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Psychiatry

Postgraduate-level comprehensive notes covering psychiatric assessment, neurobiology of mental disorders, psychopharmacology, psychotherapies, and clinical management of psychiatric conditions across the lifespan.

11 chapters · MBBS / NEET-PG

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Chapter 1 of 11

General Psychiatry Principles

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General Psychiatry Principles

General Psychiatry PrinciplesPsychiatry

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Chapter 1 of 11

Psychiatric Assessment and Classification

In 30 seconds:

A structured psychiatric assessment — history, MSE, suicide risk — is the foundation of every clinical encounter. Diagnostic classification uses DSM-5-TR and ICD-11, while the biopsychosocial model ties it all together.

Key exam topics:
  • MSE components (appearance through judgment)
  • Suicide risk assessment — SAD PERSONS vs C-SSRS
  • Sleep-wake disorders — insomnia, OSA, narcolepsy
  • Personality disorder clusters (A/B/C)
Most common trap:

Hypoactive delirium is often misdiagnosed as depression in elderly patients. Always screen with CAM.

Psychiatric Assessment

The psychiatric assessment is the cornerstone of clinical psychiatry.
Think of it as the history and physical of mental health — you cannot skip it. It begins with the psychiatric history: identifying data, chief complaints, history of present illness, past psychiatric history, medical and surgical history, family psychiatric history, social history (occupational, interpersonal, forensic aspects), and developmental history. Every piece tells a story.

Sleep-Wake Disorders

Sleep disorders commonly co-occur with psychiatric conditions and must be assessed systematically.
Insomnia disorder: difficulty initiating or maintaining sleep, or early morning awakening, at least 3 nights per week for >3 months, causing significant distress or impairment. CBT-I is first-line treatment.
Hypersomnolence disorder: excessive sleepiness despite adequate sleep duration. Narcolepsy: type 1 with cataplexy (loss of muscle tone triggered by strong emotions, associated with orexin/hypocretin deficiency due to autoimmune destruction of lateral hypothalamic neurons) and type 2 without cataplexy.
Obstructive sleep apnea (OSA) is highly comorbid with depression, anxiety, and PTSD — screening with STOP-Bang questionnaire and polysomnography is essential.
Circadian rhythm sleep-wake disorders: delayed sleep phase type (evening chronotype, common in adolescents), advanced sleep phase type (morning chronotype, elderly), irregular sleep-wake type, and non-24-hour type (common in blind individuals).
Restless legs syndrome (Willis-Ekbom disease) is associated with iron deficiency, renal failure, pregnancy, and dopamine agonist treatment.
Sleep stages: N1 (light sleep, theta waves, 5%), N2 (spindles and K-complexes, 45%), N3 (slow wave/deep sleep, delta waves, 25%), REM (rapid eye movements, low muscle tone, dreaming, 25%). REM sleep increases across the night; N3 decreases. Mnemonic: "Never (N1) Need (N2) Never (N3) REM."
The mental status examination (MSE) is a systematic assessment of the patient's appearance, behavior, speech, mood, affect, thought process, thought content, perception, cognition, insight, and judgment. The MSE is analogous to the physical examination in general medicine and must be performed at every clinical encounter.

Suicide Risk Assessment

Suicide is a major public health problem, accounting for over 700,000 deaths annually worldwide. Clinicians must assess suicide risk at every encounter with patients presenting with depression, psychosis, substance use disorders, or personality disorders.
Risk factors: male sex (3:1 ratio of completed suicide), older age, white ethnicity, unmarried status, unemployment, physical illness, family history of suicide, previous suicide attempts (strongest predictor), psychiatric illness (depression - 50%, bipolar - 20%, schizophrenia - 10%, BPD - 10%), substance use disorders, and access to lethal means.
Protective factors: strong social support, religious affiliation, children in the home, positive therapeutic alliance, and future-oriented thinking. The SAD PERSONS scale (Sex, Age, Depression, Previous attempt, Ethanol, Rational thinking loss, Social support lacking, Organized plan, No spouse, Sickness) provides a structured assessment but has limited predictive validity.
Management of acute suicidality: ensure safety (remove means, consider hospitalization), treat underlying condition, establish crisis plan, provide frequent follow-up. The C-SSRS (Columbia-Suicide Severity Rating Scale) is the gold-standard assessment instrument.

