasm of all paravertebral muscles, forcing the trunk and neck into hyperextension.  Retrocollis - spasm of paravertebral neck muscles, forcing the neck into hyperextension.  Torticollis - spasm of lateral neck muscles, twisting the neck to one side.
    • Addressing Extrapyramidal Side effects TARDIVE DYSKINESIA  Occurs with long term use of antipsychotics/ Dopamine antagonists  Risk factors for developing TD: treatment with first generation antipsychotics, More than 6 months of antipsychotic treatment, Increased length of medication therapy, Antipsychotic dose change—either increase or decrease, Diagnosis of organic mental disorder or mood disorder, Increasing age, Diabetes and Genetics  Eventhough more common with First generation (typical) antipsychotics it also copmmonly occurs with second generation drugs.  Symptoms : Involuntary movements, which develop with after long term antipsychotic exposure, are present for at least 4 weeks and may be:  Choreiform movements (rapid, jerky, nonrepetitive, purposeless)  Athetoid movements (slow, sinuous, continual)  Rhythmic movements (stereotypes)  Peri-Oral movements most common : Darting, twisting, protruding movements of the tongue (lip-licking, sucking, smacking, “fly-catching tongue), Chewing and lateral jaw movements, Lip puckering and Puffing cheeks  Other movements : Trorticollis, retrocollis, Trunk twisting, rocking, hand clenching, facial grimacing, blinking etc  There is no specific treatment once TD appears. Delaying its appearance and prevention are the only options : using atypical antipsychotics, using lowest possible dose are some strategies.
    • Addressing Extrapyramidal Side effects  Managing Tardive Dyskinesia:
    • Note :  Clozapine’s greater efficacy as an antipsychotic drug may be related to its higher affinity for the D4 than the D2 receptor. No typical neuroleptic has a similar D4/D2 ratio. This different mechanism of action may also account for its beneficial effect in treating TD  Clozapine is the drug of choice in refractory schizophrenia  ( i.e.; after no response to two different antipsychotic agents)
    • PTSD
    • PTSD  After a traumatic event normal individuals may experience symptoms for a short period such as: Nightmares, Flashbacks, Anxiety attacks , Startle reactions , Insomnia, Irritability, Anger, Depressed mood, Guilt & Poor appetite. If they last more than 1 month  PTSD.  Recurrent symptoms of Flashbacks and Hyper vigilance are characteristic to PTSD ( No flashbacks with Adjustment disorder)  Time course : < 1 mo: acute stress disorder , > 1 month  PTSD  Spontaneous recovery from acute stress disorder is common (>50%), but a high level of symptoms during the first month is a risk factor for PTSD
    • PTSD - Management  Non – Pharmacological Therapy  Cognitive-behavioral therapy, exposure therapy, and trauma-related anxiety management. Group therapy also useful  Drug Rx :  SSRIs  Start with low dose and titrate up to maximum effect.  Switch to different agents or add adjuncts if response to SSRI is inadequate.  Trazadone and sedating TCAs may be used as adjuncts to SSRIs, particularly for insomnia  In difficult cases, consider Phenelzine.
    • END
    • Anxiety Disorders  Generalized Anxiety Disorder  Panic Disorder
    • Per sonality disor der s
    •  Borderline personality Disorder  Obsessive compulsive personality Disorder
    • Borderline Personality Disorder
    • Obsessive – compulsive disorder
    • Panic Disorder
    • Generalized Anxiety Disorder
    • Bipolar disor der