‚úÖ ūü߆ Psychiatry Flashcards Preview

ūü߆ Psychiatry > ‚úÖ ūü߆ Psychiatry > Flashcards

Flashcards in ‚úÖ ūü߆ Psychiatry Deck (109)
Loading flashcards...

Mental Status

Mental Status ‚Äď Are there any cognitive or behavioral modifications you intend to use to cope? ¬†What kinds of things are important to you? Plans? Are there any important relationships you have? ‚ÄúNot discussed‚ÄĚ ‚ÄúTypical‚ÄĚ


General Chunk

1. ¬†¬†General : ūü§Ķ General appearance, grooming ("moderately"),dress ("casually"), ūüĎĀ‚Äćūü󮬆eye contact (good, fair, poor).

2.   Behavior:  Level of cooperation (e.g. "cooperative", superficially [hard time], uncooperative, hostile).

3.   Motor: Movements (Increased/decreased), agitation (increased movement), "frequent fidgeting"), Psycho Motor Agitation (PMA) / Retardation ("slowed").


4. ¬†¬†Mood: Internal subjective experience "how are you feeling?" (i.e. How patient feels; typically in quotes) ‚Äútell me what that means to you‚ÄĚ ‚Äúdepressed, anxious‚ÄĚ


5. ¬†¬†Affect: Interviewer‚Äôs experience of patient (how they express (intonation, body language, facial expression) ūüėĶ‚Äúeuphoric‚ÄĚ, ūü•į‚Äúbright‚ÄĚ, ūüėä ‚ÄĚfull range‚ÄĚ, ‚Äúrestricted range‚ÄĚ [lower baseline / fluxuation], ūüôā‚Äúblunted" (range) [ > ], ūüėź‚Äúflat" (range) [ < variation], ‚Äúlabile‚ÄĚ, ‚Äúexplosive (get punchy), ‚Äúexpansive‚ÄĚ,¬†‚ÄúMood incongruent‚ÄĚ, "irritable",¬†Ambivalence? [depressed, low, euthymic]¬†


6.¬†Thought Process: [How] Rate, organization, ‚Äúdisorganized‚ÄĚ, ‚Äúgoal orientated‚ÄĚ, "concrete", abstract, "perseveration" (loop),¬†

7.¬† Thought Content: [What] Obsessions (there or not), Delusions (e.g. paranoia, grandeur), hallucinations, Suicidal / homicidal Ideation (all-or-none), ‚ÄúIdeas of reference‚ÄĚ (news just for you (messages)

8. ¬†¬†Associations: ¬†How thoughts are linked together (e.g. linear, intact, logical, ūüėĶ "loose"¬†= "psychotic" (doesn‚Äôt make sense), "circumstantial"¬†(extra circumstances) [get back], tangential (associations) = ‚Äúmanic‚ÄĚ [rapid] ; ‚Äúflight of ideas‚ÄĚ,

Specifics under thought process

Loop (perseveration, rumination) -> thought process

9. ¬†¬†Speech: [Mechanics] ‚ÄúRate, rhythm, volume, and ¬†tone‚ÄĚ, articulation, spontaneity, interruptible vs "pressured" (cannot interrupt, talks over). "echolia"

10. Language: [Symbolic] symbolic understanding and use of words / vocabulary (expressive, receptive; "typical for age"); neologism (new words), word approximation,¬†‚ÄúIntact‚ÄĚ


11. Cognition: proverbs, serial 7s, etc (‚Äúabstract vs. concrete‚ÄĚ), Attention

12. Fund of Knowledge: Expected knowledge compared to peer group (e.g. average for age),¬†‚ÄúAware of current events‚ÄĚ,¬†

13. Memory: Recent, remote, working memory,¬†‚ÄúGrossly intact‚ÄĚ

14. Orientation: Person, place, time and situation ("Oriented X 4"), "fully oriented"

15. Concentration: Ability to stay on task,¬†"Intact", ‚ÄúEasily distracted‚ÄĚ


16. Insight: Understanding of current state (e.g. intact, good, fair, poor, absent)

17. Judgment: Ability to make decisions (good, fair, poor, impaired, very impaired)


Suicidal Ideation

Evaluate ideation

  • ūüƆ Wish to die, ūüėī not wake up (passive)
  • Thoughts of ūüĒ™ killing self (active)
  • ‚Ź≤ Frequency, duration, ūüďä intensity, ūüéģ controllability

Evaluate intent 

  • Strength of intent to attempt suicide; ability to control impulsivity
  • Determine how close patient has come to acting on a plan (rehearsal, aborted attempts).

Evaluate plan

  • Specific details:¬† Method, time, place, access to means (eg, weapons, pills), preparations (eg, gathering pills, changing will)
  • Lethality of method
  • Likelihood of rescue

Active suicidality is associated with intent AND plan for self-harm. 


  • Sex (Male)
  • Age (elderly)
  • Depression
  • ūüí™ūüŹĺ Previous suicide attempt, Self-injorious behaviors (SIB)¬†Psychiatric disorder
  • EtOH (Substance abuse, impulsivity)
  • Rational thought loss (psychosis)
  • Social Support lacking
  • Organized Plan
  • No spouse or SO, Non-suicidal self injury
  • Sickness or Injury

Anxiety, hopelessness, and disturbed sleep patterns, and ūüĎ®‚ÄćūüĎ©‚Äćūü϶‚Äćūü϶¬†¬†family history / discord, access to firearms,¬†are additional clinical risk factors.

Protective factors:

  • Social support/family connectedness
  • Pregnancy
  • Parenthood
  • Religion & participation in religious activities

ūüĒę Homicide risk factors

  • Young male (15-24)
  • Unemployed
  • Impoverished (low socieoeceonomic)
  • ūüí™ūüŹĺ Access to firearms
  • Substance abuse
  • Antisocial personality disorder
  • History of violence or criminality
  • History of childhood abuse
  • Impulsivity
  • overt stressor


High imminent risk (Ideation, intent, and plan)

  • Ensure safety: Hospitalize immediately
  • Remove personal belongings and objects that may present self harm risk¬†
  • Constant observation and security may be required

High non-imminent risk (Ideation, intent, but no plan)

  • Ensure close f/u
  • Treat modificable risk factors (underlying depression, psychosis, substance abuse, pain)
  • Recruit family or friends for support
  • Reduce access to potential means
  • Safety plan (concrete, behavioral modifications, coping strageties)
  • Normalization


ūüĎ®ūüŹĺ‚Äć‚öēÔłŹ Psychotherapy

Brief individual insight-oriented psychotherapy is characterized by a limited, predetermined number of sessions and the fact that the focus of the treatment remains on specific problematic areas in the life of the patient.

Psychoanalytic psychotherapy (months)

Interpretations are the cornerstone and are explanatory statements made by the analyst that link a symptom, a behavior, or a feeling to its unconscious meaning. Ideally, interpretations help the patient become more aware of unconscious material that has come close to the surface. Confrontation and clarification are also used in psychoanalytic psychotherapy.  In confrontation, the analyst points out to the patient something that the patient is trying to avoid.  Clarification refers to putting together the information the patient has provided so far and reflecting it back to him or her
in a more organized and succinct form.

Psychodynamic psychotherapy (years) traces problems back to their origins in childhood, daily life, replicative and unconscious conflict, may provide the patient with insight; emphasizes the role of unconscious mental processes in producing symptoms with the goal of developing insight.

  • Higher functioning
  • Personality disorders
  • Builds insight into unconscious conflicts & past relationships
  • Uses transference
  • Breaks down maladaptive defenses
  • Strongly motivated patient who can tolerate a great deal of frustration and
    has a good capacity for insight.

  Psychodynamic group therapy

Cognitive-behavioral therapy (CBT) is an evidence-based, standardized modality of psychotherapy that targets persistent maladaptive thought patterns and behaviors.  