Diagnostic Classification

Diagnostic classification in psychiatry has evolved through the Diagnostic and Statistical Manual of Mental Disorders (DSM-5-TR, published in 2022) and the International Classification of Diseases (ICD-11). The DSM-5-TR uses a multiaxial-like approach through its chapter organization, with specifiers for severity, course, and contextual factors.
Key changes in DSM-5-TR include the reorganization of trauma- and stressor-related disorders, the addition of prolonged grief disorder, and updated specifiers for mood disorders.
ICD-11, adopted by WHO member states, introduces a fully dimensional approach to personality disorders and a streamlined classification of mood disorders.

Biopsychosocial Model

The biopsychosocial model, first articulated by George Engel in 1977, remains the dominant framework in psychiatry.
It posits that biological factors (genetics, neurochemistry, neuroanatomy), psychological factors (personality, coping styles, cognitive schemas), and social factors (family dynamics, cultural context, socioeconomic status) interact to produce mental illness.
A comprehensive formulation integrates these three domains and generates a management plan that addresses each area.

Personality Disorders

A personality disorder is an enduring pattern of inner experience and behavior that deviates markedly from the expectations of the individual's culture, is pervasive and inflexible, has an onset in adolescence or early adulthood, is stable over time, and leads to distress or impairment.
DSM-5-TR organizes personality disorders into three clusters:
Cluster A (odd/eccentric): paranoid, schizoid, schizotypal. Cluster B (dramatic/erratic): antisocial, borderline, histrionic, narcissistic. Cluster C (anxious/fearful): avoidant, dependent, obsessive-compulsive.
The ICD-11 has moved to a fully dimensional model with five personality trait domains (negative affectivity, detachment, dissociality, disinhibition, anankastia) and a severity rating (mild, moderate, severe). Borderline personality disorder (BPD) is characterized by instability in interpersonal relationships, self-image, and affect, with marked impulsivity, fear of abandonment, chronic emptiness, and recurrent suicidal behavior or self-harm.
First-line treatment for BPD is dialectical behavior therapy (DBT), which combines individual therapy, group skills training, phone coaching, and therapist consultation team. Pharmacotherapy targets specific symptom domains (mood stabilizers for affective instability, SSRIs for depression/anxiety, low-dose antipsychotics for cognitive-perceptual symptoms).
BPD criteria ("SUICIDAL" mnemonic): S (Suicidal/self-harm behavior), U (Unstable relationships), I (Impulsivity), C (Chronic emptiness), I (Inappropriate anger), D (Dissociation/stress-related paranoia), A (Abandonment fears), L (Lability of mood/affect). Need ≥5 of 9 criteria.

Cultural Competence

Cultural competence is essential in psychiatric practice.
Culture influences the presentation of symptoms (e.g., somatic presentations of depression in East Asian populations), the interpretation of symptoms, and treatment-seeking behavior.
The Cultural Formulation Interview (CFI) in DSM-5-TR provides a structured approach to incorporating cultural factors into assessment.
The CFI includes domains such as cultural identity, cultural explanations of illness, cultural factors affecting psychosocial environment and functioning, and the cultural elements of the clinician-patient relationship.
Mental Status Examination (MSE) components: Appearance (grooming, posture, eye contact). Behavior (cooperation, psychomotor agitation/retardation, catatonia). Speech (rate, rhythm, volume, fluency, spontaneity). Mood (patient's subjective report, e.g., "depressed," "anxious"). Affect (objective observation: range, stability, appropriateness, intensity). Thought process (linear, circumstantial, tangential, loosening of associations, flight of ideas). Thought content (suicidal/homicidal ideation, delusions, obsessions, phobias, preoccupations). Perception (hallucinations, illusions, derealization, depersonalization). Cognition (alertness, orientation, attention, memory, executive function). Insight (absent, partial, full). Judgment (decision-making capacity).
Brain anatomy illustrating key regions involved in psychiatric disorders
Neuroanatomical regions relevant to psychiatric assessment and diagnosis

Psychopharmacology: Neurotransmitter Systems

Benzodiazepine Pharmacology Comparison

BenzodiazepineHalf-Life (hours)OnsetActive MetaboliteKey IndicationsSpecial Notes
Diazepam20-80 (long)FastYesAnxiety, alcohol withdrawal, status epilepticusPreferred for alcohol withdrawal; long-acting
Lorazepam10-20 (intermediate)IntermediateNoAnxiety, status epilepticus, catatoniaSafe in liver disease; reliable IM absorption
Alprazolam6-12 (short)FastYes (less active)Panic disorder, GADHighest abuse potential; risk of rebound
Clonazepam18-50 (long)Slow-intNoPanic, seizure, REM sleep behavior disorderSmooth pharmacokinetics; lower abuse potential
Chlordiazepoxide5-30 (long)SlowYesAlcohol withdrawalClassic agent for alcohol detoxification

