← All study guides
Guide 22 · Part V

Requested Topics

Supplement · Requested Topics. Six study modes, from notes to quick review.

Chapter 01

Requested Topics

Table of Contents

This supplement covers 6 topic clusters identified as gaps in the main 12-week study packet series. Content is exam-ready with model answer outlines and mark allocations.

01 Delirium & Consultation-Liaison Psychiatry
02 Sexual Disorders & Gender Dysphoria
03 Cultural Psychiatry & Indian Syndromes
04 Grief, Bereavement & Adjustment Disorders
05 Somatic Symptom & Related Disorders
06 Adolescent Psychiatry (Extended)
01
Delirium & Consultation-Liaison Psychiatry
Pathophysiology, assessment tools, ICU complications, and the C-L consultation model
Delirium: Pathophysiology & Assessment
Definition & Epidemiology

Delirium is an acute, fluctuating disturbance of attention, awareness, and cognition that develops over hours to days. It represents a direct physiological consequence of a medical condition, substance, or multiple aetiologies.

  • Prevalence: 10–31% of hospitalised medical patients; up to 80% in ICU patients on mechanical ventilation
  • Mortality: Associated with 10–26% in-hospital mortality; each day of delirium independently increases mortality risk
  • Post-operative delirium occurs in 15–53% of elderly surgical patients
Pathophysiology: Key Hypotheses
1. Cholinergic Deficiency Hypothesis

The most established model. Acetylcholine (ACh) is critical for attention, arousal, and memory consolidation. Delirium is associated with:

  • Reduced cholinergic transmission, anticholinergic medications are the most common pharmacological trigger
  • Serum anticholinergic activity (SAA) correlates with delirium severity
  • Physostigmine (AChE inhibitor) can transiently reverse anticholinergic delirium
  • Reciprocal relationship: ACh ↓ and dopamine ↑ → produces the hyperactive delirium phenotype
2. Neuroinflammation Hypothesis

Systemic inflammation leads to blood-brain barrier (BBB) breakdown and neuroinflammation:

  • Pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) cross a compromised BBB
  • Microglial activation → local neuroinflammation → neuronal dysfunction
  • Endothelial activation and adhesion molecule upregulation → further BBB permeability
  • Particularly relevant in sepsis-associated delirium and post-surgical delirium
3. Oxidative Stress Hypothesis

Impaired oxidative metabolism (hypoxia, hypoglycaemia, thiamine deficiency) reduces acetylcholine synthesis and increases reactive oxygen species, contributing to neuronal injury.

4. Neurotransmitter Imbalance Model (Integrated)
NeurotransmitterChange in DeliriumClinical Correlate
Acetylcholine↓ DecreasedInattention, memory impairment
Dopamine↑ IncreasedAgitation, hallucinations, psychosis
GABA↑ in hepatic / ↓ in withdrawalSedation (hepatic) or agitation (withdrawal)
Glutamate↑ ExcitotoxicityNeuronal injury, cognitive sequelae
SerotoninVariablePerceptual disturbances
Melatonin↓ Disrupted circadianSleep-wake cycle disturbance
Exam Pearl
The cholinergic deficiency hypothesis is the most frequently tested model. Remember: anticholinergic burden is the single most modifiable risk factor. Always mention the ACh-dopamine reciprocal relationship in essay answers.
Confusion Assessment Method (CAM)
CAM: Diagnostic Algorithm

The CAM (Inouye et al., 1990) is the most widely validated bedside instrument for delirium detection. Sensitivity: 94–100%, Specificity: 90–95%.

Four Core Features
FeatureDescriptionHow to Assess
1. Acute onset & fluctuating courseAbrupt change from baseline mental status, symptoms wax and wane over 24 hoursCollateral history from nursing staff/family; serial assessments
2. InattentionDifficulty focusing, sustaining, or shifting attentionDigit span, serial 7s, days of week backward, spelling WORLD backward
3. Disorganised thinkingRambling, incoherent speech, illogical flow of ideas, unpredictable topic switchingAsk simple questions: "Will a stone float on water?" "Are there fish in the sea?"
4. Altered level of consciousnessAny level other than normal alert, hyperalert, lethargic, stuporous, or comatoseRASS (Richmond Agitation-Sedation Scale) or clinical observation
Diagnostic Rule
CAM+ = Feature 1 + Feature 2 + (Feature 3 OR Feature 4)

Both Feature 1 (acute onset/fluctuation) AND Feature 2 (inattention) must be present, PLUS either Feature 3 or Feature 4.