  • Depression
  • Generalized anxiety disorder
  • PTSD
  • Panic disorder
  • OCD
  • Eating disorders
  • Negative thought patterns
  • Combines cognitive & behavioral therapy
  • Challenges maladaptive cognitions
  • Targets avoidance with behavioral techniques (relaxation, exposure, behavior modification)
  • Used as monotherapy or in combination with medication.
  • Combines cognitive approaches and social skills training.

Treatment is generally time limited (approximately 5-20 sessions) and structured, and involves homework.  Therapists work with patients to identify and change cognitive distortions, such as overgeneralization (eg, believes nothing ever works out) and catastrophizing (eg, assumes the worst outcome).  Behavioral techniques such as graded exposure target the avoidance behaviors that stem from these distortions.

Cognitive-behavioral therapy based on exposure and response prevention (ERP) and/or ERP therapy involves repeated exposure to thoughts, images, and situations that provoke obsessional fears followed by prevention of the accompanying compulsion. 

Supportive psychotherapy is a broadly applicable approach that helps to reduce stress, improve coping skills, and maintain hope.  Duration evidence lacking? 

  • No interpretations; concrete suggestions
  • Used to reinforce a patient's ability to cope with stressors and is commonly used for low-functioning patients or those in crisis who are at risk of decompensation.¬†
  • Lower functioning; psychotic disorders
  • Patients in crisis
  • Maintains hope; provides encouragement
  • Reinforces coping skills, adaptive defenses
  • Normalization,¬†Validation, problem solving, psychoeducation.
  • Behavioral Chain Analysis (RCA)

Dialectical behavioral therapy was developed for borderline personality disorder that integrates standard cognitive-behavioral therapy techniques with principles of mindfulness, distress tolerance, and emotion regulation.  

  • Borderline personality disorder
  • Improves emotion regulation, distress tolerance, mindfulness
  • Decreases self harm; builds skills

Interpersonal psychotherapy is an evidence-based therapy primarily used for depression that focuses on the interplay between depressive symptoms and interpersonal stressors.  

  • Depression
  • Links symptoms to current relationship conflicts & interpersonal skill deficits

Motivational interviewing is commonly used to treat substance abuse and involves the therapist assuming a nonjudgmental stance, acknowledging ambivalence, focusing on the patient's motivation for change, and tolerating resistance to change.

  • Substance use disorders
  • Nonjudgmental; acknowledges ambivalence & resistance
  • Enhances intrinsic motivation to change

Behavioral therapy focuses on decreasing or ameliorating people’s maladaptive behavior without theorizing about their inner conflicts. Behaviorists look for observable factors that have been learned or conditioned and can therefore be unlearned.

Biofeedback involves using signals from the body (ie, heart rate, muscle tension, skin temperature, blood pressure) as indicators of emotional distress.  Patients are taught to identify and control their responses to various stimuli.

  • Prominent physical symptoms; pain disorders

  • Improves control over physiological reactions to emotional stressors

Eye movement desensitization and reprocessing (EMDR) Based on the concentration necessary to watch the therapist’s laterally moving finger helps create a state of deep relaxation, during which traumatic events can be worked through.

Eclectic/Integrated therapy

  • History of sexual abuse and the long-standing history of these symptoms

ūüĎ©‚ÄćūüĎ©‚ÄćūüĎß‚Äćūü϶¬† Family therapy¬†(psycho-dynamic, solution-oriented, narrative,¬†systemic, strategic, structural, and transgenerational, to name only a¬†few).¬†¬†Each school focuses on a particular aspect of the family dynamics and¬†uses different techniques to obtain the desired results. For example, the¬†structural school focuses on patterns of engagement-enmeshment and on
family boundaries and hierarchies. The solution-oriented approach focuses on solutions and minimizes the importance of problems. 


Acute Psychosis

Grossly ūüĒÄ disorganized speech and behavior, probable hallucinations ūüėĶ.

The acute onset of psychosis in a child or adolescent is rare, and it is essential to rule out medical or substance-induced conditions that are potentially reversible:

CNS Injury

  • Trauma
  • Space-occupying lesion
  • Infection
  • Stroke
  • Epilepsy
  • Cerebral hypoxia

Metabolic Electrolyte disturbances

  • Urea cycle disorders
  • Acute Intermittent porphyria
  • Wilson Disease
  • Kidney/liver failure
  • Hypoglycemia
  • Sodium/Calcium/Magnesium disturbance

Systemic Disorders

  • SLE
  • Tyroiditis

Illicit Substance

  • ūüćĄ Hallucinogens
  • Marijuana
  • Sympathomimetics
  • Alcohol Withdrawl
  • Bath Salts


  • Intoxication
  • Anticholinerics: Many¬†over-the-counter cold preparations¬†ūü§ß contain antihistamines (eg, diphenhydramine, doxylamine) that decrease nasal discharge but also have anticholinergic properties that can cause confusion and hallucinations.¬†
  • Serotonin Syndrome ūüôā
  • Amoxicillin/erythromycin/clairitromycin
  • Anticonvulsants
  • Corticosteroids: High-dose ūüĆĎ glucocorticoids, often given for allergic, inflammatory, or autoimmune conditions, may cause¬†glucocorticoid-induced psychosis.¬†¬†
  • Isoniazid
  • Alpha-adrenergic agents¬†ūüēĮ (eg, phenylephrine, pseudoephedrine) constrict blood vessels, decreasing nasal congestion, but can result in agitation and psychosis via their sympathomimetic properties.


  • Baclofen
  • Benzodiazepines

Dx: Basic medical workup for new-onset psychosis commonly includes a complete physical and mental status examination, metabolic panel, complete blood count, and urine toxicology screen; it may also include a screen for syphilis, HIV, vitamin B12 levels, thyroid function tests, and antinuclear antibody imaging and neuroimaging depending on specific findings and risk factors.


1st generation antipsychotics:¬†High-potency (ūüėá haloperidol and ūüĆüfluphenazine, being low in anticholinergic side effects¬†and less likely to cause postural hypotension, are preferred to low-potency¬†medications such as ūü鮬†chlorpromazine in elderly patients with cardiovascular¬†problems and prostatic hypertrophy.

Second-generation antipsychotics¬†(ūüôā serotonin- dopamine antagonists) are¬†often chosen [first-line] due to their lower risk of extrapyramidal side effects and tardive dyskinesia compared with first-generation antipsychotics.¬†¬†

All are associated with ūüć≠¬†metabolic adverse effects:

  • Weight gain
  • Dyslipidemia
  • Hyperglycemia (including new-onset diabetes)

‚úĒ Ziprasidone (Geodon)¬†has a low¬†metabolic risk profile; QT ūüďą prolonging

Highest-risk drugs (avoid in T2DM)

  • ‚Ěó Clozapine¬†
  • ‚Ěó Olanzapine (Zyprexa) ūü•ą
  • Quetiatpine

Monitoring guidelines

  • Baseline & regular follow-up
  • BMI
  • Fasting glucose & lipids
  • Blood pressure
  • Waist circumference

q3 months, and then annually.  Earlier and more frequent monitoring is recommended for patients with diabetes or those who have gained >5% of initial weight.

Quetiapine (Seroquel) low-potency antipsychotic with minimal dopamine-2 receptor antagonism.

ūüö™ Clozapine (Clozaril)¬†is a second-generation antipsychotic used in ūüí™ūüŹĺ¬†treatment-resistant schizophrenia [ūü•ágold standard]¬†and schizoaffective disorder (ie, patients who have failed ‚Č•2 antipsychotic trials).¬† Minimal dopamine-2 receptor antagonism.¬†It is associated with risk of¬†neutropenia.¬† Life-threatening¬†agranulocytosis¬†(ie, complete absence of neutrophils) has been reported in approximately 1% of patients treated, but this rate has been reduced with regular blood monitoring.¬† Patients must participate in a computer-based registry that requires¬†regular monitoring¬†of the¬†absolute neutrophil counts¬†(ANCs) before dispensing of the drug.¬†¬†

Other adverse effects of clozapine include weight gain, metabolic syndrome, seizures, ūüí© ileus, myocarditis,¬†hypotension and¬†‚ėē ūüÉŹ¬†anticholinergic effects.¬† Compared to other antipsychotics, clozapine is the least likely to cause extrapyramidal symptoms and has not been shown to cause tardive dyskinesia.¬† Clozapine is also indicated in schizophrenic ūüėĶ¬†and schizoaffective patients with recurrent ūüĒ™¬†suicidality. ūüö¨ smoking 1A2, 2D6, 3A4 receptor and SIP enzyme.¬†¬†The occurrence¬†of seizures during clozapine treatment is dose related and increases¬†considerably with dosages greater than 400 mg/day. ūüíąPhenobarbital is considered¬†the safest and the best-tolerated anticonvulsant for patients taking¬†clozapine who experience seizures.

