USMLE Step 3 (Subject) / Psychiatry (Lesson)

First Aid Step 3

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• Benzodiazepines Short duration of action: Midazolam, Triazolam, Alprazolam, Oxazepam- Indications: Procedural sedation, Anesthesia induction, Sleep-onset insomnia   Intermediate duration of action: Tamazepam, Lormetazepam- Indications: Sleep-onset as well as sleep-maintenance insomnia, Anxiety disorders Long duration of action: Lorazepam, Diazepam, Clonazepam, Chlordiazepoxide, Tetrazepam- Indications: Anxiety and panic attacks, Stress disorders, Night terrors, Eclampsia (second line), Acute episodes of paranoia, Muscle relaxation, Epilepsy (including status epilepticus), Alcohol withdrawal syndrome Lorazepam, Oxazepam, and Temazepam are preferred in those who drink a LOT because they are not metabolized by the liver and therefore safe in alcoholic liver disease.
• Benzodiazepine-like substances (Z-drugs) Agents:- Zolpidem (imidazopyridine): half-life up to 4.5 hours- Zaleplon (pyrazolopyrimidine): half-life ∼ 1 hour- Eszopiclone: half-life ∼ 6 hours Indication: Sleep disorders (especially with difficulty falling asleep) Mechanism of action:- Similar to benzodiazepines: Show selectivity for GABAA receptors containing α1 subunits- Less of an effect on sleep architecture compared to benzodiazepines
• Buspirone Mechanism of action: A5-HT1A partial agonist. Indications:- GAD and chronic anxiety- Augmentation of depression or OCD therapy- Patients with a history of substance abuse. - May also be used when sedation poses a potential risk. - Unlike benzodiazepines, it has no anticonvulsant or muscle relaxant properties. - Few side effects and no tolerance, dependence, or withdrawal. Relative contraindications: - Has slow onset of action and lower efficacy than benzodiazepines.- Should not be used with MAOIs. - Not effective as a PRN anxiolytic (chronic increases in 5-HT are anxiolytic, but acute increases cause anxiety).
• Selective serotonin reuptake inhibitors Drugs: Fluoxetine, Paroxetine, Sertraline, Citalopram, Escitalopram, Fluvoxamine Indications:- Major depressive disorder (first-line therapy)- Generalized anxiety disorder (GAD)- Obsessive-compulsive disorder (OCD)- Post-traumatic stress disorder (PTSD)- Panic disorder- Premature ejaculation- Premenstrual dysphoric disorder- Binge-eating disorder- Bulimia nervosa- Gambling disorder- Somatic symptom disorder- Irritable bowel syndrome Side effects:- Sexual dysfunction (e.g., anorgasmia, erectile or ejaculatory dysfunction, ↓ libido)- Diarrhea, nausea, vomiting  - Agitation- Insomnia- Headache- Serotonin syndrome Drug interactions: increased risk of serotonin syndrome if used concomitantly with other serotonergic drugs (e.g., MAOIs, linezolid, St. John's wort, dextromethorphan, meperidine, methylene blue)- Can ↑ warfarin levels because of P-450 interactions. Additional information:- Typically takes 4-6 weeks before SSRIs begin to reduce symptoms- In the first trimester of pregnancy, paroxetine increases the risk of fetal cardiovascular malformations; in the third trimester, it increases the risk of pulmonary hypertension in the fetus.
• Bupropion Mechanism of action: not fully understood, but thought to increase dopamine and norepinephrine levels via reuptake inhibition   Indications:- Smoking cessation: used in conjunction with counseling and nicotine replacement- Major depressive disorder- Effective or patients who have had sexual side effects rom other antidepressants. Side effects:- Reduction of seizure threshold: Bupropion should be avoided in patients at increased risk for seizure (e.g., history of epilepsy, anorexia/bulimia, alcohol or benzodiazepine withdrawal).- Tachycardia, palpitations- Dry mouth- Weight loss- Neuropsychiatric symptoms: insomnia, agitation, headache Drug interactions: risk of serotonin syndrome if used concomitantly with other serotonergic drugs
• Serotonin-norepinephrine reuptake inhibitors Mechanism of action: inhibition of serotonin and norepinephrine reuptake in synaptic cleft → ↑ serotonin and norepinephrine levels   Drugs: Venlafaxine, Duloxetine, Desvenlafaxine, Levomilnacipran, Milnacipran Indications:- Major depressive disorder (second-line therapy)- Generalized anxiety disorder- Neuropathic pain- Fibromyalgia: duloxetine and milnacipran- Stress incontinence in women: duloxetine  - Social anxiety disorder, OCD, panic disorder, and PTSD: venlafaxine Side effects:- Similar profile to SSRIs - Increased blood pressure- Sedation- Nausea Drug interactions: risk of serotonin syndrome if used concomitantly with other serotonergic drugs Additional information: Blood pressure should be well-controlled before initiating SNRI therapy.
• Mirtazapine Mechanism of action:- Selective α2-adrenergic antagonist → ↑ serotonin and norepinephrine release- 5-HT2 and 5-HT3 receptor antagonists → ↑ effect of serotonin on free 5-HT1 receptor → likely causes antidepressant effects- H1 antagonist Indications: major depressive disorder, especially in patients who are underweight and/or who have insomnia Side effects:- ↑ Appetite and weight gain- Sedation (due to H1 antagonism)- ↑ Serum cholesterol and triglyceride levels- Minimal sexual side effects- Dry mouth Drug interactions: risk of serotonin syndrome if used concomitantly with other serotonergic drugs
• Serotonin antagonist and reuptake inhibitors Mechanism of action:- Block postsynaptic type 2 serotonin receptors (5-HT2) - Weak inhibition of serotonin reuptake → ↑ serotonin levels- Antagonist of H1 and α1-adrenergic receptors Drugs: Trazodone, Nefazodone Indications:- Insomnia- Major depressive disorder (high doses required) Side effects:- Priapism- Sedation (due to H1 antagonism)- Orthostatic hypotension- Nausea Drug interactions: risk of serotonin syndrome if used concomitantly with other serotonergic drugs Additional information:- Mainly used as an adjunct to other antidepressants for treating insomnia associated with depression  - Two-week washout period before starting other serotonergic drugs
• Tricyclic antidepressants Mechanism of action: inhibition of serotonin and norepinephrine reuptake in synaptic cleft → ↑ serotonin and norepinephrinelevels   Drugs:- Secondary amines: Nortriptyline, Desipramine, Protriptyline, Amoxapine- Tertiary amines: Amitriptyline, Clomipramine, Doxepin, Imipramine, Trimipramine Indications:- Major depressive disorder (third- or fourth-line therapy)- Neuropathic pain (e.g., peripheral neuropathy, diabetic neuropathy, postherpetic neuralgia)- Chronic pain (including fibromyalgia)- Migraine prophylaxis- OCD: clomipramine- Nocturnal enuresis: imipramine Side effects:- Orthostatic hypotension  - Cardiotoxicity due to Na+ channel inhibition in the myocardium: changes in cardiac conductivity velocity, arrhythmias, prolonged QT interval (predisposes to torsades de pointes), wide QRS complex- Tremor- Respiratory depression- Hyperpyrexia- Anticholinergic symptoms (more common with tertiary amines)→ Cardiovascular: tachycardia, arrhythmia (including ventricular fibrillation), hypotension→ CNS: confusion, hallucinations, sedation, coma, seizures→ Gastrointestinal: intestinal ileus, constipation→ Genitourinary: urinary retention→ General: xerostomia, mydriasis, hyperthermia, dry skin- Certain TCAs (e.g., clomipramine) are associated with hyperprolactinemia.   Contraindications: Tertiary amines should be avoided in the elderly because of their side-effect profile. Drug interactions:- Risk of serotonin syndrome if used concomitantly with other serotonergic drugs- Risk of anticholinergic toxicity Additional information: rarely used as a first- or second-line antidepressant today because of extensive side-effect profile and risk of lethal overdose (ingestion of a one-week supply can be fatal)
• Monoamine oxidase inhibitors Mechanism of action  :- Inhibition of monoamine oxidase → ↓ breakdown of epinephrine, norepinephrine, and serotonin → ↑ levels of epinephrine, norepinephrine, and serotonin- Selegiline: selective MAO-B inhibitor → ↑ levels of dopamine Drugs: Tranylcypromine, Phenelzine, Selegiline, Isocarboxazid Indications:- Major depressive disorder (third- or fourth-line therapy); particularly effective treatment for atypical depression- Parkinson disease: selegiline (as an adjunct to carbidopa-levodopa) Side effects:- CNS stimulation- Sexual dysfunction- Orthostatic hypotension- Weight gain- Hypertensive crisis with ingestion of foods containing tyramine (e.g., aged cheeses, smoked/cured meats, alcoholic beverages, dried fruits)   Drug interactions: risk of serotonin syndrome if used concomitantly with other serotonergic drugs Additional information:- Rarely used due to poor side-effect profile- For the treatment of depression, selegiline is available as a transdermal patch (the oral form is only used for Parkinson disease).