CAM-ICU (for intubated/non-verbal patients)
  • Feature 1: Assessed via RASS fluctuation or GCS change
  • Feature 2: Attention Screening Exam (ASE), visual (picture recognition) or auditory (letter 'A' squeeze test)
  • Feature 3: Yes/no questions + simple commands
  • Feature 4: RASS score ≠ 0
Delirium Subtypes
SubtypePrevalenceFeaturesPrognosis
Hyperactive~25%Agitation, restlessness, hallucinations, combativeness, pulling at linesBetter (detected earlier)
Hypoactive~25%Lethargy, reduced motor activity, flat affect, withdrawalWorse (often missed, higher mortality)
Mixed~45%Fluctuates between hyperactive and hypoactive features within hoursIntermediate
No motor subtype~5%CAM-positive but no motor disturbanceVariable
Exam Strategy
Hypoactive delirium is the most commonly missed subtype and carries the worst prognosis. Examiners frequently ask why it is underdiagnosed, answer: mistaken for depression or fatigue, no behavioural disturbance to alert staff.
Delirium Management Algorithm
Step 1: Identify and Treat the Underlying Cause
Mnemonic, I WATCH DEATH
I WATCH DEATH

Infection · Withdrawal · Acute metabolic · Trauma · CNS pathology · Hypoxia · Deficiencies · Endocrine · Acute vascular · Toxins/drugs · Heavy metals

Step 2: Non-Pharmacological Interventions (First-Line for ALL Subtypes)
  • Reorientation, clocks, calendars, familiar objects, consistent caregivers, family presence
  • Sleep hygiene, minimise night-time interventions, lights off, reduce noise, avoid sedating medications as sleep aids
  • Sensory optimisation, ensure hearing aids and glasses are in place
  • Mobilisation, early and frequent ambulation where medically safe
  • Hydration and nutrition, correct dehydration, ensure adequate caloric intake
  • Minimise restraints, physical restraints worsen agitation and prolong delirium
  • Medication review, discontinue or reduce anticholinergics, benzodiazepines, opioids where possible
Step 3: Pharmacological Management (When Non-Pharmacological Measures Insufficient)
Indications for pharmacotherapy: severe agitation threatening safety, distressing hallucinations/delusions, risk of self-harm or harm to staff
AgentDoseRouteNotes
Haloperidol0.5–2 mg, repeat q30min PRNPO/IM/IVFirst-line for hyperactive delirium. Monitor QTc. Avoid in Parkinson's and DLB.
Quetiapine12.5–50 mg BDPOPreferred in Parkinson's/DLB. Good for mixed subtype. Sedating at low doses.
Olanzapine2.5–5 mgPO/IMAlternative to haloperidol. Avoid with benzodiazepines IM (respiratory depression).
Lorazepam0.5–2 mgPO/IM/IVONLY for alcohol/benzodiazepine withdrawal delirium and hepatic encephalopathy.
DexmedetomidineIV infusion 0.2–0.7 μg/kg/hrIVICU setting only. α2-agonist. Reduces delirium duration in ventilated patients.
Exam Pearl
Benzodiazepines worsen delirium, except in alcohol/BZD withdrawal and hepatic encephalopathy. This is the most tested pharmacological principle in delirium management.
Consultation-Liaison Model
The C-L Consultation Process
  1. Referral receipt, clarify the question being asked (not just "psychiatry consult")
  2. Record review, medications (anticholinergic burden), labs, vitals, nursing notes for fluctuation
  3. Patient assessment, cognitive screening (CAM, MMSE/MoCA), mental status exam, physical exam for medical causes
  4. Collateral history, baseline cognitive function, timeline of changes, substance use
  5. Formulation, biopsychosocial, with emphasis on medical contributors
  6. Recommendations, written clearly, prioritised, with specific medication doses and monitoring parameters
  7. Follow-up, daily re-assessment until delirium resolves or patient is discharged
Differential: Delirium vs Dementia vs Depression vs Psychosis
FeatureDeliriumDementiaDepressionPsychosis
OnsetAcute (hours–days)Insidious (months–years)WeeksDays–weeks
CourseFluctuatingProgressiveDiurnal variationSustained
AttentionMarkedly impairedRelatively preserved earlyMildly impairedVariable
ConsciousnessAltered (clouded)Clear until late stagesClearClear
HallucinationsVisual (common)Visual (DLB)Rare (mood-congruent)Auditory (common)
ReversibilityUsually reversibleIrreversible (mostly)TreatableTreatable
EEGDiffuse slowingNormal or mild slowingNormalNormal
ICU Psychiatric Complications
ICU Delirium

ICU delirium affects up to 80% of mechanically ventilated patients and is independently associated with longer ICU stay, higher mortality, and long-term cognitive impairment.