Risperidone (Risperdal) is a commonly used¬†second-generation antipsychotic¬†(SGA) that has mixed¬†serotonin-dopamine antagonist¬†activity with binding at both¬†serotonin 2A¬†and¬†dopamine D2 receptors. [known for ūüí™ūüŹĺstronger dopamine receptor antagonism relative to other second-generation antipsychotics.]¬†The addition of serotonin antagonism to dopamine antagonism is believed to contribute to the comparatively decreased risk of extrapyramidal side effects when compared with first-generation antipsychotics that primarily block D2 receptors.¬†ūüćľ Breast formation.

ūüíČ Long-acting injectable¬†(LAI) (depot)¬†antipsychotics are administered¬†intramuscularly¬†every¬†2-4 weeks, eliminating the need to take oral medication daily.¬† Both first-generation (haloperidol, trifluoperazine ["An angel with a¬†halo¬†will¬†tri¬†to¬†fly"]¬†fluphenazine, perphenazine, chlorpromazine) and second-generation (risperidone, paliperidone (INVEGA)¬†SUSTENNA¬ģ]{234 mg on day one followed by another deltoid injection of 156 mg one week later; maintenance dose of 117 mg is begun four weeks after the second injection; Initiation of paliperidone 12-week-LAI may occur only after a patient has been established on monthly paliperidone-LAI for a period of at least four months,}, olanzapine, aripiprazole) antipsychotics are available in LAI formulations.¬†

Patients with unstable illnesses who live alone and have poor social support systems, poor insight, and frequent medication nonadherence are good candidates for LAI antipsychotics.  These medications can be administered on an outpatient basis with the support of assertive community treatment programs (eg, clinician can administer the drug in the patient's home, or facilitate the patient's adherence to scheduled medication appointments).

ūü߆ Pathways

The tuberoinfundibular dopamine pathway¬†projects from the hypothalamus to the pituitary gland.¬† Normally, neurons in the tuberoinfundibular pathway secrete dopamine, which inhibits prolactin release from the anterior pituitary gland.¬† Most antipsychotics act as dopamine antagonists, ūüĎáūüŹĺ¬†decreasing activity in this pathway by preventing dopamine from binding to D2 receptors.¬† When dopamine is blocked in the tuberoinfundibular pathway, the production of ūü澬†prolactin increases, which can result in¬†galactorrhea, gynecomastia,¬†menstrual¬†irregularities,¬†¬†infertility, and sexual dysfunction.

The antipsychotics with the highest potential for increasing prolactin are high-potency, first-generation medications (eg,¬†‚Ěó haloperidol, ‚Ěó fluphenazine) and the second-generation agents ‚Ěó¬†risperidone¬†and ‚Ěó¬†paliperidone (a metabolite of risperidone).¬†¬†

Among second-generation antipsychotics, ‚úĒ¬†aripiprazole (a partial D2R agonist) and ‚úĒ¬†quetiapine (a low-potency D2R antagonist) are two of the least likely drugs to produce hyperprolactinemia¬†

The mesolimbic pathway extends from the ventral tegmental area to the limbic system.  Decreased dopamine activity in this pathway accounts for the therapeutic effects of antipsychotics.  Increased dopamine activity in the mesolimbic pathway accounts for the euphoria that accompanies drug use, as well as the delusions and hallucinations experienced in schizophrenia.


Medications that block the dopamine (D2) receptor may cause ūüĒļ¬†extrapyramidal symptoms (EPS).¬† The most common offending agents include first-generation¬†antipsychotics¬†(eg, haloperidol), second-generation antipsychotics (eg, risperidone) to varying degrees, and antiemetics (eg,¬†metoclopramide).¬†¬†The onset of extrapyramidal symptoms in antipsychotic toxicity occurs¬†in the following timeframes (mnemonic:¬†ADAPT):

Hours to days:¬†Acute¬†dystonia:¬†Sudden, sustained contraction of the ūüĎ®ūüŹĹneck, mouth, tongue & eye muscles; torticollis

Tx: ūüöó Benztropine (anticholinergic), ūüźĚ¬†Diphenhydramine

Days to months:¬†ūüíļ¬†Akathisia:¬†Subjective restlessness, inability to sit still; moving doesn't help (vs RLS)

Tx: ūüéļ¬†Beta blocker (propranolol),¬†Benzodiazepine (lorazepam), ūüöó¬†Benztropine

Secondary Parkinsonism: Gradual-onset tremor, rigidity, bradykinesia

Tx:¬†ūüöó¬†Benztropine, ūüźü¬†Amantadine (a dopaminergic medication, and a weak N-methyl-D-aspartate receptor antagonist)

Months to years:¬†Tardive¬†dyskinesia:¬†Gradual onset after prolonged therapy (> 6ÔłŹ‚É£¬†months): Dyskinesia of the ūüĎĄ mouth ūüźá (rabbit syndrome), face (orofacial),¬†trunk & extremities [typically occurs after prolonged (>6 months)], Limb dyskinesia (dystonic postures, foot tapping, chorea), trunk dyskinesias (rocking, thrusting, shoulder shrugging).¬† The pathophysiology of TD is thought to involve¬†dopamine D2 receptor UPREGULATION¬†and supersensitivity¬†resulting from chronic blockade of dopamine receptors.¬† Other hypotheses include an imbalance between dopamine D1 receptor and dopamine D2 receptor effects in the basal ganglia as well as excitotoxic destruction of GABA neurons in the striatum.¬†¬†Typical antipsychotic medications¬†(such as perphenazine) and, in particular, high-potency drugs carry the¬†highest risk of TD. Atypical antipsychotics are thought to be less likely to¬†cause this disorder.


  • Valbenazine or deutetrabenazine, reversible inhibitors of the vesicular monoamine transporter 2 (VMAT2) recently approved by the FDA for use in¬†TD.
  • Switching¬†(cross-tapering) to an antipsychotic with a lower tendency to cause TD, such as quetiapine or¬†ūüö™¬†clozapine.¬†

Neuroleptic malignant syndrome¬†(NMS)¬†is a rare, idiosyncratic, and potentially life-threatening complication of treatment with antipsychotics.¬† Although it is more commonly associated with the use of high-potency, first-generation antipsychotics (eg, haloperidol), NMS can occur with¬†every class of antipsychotics, including second-generation drugs (eg, olanzapine).¬†¬†It may occur at any time but usually develops within the first 2 weeks of treatment.¬†¬†Hx: The cardinal features of NMS include¬†severe hyperthermia, autonomic instability, muscular (lead-pipe) rigidity, and altered sensorium.¬† Laboratory findings include elevated creatine phosphokinase level and white blood cell count.¬† Rhabdomyolysis, followed by myoglobinuria that can cause acute renal failure, is a known complication.¬†¬†Dx: Creatine kinase¬†level and white blood cell count may be elevated.¬† Tx: Treatment of NMS includes prompt ‚ĚƬ†discontinuation of the offending agent (the antipsychotic) followed by supportive care (ie, aggressive cooling, antipyretics, fluid and electrolyte repletion).¬† Dopaminergic agents that can reverse dopamine blockade, such as ūüßĻbromocriptine¬†or ūüźü¬†amantadine, can be considered in patients who do not respond to supportive care and withdrawal of medication.¬† Dantrolene, a direct-acting muscle relaxant, has also been used.