Monoamine Systems

The monoamine hypothesis has been central to psychopharmacology for over five decades.
The three major monoamine systems relevant to psychiatry are serotonin (5-HT), norepinephrine (noradrenaline), and dopamine.
Serotonin is synthesized from tryptophan and is involved in mood regulation, appetite, sleep, pain perception, and impulse control. The 5-HT1A receptor is a key autoreceptor, while 5-HT2A receptors are targets of atypical antipsychotics and psychedelics. The serotonin transporter (SERT) is the primary target of SSRIs.
Norepinephrine is synthesized from tyrosine via dopamine and is critical for arousal, attention, vigilance, and the stress response.
Dopamine is synthesized from tyrosine and is involved in reward, motivation, motor control, and the pathophysiology of psychosis.

Dopaminergic Pathways

The four major dopaminergic pathways are:
  1. Mesolimbic pathway (VTA to nucleus accumbens — positive symptoms of schizophrenia and reward processing)
  2. Mesocortical pathway (VTA to prefrontal cortex — negative symptoms and cognitive deficits)
  3. Nigrostriatal pathway (substantia nigra to striatum — motor control and extrapyramidal side effects)
  4. Tuberoinfundibular pathway (hypothalamus to pituitary — regulates prolactin secretion)
D2 receptor blockade is the common mechanism of all antipsychotics.

GABA-Glutamate Balance

The GABA-glutamate balance is increasingly recognized as fundamental to psychiatric disorders.
GABA is the primary inhibitory neurotransmitter, acting through GABA-A (ligand-gated ion channel) and GABA-B (G-protein coupled) receptors.
Benzodiazepines enhance GABA-A receptor function by increasing the frequency of chloride channel opening.
The NMDA receptor hypofunction hypothesis of schizophrenia proposes that reduced NMDA receptor function on GABAergic interneurons leads to disinhibition of glutamatergic neurons, resulting in excitotoxicity and psychotic symptoms.
Ketamine, an NMDA receptor antagonist, produces psychotomimetic effects that model schizophrenia.

Neuroplasticity and Neurotrophic Factors

Brain-derived neurotrophic factor (BDNF) plays crucial roles in the mechanism of action of antidepressants and mood stabilizers.
Chronic stress reduces BDNF expression in the hippocampus, while antidepressants increase BDNF through cAMP-CREB signaling. The neurogenic hypothesis of depression proposes that reduced hippocampal neurogenesis contributes to depressive symptoms and that antidepressants work in part by increasing neurogenesis.
Lithium, the gold-standard mood stabilizer, inhibits glycogen synthase kinase-3 (GSK-3) and modulates inositol monophosphatase.
Valproate increases GABA levels and inhibits histone deacetylases.
Synaptic transmission at a chemical synapse
Synaptic neurotransmission and sites of psychotropic drug action
Drug-receptor interaction at the synapse
Receptor pharmacology of psychotropic medications

Electroconvulsive Therapy and Neuromodulation

Electroconvulsive Therapy (ECT)

Electroconvulsive therapy (ECT) is the most effective biological treatment in psychiatry, producing a generalised tonic-clonic seizure under general anaesthesia via brief electrical stimulation of the brain. It was first developed by Cerletti and Bini in 1938.
Established indications for ECT: severe major depressive disorder (especially with psychotic features, severe suicidality, food/fluid refusal, or failure to respond to two adequate antidepressant trials), severe mania unresponsive to medication, acute schizophrenia (particularly catatonic or treatment-refractory), neuroleptic malignant syndrome, and Parkinson's disease with severe "on-off" fluctuations.
ECT response rates: major depression 70–90%, psychotic depression 80–90%, acute mania 80%, catatonia 80–85%.

Mechanism of Action

The exact mechanism of ECT is not fully understood. Proposed mechanisms include: (1) generalised seizure causing downregulation of postsynaptic β-adrenergic receptors and upregulation of 5-HT₁A receptors (similar to antidepressants but faster); (2) increased BDNF and hippocampal neurogenesis; (3) modulation of the HPA axis; (4) anticonvulsant effects (raising the seizure threshold, explaining why bilateral ECT reduces the risk of status epilepticus); (5) antiinflammatory and neuroprotective effects via adenosine and GABA signalling.