• First-generation antipsychotics High potency: Haloperidol, Fluphenazine, Perphenazine, Trifluoperazine, PimozideIndications:- Schizophrenia- Bipolar disorder- Acute psychosis- Delirium- Acute agitated states  - Tourette syndrome- OCD (concomitant therapy)Side effects:- Hyperprolactinemia  - Extrapyramidal symptoms most common in high-potency FGAs- Prolonged QT interval- Neuroleptic malignant syndrome- Metabolic and anticholinergic effects less pronounced Low-potency antipsychotics: Chlorpromazine, Thioridazine, PromethazineIndications:- Acute agitation- DeliriumSide effects:- Anticholinergic effects, sympatholytic effects, metabolic effects, and sedation dominate- EPS less common
• Second-generation antipsychotics Drugs: Clozapine, Olanzapine, Risperidone, Quetiapine, Amisulpride, Ziprasidone, Aripiprazole, Lurasidone, Asenapine, Iloperidone, Paliperidone Indications:- Schizophrenia- Bipolar disorder- Acute psychosis- Postpartum psychosis- MDD with psychotic features- OCD (concomitant medication)- Tourette syndrome- Huntington disease Side effects:- Metabolic effects (usually weight gain, hyperglycemia, dyslipidemia) most prominent- Sedation, somnolence- Prolonged QT interval- Hyperprolactinemia (less pronounced than in FGAs)- EPS less common- Anticholinergic and sympatholytic effects- Neuroleptic malignant syndrome- Clozapine can cause agranulocytosis.
• Extrapyramidal symptoms (EPS) A collection of movement disorders that are typically due to disruption of dopaminergic pathways in the basal ganglia, resulting in bradykinesia, rigidity, dystonia, athetosis, chorea, ballismus, akathisia, tics, and tremors. Etiology: All antipsychotics that interact with the D2 receptor may cause EPS, but the probability of this side effect is significantly higher with high-potency antipsychotics.- Metoclopramide, although not an antipsychotic, may also cause extrapyramidal symptoms. Pathophysiology: Inhibition of the nigrostriatal dopaminergic pathways results in EPS.- First-generation high-potency antipsychotics: D2 antagonism → EPS- Second-generation antipsychotics: weaker D2 antagonism → fewer EPS Acute dystonia:- Onset: Hours to days- Painful and lasting muscle spasmspredominantly affecting the head, neck, and tongue  → Facial grimacing, torticollis→ Tongue protrusion or twisting→ Oculogyric crisis  → Opisthotonus of the back- Acute treatment: anticholinergics or antihistamines→ First-line: benztropine→ Alternatives: Diphenhydramine, Benzodiazepines (e.g., diazepam)- Switch to an antipsychotic drug with lower risk of EPS (SGA) or begin secondary prophylaxis with benztropine- Prophylaxis using benztropine or diphenhydramine is recommended for patients who receive intramuscular haloperidol (especially individuals with little prior exposure to FGA). Pseudoparkinsonism:- Onset: Week 1- Cogwheel rigidity, stiff gait, tremor- Dose reduction or switch to an antipsychotic drug with lower risk of EPS (SGA)- Anticholinergic (e.g., benztropine) or a dopamine agonist (e.g., amantadine) Akathisia:- Onset: Weeks 1-8- Restlessness/compelling urge to move- Inability to sit or stand still- Dose reduction or switch to an antipsychotic drug with lower risk of EPS (SGA)→ First-line: propranolol→ Alternative: Benztropine, Benzodiazepines Tardive dyskinesia:- Onset: Months-years- Involuntary movements of the mouth and tongue; limbs, face, and respiratory muscles caused by chronic use of antipsychotic drugs→ Repetitive chewing and lip smacking→ Choreic movements- Discontinuation of antipsychotic drug- Switch to SGA (less EPS)- Anticholinergics or antipsychotic dose reduction may initially worsen the condition.- Treatment: valbenazine and tetrabenazine (VMAT inhibitor)
• Lithium Indications:- First-line therapy for bipolar disorder- Treatment-resistant depression to augment antidepressants Side effects: Side effects occur at therapeutic levels (0.8-1.2 mEq/L) but tend to be more severe at peak serum concentration of the drug.- Fine tremor: One of the most common side effects of lithium use- Nausea, diarrhea- Polyuria, polydipsia- Weight gain  - Acne- Worsens psoriasis- Muscle weakness- Dry oral mucosa- Leukocytosis- Hair thinning- ECG changes: T-wave depressions (most common), U waves, repolarization abnormalities- Sinus node dysfunction (most commonly sinus bradycardia)- Hypothyroidism  - Goiter (particularly in second and third trimester of pregnancy)  - Hyperparathyroidism causing hypercalcemia- Nephrogenic diabetes insipidus→ Pathophysiology: lithium interferes with ADH signaling → reduces aquaporins (water channels) on the collecting duct cell's surface → fewer water molecules are reabsorbed and kidneys are unable to concentrate urine → increased free water excretion→ Clinical features: polyuria, nocturia, and polydipsia → increased risk of dehydration and subsequent lithium toxicity→ Treatment: amiloride  - Chronic interstitial nephritis (lithium-associated nephropathy) → Can progress to chronic kidney disease- Teratogenicity: cardiac malformations, in particular Ebstein anomaly (0.1% risk)
• Valproate Indications:- First-line long-term treatment for tonic-clonic generalized seizures- Partial (focal) seizures- Absence seizures- Myoclonic seizures- Bipolar disorder Mechanism of action:- Inhibits GABA transaminase → ↑ GABA → decreased neuronal excitability- Inactivates Na+ channels Side effects:- Gastrointestinal upset (e.g., abdominal discomfort)- Hepatotoxicity (rare)  - Teratogenicity- Tremor- Sedation- Ataxia- Alopecia- Pancreatitis- Skin rash- Agranulocytosis- Weight gain
• Carbamazepine Indications:- First-line treatment for tonic-clonic generalized and focal seizures- First-line treatment of trigeminal neuralgia Mechanism of action: Inactives Na+ channels Side effects:- Nausea- Skin rash- Hyponatremia, hyperhydration, and edema (due to SIADH)- Blood count abnormalities (e.g., agranulocytosis, aplastic anemia)- Teratogenicity during the first trimester - Diplopia- Ataxia- Hepatotoxicity- Stevens-Johnson syndrome- Induces cytochrome P-450
• Lamotrigine Indications:- First-line treatment for long-term therapy of focal seizures- Second-line treatment for generalized seizuresand absence seizures- Mood stabilizer for bipolar disorder treatment Side effects:- Exanthema, exfoliative dermatitis, Stevens-Johnson syndrome (slow dose increase necessary to prevent skin and mucous membrane reactions)- Rarely hepatotoxic or nephrotoxic- Blurry vision- Gastrointestinal symptoms
• Autism spectrum disorder Epidemiology:- Prevalence: 14.7/1000 in the US  - Sex: ♂ > ♀ (4:1)- Age: symptoms typically evident before 2-3 years of age Clinical features:- Persistent impairment in communication and social interaction (inability to form relationships, abnormal language development, reduced empathy, difficulties in adjusting behavior to social situations, and poor eye contact)- Restricted, stereotyped patterns of behavior, interests, and activities (e.g., hand flapping, excessive touching/smelling, lining up toys, adverse response to sounds, and echolalia)- Intellectual impairment- Language impairment  - Associated conditions:→ Epilepsy→ Other neurodevelopmental and psychiatric disorders, e.g.: Pica, ADHD, Anxiety disorder- Genetic disorders, e.g., tuberous sclerosis, fragile X syndrome, Rett syndrome   Diagnostics:- Comprehensive evaluation of→ Social interaction and communication skills→ Language and comprehension skills→ Behavior→ Cognitive development→ Associated conditions- Hearing and vision testing: to rule out comorbidities or other causes of developmental delays and behavioral disorders.- Genetic testing: fragile X syndrome, tuberous sclerosis (if any of these conditions is suspected) Treatment:- Early behavioral and educational management  → Competence training: social skills, communication skills→ Establishing clear and consistent structures- Family support and counseling: e.g., parental education on interaction with the child and acceptance of his/her behavior  - Medical treatment  → SSRIs: repetitive stereotyped behavior, anxiety→ Antipsychotic drugs: aggression, self-injury→ Methylphenidate: ADHDRisperidone and aripiprazole are the only FDA-approved drugs for controlling irritability in patients with autism spectrum disorder!