Fu: Patients that have remained symptom free on her medication for over 3 years should be discontinued from antipsychotic medication.  In addition, it is recommended that the patient and family be encouraged to develop early intervention strategies prior to medication discontinuation, should a relapse occur.


Neuroleptic malignant syndrome (NMS)

A rare but potentially lethal adverse reaction to antipsychotic medications.  Both first-generation (eg, haloperidol) and second-generation antipsychotics can cause NMS.  It may occur at any time but usually develops within the first 2 weeks of treatment. 

The cardinal features of NMS include severe hyperthermia, autonomic instability, muscular (lead-pipe) rigidity, and altered sensorium.  Laboratory findings include elevated creatine phosphokinase level and white blood cell count.  Rhabdomyolysis, followed by myoglobinuria that can cause acute renal failure, is a known complication.

Treatment of NMS includes prompt discontinuation of the offending agent (the antipsychotic) followed by supportive care (ie, aggressive cooling, antipyretics, fluid and electrolyte repletion).  Dopaminergic agents that can reverse dopamine blockade, such as bromocriptine or amantadine, can be considered in patients who do not respond to supportive care and withdrawal of medication.  Dantrolene, a direct-acting muscle relaxant, has also been used.



is characterized by the acute onset of mental status changes that wax and wane. It may present as impaired awareness, easy distraction, confusion, and/or disturbances of perception such as: illusions, misinterpretations, and visual hallucinations. Recent memory is usually impaired, and speech may be rambling, perseverating, nonsensical, pressured, or incoherent. Patients may also be agitated or obtunded. Keep in mind that one of the most important features of delirium is that it is reversible. Patients' degree of awareness of their condition may fluctuate with time. 


Delirium is characterized by:

Rapid decrease in attention span and level of arousal

Disorganized thinking, cognitive dysfunction

Hallucinations, illusions, misperceptions

Disturbance in sleep-wake cycle


Several causes of delirium include (AEIOU TIPS):


Electrolytes or metabolic disturbances

Iatrogenic (anticholinergics, anticonvulsants, antihypertensives, anti-Parkinson drugs, antibiotics, benzodiazepines, disulfiram, H2receptor blockers, hypoglycemics, insulin, narcotics, NSAIDs, steroids)

Oxygen hypoxia (bleeding, pulmonary disease, carbon monoxide poisoning)

Uremia and/or Urinary/fecal retention




Substance abuse/withdrawal


Physical examination or laboratory studies usually reveal some organic cause for the delirium. Common causes of delirium include intoxication, occult infection, head trauma, seizure, mania, thyrotoxicosis, renal failure, hepatic failure, neoplasm, stroke, and shock. When delirium is diagnosed, the underlying causes should be sought and treated.  Components of delirium management include supportive therapy and pharmacologic management with short-acting neuroleptics (risperidone, haloperidol).


The treatment of delirium consists of the following:

Identify underlying cause

Oxygen, hydration, pain control

Haloperidol (with agitation)

Benzodiazepines (for alcohol withdrawal)


Major depressive Disorder [MDD](Clinical depression)

"recurrent", "single episode"; mild, moderate, severe

Dx: Depressed mood must be present most of the day, almost every day for > 2ÔłŹ‚É£ weeks:¬†

‚Č• 5 of 9 symptoms: Depressed mood + SIGECAPS

ūüí§ Sleep changes: increase during day or decreased sleep at night.

Interest (loss): of interest in activities that used to interest them

Guilt (worthlessness): depressed persons may devalue themselves

Energy (lack): common presenting symptom (fatigue)

Cognition/Concentration: reduced cognition and/or difficulty concentrating

ūüćó Appetite (weight loss); usually declined, occasionally increased

Psychomotor: agitation (anxiety) or lethargic

ūüĒ™ Suicide/preoccupation with death

Hopelessness is one of the most accurate indicators of long-term suicidal risk.

No lifetime history of mania


Pediatric depression often presents with symptoms of irritability rather than depressed mood.  Treatment is warranted if they have resulted in a marked change from baseline as well as significant academic and social impairment.  Depressed preschoolers tend to be irritable, aggressive, withdrawn, or clingy instead of sad.

Psychotic symptoms are common in depressed children, most commonly one voice that makes depreciative comments and mood-congruent delusional ideations. Up to one-third of children diagnosed with major depression receive a diagnosis of bipolar disorder later in life.

School-age children may experience a significant loss of interest in friends and school.

Adolescents present more similar to adults. 

Older adults with depression initially present to primary care providers and focus more on somatic complaints than on subjective changes in mood and interest. 


Major depressive disorder is a highly recurrent illness for most patients. 

Continuation phase =¬†6ÔłŹ‚É£ months following remission

Due to the high risk of recurrence, patients with ‚Č•2 episodes are candidates for Maintenance antidepressant treatment ¬†Other indications for maintenance therapy (due to high risk of recurrence) include early age of onset (‚ȧ18), persistent residual depressive symptoms, and comorbid psychiatric disorders.¬† Maintenance therapy can be continued for 1-3 years.¬†

However, patients with a history of¬†highly recurrent illness¬†(eg, ‚Č•3 lifetime depressive episodes),¬†chronic episodes¬†(‚Č•2 years), severe ongoing psychosocial stressors, or¬†severe episodes¬†(eg, suicide attempts) are candidates for¬†maintaining antidepressant¬†treatment¬†indefinitely.

Doses of antidepressants should generally be raised to their maximal doses and kept there for 4 to 5 (6ÔłŹ‚É£)weeks before a drug trial is considered unsuccessful.¬† Patients with minimal to no improvement with initial antidepressant treatment can be¬†switched¬†to another antidepressant.

Patients with anxiety disorders are especially sensitive to activating effects of antidepressants.  They should generally be started at lower doses than are typically used to treat depression (eg, half the normal starting dose) with a gradual increase to a therapeutic level over several weeks.


Selective serotonin reuptake inhibitors (SSRIs) are frequently used as first-line treatment for depressive and anxiety disorders due to their efficacy, tolerability, and general safety in overdose.  Common early side effects of SSRIs include nausea, diarrhea, headache, increased anxiety, and insomnia or somnolence.  These effects most commonly occur shortly after initiation and diminish or resolve over time for most patients.  Sexual dysfunction (retarded ejaculation?) is the most common long-term side effect and is more likely to be persistent.

Selective serotonin reuptake inhibitors¬†(SSRIs) are used as first-line treatments after an acute MI because they are generally well tolerated and less likely to cause adverse cardiac effects compared with other classes of antidepressants.¬† Among the SSRIs, ūüíó¬†sertraline (Zoloft)¬†and¬†escitalopram¬†(Lexapro) are preferred because they carry a very low risk of drug interactions, especially with cardiac medications.¬†

ūüŹô Citalopram is generally avoided in patients with a recent MI due to its potential for dose-dependent QT prolongation

ūü¶ú Paroxetine has a¬†potential for anticholinergic effects, drug-drug interactions through inhibition of cytochrome P-450 enzymes, and weight gain.

‚úą Fluoxetine (Prozac)¬†is considered the medication of choice for ūüĎ∂ūüŹĺ pediatric depression;¬†has the least potential to cause ‚ĚƬ†weight gain.

ūüö≤ Tricyclic antidepressants such as amitriptyline can slow cardiac conduction by inhibition of fast sodium channels.¬†¬†Amitriptyline is associated with a great tendency to gain weight.

ūüć∑ Phenelzine is a monoamine oxidase inhibitor (MAOI) that is not used as a first-line antidepressant due to its unfavorable side effect profile and required dietary restrictions.¬† At therapeutic doses, MAOIs commonly cause hypotension, not hypertension.¬† Hypertensive crisis refers to severe hypertension that can occur after patients on MAOIs ingest foods containing the sympathomimetic tyramine.¬†¬†Tyramine metabolism is inhibited in the presence of MAOIs, causing an increased¬†sympathomimetic (ie, adrenergic) effect¬†that can result in severe hypertension.¬† This commonly presents first as a headache but can lead to intracranial bleeding, stroke, and death.¬†¬†Foods to be avoided by¬†patients on MAOIs include tyramine-rich foods such as aged cheese,¬†salami, ūüćēpepperoni, sausage, overripe fruit, liquors, red wine, pickled fish,¬†sauerkraut, and brewer‚Äôs yeast. Chocolate, coffee, tea, beer, and white wine¬†can be consumed in small quantities.