Practical Aspects and Side Effects

ECT is administered 2–3 times per week (typically 6–12 sessions for depression; up to 20 for schizophrenia). Electrode placement: bilateral (bitemporal, bifrontal) — more effective, more cognitive side effects; right unilateral (ultrabrief pulse) — fewer cognitive effects, slightly less effective at standard dose.
The only absolute contraindication is raised intracranial pressure (risk of cerebral herniation during ECT-induced mPAP surge). Relative contraindications: recent MI or stroke, severe cardiorespiratory disease, and space-occupying lesions. A common misconception is that pacemakers and prosthetic heart valves are absolute contraindications — they are not.
The most common side effect is transient anterograde and retrograde amnesia (more with bilateral electrode placement); permanent memory loss is rare. Other adverse effects: headache, nausea, post-ictal confusion, cardiovascular (transient hypertension, arrhythmias), myalgia.

Other Neuromodulation Techniques

Repetitive transcranial magnetic stimulation (rTMS): delivers focused magnetic pulses to the dorsolateral prefrontal cortex (DLPFC); high-frequency (10–20 Hz) stimulation of the left DLPFC is excitatory and FDA-approved for MDD and OCD. Deep brain stimulation (DBS): continuous electrical stimulation via implanted electrodes; targets include the subgenual cingulate cortex (Area 25, depression), the nucleus accumbens and anterior limb of internal capsule (OCD), and the subthalamic nucleus (Parkinson's). Vagus nerve stimulation (VNS): implanted device delivering electrical impulses to the left vagus nerve, FDA-approved for treatment-resistant epilepsy and depression.
ECT: most effective Rx in psychiatry; bilateral = more effective but more amnesia; absolute CI = raised ICP; rTMS = left DLPFC for MDD; DBS = Area 25 for refractory depression.
ECT and neuromodulation targets in the brain
Brain targets for ECT, rTMS, DBS, and VNS in treatment-resistant psychiatric disorders

Psychotherapeutic Modalities

Cognitive Behavioral Therapy (CBT)

Cognitive behavioral therapy (CBT) is one of the most empirically supported psychotherapies.
It is based on the cognitive model developed by Aaron Beck, which proposes that distorted thinking patterns (cognitive distortions) mediate emotional and behavioral responses. Common cognitive distortions include catastrophizing, overgeneralization, all-or-nothing thinking, mind reading, and emotional reasoning. CBT involves identifying these distortions, challenging them through Socratic questioning, and replacing them with more balanced thoughts.
Behavioral activation, a core component of CBT for depression, involves scheduling rewarding activities and breaking the cycle of avoidance.
CBT has established efficacy for major depressive disorder, anxiety disorders, PTSD, OCD, and bulimia nervosa, with effect sizes comparable to medication for mild-to-moderate depression.

Psychodynamic Psychotherapy

Psychodynamic psychotherapy, rooted in the work of Freud, Jung, and their successors, focuses on unconscious processes, defense mechanisms, and the therapeutic relationship.
Key concepts include the therapeutic alliance, transference (the patient's unconscious redirection of feelings from past relationships onto the therapist), countertransference (the therapist's emotional response to the patient), and resistance (unconscious defenses that impede therapy).
Mentalization-based therapy (MBT), developed by Bateman and Fonagy for borderline personality disorder, integrates psychodynamic and attachment theory concepts, focusing on the capacity to understand one's own and others' mental states.

Third-Wave Behavioral Therapies

  • Dialectical behavior therapy (DBT), developed by Marsha Linehan for borderline personality disorder, combines CBT techniques with mindfulness, distress tolerance, interpersonal effectiveness, and emotion regulation skills.
  • Acceptance and commitment therapy (ACT) uses acceptance, defusion, and values-based action to increase psychological flexibility.
  • Mindfulness-based cognitive therapy (MBCT), developed by Teasdale and Segal, combines mindfulness meditation with CBT techniques and is recommended by NICE for preventing relapse in recurrent depression.

Interpersonal Therapy (IPT)

Interpersonal therapy (IPT) was developed by Klerman and Weissman for depression and is based on the theory that interpersonal problems trigger or maintain depressive episodes.
IPT focuses on four interpersonal problem areas: grief (complicated bereavement), role disputes (conflicts with significant others), role transitions (life changes), and interpersonal deficits (social isolation or chronic relationship difficulties).
IPT is structured in three phases: initial phase (assessment and formulation), middle phase (addresses the identified problem area), and termination phase (consolidates gains and prepares for future challenges).
Neuron illustrating neural connectivity and networks
Neural networks underlying cognitive and emotional processing in psychotherapy