• Fragile X syndrome X-linked dominant disease caused by a change in the expression of the FMR1 gene (fragile X mental retardation 1 gene) → inability to express gene product due to CGG trinucleotide repeat expansion during oogenesis Epidemiology:- After trisomy 21, fragile X syndrome accounts for the most cases of intellectual disability due to a genetic cause. Fragile X syndrome is the most common inherited cause of intellectual disability.- Sex distribution: ♂ >> ♀   Clinical features:- Intellectual disability of varying severity- Delayed language development, autistic behavior- Body structure anomalies: e.g., long and narrow face, big ears, hypermobile joints→ In men: postpubertal macroorchidism (enlarged testes; rarely occurs prior to puberty)- Beyond average height and head circumference- Mitral valve prolapse: can lead to mitral regurgitation- Hyperactivity- Focal seizures Diagnosis:- Molecular genetic detection (PCR, Southern blot)- Cytogenetic detection (not very sensitive)- Echocardiography   Treatment: symptomatic
• Rett's syndrome X-linked disorder with progressive loss of intelligence and cognitive abilities such as language, locomotion, and fine motor skills Etiology: X-linked dominant gene mutation (in methyl-CpG binding protein 2 [MECP2] gene)- Usually not an inherited gene defect, but rather a sporadic mutation. The mutated copy of the MECP2 gene is often associated with the paternal allele, as it occurs randomly during spermatogenesis → primarily females are affected   Clinical features:- Affects females almost exclusively  - Normal development and then onset between 7-24 months of age  - Loss of targeted hand movements with characteristic hand wringing- Truncal ataxia, apraxia, choreatic movements- Intellectual and verbal disability- Seizures- Growth failure Diagnosis: a combination of typical clinical presentation and gene mutation detection  
• Attention deficit hyperactivity disorder (ADHD) Epidemiology:- Sex: ♂ > ♀- Age of onset: usually before age 6- Prevalence: estimated to be 8-11% Comorbidities:- Oppositional defiant disorder- Conduct disorder- Depression- Anxiety disorders- Learning disabilities Diagnostic criteria (according to the DSM-5)A: Pattern of inattention and/or hyperactivity that is inconsistent with the developmental level of the individual and lasts for ≥ 6 months- Inattention is characterized by ≥ 6 of the following in children or ≥ 5 of the following in adolescents and adults (≥ 17 years of age):→ Poor attention to details at work/school→ Difficulty sustaining attention during tasks→ Does not listen when spoken to directly (e.g., distraction in the absence of an obvious interruption)→ Inability to complete tasks/instructions at work/school (e.g., easily sidetracked)→ Struggles to organize tasks/activities (e.g., disorganized work, misses deadlines)→ Prefers to avoid tasks that require a high amount of mental effort (e.g., homework, preparing reports)→ Loses things necessary to complete tasks (e.g., stationery, documents)→ Easily distracted→ Forgetful (e.g., doesn't pay bills, doesn't do homework)- Hyperactivity is characterized by ≥ 6 of the following in children or ≥ 5 of the following in adolescents and adults (≥ 17 years of age):→ Fidgets or squirms in seat→ Often leaving their seat during inappropriate situations (e.g., meetings or in class)→ Restless; runs about in inappropriate situations→ Unable to carry out tasks quietly→ Talks excessively→ Answers questions prematurely or for others→ Difficulty waiting their turn (e.g., has problems with lines)→ Interrupts other people (e.g., in conversation, during activities)B: Several symptoms were present at < 12 years of age.C: Symptoms present in ≥ 2 settings (e.g., school, home, work)D: Interfere with important levels of functioning (e.g., school or work)E: Not due to a mental disorder Treatment:- Behavioral interventions→ Indications: first-line therapy for preschool-aged children, and adjunct therapies for school-aged children and adults→ Socio-educational measures  → Behavioral parent training (BPT): teaches parents how to understand and manage their child's condition, how to manage problematic situations, and how to support positive behavior using operant conditioning.→ Operant conditioning: an approach in which the desired behavior is modified by positive reinforcement (reward) or negative reinforcement (absence of punishment).- Medication→ Methylphenidate. Indication: first-line therapy for patients ≥ 6 years of age→ Atomoxetine. Indications: second-line therapy for patients ≥ 6 years of age; preferred in cases of substance abuse (patient or family member) Prognosis:- The persistence of symptoms after treatment predicts prognosis into adulthood.- In 35-65% of patients, symptoms of ADHD and their associated functional impairment will persist into adulthood.- Patients with ADHD are at higher risk of injury (both unintentional and self-injury), substance use disorder, and antisocial personality disorder.