ūüéļ Trazodone, a serotonin-modulating antidepressant, is extremely sedating.¬† It is used primarily at low dose for sleep induction rather than for its antidepressant effects.¬† Its orthostatic effects are problematic in the elderly. [vilazodone]

ūüď† Venlafaxine (Effexor); Duloxetine (Cymbalta)¬†a serotonin-norepinephrine reuptake inhibitor, is associated with tachycardia and has been associated with¬†dose-dependent hypertension.¬† At lower doses, venlafaxine primarily inhibits the reuptake of serotonin.¬† As the dose is increased, the drug also inhibits norepinephrine reuptake with the potential effect of increasing systolic and diastolic blood pressure.¬† The hypertensive effect is dose dependent and is especially significant at doses above 300 mg daily, where the incidence may be >10%.

ūü§° Mirtazapine (Remeron)¬†is a first-line antidepressant medication whose side effects include stimulation of appetite, weight gain, and somnolence.

⚡ Electroconvulsive therapy is generally indicated for patients with very severe depressive symptoms (eg, persistent suicidality, malnutrition/dehydration), major depression with psychotic features, or failure to respond to multiple medication trials.  ECT is a safe procedure with very few contraindications (recent myocardial infarcts, increased intracranial pressure, aneurysms, bleeding disorders, and any condition that disrupts the blood-brain barrier).  Unilateral electrode placement is less efficacious than bilateral electrode placement but is associated with less cognitive side effects, including short-term memory impairment and confusion.

ūüŹÄ Bupoprion (Wellbutrin, Zyban):¬†Side effects most common include headache, insomnia,¬†dry mouth, tremor, and nausea. Severe anxiety and panic disorder can be worsened by bupropion. Can¬†worsen psychosis and delirium due to dopaminergic activity. Have seen severe psychosis with use of¬†bupropion in pregnancy.¬† Seizure risk is 2% with 600 mg and 0.1% with 300-450 mg .

ūüö© Half-lives

Fluvoxamine: 15.6 hours

ūü¶ú Paroxetine: 21 hours

Escitalopram: 27-32 hours

Citalopram: 35 hours

‚úą Fluoxetine: 4-6 days (9.3 days for active metabolite)


Antidepressant discontinuation syndrome¬† Sudden onset of dysphoria, fatigue, insomnia, and myalgias.¬†Other physical symptoms may include dizziness, flu-like and gastrointestinal symptoms, tremor, and neurosensory disturbances (eg, ‚ö°¬†"electric shock" and "rushing" sensations in the head, paresthesias, hyper-responsivity to light and noise, vivid dreams).¬† Symptoms typically begin within 2-4 days of the medication being abruptly stopped or rapidly tapered.¬†¬†Serotonergic antidepressants¬†with a¬†shorter elimination half-life¬†(eg, ūü¶ú paroxetine, venlafaxine), higher doses, and longer duration of treatment are associated with more severe discontinuation symptoms.

Tx: The best approach to manage discontinuation syndrome is to re-institute the same antidepressant and taper the dose gradually over 2-4 weeks (or longer in severe cases). 

In 2007 the US Food and Drug Administration extended its warning that all patients age <25 should be informed about the small risk of becoming suicidal during initial antidepressant treatment.  The warning was based on studies showing a slightly increased risk of suicidal thoughts and behaviors (not completed suicide) among a small group of child and adolescent patients treated with antidepressants compared with placebo.

ūüė†Serotonin syndrome is characterized by hyperthermia ūüĒ•(although fevers are not as high as in NMS), autonomic instability, mental status changes, prominent gastrointestinal symptoms, and neuromuscular irritability (including hyperreflexia and myoclonus).

Antidepressant-induced mania: All antidepressants carry the risk of inducing mania in susceptible patients, and many patients who experience this are ultimately diagnosed with a bipolar spectrum disorder.  If manic symptoms persist despite discontinuing the antidepressant, treatment with a mood stabilizer (eg, lithium, valproate) or an antipsychotic should be considered.

ūü߆¬†Hyperactivity¬†of the¬†hypothalamic-pituitary-adrenal axis, resulting in¬†increased ūüĆĎcortisol levels, has been associated with depression.¬† The neurocytotoxic effects of hypercortisolemia may play an important role in the pathogenesis of depressive symptoms and associated cognitive deficits.¬† These effects may also explain the association of stress and ūüöϬ†trauma with an increased risk for the development of depression.

Positron emission tomography (PET) scan has consistently demonstrated a decrease in blood flow and metabolism in the frontal lobe of depressed patients.

Other findings in depressed patients include decreased hippocampal and frontal lobe volumes

ūüí§ Sleep architecture: REM sleep latency (the time from sleep onset until the start of the first REM sleep period) and slow-wave sleep are both decreased in depression¬† ¬†Patients with¬†major depressive disorder have increased REM sleep (duration) ???


MDD w/ psychotic features

In this severe subtype of unipolar major depression, the depressive episode is accompanied by delusions and/or hallucinations, typically with depressive themes (eg, deserving punishment, worthlessness, nihilism).

The diagnosis is differentiated from psychotic disorders in that the psychotic symptoms are present only during the episode of major depression.  Identification of psychotic features has important implications as effective treatment of major depressive disorder with psychotic features requires the combination of an antidepressant and antipsychotic or electroconvulsive therapy.

Tx: ūü•á¬†First-line treatment of major depressive disorder with psychotic features is¬†combination¬†pharmacotherapy with an ūüėʬ†antidepressant AND ūüėĶ antipsychotic (sertraline and risperidone)¬†or ‚ö°¬†electroconvulsive therapy (ECT).¬† Because ECT is generally faster than pharmacotherapy, it is used to achieve a¬†rapid response¬†in depressed¬†elderly patients¬†who are¬†unable to eat and drink,¬†psychotic, or actively¬†suicidal.¬†¬†ECT involves inducing a 30- to 60-second generalized tonic-clonic seizure.¬† Hemodynamic changes are brief and cardiac complications are rare.¬†¬†Methohexital (barbiturate) is commonly used for anesthesia prior to ECT.


Persistent depressive disorder (Dysthymia)

Can be thought of as a chronic, low-grade depression that lasts for years. 

Clinical Features:

  • Persistent depressive symptoms for > 2ÔłŹ‚É£ years (1 year in adolescents)
  • No symptom-free period for¬†for > 2 months ūüďÜūüďܬ†at a time.¬†¬†
  • Presence of 2 of the following:
    • Poor appetite or overeating
    • insomnia / hypersomnia
    • Low energy or fatigue
    • Low self-esteem
    • Poor concentration or¬†difficulty making decisions
    • Feelings of hopelessness


"Pure dysthymic syndrome": criteria for major depressive episode never met

Dysthymia with "intermittent" major depressive episodes

Dysthymia with "persistent" major depressive episodes: criteria for major depressive episode met throughout previous 2 years

Tx: Antidepressants, psychotherapy, or a combination of these.


Acute stress disorder

Acute stress disorder is characterized by symptoms of reexperiencing (intrusive memories and flashbacks), avoidance, negative mood, dissociation, and hyperarousal lasting from 3 days to 1 month¬†ūüďÜ following a traumatic event.

Can follow trauma related to threatened death, serious injury, or sexual violation. Symptoms of acute stress disorder can be broken down into 5 categories which include intrusive thoughts, negative mood, dissociation, avoidance, and arousal.

Patients with ASD may have difficulty recalling part or all of a specific traumatic event; this does not require a comorbid diagnosis of dissociative amnesia unless the amnesia extends beyond the immediate time of the trauma.