General Psychiatry: NEET PG Rapid Revision Compendium

Psychiatric History Taking: NEET PG High-Yield Framework

History DomainKey QuestionsClinical Pearl
Chief Complaint"What brings you here today?" — in patient s own wordsAlways document verbatim; include duration of each complaint
History of Present IllnessOnset (acute/subacute/insidious), precipitating factors, course (episodic/continuous/fluctuating), severity, impact on functioningUse chronological narrative; include collateral information from family
Past Psychiatric HistoryPrevious diagnoses, hospitalizations (number, dates, voluntary vs involuntary), suicide attempts (methods, lethality, intent), self-harm, medications (doses, duration, response, side effects)Check old records; medication trials must specify dose + duration to assess adequacy
Medical/Surgical HistoryHead injury/LOC, seizures, thyroid, diabetes, cardiac, neurological, chronic painMany medical conditions cause psychiatric symptoms (e.g., hypothyroidism → depression, hyperthyroidism → anxiety, Cushing → depression/psychosis)
Medication HistoryCurrent medications, allergies, adherenceCheck for drug interactions; ask specifically about OTC drugs, supplements, herbal remedies (St. John s wort interacts with SSRIs)
Family Psychiatric HistoryPsychiatric diagnoses, hospitalizations, suicide, substance use in first- and second-degree relativesDraw a genogram (3 generations); bipolar and schizophrenia have high heritability (60-80%)
Social HistoryEducation, occupation, living situation, relationships, legal issues, trauma history, cultural and religious backgroundDocument ACEs (Adverse Childhood Experiences); trauma history essential for PTSD differential
Substance Use HistoryAlcohol (quantity, frequency, CAGE), tobacco, cannabis, opioids, stimulants, benzodiazepines, othersQuantify in standard units; calculate weekly alcohol units; ask about route of administration
Developmental HistoryPregnancy/birth complications, milestones (motor, language, social), childhood temperament, school performanceEssential for neurodevelopmental disorders (ADHD, ASD, ID); birth complications → hypoxia risk
Premorbid PersonalityDescribe personality before onset of illness: relationships, coping style, interests, valuesHelps distinguish personality disorder (lifelong) from illness-related personality change (recent)

The Mental Status Examination: Systematic Documentation

MSE DomainComponents to AssessDocumentation Example
AppearanceAge (apparent vs stated), grooming, hygiene, dress, posture, eye contact, distinguishing features (scars, tattoos)"Well-groomed 45-year-old woman appearing stated age, dressed in casual clothes, maintained eye contact, no psychomotor abnormalities"
BehaviorCooperativeness, psychomotor activity (retardation vs agitation), catatonic signs (posturing, waxy flexibility, negativism, echopraxia), tics, mannerisms, stereotypies"Cooperative throughout interview. Psychomotor retardation noted — slow movements, prolonged response latency. No catatonic features."
SpeechRate (rapid/slow/normal), rhythm, volume (loud/soft), fluency, spontaneity (talkative vs paucity), prosody (monotone vs normal)"Pressured speech — rapid, difficult to interrupt, increased volume. Normal prosody. No dysarthria."
MoodPatient s subjective report: "How is your mood?" Document in patient s own words"Mood: 'depressed,' 'hopeless,' 'like nothing matters anymore' — per patient."
AffectRange (full/restricted/flat), stability (stable vs labile), appropriateness (congruent vs incongruent with mood/content), intensity"Affect: restricted range, mood-congruent (tearful when discussing losses), stable throughout interview."
Thought ProcessRate and flow: linear/goal-directed, circumstantial, tangential, flight of ideas, loosening of associations (derailment), word salad, thought blocking, perseveration"Thought process: linear and goal-directed. No formal thought disorder."
Thought ContentSuicidal/homicidal ideation (intent, plan, means, preparatory acts), delusions (type, conviction, preoccupation), obsessions, phobias, preoccupations, overvalued ideas"Thought content: passive death wishes ('I d be better off dead') without active suicidal ideation, plan, or intent. No homicidal ideation. No delusions."
PerceptionHallucinations (modality: auditory, visual, olfactory, gustatory, tactile; content; frequency; distress), illusions, depersonalization, derealization"Perception: No hallucinations or illusions. Reports occasional derealization ('feeling detached, like watching a movie') when anxious."
CognitionAlertness, orientation (time, place, person), attention (digit span forward/backward), concentration (serial 7s, WORLD backwards), memory (immediate, recent, remote), abstraction (proverb interpretation), fund of knowledge, MMSE/MoCA score"Cognition: Alert. Oriented ×3. Attention: digit span 6 forward, 4 backward. Recent memory: 3/3 objects at 5 minutes. MMSE 28/30 (lost 2 points on recall)."
InsightDegree of awareness of illness: (1) complete denial, (2) vague awareness, (3) intellectual insight (acknowledges illness but doesn t apply to behavior), (4) true emotional insight"Insight: Grade 3 — acknowledges depression and need for treatment intellectually, but minimizes impact on functioning."
JudgmentAbility to make reasoned decisions: test with hypothetical scenarios ("What would you do if you smelled smoke in a cinema?"), assess from history and behavior"Judgment: Fair — able to articulate reasonable responses to hypothetical scenarios, though recent decision-making impaired by depressive symptoms."