• Sporadic transient tic disorder - Motor and/or vocal tics - Onset before 18 years of age - Symptoms occur for less than 1 year (resolve spontaneously) - Not explained by any other medical conditions or substance abuse - Do not meet the criteria for Tourette's syndrome
• Persistent motor tic disorder or persistent vocal tic disorder - Motor or vocal tics (not both) - Onset before 18 years of age - Persist > 1 year - Not explained by any other medical conditions or substance abuse - Do not meet the criteria for Tourette's syndrome
• Stereotypic movement disorder - Stereotypic, uncontrolled, repetitive movements lasting ≥ 4 weeks - More common in children, especially boys, with neurological disorders and developmental retardation - Includes rocking movements, hair pulling, hair twisting, and self-destructive behavior (e.g., head banging, picking at skin, hitting oneself)
• Tourette syndrome Epidemiology:- Sex: ♂ > ♀- Age of onset: usually 2-15 years of age Associations:- ADHD and/or OCD (most common)- Learning disabilities- Sleep disorders- Conduct disorder and oppositional defiant disorder- Mood and anxiety disorders Clinical features:- Tics→ Sudden and rapid involuntary, intermittent, nonrhythmic movements or vocalizations without any recognizable purpose→ Temporarily suppressible→ An urge or sensation preceding the tic is relieved by its onset. Vocal tics:- Simple: Throat clearing, Grunting, Lip smacking, Barking, Sniffing- Coprolalia: uttering obscene or socially inappropriate words or phrases  - Echolalia: repeating vocalizations of others Motor tics:- Simple: Facial grimacing, Blinking, Shoulder shrugging, Head jerking- Complex: Jumping, Twisting the body- Echopraxia: repeating movements of others Clinical diagnosis based on all of the following:- Multiple motor tics and at least 1 vocal tic with a variable anatomical location, frequency, number, frequency, complexity, type, or severity over time- Onset before 18 years of age- Lasting > 1 year- Not explained by other medical conditions or substance use (e.g., cocaine) Treatment:- Support: Counseling and education (caregivers and patients)- Behavioral therapy→ Indicated for mild, nondisabling symptoms→ Involves habit reversal training or Comprehensive Behavioral Intervention for Tics (CBIT)- Medical therapy→ Indicated for severe or refractive cases despite behavioral therapy  → Alpha-adrenergic agonists: guanfacine (often first-line therapy), clonidine (very sedating)  → Typical neuroleptic drugs: pimozide or haloperidol (FDA-approved but may cause tardive dyskinesia)  → Atypical neuroleptic drugs: risperidone (increasingly preferred because of fewer side effects)→ Dopamine depleting drugs: tetrabenazine (may be used as first-line therapy to avoid side effects of neuroleptic drugs i.e., dopamine blockade)   Prognosis:- Symptoms peak during adolescence and improve during adulthood.- May resolve spontaneously by 18 years of age (50% of cases)
• Schizophrenia Epidemiology:- Prevalence: < 1% - Sex: ♂ = ♀  - Age of onset: late teens to mid-30s  Risk factors:- Genetic factors: risk significantly increased if relatives are also affected- Environmental factors: Stress and psychosocial factors, frequent use of cannabis, urban environment, birth in late winter or early spring, advanced paternal age at conception Clinical features:- Schizophrenia typically manifests with a prodrome of negative symptoms and psychosis (e.g., social withdrawal) that precedes the positive psychotic symptoms (e.g., hallucinations and bizarre delusions).- Positive symptoms of psychosis→ Hallucinations: perceptual abnormalities in which sensory experiences occur in the absence of external stimuli.→ Illusions: a perceptual abnormality, in which real external stimuli are misinterpreted→ Delusions: fixed, false beliefs that are maintained despite being contradicted by reality or rational arguments.→ Disorganized thought and speech processes- Negative symptoms of psychosis→ Flat affect: reduced or absent emotional expression→ Avolition: reduced or absent ability to initiate purposeful activities→ Alogia: impaired thinking that manifests with reduced speech output or poverty of speech (e.g., always replying to questions with one-word answers)→ Anhedonia: inability to feel pleasure from activities that were formerly pleasurable or from any new positive stimuli→ Apathy: lack of emotion or concern, especially with regards to matters that are normally considered important→ Emotional and social withdrawal- Cognitive symptoms- Mood symptoms and anxiety- Catatonia: A behavioral syndrome characterized by abnormal movements and reactivity to the environment   Diagnostic criteria include (according to DSM-5): At least two of the following symptoms, at least one of which is from the top three:1. Delusions2. Hallucinations3. Disorganized speech4. Grossly disorganized or catatonic behavior5. Negative symptoms- The above symptoms persist for ≥ 1 month over a period of ≥ 6 months.- Symptoms must cause social, occupational, or personal functional impairment lasting ≥ 6 months.- Schizoaffective disorder and mood disorder with psychotic features have been ruled out.- Medical or substance use disorder has been ruled out. Treatment:- Establish a therapeutic alliance when taking care of patients with delusions.- Acknowledge the patient's emotional state.- Avoid validation of delusions or confronting patients about the delusional nature of their symptoms.- Initial response to treatment during the first 2-4 weeks is associated with a better long-term response.  - Hospitalization if acutely psychotic  - Pharmacotherapy → Acute psychotic episode: short-acting antipsychotics  → Acute manic episode: mood stabilizers (e.g., lithium, valproate, carbamazepine)→ First-line treatment: second-generation antipsychotics (e.g., risperidone, quetiapine), which are especially effective at treating positive psychotic symptoms→ Alternative treatment: first-generation antipsychotics in depot form for those at risk of poor adherence (e.g., fluphenazine, haloperidol, chlorpromazine)→ Treatment-resistant schizophrenia: clozapine for persistent positive symptoms (i.e., delusions, hallucinations, and/or disorganized speech) despite trials of ≥ 6 weeks of 2 different antipsychotics at their maximum doses  → Treatment during pregnancy: first-generation antipsychotics (e.g., haloperidol) as a first-line treatment→ Treatment of depression: SSRIs or tricyclic antidepressants (e.g., sertraline, imipramine)→ Treatment of anxiety: SSRIs- Psychoeducation (used as an adjunct to avoid relapse)
• Major depressive disorder Epidemiology:- Sex: ♀ > ♂- Lifetime prevalence: 10-20% - Age of onset: 3rd decade of life Diagnostic criteria for major depressive disorder (according to DSM-5)A: Five or more of the nine symptoms listed below, for at least 2 weeks, with at least one of the symptoms being depressed mood or anhedonia- Depressed mood for most of the day, almost every day- Sleep disturbance (insomnia or hypersomnia)- Anhedonia- Feelings of worthlessness or disproportionate guilt- Fatigue or loss of energy- Diminished concentration, cognition, and ability to make decisions (pseudodementia)- Weight change due to appetite change- Psychomotor changes (observed by others): Agitation, Retardation  - Suicidal ideationB: There is clinically significant distress or impaired functioning in important areas of life (e.g., work, school).C: Symptoms are not due to the effects of psychoactive substances or organic disease.D: Symptoms are not due to another psychiatric disorder.E: There is no history of a manic or hypomanic episode. Laboratory evaluation: indicated to rule out organic disease- Thyroid function tests: to rule out hypothyroidism, which can manifest with lethargy, cognitive impairment (slowed mentation, poor concentration), psychomotor retardation, social withdrawal, and depressed mood- Urine toxicology: to screen for drug use causing depressive symptoms, such as benzodiazepine withdrawal, amphetamine use, and cocaine “crash”- Neuroimaging: to evaluate for structural brain disease if suspected Treatment approach:- For initial treatment of adult patients, pharmacotherapy and psychotherapy can be used alone or in combination.- For nonresponders to initial pharmacotherapy, consider one of the following:→ Switching the modality to psychotherapy→ Adding psychotherapy→ Switching to another antidepressant  → Adding an augmenting agent  - Therapy should be continued until the patient is in remission.- Patients with ≥ 3 prior major depressive episodes or chronic MDD (≥ 2 years) should receive maintenance therapy. Therapeutic principles:- Initial treatment: 6-12 weeks- If the patient is in remission, continue antidepressants for at least 4-9 months (continuation phase).- If the patient has had ≥ 3 prior major depressive episodes or severe episodes (e.g., including suicide attempt or psychosis) or has risk factors for recurrence, or chronic MDD, continue antidepressants for at least 1-3 years (maintenance phase).  