Although ASD will remit in some individuals without intervention, others can benefit from treatment designed to alleviate symptoms and prevent development of post-traumatic stress disorder (diagnosed when symptoms persist for ‚Č•4 weeks).¬† The best¬†initial approach¬†is to provide¬†education on symptoms¬†and the course of acute and post-traumatic stress disorders, as well as to encourage the patient to seek help if the symptoms persist.¬†¬†Normalizing¬†the¬†stress response, while explaining that symptoms can sometimes cause distress and impairment, would be helpful.¬†¬†


Adjustment disorder

An adjustment disorder involves emotional or behavioral symptoms (eg, anxiety, depression, disturbance of conduct) developing within 3 months of an identifiable stressor and lasting no longer than 6 months once the stressor ceases.

  • Depressive symptoms develop within 3ÔłŹ‚É£ months of the onset of an identifiable stressor.¬†
  • Marked distress out of proportion to the stressor and/or impaired social or occupational functioning.
  • ‚Ěó Does not meet criteria for another DSM-5 disorder

‚Ěď What is ther worst thing that has ever happened to you ‚Ěď

The treatment of choice for adjustment disorder is psychotherapy, which focuses on developing coping mechanisms and improving the individual's response to and attitude about the stressful situation.  


Atypical depression

Another variant of major depressive disorder, is characterized by mood reactivity ‚õÖ¬†(ie, feeling better in response to positive events), self-pity, excessive sensitivity to rejection, reversed diurnal mood fluctuations (patients feel better in the ūüēó morning), and reversed vegetative symptoms (ūüćó¬†increased appetite and¬†ūüí§ increased sleep),¬†leaden paralysis¬†(patient's arms and legs feel extremely heavy).¬†¬†Approximately 15% of patients with depression have atypical features.

Tx: ūüźĀ MAOIs are considered to be more effective than other classes of antidepressants in atypical depression.



(1) guilt about things other than actions taken or not taken by the survivor at the time of the loved one’s death, (2) thoughts of death other than the survivor feeling he/she would be better off dead  without the loved one, (3) a morbid preoccupation with worthlessness, (4) marked psychomotor retardation, (5) marked and prolonged functional impairment, and (6) hallucinations other than the survivor believing he/she can hear the voice or see the loved one.



Characterized by an irritable or depressed mood for at least 1 year

(In adults, the time requirement for the diagnosis would be 2 years)

Venlafaxine and bupropion are generally believed to be the treatments of choice, though there is a subgroup of patients that will respond to the MAOIs as well.

Double depression is diagnosed when a major depressive episode develops in a patient with dysthymic disorder.


Melancholic depression

A variant of major depressive disorder, is characterized by loss of pleasure in all activities (anhedonia), lack of reactivity (nothing can make the patient feel better), intense guilt, significant weight loss, ‚Źį¬†early morning awakening, and marked psychomotor retardation.¬† TCAs have been considered to be more effective than other antidepressants in the treatment of melancholic depression.


Postpartum blues

Frequent, with a prevalence estimated between 20% and 40%. Symptoms include tearfulness, irritability, anxiety, and mood lability. Symptoms usually emerge during the first 2 to 4 days after birth, peak between days 5 and 7, and resolve by the end of the second week postpartum. 

t is a normal and self-limited response that typically peaks at 5 days postpartum and resolves within 2 weeks. 

Anhedonia is NOT seen in postpartum blues. 

Tx: Resolves spontaneously, and usually the only interventions necessary are support and reassurance.


Normal stress response

Symptoms are mild rather than excessive given the nature of the stressor; does not meet the full criteria for any disorder; not markedly distressed.  Most importantly no impairment of social and occupational functioning, a key feature of psychiatric illness. 

  • Not excessive or out of proportion to severity of stressor
  • No significant functional impairment

Patient continues to function well (eg, still performs at work, enjoys socializing and leisure activities).


Substance-induced depressive disorder

A substance (eg, drug of abuse, medication, toxin) is judged to be etiologically related to the mood disturbance (eg, depressed mood that occurs only during cocaine withdrawal would be diagnosed as cocaine-induced depressive disorder).


Seasonal affective disorder (SAD)

A depressive disorder that is associated with seasonal changes and is worse during winter months.

Patients usually exhibit typical signs and symptoms seasonally, most often¬†during the winter, with symptoms remitting in the spring. ūüõĆūüŹĺ Hypersomnia¬†and ūüćó hyperphagia (atypical signs of a depression) are classically seen.

Tx: Bright light therapy is typically administered with a 10,000-lux light box shortly after awakening.  Most patients experience clinical improvement in 1-4 weeks and continue treatment through the fall or winter until spontaneous remission in the spring or summer.  Light therapy alone is a reasonable alternative for patients with mild to moderate SAD.


Normal Grief

Clinical features:

  • Normal reaction to loss (bereavement)
  • Sadness more specific to thoughts of the deceased¬†
  • "Waves" of grief at reminders
  • Worthlessness &¬†self-loathing;¬†guilt less common
  • Functional decline less severe
  • Thoughts of dying involve wish to join the deceased; active suicidality uncommon

Normal grief¬†can last up to 1 year¬†(although DSM IV and especially DSM V seem to be shortening the "allowable" time for grieving and encouraging consideration of a diagnosis of ūüėĘdepression after 2 months, or in DSM V, 2 weeks in some patients with additional symptoms of depression).¬†Grief should not be medicated


Persistent complex bereavement disorder (also known as complicated grief, prolonged grief, or complex grief).

>12 months¬†ūüďÖ after the loss¬†

Difficulty accepting the death, persistent yearning for the deceased, and avoidance of reminders of the deceased.

The estimated incidence of complicated grief in bereaved individuals is 7%, with increased risk associated with unexpected or violent death of a loved one and death of a spouse or child.  Difficulty envisioning a meaningful life without the deceased, suicidal ideation or wish to join the deceased, and guilty ruminations about the circumstances of the death are also common.

If left untreated, persistent complex bereavement disorder can continue for years or decades after the loss and result in poor quality of life, increased substance use, and increased mortality due to medical conditions or suicide. 

Tx: Psychotherapy specifically geared to helping the patient come to terms with the loss and re-engage in a meaningful life without the deceased.



"current episode", "most recent episode"; manic, depressed, mixed

Acute mania:

Clinical features

  • Elevated, irritable, labile mood, Distractability, Impulsivity
  • Increased energy & Activity (increased goal-directed activity / psychomotor agitation), decreased need for Sleep
  • Talkativeness / Pressured speech, racing thoughts (Flight of Ideas), distractibility
  • Grandiosity, Impulsivity (high-risk¬†behavior [spending, sexual])
  • Marked impairment, may have ūüėĶ¬†psychotic symptoms
  • 1ÔłŹ‚É£ week unless hospitalized
  • Marked impariement in social or occupational functioning or hospitilization necessary.


  • Antipsychotics (first- & second-generation)
  • Lithium (avoid in renal disease)
  • Valproate (avoid in liver disease)
  • Combinations in severe mania (eg, antipsychotic plus lithium or valproate)
  • Adjunctive benzodiazepines for insomnia, agitation

Brief auditory hallucinations are likely related to the manic phase.  In fact, auditory hallucinations are seen in a variety of psychiatric disorders. It has been estimated that around 75% of patients with schizophrenia experience auditory hallucinations. These hallucinations are also relatively common in bipolar disorder (20% to 50%), major depressive disorder with psychotic features (10%), and in posttraumatic stress disorder (40%). 

Hypomania is differentiated from mania by a lesser degree of severity and functional impairment and the absence of psychosis.  Patients experiencing hypomania exhibit a noticeable change in behavior but are often very productive despite requiring less sleep.  Hypomanic patients are often able to work and are rarely hospitalized.

‚Č• 4ÔłŹ‚É£ days (consecutive)

  • Unequivocal, observable change in functioning from patient's baseline
  • Symptoms not severe enough to cause marked impairment or necessitate hospitalization
  • No psychotic features

Bipolar I disorder is diagnosed in patients who experience 1 or more lifetime manic episodes (irritable mood, hyperactivity, pressured speech, decreased need for sleep, and¬†grandiose delusions).¬†¬†Major depressive episodes are common but ‚õĒ NOT required for diagnosis.¬† Delusions, if present, are often mood congruent and have manic themes (eg, grandiose themes involving special talent and powers).