Clinical Pearls: Psychopathology Phenomenology

PhenomenonDefinitionAssociated ConditionsNEET PG Trap
CircumstantialityOverinclusive detail but eventually reaches the goal — patient will answer the question after excessive detailAnxiety, OCD, obsessive personality traitsvs Tangentiality: never reaches goal (schizophrenia, mania)
TangentialityPatient goes off on tangents and never returns to the original point — never answers the questionSchizophrenia, mania, organic brain syndromesvs Circumstantiality: eventually reaches the goal after detailed detours
Loosening of associations (derailment)Ideas slip from one track to another without logical connection; speech may become incomprehensibleSchizophrenia (pathognomonic for formal thought disorder)vs Flight of ideas: connections between topics are UNDERSTANDABLE (though rapid) in mania; in loosening, connections are incomprehensible
Flight of ideasRapid, continuous verbalizations with understandable associations between ideas; may be triggered by environmental stimuliMania (bipolar disorder), occasionally stimulant intoxicationConnections between ideas are LOGICAL and understandable — this distinguishes from loosening of associations
Thought blockingSudden, involuntary interruption in the train of thought; patient stops mid-sentence and cannot recall what they were sayingSchizophrenia (classic feature)Patient experiences this as if the thought was "removed" — differentiates from simple forgetfulness
PerseverationPersistent repetition of words, phrases, or behaviors beyond the point of relevanceFrontal lobe damage, dementia, organic brain syndromesNot a psychotic phenomenon — indicates organic brain dysfunction
EcholaliaInvoluntary repetition of another person s words or phrasesCatatonia, autism, frontal lobe damage, transcortical aphasiaCan be part of catatonic syndrome; differentiate from voluntary mimicry
VerbigerationMeaningless, stereotyped repetition of words or phrasesSchizophrenia (catatonic type), severe dementiaDifferentiated from perseveration by the meaningless quality
Thought disorder mnemonic: "CLAT-FP": Circumstantiality, Loosening of associations, Alogia (poverty of speech), Tangentiality, Flight of ideas, Perseveration. Plus blocking.
Hallucination types by disorder: "Auditory = Schizophrenia (especially 3rd person running commentary), Visual = Delirium/Organic (consider Lewy body dementia in elderly with detailed visual hallucinations), Tactile = Cocaine/amphetamine intoxication (formication — 'cocaine bugs'), Olfactory = Temporal lobe epilepsy (uncinate fits), Gustatory = Temporal lobe epilepsy." Mnemonic: "AVTOG" — Auditory (Schizophrenia), Visual (Delirium/DLB), Tactile (Stimulants), Olfactory (TLE), Gustatory (TLE).
General psychiatry NEET PG rapid revision: MSE = psychiatric "physical exam" — perform at EVERY encounter. Psych history: chief complaint → HPI → past psych → medical → family → social → substance → developmental → premorbid. Insight grades (1-4): denial → vague → intellectual → true emotional. Hallucination modality guides differential: auditory (functional psychosis), visual (organic), tactile (substance), olfactory/gustatory (TLE). Thought disorder: circumstantial vs tangential (reaches goal?), loosening vs flight of ideas (understandable connections?). Pseudo-hallucinations: perceived in inner subjective space (vs true hallucinations in external objective space) — seen in grief, BPD, PTSD.