• Bipolar disorder Epidemiology:- Sex: ♀ = ♂  - The average age of onset is 20 years; the frequency of depressive and manic episodes increases with age. Diagnostic criteria according to DSM-V- Abnormally elevated, expansive, or irritable mood and increased goal-directed behavior not attributable to an organic psychic disorder or psychotropic substances.- ≥ 3 of the following:→ Increased goal-directed activity (sexually, at work, and/or socially) or psychomotor agitation→ Increased talkativeness or pressure of speech→ Flight of ideas or racing thoughts→ Loss of social inhibitions, socially inappropriate and reckless behavior, aggressiveness, and hostility→ Decreased need for sleep→ Heightened self-esteem or grandiosity→ Distractibility Manic episode:- Duration: Most of the day for at least 1 week- Significant dysfunction (work/school), patient requires hospitalization (risk of harm to self or others), or there are psychotic features Hypomanic episode:- Duration: Most of the day for at least 4 consecutive days- Does not result in significant dysfunction, hospitalization, or present with psychotic features Bipolar I disorder: at least one episode of mania; major depressive episodes usually occur but are not required for diagnosisBipolar II disorder: at least one episode of hypomania and one major depressive episode; no episodes of mania (distinguishing feature from bipolar I) Acute treatment:- Reduce external stimuli.- Assess for possible contributing substances (e.g., cocaine, alcohol, phencyclidine, etc.).- Limit access to cars, bank accounts/credit cards, cell phones, etc., because of the potential for reckless behavior.- Mild to moderate mania: lithium monotherapy or atypical antipsychotics (olanzapine, quetiapine)- Severe mania: mood stabilizer (lithium or valproate) PLUS antipsychotic→ If a patient doesn't respond to medication within 1-3 weeks, continue with the antipsychotic and switch lithium to valproate or vice versa.→ If a patient is still not responsive, switch the antipsychotic to another antipsychotic drug.→ If a patient has refractory mania, discontinue pharmacotherapy and switch to ECT.- Mania/hypomania in pregnancy: typical antipsychotics (e.g., haloperidol) or ECT (if severe or refractory mania) → Management of agitation: rapid-acting intramuscular atypical antipsychotics (olanzapine, aripiprazole) or benzodiazepines (e.g., lorazepam)  Long-term maintenance treatment:- Maintenance therapy is indicated following even a single manic episode.- Treat for at least 1 year following an acute manic episode.- In patients who experience 2 or more episodes, long-term or lifetime therapy should be considered.- First-line: mood stabilizers→ Lithium  → Valproic acid (useful for patients with renal dysfunction) → Lamotrigine→ Carbamazepine- Refractory or severe bipolar episodes: combination therapy with lithium or valproic acid PLUS atypical antipsychotic (e.g., quetiapine, aripiprazole, olanzapine, risperidone)- Severe depression or predominantly depressive bipolar II disorder: Antidepressants may be started after initiating mood stabilizers.
• Specific phobias Persistent and intense fears of one or more specific situations or objects (phobic stimuli); always occurs during encounters with the phobic stimulus but may already surge in anticipation of an encounter. Epidemiology:- Lifetime prevalence: approx. 5-10% of the population- The average age of onset depends on the specific phobia (e.g., animal phobias more commonly develop in early childhood).- ♀ > ♂ (2:1)   Common phobias:- Animal: spiders (arachnophobia), insects (entomophobia), dogs (cynophobia)- Natural environment: heights (acrophobia), storms (astraphobia)- Blood-injection-injury: blood (hematophobia), needles (blenophobia), dental procedures (odontophobia), fear of injury (traumatophobia)- Situational: enclosed places (claustrophobia), flying (aviophobia)- Other: fear of vomiting (emetophobia), the number 13 (triskaidekaphobia), costumed characters (masklophobia), fear of clowns (coulrophobia) Treatment:- First-line: CBT- Alternative: benzodiazepine or SSRIs  
• Agoraphobia Pronounced fear or anxiety of being in situations that are perceived as difficult to escape from or situations in which it might be difficult to seek help Epidemiology:- ♀ > ♂ (2:1)- Age of onset: < 35 years (60-70% of cases) Clinical features:- Fear, anxiety, or even panic attacks over a period of ≥ 6 months in ≥ 2 of the following 5 situations:→ Using public transportation→ Being in open spaces→ Being in enclosed places→ Standing in line or being in a crowd→ Being outside of the home alone- Active avoidance of these settings unless a companion is present- Some patients can have comorbid panic disorder. Treatment:- CBT- SSRIs
• Panic disorder Recurrent spontaneous and unexpected panic attacks that often occur without a known trigger Epidemiology:- Lifetime prevalence: approx. 5% of the population- Most common in patients aged 26-34 years- ♀ > ♂ (2:1) Associations:- Agoraphobia- Substance use- Depression- Bipolar disorder Symptoms:- Recurrent panic attacks:→ Episodes of intense fear and discomfort that last for several minutes→ Fear of dying- Overstimulation of the sympathetic system→ Sweating, palpitations→ Paresthesias, abdominal pain, nausea, light-headedness, chest pain, shortness of breath, choking sensation- There is a concern about future attacks and their consequences, and/or a significant change in behavior related to the attacks, for at least one month. Treatment:- Acute panic attack:→ Short-acting benzodiazepine (e.g. alprazolam)→ If hyperventilation: breathing in a paper bag  - Long-term management:→ CBT→ Antidepressants: SSRIs, SNRIs, TCAs→ Benzodiazepines may be used until antidepressants take effect.
• Generalized anxiety disorder Prolonged and excessive anxiety that is either unspecific or revolves around certain themes (e.g., health, work); not focused on a single specific fear Epidemiology:- Most common anxiety disorder among the elderly population- Lifetime prevalence: 5-10%- ♀ > ♂(2:1) Symptoms:- Prolonged (≥ 6 months, occurring more days than not) and excessive anxiety- Anxiety causes clinically significant distress- Not caused by substance use, medication, or underlying medical condition- Fatigue and muscle tension- Restlessness and irritability- Sleep disturbances and difficulty concentrating Treatment:- First-line: psychotherapy, pharmacotherapy, or both  → Psychotherapy: CBT, applied relaxation therapy, biofeedback→ Pharmacotherapy: SSRIs/SNRI- Second-line: → Benzodiazepines can be used until SSRIs take effect but should never be used for long-term management, as they increase the risk of benzodiazepine dependence.→ Buspirone: requires consistent, daily intake for at least two weeks because of its delayed onset of action→ Antipsychotics only for refractory cases
• Obsessive-compulsive disorder (OCD) Epidemiology:- Sex: ♀ ≥ ♂- Age of onset: average is 20 years of age- Lifetime prevalence: approx. 2% Symptoms:- Egodystonic: behavior patterns are not in agreement with ideal self-image- Obsessions: recurring and intrusive thoughts- Compulsions: repetitive actions to provide relief from anxiety caused by obsessions Comorbidities:- Anxiety disorders- Depressive disorders- Bipolar disorders- Tic disorders- Personality disorders- Schizophrenia or schizoaffective disorder Diagnostic criteria (according to the DSM-5- Obsessions (e.g., thoughts about contamination, harm, or symmetry) defined by both: → Recurrent/persistent, intrusive thoughts, or urges that cause anxiety or distress→ Attempts to suppress these thoughts or urges- Compulsions (e.g., repeatedly washing hands, opening and closing a door multiple times, or rearranging objects on a desk) defined by both: → Repetitive behaviors or mental actions (e.g., counting, repeating words) that the individual feels compelled to perform, in order to relieve anxiety brought upon by the obsessions.→ These behaviors or mental actions may be performed in an attempt to prevent some perceived dreaded event, though they tend to be excessive and not connected in any realistic way to the event.- Time-consuming (E.g., ≥ 1 hour/day), or result in significant distress/impairment (school, work)- Not due to substance-use disorders or another medical condition- Not due to another mental disorder (e.g., anxiety disorders, eating disorders) Treatment:- Cognitive-behavioral therapy (CBT)→ Cognitive therapy techniques→ Exposure therapy- Pharmacotherapy→ SSRIs are the preferred treatment (e.g., sertraline, paroxetine, fluoxetine, fluvoxamine).→ Alternatively, tricyclic antidepressants with serotonergic action (e.g., clomipramine)→ Atypical antipsychotics (e.g., risperidone, aripiprazole, quetiapine)
• Body dysmorphic disorder Epidemiology- Point prevalence: ∼ 2%- ♂ ≈ ♀  - Mean age of onset: ∼ 17 years Diagnostic criteria (according to the DSM-5)- Persistent preoccupation with a perceived flaw in one's physical appearance- Flaws are mild or not observable by others.- Repetitive behaviors (e.g., skin scratching) or thoughts (e.g., comparing oneself to others)- Clinically relevant impairments in functioning and/or clinically relevant distress- In order to diagnose BDD, an eating disorder that might also explain the symptoms should be ruled out. Treatment: cognitive behavioral therapy, SSRIs