Tx: It is a lifelong illness that requires maintenance pharmacotherapy to reduce the risk of recurrent mood episodes.  Most patients require maintenance for many years, and lifelong maintenance is indicated for those with a severe course (eg, frequent episodes, suicide attempts, severe symptoms, hospitalization).  A strong therapeutic alliance, psychoeducation, and adjunctive psychotherapy can help the patient accept the chronic nature of the illness and enhance adherence. 

Bipolar II disorder involves hypomanic episodes (less severe than mania, no psychosis) AND¬†ūüėĘ one or more¬†major depressive episodes.

Tx: Maintenance treatment to delay or prevent recurrence of new mood episodes.  

‚Ěď Have there been times, lasting at least a few days when you felt the opposite of depressed, where you were very cheerful or happy and this felt different from your normal self ‚Ěď

ūüíä Rx:¬†Evidence-based maintenance monotherapy options for bipolar disorder include lithium, valproate, quetiapine, and lamotrigine.¬† However, those with¬†severe illness¬†(ie, psychosis, aggression, frequent episodes/hospitalization), often require¬†combination therapy¬†to maintain stability.¬†¬†

ūüėĶ Acute mania:

ūüĒė Lithium OR valproate¬†combined with a¬†second-generation antipsychotic (eg, quetiapine)¬†is ūü•á¬†first-line combination therapy.

First- and second-generation antipsychotics are effective in managing mania and associated acute behavioral agitation. 2nd [quetiapine and lurasidone]

Olanzapine can be administered intramuscularly and has more rapid onset of action. 

Antipsychotics and benzodiazepines should be discontinued as soon as the patient is in a stable state, given the risk of movement disorders and dependence, respectively.

ūüźĎ Lamotrigine (anticonvulsant)ūü•ą¬†[second-line] has the greatest efficacy in treating bipolar depressive (not manic) episodes.¬† The most significant adverse effect is rash that can develop into a life-threatening mucocutaneous reaction (ie, Stevens-Johnson syndrome)(<10% body surface area skin detachment) and toxic epidermal necrolysis (>30% detachment) occur at a rate of 0.1% (10%-30% detachment is known as Stevens-Johnson syndrome/toxic epidermal necrolysis overlap). in approximately 0.1% of patients.

Long-term maintenance:

Valproate (Depacote)[first line] : Periodic monitoring of liver function tests and platelets is necessary due to the medication's rare association with hepatotoxicity and thrombocytopenia.

ūüźĄ Drug-induced liver injury: Patients receiving valproate should have liver tests prior to therapy and regularly thereafter.¬† In addition to hepatotoxicity, valproate is also associated with tremor, thrombocytopenia, and alopecia.

ūüĒė Lithium [first line]¬†


  • Acute mania, bipolar maintenance

‚ĚĆ Contraindications

  • Chronic kidney disease
  • Heart disease
  • Hyponatremia or diuretic use

Baseline studies

  • Blood urea nitrogen (BUN)[yearly], creatinine, calcium, urinalysis
  • TSH¬†(Thyroid function tests)¬†q6¬†months; T3RU (yearly)
  • ECG in patients with coronary risk factors

‚ė† Adverse¬†effects


  • Tremor, ataxia, weakness
  • Polyuria, polydipsia
  • GI: Nausea, vomiting, diarrhea ūüí©
  • Cognitive impairment (confusion, agitation)


  • Nephrogenic diabetes insipidus:¬†lithium¬†antagonizes the effects of ADH in the distal kidney. The primary treatment is discontinuation of treatment or addition of ūü¶Ķ¬†HCTZ (thiazide diuretic). Thiazides, in addition to effects on Na in the proximal kidney, increase¬†expression of distal aquaporins, thus¬†reversing the effects of lithium. Because HCTZ decreases NA reabsorption, it ultimately leads to¬†increased lithium absorption (a positive ion) and can be associated with lithium toxicity. Thus lithium¬†coadministered with HCTZ must be decreased in dose.
  • Chronic kidney disease
  • ūüéÄ Thyroid dysfunction: Approximately 25% of patients treated with lithium will develop¬†hypothyroidism (fatigue, constipation, myalgias, and bradycardia).¬† A much smaller percentage will experience hyperthyroidism.¬† Tx: Patients who develop hypothyroidism are generally managed symptomatically with addition of T4 (eg, levothyroxine) rather than discontinuation of lithium.
  • Hyperparathyroidism

Weight gain, metallic taste, acne, and polyuria,

Drug interactions

  • ūü¶Ķ Thiazide diuretics¬†can cause a decrease in the renal clearance of lithium and lead to lithium toxicity.¬† The risk of lithium toxicity is higher in patients with dehydration from any cause (eg, vomiting, diarrhea, fever, diuresis) and in elderly patients due to a lower glomerular filtration rate and reduced volume of distribution.
  • NSAIDs (not aspirin)
  • ACE inhibitors
  • Tetracyclines, metronidazole

ECG is also recommended in patients with coronary artery disease risk factors (eg, diabetes, hypertension, smoking) as lithium may cause dysrhythmias in these patients.  These studies should also be reassessed periodically after starting the medication.

The lithium level considered effective for acute mania is between 1 and 1.5 meq/L.  Since the half-life of lithium is about 20 hours, equilibrium is reached after 5 to 7 days of regular intake.  Mild lithium toxicity (serum levels below 3 meq/L with symptoms of tremor, mild confusion, and gastrointestinal distress); severe toxicity requires dialysis


Neurologic (eg, altered mental status, seizure, fasciculations, tremor) and gastrointestinal (eg, vomiting, diarrhea) signs are common in cases of acute intoxication.  Tx: Although mild overdoses can frequently be managed supportively with hydration and monitoring, hemodialysis is the treatment of choice for patients with lithium levels >2.5 mEq/L and prominent signs of toxicity.  Patients with levels >4 mEq/L and creatinine >2.0 mg/dL should generally be prescribed dialysis regardless of symptoms.

Because lithium is renally excreted, common precipitants of toxicity include medications that affect the excretion rate (eg, nonsteroidal anti-inflammatory drugs, ACE inhibitors, angiotensin receptor blockers) as well as dehydration by any cause (eg, diuretics, gastrointestinal illness).  Intentional overdose should also always be on the differential.

Carbamazepine:¬†can cause ūü¶ī aplastic¬†anemia, agranulocytosis, thrombocytopenia, and leucopenia. It also has¬†a risk of hepatotoxicity. Because of these possibly side effects, a CBC,¬†platelet count, reticulocyte count, serum electrolytes, SGOT, SGPT, LDH,¬†and a pregnancy test (in appropriate patients, since carbamazepine raises¬†the risk a baby will be born with spina bifida) should all be drawn before¬†treatment with carbamazepine is instituted. SGOT, SGPT, and LDP should¬†be drawn every month for the first 2 months, and thereafter, every 3¬†months.

Sleep deprivation has an antidepressant effect in depressed patients and may trigger a manic episode in bipolar patients. 

The use of a long-acting benzodiazepine will allow patients to return to a normal sleep pattern and generally will abort manic episodes.

‚ĚĆ Antidepressant monotherapy¬†should generally be¬†avoided¬†in patients with¬†bipolar I¬†disorder due to the¬†risk¬†of precipitating¬†mania.¬†

Medications commonly used in the treatment of¬†acute bipolar depression¬†include the second-generation antipsychotics¬†quetiapine¬†and¬†lurasidone¬†and the anticonvulsant¬†lamotrigine.¬† Lithium, valproate, and the COMBINATION of olanzapine and fluoxetine have also demonstrated efficacy.¬† [If necessary, antidepressants should be used in combination with mood stabilizers (eg, lithium, valproate, second-generation antipsychotics) as these appear to decrease the risk of an antidepressant-induced switch from depression to mania.]¬† Other risks of using antidepressants in patients with bipolar depression include the development of rapid cycling (‚Č•4 mood episodes/year) and increased mood cycle frequency.