Psychiatry Pharmacology: NEET PG Rapid Revision Compendium

Psychotropic Drug Interactions: High-Yield for NEET PG

CombinationInteractionMechanismClinical Consequence
SSRI + MAOISerotonin syndrome (most dangerous psychotropic interaction)Synergistic serotonin excess (reuptake inhibition + metabolism inhibition)Potentially fatal; minimum 14-day washout between SSRI and MAOI (5 weeks for fluoxetine due to long half-life)
SSRI + TramadolSerotonin syndrome risk; reduced tramadol efficacyTramadol is SNRI + mu-opioid; SSRIs inhibit CYP2D6 (tramadol to active M1 metabolite)Serotonin toxicity; reduced analgesia
Lithium + NSAIDs/ACEi/ARBs/thiazidesIncreased lithium levels (toxicity risk)Decreased renal clearance of lithium (NSAIDs reduce GFR; ACEi/ARBs reduce tubular secretion; thiazides increase proximal reabsorption)Lithium toxicity at previously therapeutic doses; monitor levels closely
Lithium + dehydration/vomiting/diarrheaIncreased lithium levelsVolume depletion reduces renal lithium clearanceAvoid dehydration in lithium patients; hold lithium during gastroenteritis
Clozapine + carbamazepineAdditive agranulocytosis risk (CONTRAINDICATED)Both cause bone marrow suppressionSevere neutropenia/agranulocytosis; never combine
Clozapine + smoking cessationIncreased clozapine levels (up to 50% increase within days)Smoking induces CYP1A2 (metabolizes clozapine); cessation reverses induction rapidlyToxic clozapine levels; reduce clozapine dose by 30-50% when patient quits smoking
Lamotrigine + valproateDoubles lamotrigine levels (increased SJS risk)Valproate inhibits lamotrigine glucuronidationIncreases lamotrigine level 2x; start lamotrigine at 25 mg every OTHER day when combined with valproate
Lamotrigine + OCPs/carbamazepineDecreased lamotrigine levels (up to 50% reduction)Estrogen and carbamazepine induce lamotrigine glucuronidationMay need to double lamotrigine dose; when OCPs stopped during placebo week, lamotrigine levels rise
SSRI + antiplatelet/anticoagulantIncreased bleeding risk (GI, intracranial)SSRIs deplete platelet serotonin (needed for platelet aggregation)GI bleeding risk increased ~2x; add PPI or consider mirtazapine/bupropion
SSRI + tamoxifenReduced tamoxifen efficacy (increased breast cancer recurrence)Strong CYP2D6 inhibitors (paroxetine, fluoxetine, bupropion) block tamoxifen → endoxifen (active metabolite)Use citalopram, escitalopram, or venlafaxine instead (weak CYP2D6 inhibition)
MAOI + tyramineHypertensive crisisTyramine displaces NE from vesicles; MAO-A inhibition prevents NE metabolism → massive NE releaseSevere hypertension, headache, intracranial hemorrhage; avoid aged cheese, cured meats, tap beer, soy sauce, sauerkraut
MAOI + sympathomimeticsHypertensive crisisPotentiation of sympathomimetic effectAvoid pseudoephedrine, phenylephrine, amphetamines, methylphenidate; avoid stimulants with MAOIs
Carbamazepine + OCPsContraceptive failureCarbamazepine induces CYP3A4 → increased estrogen metabolismUnplanned pregnancy risk; use alternative/additional contraception
Carbamazepine + any CYP3A4 substrateAuto-induction + hetero-inductionInduces CYP3A4, 1A2, 2C9, UGTs; also induces its own metabolism (auto-induction complete by 3-5 weeks)Many drug levels reduced (APs, OCPs, warfarin, anticonvulsants); dose adjustments needed

Antidepressant Discontinuation Syndrome Comparison

FeatureSSRI WithdrawalSNRI Withdrawal (venlafaxine)MAOI WithdrawalRelapse (Recurrence)
Onset1-7 days after discontinuation1-3 days (shorter T1/2 of venlafaxine)2-7 daysWeeks-months after remission
FINISH mnemonicFlu-like symptoms, Insomnia, Nausea, Imbalance (dizziness, vertigo), Sensory disturbances (electric shock sensations, "brain zaps"), Hyperarousal (anxiety, agitation)More severe FINISH; prominent "brain zaps" and dizzinessAgitation, psychosis, delirium, catatonia (severe — cholinergic/DA rebound)Return of original depressive symptoms (SIGECAPS)
Risk factorsHigh potency + short half-life (paroxetine most; fluoxetine least due to long half-life)Venlafaxine > duloxetine > desvenlafaxine (longer T1/2)Phenelzine > tranylcypromine (tranylcypromine has amphetamine-like structure — withdrawal can be severe)Residual symptoms, prior episodes, chronic stress, non-adherence
ManagementTaper over 4-12 weeks; switch to fluoxetine (long half-life self-tapers); restart drug if severeSlow taper (10% dose reduction every 2 weeks); if severe, switch to fluoxetine first, then taperSlow taper over 4-8 weeks; may need BZD cover for agitationRestart antidepressant; continue maintenance treatment for longer duration
FINISH for SSRI discontinuation: Flu-like, Insomnia, Nausea, Imbalance (dizziness), Sensory (brain zaps), Hyperarousal.