• Hoarding disorder Epidemiology:Point prevalence: ∼ 2-6%- ♂ > ♀ Diagnostic criteria (according to the DSM-5):- Persistent urge to keep items; distress associated with getting rid of items- Difficulty discarding belongings- Accumulation of belongings → intended use of belongings is compromised and living areas are cluttered- Clinically relevant impairment in functioning and/or clinically relevant distress- Not explained by other medical conditions (e.g., brain injuries) or mental illness (e.g.; OCD) Treatment: cognitive behavioral therapy, if CBT fails: trial of SSRI (off-label use)  
• Hoarding disorder Epidemiology:Point prevalence: ∼ 2-6%- ♂ > ♀ Diagnostic criteria (according to the DSM-5):- Persistent urge to keep items; distress associated with getting rid of items- Difficulty discarding belongings- Accumulation of belongings → intended use of belongings is compromised and living areas are cluttered- Clinically relevant impairment in functioning and/or clinically relevant distress- Not explained by other medical conditions (e.g., brain injuries) or mental illness (e.g.; OCD) Treatment: cognitive behavioral therapy, if CBT fails: trial of SSRI (off-label use)  
• Post-traumatic stress disorder (PTSD) Distressing symptoms related to a specific traumatic event and lasting > 1 month following the event Epidemiology:- Lifetime prevalence: 6-9%- Sex: ♀ > ♂ (4:1) Triggers (either through direct experience or as a witness): Sexual abuse (most common), physical abuse, accidents, natural disasters, war, diagnosis of a severe disease Risk factors:- Psychiatric comorbidities- Lower socioeconomic status- Younger age at time of trauma- Lack of social support- Prior traumatic exposure and/or subsequent reminders, including childhood experiences- Initial severe reaction to the traumatic event Common comorbidities: depression, substance use disorders, somatic symptom disorder Diagnostic criteria (according to DSM-5):- Experience of a traumatic event involving death (actual or threatened), serious injury, or sexual violence that occurs in ≥ 1 of the following ways:→ Direct experience of these events→ Witnessing these events→ Hearing about these events happening to close friends or family→ Repeated exposure to unpleasant details of traumatic events occurring to others  - ≥ 1 of the following intrusion symptoms that begin after the traumatic event:→ Intrusive thoughts: recollection of psychotraumatic events→ Recurrent, distressing dreams→ Flashbacks: reexperiencing the traumatic event. Flashbacks can last from seconds to days.→ Intense and persistent distress due to internal or external cues related to the traumatic event→ Physiological reactions due to internal or external cues related to the traumatic event- Avoidance of triggering stimuli following the event in ≥ 1 of the following ways:→ Avoidance of memories, thoughts, or feelings associated with the event→ Avoidance of external reminders (e.g., places, people, conversations, objects) related to the event- Negatively affected mood and cognition that begins or worsens after the event in ≥ 2 of the following ways:→ Inability to remember important details of the event→ Severe negative thoughts or expectations about oneself or the world→ Distorted memories of the cause and/or consequences of the event→ Constant negative emotions (e.g., fear, guilt)→ Reduced or absent interest in important life activities→ Detachment from others→ Inability to feel positive emotions (e.g., happiness, satisfaction, or love)- Altered reactivity or arousal beginning or worsening after the event in ≥ 2 of the following ways:→ Irritability or angry outbursts→ Self-destructive behavior→ Hypervigilance→ Heightened startle reflex→ Poor concentration→ Sleep disturbance- Duration: Symptoms in groups B-E last > 1 month following the traumatic event.- The affected individual has been experiencing significant distress or impaired social and/or occupational functioning since the traumatic event.- Symptoms are not explained by substance misuse or another medical condition. Treatment:- Psychotherapy: first-line treatment; with or without adjunctive pharmacotherapy → Exposure therapy (e.g., showing war veterans images of war, returning to the scene of an accident)→ Cognitive processing therapy→ Eye movement desensitization and reprocessing: Under the guidance of a therapist, the patient recalls traumatic images while following the therapist's fingers with their eyes from left to right.  - Pharmacotherapy:→ SSRIs, SNRIs→ Prazosin: for nightmares→ Consider atypical antipsychotics to augment SSRIs and SNRIs.→ Benzodiazepines are rarely used for hyperarousal and anxiety. Their use should be closely monitored because many patients with PTSD are at risk for drug dependence. Prognosis: Approximately 60% of patients have reported a full recovery within an average of 4.5 years following the event with psychotherapy and/or pharmacotherapy.
• Adjustment disorder A maladaptive emotional or behavioral response to a stressor, lasting ≤ 6 months following resolution of the stressor Epidemiology:- Occurs in ∼ 5-20% of individuals undergoing outpatient mental health treatment- Up to one-third of patients with a cancer diagnosis develop this disorder.  Etiology: a combination of intrinsic and extrinsic stressors (e.g., divorce, losing a job, academic failure, difficulties with peer group) Diagnostic criteria (according to DSM-5):- Emotions or behaviors in response to a stressor that occur within 3 months of onset- Clinically significant responses that include ≥ 1 of the following:→ A level of distress that is disproportionate to the expected response to the stressor→ Impaired functioning in social, occupational, and/or other important areas- Symptoms are not explained by another mental disorder.- Symptoms are not explained by a normal response to grief.- Symptoms last ≤ 6 months following resolution of the stressor. Treatment:- Psychotherapy→ First-line treatment: cognitive-behavioral therapy or psychodynamic psychotherapy→ May be provided as individual, family, or group support therapy→ Interpersonal psychotherapy- Pharmacotherapy→ SSRIs: for depressed mood→ Benzodiazepines: for anxiety or panic attacks→ Benzodiazepines or other sedative-hypnotic agents (e.g., zolpidem): for insomnia
• Dissociative identity disorder Epidemiology:- Rare (prevalence < 1%)- More prevalent in women- May manifest at any age- Very common in patients with a history of physical/sexual abuse and/or neglect during childhood (90% of patients) Diagnostic criteria:1. Alternation of at least two separate personality states that cause identity disruption and dominate at different times- Involves discontinuity in sense of self (depersonalization) and agency; altered affect, memory, behavior, perception, consciousness, cognition and/or sensory-motor functioning (derealization)2. Frequent gaps in recall of normal daily events or personal information that are significantly different from ordinary forgetfulness3. Symptoms cause the patient significant social or occupational impairment.4. Symptoms are not related to substance use, another medical condition, or a broadly accepted religious or cultural practice. Treatment: psychotherapy; SSRIs for comorbid conditions (depression, PTSD) Prognosis:- Chronic disease course with fluctuations in severity- Increased risk of other psychiatric conditions (major depression, borderline personality disorder, PTSD, eating disorders, substance use disorders)- High rates of self-harm and suicide
• Depersonalization/derealization disorder Epidemiology: lifetime prevalence ∼ 2%; average age at onset 16 years Diagnostic criteria:1. Recurrent or persistent episodes of depersonalization and/or derealization- Depersonalization: sense of unreality with detachment from oneself (e.g., body perception, feelings, thoughts, actions)- Derealization: sense of unreality with detachment from one's environment2. Reality testing is intact during these episodes.3. Symptoms cause significant social or occupational impairment.4. Symptoms are not due to substance use or another medical condition.5. Symptoms cannot be better explained by another psychiatric disorder (e.g., schizophrenia, major depressive disorder, panic disorder, acute stress disorder, PTSD, other dissociative disorders) Treatment: cognitive behavioral therapy, hypnotherapy, psychodynamic therapy Prognosis:- Often persistent, with fluctuations in severity- Increased risk for concurrent major depression and anxiety disorders
• Somatic symptom disorder Patients with somatic symptom disorder often have multiple physical symptoms that cause significant distress and have a history of extensive (and fruitless) diagnostic testing and medical procedures. Affected patients maintain a preoccupation with their symptoms and health concerns over an extended period. Epidemiology:- ♀ > ♂- Prevalence in adults: ∼ 5-7% Diagnostic criteria (according to DSM-5)- ≥ 1 somatic symptom that causes significant distress or impairment- The patient exhibits excessive thoughts, feelings, or behaviors related to the somatic symptoms or health manifested by ≥ 1 of the following:→ Disproportionate and constant thinking about the severity of symptoms→ Constant anxiety about symptoms or general health→ Excessive amounts of time and energy attending to symptoms or health concerns- Duration: ≥ 6 months Management:- Establish regular visits with a single primary care physician in order to minimize unnecessary testing and procedures.- Gradually begin to address psychological issues with psychotherapy.