Involves > 2ÔłŹ‚É£ years of numerous periods with hypomanic and depressive symptoms that do not meet the full criteria for hypomanic and depressive symptoms that do not meet the full criteria for hypomanic or major depressive episodes.¬†

Characterized by recurrent periods of mild depression alternating with periods of hypomania.



Disorganized type

‚Č• 6ÔłŹ‚É£ months¬†(includes ‚Č•1 month of active symptoms, can include prodromal & residual periods), requires functional decline.¬†¬†‚Č•2 of the following:

  • Delusions¬†
  • Prominent ūüĎāūüŹĺ¬†auditory or ūüĎĀ¬†visual hallucinations
  • Disorganized speech (ūüßĶ¬†loosening of associations, nonsensical words)
  • Grossly disorganized or catatonic behavior (unpredictable agitation, bizarre behaviors, inappropriate affect), functional impairment, grimacing, silly/odd behaviors and mannerisms.
  • Negative symptoms (affective flattening, avolition, alogia [poverty of speech], anhedonia, asociality), 1 of which must be delusions, hallucinations, or disorganized speech.¬† Mood symptoms (meeting criteria for manic or depressive episodes) are absent.¬† These active symptoms must be present for ‚Č•1 month during a period of ‚Č•6 months, with prodromal or residual symptoms occurring the rest of the time.

The psychotic features of schizophrenia typically emerge between the late teens and mid-30s; childhood onset is rare and is associated with a poorer prognosis.¬† ūü϶ūüŹĹAdolescents commonly have a¬†prodromal¬†phase marked by¬†social withdrawal¬†and academic decline, which can last for weeks to years prior to the onset of active psychotic symptoms.¬† Youth with schizophrenia frequently name their hallucinations, which need to be differentiated from imaginary friends.¬† Imaginary friends typically decline in prevalence around age 6 and are not associated with functional decline.

Factors weighting toward ‚úÖ¬†good prognosis in schizophrenia include: late onset of the disease (>25y), obvious precipitating factors/stressors, an acute onset, good premorbid functioning, the presence of mood disorder symptoms, the patient being married, a ūüĎ®‚ÄćūüĎ©‚ÄćūüĎß‚ÄćūüĎßfamily history of mood disorders, good support systems, and the presence of positive symptoms (as opposed to negative symptoms).

Patients with schizophrenia can have grandiose delusions that they possess special powers or are related to or have become someone famous.  Other common types of delusions include paranoid delusions and delusions of reference (receiving special messages from electronic media).

ūü߆ Neuroimaging studies have frequently shown loss of cortical tissue volume with ventricular enlargement

Tx: Family interventions that have been shown to be effective in the treatment of schizophrenic patients include teaching the family members about schizophrenia, emphasizing the importance of keeping interpersonal communication at a low emotional quotient (schizophrenic patients tend to relapse when exposed to the intense negative emotions of family members), and helping the family learn more adaptive ways to cope with stress.


Brief psychotic Disorder

ūüėĶ Psychotic symptoms (delusions, hallucinations, disorganized speech and behavior, negative symptoms) last at >1 day but <1 month ūüďܬ†with full return to premorbid functioning;¬†normal functioning apart from direct impact of delusions


Schizoaffective Disorder

"depressed-type", "bipolar type"

Diagnostic Criteria:

  • Major depressive OR¬†manic episode concurrent with symptoms of schizophrenia
  • ‚ěē Lifetime history of¬†delusions or hallucinations ūüėĶ¬†for¬†‚Č•2 weeks in the ABSENCE of major depressive or manic episode
  • Mood episodes are prominent & recur throughout illness
  • Not due to substances or another medical condition

Schizoaffective disorder can be differentiated from schizophrenia and bipolar disorder by assessing the relationship of mood and psychotic symptoms over the course of the illness. 

Differential diagnosis

  • Major depressive or bipolar disorder with psychotic features:¬†¬†Psychotic symptoms occur exclusively during mood episodes
  • Schizophrenia:¬†¬†Mood symptoms may be present for relatively brief periods

Concurrent Mania/mood episode (elevated mood, decreased need for sleep, hypersexuality, grandiose delusions) with a history (at least 2 weeks) of delusions and hallucinations occurring in the absence of a major mood episode (manic or depressive).  A lifetime history of psychotic symptoms without significant mood disturbance.


Schizophreniform Disorder

Psychotic symptoms with a duration of > 1 month and < 6ÔłŹ‚É£ months

Psychotic symptoms such as auditory or visual hallucinations are common, as is a
premorbid history of being ‚Äúweird‚ÄĚ or a ‚Äúloner.‚ÄĚ


Delusional Disorder

Clinical features:

  • ‚Č•1 delusions for ‚Č• 1ÔłŹ‚É£ month
  • Other psychotic symptoms absent or not prominent
  • Behavior not obviously odd/bizarre; ability to function apart from delusion's impact
  • Subtypes: Erotomanic, grandiose, jealous, persecutory & somatic

Delusional disorder may be subtyped based on delusional themes:¬† persecutory (eg, being poisoned, harassed, plotted against)[pt. is commonly verbally/physically abusive], ūüíĖ¬†erotomanic (false belief that someone of higher status is in love with them), grandiose (great talent, insights, or achievements), jealous (unfaithful partners), and somatic (bodily functions and sensations [eg. odor]), Unspecified (Capgras syndrome), mixed.¬†¬†

Autoscopic psychosis (visual hallucination of a transparent phantom of one’s
own body). Capgras syndrome (delusion of doubles) familiar persons have been replaced by identical imposters who behave exactly like the original person. Lycanthropy is the delusion that the person is a werewolf or other animal. Cotard syndrome is the false perception of having lost everything, including money, status, strength, health, and internal organs. Folie á deux is a shared psychotic disorder in which one person develops psychotic symptoms similar to the ones a long-term partner has been experiencing.


  • Schizophrenia: Other psychotic symptoms present (eg, hallucinations, disorganization, negative symptoms); greater functional impairment
  • Personality disorders: Pervasive pattern of suspiciousness (paranoid), grandiosity (narcissistic), or odd beliefs (schizotypal), but no clear delusions.


  • Antipsychotics
  • Cognitive-behavioral therapy


Oppositional defiant disorder (ODD)


Pattern of angry/irritable mood, argumentative/defiant behavior, or vindictiveness for ‚Č•6 months

  • Argues with adults, defies authority figures, refuses to follow rules
  • Deliberately annoys others
  • Blames others for own mistakes or misbehavior
  • Easily annoyed, angry, resentful, or vindictive
  • Not due to another mental disorder

The oppositional behaviors must be excessive compared to normative, age-appropriate behaviors and observed during interactions with individuals other than siblings. 


  • Parent management training
  • Psychotherapy (anger management, social skills training)
  • No pharmacotherapy for ODD but assess for comorbid ADHD & treat if present

Management programs in which parents are trained to reward prosocial behavior and use brief, non-aversive consequences for misbehavior. 

Individual or group psychotherapy focusing on anger management and problem-solving and social skills is also beneficial. 

Children with ODD should be assessed for attention-deficit hyperactivity disorder (ADHD), a common comorbid condition.  Treating ADHD can help to reduce behaviors that frequently put them in conflict with parents and other adults.


Conduct Disorder

Characterized by more severe and aggressive behaviors (eg, physical aggression or cruelty toward people or animals, destruction of property, stealing, lying).  However, ODD can precede the development of conduct disorder and increases the risk of adult antisocial behavior, impulse control problems, substance abuse, anxiety, and depression.

Infants with ‚Äúdifficult‚ÄĚ temperaments, as¬†opposed to ‚Äúeasy‚ÄĚ temperaments, have been shown to be at risk in the early¬†school years for conduct problems. This correlation, although somewhat¬†weaker, is also present through adolescence.