Psychotropic Monitoring Guidelines: NEET PG Must-Know

MedicationMonitoring TestFrequencyAction Level
LithiumSerum level, TSH, Cr, Ca, PTHLevel: every 3-6 months (stable); weekly during dose change; TSH/Cr: every 6-12 monthsLevel >1.5 mEq/L = toxic; CrCl decrease >30% = referral; TSH >10 = treat hypothyroidism
ValproateSerum level, LFTs, CBC (platelets), ammoniaLFTs at baseline, 1 month, 3 months, then every 6 months; CBC same scheduleLFTs >3x ULN = discontinue; Platelets <100,000 = dose reduce; Ammonia >65 = hyperammonemia evaluation
CarbamazepineSerum level, CBC, LFTs, Na, HLA-B*1502Baseline CBC, LFTs, Na; CBC/LFTs q2 weeks x 2 months, then q3 months; HLA-B*1502 before starting (Asian ancestry)WBC <3000 or ANC <1500 = discontinue; Na <125 = dose reduce or discontinue
ClozapineANC (absolute neutrophil count), troponin, CRP, fasting glucose, lipids, weightANC weekly x 18 weeks, biweekly x 18-52 weeks, monthly thereafter; troponin/CRP week 2, 4, 8, 12; glucose/lipids/weight q3 monthsANC <1500 (<1000 for BEN) = discontinue clozapine; troponin >ULN = hold clozapine, echo, cardiology consult
SGAsWeight, BMI, waist, fasting glucose, HbA1c, lipidsWeight: weekly x 1 month, then monthly; Glucose/lipids: baseline, 3 months, then annually (more often with olanzapine/clozapine)Weight gain >5% = intervention (diet, exercise, switch); Fasting glucose >126 = DM management
SSRIsECG (citalopram — QTc), Na (elderly — SIADH)Baseline ECG for citalopram if >40 mg dose or CV risk; Na in elderly on SSRIs if symptomsQTc >500 ms = discontinue; Na <130 = SIADH evaluation; Hyponatremia risk in elderly, especially first 2 weeks
TCAsECG (QTc, QRS), serum level (nortriptyline, imipramine, desipramine), orthostatic BPBaseline ECG; level if non-response or toxicity suspectedQRS >100 ms = risk of heart block/arrhythmia; QTc >500 ms = discontinue; TCA level >500 ng/mL = toxic

Key NEET PG Psychopharmacology Principles

Principle 1 (D2 occupancy and EPS): Therapeutic window for D2 blockade is 65-80%. Below 65%: ineffective. Above 80%: EPS risk (striatal D2 >80% = parkinsonism, dystonia, akathisia). Above 95%: prolactin elevation. Clozapine has D2 occupancy of only 40-60% (explains low EPS and prolactin) but superior efficacy (5-HT2A, D4, noradrenergic mechanisms compensate).
Principle 2 (Antidepressant onset): All antidepressants take 2-4 weeks for initial response and 6-12 weeks for full response. This delay is explained by receptor adaptation: acute SERT/NET blockade → increased synaptic monoamines → desensitization of presynaptic autoreceptors (5-HT1A, alpha-2) → increased neuronal firing → downstream gene expression (BDNF, CREB) → neurogenesis and synaptogenesis.
Principle 3 (Tapering principles): All psychotropics should be tapered, not abruptly discontinued. SSRIs/SNRIs: taper over 4-12 weeks (paroxetine = worst withdrawal, fluoxetine = self-tapering). Benzodiazepines: taper by 10-25% every 1-2 weeks. Antipsychotics: taper over weeks-months (rebound psychosis, cholinergic rebound, withdrawal dyskinesia can occur if stopped abruptly). Mood stabilizers: lithium → rebound mania; valproate/carbamazepine → rebound seizures.
Principle 4 (Polypharmacy pitfalls): Each additional psychotropic increases side effect burden, drug interactions, and cost. Before adding a medication: (1) Optimize current medication (dose, duration), (2) Confirm adherence, (3) Address substance use and psychosocial factors, (4) Consider psychotherapy augmentation before pharmacotherapy augmentation.
Psychopharmacology NEET PG rapid revision: SSRI + MAOI = serotonin syndrome (14-day washout, 5 weeks for fluoxetine). Lithium + NSAIDs/ACEi/thiazides = toxicity. Clozapine + carbamazepine = CONTRAINDICATED (agranulocytosis). Smoking = induces CYP1A2 → higher clozapine/olanzapine doses needed. Paroxetine/fluoxetine/bupropion = inhibit CYP2D6 → avoid with tamoxifen. Valproate = inhibit lamotrigine → double lamotrigine level (use 25 mg alternate day dosing). Estrogen/carbamazepine = induce lamotrigine → need higher doses. FINISH = SSRI withdrawal (flu-like, insomnia, nausea, imbalance, sensory, hyperarousal). D2 occupancy: 65-80% therapeutic, >80% EPS. Antidepressant onset delayed = receptor adaptation + neurogenesis. Always taper psychotropics slowly.

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