• Illness anxiety disorder In illness anxiety disorder (previously known as hypochondriasis), patients present with a persistent preoccupation with having or developing a serious illness. Somatic symptoms are usually absent or mild, but patients spend large amounts of time and energy obsessing over their health and over the possibility of developing a disease. Epidemiology:- ♀ = ♂- Age of onset: usually early adulthood- Strongly associated with comorbid anxiety or depressive disorders Diagnostic criteria (according to DSM-5)- Preoccupation with having or acquiring an illness- Somatic symptoms absent or mild- Significant anxiety over health- Excessive health-related behaviors (e.g., constantly checking for minor signs of illness) or maladaptive avoidance behaviors (e.g., avoiding doc­tor appointments and hospitals)- Duration: ≥ 6 months  - Not better explained by another mental disorder Management:- Cognitive behavioral therapy- Schedule regular visits to one primary care physician.- Treat comorbid disorders (e.g., depression), if present.
• Conversion disorder Patients with conversion disorder (also known as functional neurological symptom disorder) present with neurological symptoms that cannot be fully explained by a neurological condition.   Epidemiology:- ♀ > ♂- Age of onset: ∼ 10-35 years- Strongly associated with comorbid psychiatric or neurological disorders Diagnostic criteria (according to DSM-5):- ≥ 1 neurological symptom (altered motor or sensory function): e.g., paralysis, blindness, muscle spasms, mutism, lump in throat, weakness, gait disorder- Reported symptoms must be incompatible with recognized neurological or medical conditions.- Reported symptoms are not explained better by another medical disorder.- Symptoms cause significant distress or psychosocial impairment. Management:- Patient education- Cognitive behavioral therapy
• Factitious disorder Previously known as Münchhausen syndromePatients intentionally falsify signs and symptoms, even through self-harm (e.g., injecting insulin), to assume the role of a patient Epidemiology:- ♀ > ♂- Associated with history of significant exposure to health care and personality disorders (e.g., narcissistic, borderline, or antisocial personality disorder) Diagnostic criteria (according to DSM-5):A: Intentionally deceptive falsification of disease signs or symptoms, inducing injury, or promoting disease in self  B: Presents himself, herself to others as ill, impaired, or injuredC: Even occurs in the absence of external rewardsD: Behavior is not better explained by another mental disorder.   Factitious disorder imposed on another: Patients intentionally produce symptoms in someone else (usually their child).- ♀ = ♂- Associated with a history of maternal abuse and personality disorders (e.g., narcissistic or borderline personality disorder) In factitious disorders, there is evidence that the individual is intentionally falsifying injury or disease in the absence of external rewards. They can be contrasted with somatic symptom disorder, in which there is no evidence that the individual is behaving deceptively and malingering and external rewards are an incentive!
• Malingering Individuals displaying malingering behavior present with vague complaints, either false or grossly exaggerated, that do not conform to a known medical condition. This is an intentional behavior motivated by an external reward (e.g., avoiding the police; obtaining narcotics, insurance money, sympathy from others, time off work, etc.). Malingering individuals are typically uncooperative and insist on undergoing an extensive medical evaluation. Not classified as a mental disorder.  Epidemiology: ♂ > ♀ Diagnostics: Any combination of the following is suggestive of the condition.- The individual presents under medicolegal circumstances (e.g., self-referral while criminal charges are pending).- Clinical findings do not match up with the individual's complaints.- Lack of patient cooperation during diagnostic evaluation and/or treatment- Features of antisocial personality disorder Management- Confront the patient in a nonthreatening manner (give the patient the opportunity to be honest).- Avoid unnecessary referral (which perpetuates malingering).
• Pica An eating disorder characterized by the appetite for and ingestion of nonnutritive substances (e.g., hair, clay, soil, ice, paint chips). Epidemiology:- Prevalence: highest in children, during pregnancy, and in individuals with psychiatric conditions- Sex: ♀ = ♂ Associations:- Nutritional deficiencies (iron deficiency, zinc deficiency)  - Pregnancy  - Low socioeconomic status- Psychosocial trauma: neglect, abuse, separation  - Intellectual disability- Autism spectrum disorder- Dementia- Schizophrenia Features:- Persistent ingestion of nonnutritive substances for > 1 month that is inappropriate for developmental age and not part of culturally or socially normative practice.  - Possibly, underlying zinc or iron deficiency anemia Complications: e.g., lead poisoning (paint ingestion), GI complications (e.g., bowel obstruction, bowel perforation, bacterial or parasitic infections) Treatment:- Behavioral interventions and nutritional rehabilitation (first-line)- Pharmacotherapy: SSRIs (second-line)
• Anorexia nervosa Epidemiology:- Sex: ♀ > ♂ (10:1)- Peak age: 10-25 years of age   Features:- Significant deliberate reduction in body mass (as measured by BMI) using strategies that include restrictive eating, purging, and excessive exercise.- Fear of weight gain motivates compensatory behavior that promotes weight loss, even if the patient already has low body weight.- Body image disturbance- Lack of awareness of the seriousness of low body weight   Restricting type: No binge eating or purging over a 3-month period→ Suggests weight loss is achieved by excessive dieting, exercise, or fastingBinge-eating/purging type: Presence of binge eating or purging over a 3-month period→ Suggests weight loss is achieved by vomiting, diuretic and laxative abuse, or enemas Severity based on BMIPatients ≤ 20 years of age: BMI below the 10th percentile for sex and age is considered the threshold for being underweight.Patients > 20 years of age- Mild: BMI 17-18.4 kg/m2- Moderate: BMI 16-16.99 kg/m2- Severe: BMI 15-15.99 kg/m2- Extreme: BMI < 15 kg/m2 CNS:- Hypothermia  - Cortical pseudoatrophy with enlargement of the subarachnoid space → possible organic psychosyndrome → disturbed concentration and memory, changes in personality- Seizures   Endocrine disorders:- Stress hormones: ↑ cortisol, ↑ adrenaline- Thyroid: euthyroid sick syndrome- Secondary amenorrhea (severe weight loss suppresses the hypothalamic-pituitary-gonadal axis → hypogonadotropic hypogonadism)- Impaired glucose tolerance- Electrolyte abnormalities (e.g., hypokalemia) Heart: bradycardia, hypotension, cardiac arrhythmia  Bones: secondary osteoporosis and stress fracturesSkin and hair: dry skin, wound healing disorders, hair loss, lanugo body hair, Russell signSalivary glands: sialadenosis with dystrophyDental status: caries and perimolysis due to frequent vomiting   Diagnostics:- Physical exam: BMI < 18.5- Electrolyte imbalances: ↓ potassium, ↓ sodium, ↓ chloride, ↓ phosphate, ↓ magnesium, ↑ bicarbonate (metabolic alkalosis)- ↓ Glucose, pathological tolerance of low glucose levels- Liver enzymes: ↑ AST/ALT- ↑ Serum α-amylase  - Renal function parameters: ↓ creatinine  - Lipids: ↑ cholesterol  - Proteins: hypoproteinemia, hypoalbuminemia- Blood count: pancytopenia Treatment:- Psychotherapy (first-line): Cognitive behavioral therapy, Psychodynamic psychotherapy  - Nutritional support: Monitor weight gain and provide nutritional support; usually through oral intake  (hospitalization if necessary)- Indications for hospitalization:→ < 70% ideal body weight or BMI < 15 kg/m2→ Unstable vital signs: Hypothermia (< 35.5°C), Bradycardia (< 40 bpm), Hypotension or symptoms of lightheadedness→ Acute medical complications (e.g., syncope, seizures, pancreatitis, liver failure)→ Arrhythmia→ Hypoglycemia→ Electrolyte disturbances, marked dehydration→ Severe refeeding syndrome- Contract governing medical treatment: agreement between the patient and caregivers on target weight development and daily number of meals (usually 3-5 meals/day, 500-1000 g weight gain/week) Prognosis:- Chronic, relapsing disease course with various outcomes (complete recovery, symptom fluctuation and relapses, progressive deterioration)   Mortality:- Cumulative mortality rate (∼ 5% per decade)- Most commonly due to severe cachexia/starvation, cardiac failure, or suicide- Increased risk of comorbidities→ Mood disorders (e.g., depression, bipolar disorder)→ Anxiety disorders (e.g., generalized anxiety disorder, social anxiety disorder)→ Personality disorders→ Obsessive-compulsive disorder
• Bulimia nervosa Epidemiology:- Sex: ♀ > ♂ (> 90% of affected individuals are young women)- Peak age: 20-24 years of age Features:- Recurrent binge eating- Recurrent compulsive compensatory behavior to counteract weight gain→ Most frequent: self-induced vomiting after binge eating→ Laxative abuse→ Transient starvation periods→ Other weight-loss measures  - Binge eating and compulsive compensatory behavior both occur at least once a week over a 3-month period.- Sense of self-worth pathologically influenced by the perception of physical appearance (body weight and shape)- Binging and purging do not occur exclusively during episodes of anorexia nervosa Additional clinical features- By definition, the BMI in individuals with bulimia is normal or elevated (≥ 18.5 kg/m2 or ≥ 10th percentile for pediatric patients)  - Dental status: caries and perimolysis due to frequent vomiting  - Esophagitis and/or gastritis- Salivary gland swelling (parotitis)  - Metabolic imbalances: ↓ Potassium, ↓ sodium, ↓ chloride, and ↓ calcium- ↑ Blood pH (metabolic alkalosis)  - Calluses on the knuckles (Russell sign)  - Dry skin and brittle nails- Cardiac arrhythmias  - Hypotension  - CNS: seizures   Treatment:- Psychotherapy (first-line): cognitive behavioral therapy  - Nutritional rehabilitation- Pharmacotherapy: treatment with selective serotonin reuptake inhibitors (e.g., fluoxetine) may help decrease binging/purging cycles.   Prognosis:- The disease course is chronic with relapses.- Mortality: 2-8 times higher than the general population- Increased risk of psychological comorbidities  → Most common: depression, anxiety, and panic disorders (particularly social phobias)→ Attention deficit hyperactivity disorder→ Alcohol and drug addiction or abuse
• Enuresis Repeated involuntary elimination of urine that is inappropriate for developmental age (e.g., pants- or bed-wetting) Epidemiology: affects 5-10% of 5-year-olds; prevalence decreases with age   Risk factors: psychosocial stressors (e.g., recent move, sexual abuse, conflicts in the family), positive family history Associations: other psychiatric disorders, e.g., ADHD, conduct disorders, autism Diagnostic criteria:- Occurs 2x/week for ≥ 3 months or causes clinical distress- Patient's developmental age must be ≥ 5 years- Symptoms not caused by a medication or another medical condition Types:- Nocturnal (♂ > ♀) or diurnal (♀ > ♂)- Primary (patient never achieved continence) or secondary (onset of symptoms after patient had achieved continence) Therapy:- Treatment not typically recommended in children under 5 years of age- In children, treatment may become indicated as soon as enuresis causes distress or impairs social function- Organic causes (e.g., urinary tract infections, urinary tract abnormalities, renal disorders) must be excluded before any treatment is started.- First-line:→ Psychoeducation→ Parent management training→ Fluid restriction at night→ Behavioral training with a urine alarm- Second-line: pharmacological treatment (e.g., desmopressin, imipramine) if first-line treatments fails or to control nighttime enuresis in combination with first-line treatmentsTreatment of enuresis is not indicated before 5 years of age! Most cases resolve spontaneously!
• Insomnia disorder Prevalence: ∼ 10% (most common sleep-wake disorder) Etiology:- Poor sleep hygiene- Subclinical mood or anxiety disorders Classification:- Acute or transient: < 3 months (associated with stress or a disrupted sleep schedule)- Chronic: ≥ 3 months (associated with an increased risk of psychiatric illness and functional impairment) Clinical features:- Initial or sleep-onset insomnia: difficulty initiating sleep- Middle or sleep-maintenance insomnia: frequently waking from sleep- Late or sleep-offset insomnia: awakening early in the morning- Nonrestorative sleep: feeling fatigued after waking DSM-5 diagnostic criteria (primary insomnia is a diagnosis of exclusion)- Problems initiating or maintaining sleep, or awakening in the early morning and being unable to return to sleep- Symptoms occur ≥ 3 days/week for ≥ 3 months- Symptoms cause functional impairment or distress- Symptoms are not caused by an underlying substance or medication use- Symptoms occur despite having enough time to sleep- No underlying or coexisting psychiatric or medical disorder that explains symptoms Treatment:- Improve sleep hygiene→ No alcohol 4-6 hours preceding sleep  → No stimulants (caffeinated drinks and nicotine should be avoided 3-4 hours before bedtime)→ Quiet, dark, pleasantly cool bedroom and a comfortable bed→ No large meals before bedtime→ Regular exercise is beneficial but should be avoided 6 hours before bedtime.- Stimulus control therapy: Insomnia disorder may cause the bed and bedroom to become cues for arousal rather than sleep. Stimulus control instructions aim to correct this by re-establishing the association of the bed and bedroom with sleep. → Advise waking up at regular times (also during the weekend and holidays).→ Discourage engaging in other activities in bed such as working or reading.→ Leave the bedroom when unable to fall asleep within 20 minutes (e.g., to read or listen to music) and return only when sleepy.→ Advise against afternoon naps; if taken, this should not take place after 3 pm and naps should be no longer than 1 hour.- Sleep restriction therapy: A cognitive behavior therapy for patients with chronic insomnia, where the amount of time spent in bed is restricted to their average estimated sleep time. When sleep efficacy (total sleep divided by time spent in bed) is greater than 90%, the amount of time spent in bed is increased. This has been shown to reduce sleep latency.- Cognitive-behavioral therapy (CBT): preferred treatment for chronic insomnia- Pharmacotherapy (use sparingly and short-term)→ Benzodiazepines: ↓ Sleep latency; ↓ awakenings during sleep→ Only for short-term use due to high risk of addiction→ For sleep onset insomnia: short-acting agent, e.g., triazolam→ Antidepressants: trazodone (most commonly prescribed antidepressant for chronic insomnia and depressive symptoms) or amitriptyline→ Non-benzodiazepine sedatives: Zolpidem, eszopiclone, zaleplon→ Lower risk of daytime sleepiness, although falls and cognitive impairment are still a concern (especially in the elderly and individuals using zolpidem)

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