Risk Factors Specific to ICU
  • Predisposing: Age >65, pre-existing cognitive impairment, alcohol use disorder, high APACHE II score
  • Precipitating: Sedation (especially benzodiazepines), mechanical ventilation, sleep deprivation, immobilisation, pain, sepsis
Prevention: ABCDEF Bundle (ICU Liberation)
LetterComponentAction
AAssess, prevent, and manage painRegular pain assessment (BPS/CPOT); analgesia-first sedation
BBoth SATs and SBTsDaily spontaneous awakening + breathing trials
CChoice of analgesia and sedationAvoid benzodiazepines; prefer propofol or dexmedetomidine
DDelirium: assess, prevent, manageCAM-ICU every shift; non-pharmacological prevention
EEarly mobility and exerciseProgressive mobilisation from passive ROM to ambulation
FFamily engagement and empowermentOpen visitation, family involvement in care, orientation cues
Clinical Anchor
Agitation management in ICU: First rule out pain, full bladder, constipation, hypoxia, and drug withdrawal before reaching for sedation. Use the RASS to target light sedation (RASS 0 to -1) rather than deep sedation.
Post-ICU Psychiatric Sequelae
  • Post-intensive care syndrome (PICS): cognitive impairment (25–80%), depression (30%), PTSD (10–50%), anxiety (70%)
  • Duration of delirium correlates with severity of long-term cognitive impairment
  • ICU diaries and psychological follow-up at 3 months recommended
Model Answer Outline, "Discuss the pathophysiology and management of delirium" (10 marks)
Introduction (1 mark)
  • Define delirium; state prevalence (10–31% medical, 80% ICU)
Pathophysiology (3 marks)
  • Cholinergic hypothesis, reduced ACh, anticholinergic burden as top modifiable risk factor
  • Neuroinflammation, cytokines cross BBB, microglial activation
  • Neurotransmitter imbalance, ACh ↓, DA ↑, GABA variable, melatonin disruption
  • Oxidative stress, impaired oxidative metabolism
Assessment (2 marks)
  • CAM algorithm, 4 features, diagnostic rule (1+2+3or4)
  • Subtypes: hyperactive, hypoactive (worst prognosis, most missed), mixed
Management (3 marks)
  • Identify and treat cause (I WATCH DEATH mnemonic)
  • Non-pharmacological, reorientation, sleep hygiene, mobilisation, sensory optimisation
  • Pharmacological, haloperidol first-line, quetiapine for PD/DLB, BZDs ONLY for withdrawal
Prognosis (1 mark)
  • Usually reversible; persistent delirium associated with dementia risk; mention PICS for ICU delirium
02
Sexual Disorders & Gender Dysphoria
ICD-11 classification, medication-induced dysfunction, paraphilias, and gender incongruence
Sexual Dysfunction: ICD-11 Classification
ICD-11 Sexual Dysfunctions (Block 17: Conditions Related to Sexual Health)

ICD-11 moved sexual dysfunctions out of the mental disorders chapter into Conditions Related to Sexual Health, a deliberate destigmatisation parallel to gender incongruence reclassification.

CategoryMaleFemale
Desire disordersHypoactive sexual desire dysfunctionSexual interest/arousal dysfunction
Arousal disordersErectile dysfunction(Merged with desire in female)
Orgasmic disordersMale early ejaculation; Delayed ejaculationAnorgasmia
Pain disordersSexual pain-penetration disorder
Key ICD-11 vs DSM-5 Differences
  • ICD-11 merges female desire + arousal into one entity; DSM-5 does the same (FSIAD)
  • ICD-11 requires the dysfunction to be not better explained by a medical condition, substance, or relationship distress
  • ICD-11 uses "dysfunction" rather than "disorder", less pathologising language
  • Duration criterion: several months (ICD-11); approximately 6 months (DSM-5)
Antipsychotic/SSRI-Induced Sexual Dysfunction
Hyperprolactinaemia Pathway

Dopamine D2 blockade in the tuberoinfundibular pathway → prolactin elevation → downstream sexual effects:

  • ↑ Prolactin → ↓ GnRH pulsatility → ↓ LH/FSH → ↓ testosterone/oestrogen
  • Men: decreased libido, erectile dysfunction, gynaecomastia, galactorrhoea
  • Women: amenorrhoea, galactorrhoea, decreased libido, anorgasmia
  • Long-term: osteoporosis risk from chronic hypogonadism
Prolactin-Sparing vs Prolactin-Raising Antipsychotics
High Prolactin RiskModerateProlactin-Sparing
Risperidone, Paliperidone, Amisulpride, Sulpiride, HaloperidolOlanzapine, ZiprasidoneAripiprazole (partial D2 agonist → may lower prolactin), Quetiapine, Cariprazine, Clozapine
SSRI-Induced Sexual Dysfunction
  • Prevalence: 30–70% of patients on SSRIs (often under-reported)
  • Mechanism: serotonin ↑ → inhibits dopamine and norepinephrine pathways involved in arousal and orgasm; 5-HT2A/2C stimulation inhibits NO-mediated vasodilation
  • Most common complaints: delayed orgasm/anorgasmia > decreased libido > erectile dysfunction
  • Post-SSRI Sexual Dysfunction (PSSD): rare but recognised, persists after SSRI discontinuation
Exam Pearl
Management of SSRI-induced sexual dysfunction: (1) Wait and watch, may improve over 1–3 months; (2) Dose reduction; (3) Drug holiday (weekend breaks, risky with short-half-life SSRIs); (4) Switch to bupropion or mirtazapine; (5) Augment with bupropion or sildenafil. Bupropion is the antidepressant with the lowest sexual side-effect profile.
Paraphilic Disorders & Gender Incongruence
Paraphilic Disorders: ICD-11 Classification

ICD-11 distinguishes between paraphilias (atypical sexual interests, not disorders per se) and paraphilic disorders (cause distress OR involve non-consenting individuals).

DisorderFocusForensic Relevance
ExhibitionisticExposing genitals to unsuspecting personsIPC Section 354 (outraging modesty), POCSO if minor
VoyeuristicObserving unsuspecting persons undressing/sexual activityIPC Section 354C (voyeurism, added 2013)
PaedophilicPrepubescent childrenPOCSO Act, IPC 376, mandatory reporting
Coercive sexual sadismNon-consenting victims; physical/psychological sufferingIPC 354, 375, 376
FrotteuristicTouching/rubbing against non-consenting personIPC 354 (sexual harassment)
OtherFetishistic, transvestic (only if causing distress)Generally not forensic unless involving non-consent
Exam Strategy
For forensic questions, always mention: (1) legal framework (IPC sections, POCSO Act), (2) fitness to stand trial, (3) criminal responsibility, (4) risk assessment (static + dynamic factors), (5) treatment (CBT, anti-androgens for severe cases, relapse prevention).
Gender Incongruence: ICD-11 Reclassification
The Landmark Change

ICD-11 moved gender identity conditions from "Mental and Behavioural Disorders" (ICD-10 F64) to a new chapter: "Conditions Related to Sexual Health". This is one of the most significant reclassifications in ICD-11.

Rationale for Reclassification
  • Destigmatisation, being transgender is not a mental disorder
  • Evidence-based, distress in gender incongruence largely arises from social stigma and barriers to care, not from the experience itself
  • Retained in ICD (not removed entirely) to ensure access to healthcare services, hormonal treatment, and surgical care
  • Parallel: homosexuality was removed from ICD-10 in 1990; gender incongruence retained but reclassified
ICD-11 Terminology
ICD-10 (Old)ICD-11 (New)Code
Transsexualism (F64.0)Gender incongruence of adolescence and adulthoodHA60
Gender identity disorder of childhood (F64.2)Gender incongruence of childhoodHA61
Dual-role transvestism (F64.1)Removed
Management of Gender Dysphoria
  • Assessment: Comprehensive psychiatric evaluation to rule out comorbid conditions, confirm persistent gender incongruence, assess capacity for informed consent
  • Psychological support: Affirmative therapy approach; address minority stress, family dynamics, and social transition
  • Hormonal treatment: Cross-sex hormones under endocrinology guidance (testosterone for trans men, oestrogen + anti-androgens for trans women)
  • Surgical: Referral after sustained gender incongruence (WPATH Standards of Care 8, no mandatory time period)
  • Indian context: Transgender Persons (Protection of Rights) Act, 2019, legal recognition, identity certificate, prohibition of discrimination
Model Answer Outline, "Discuss the ICD-11 reclassification of gender identity disorders" (10 marks)
ICD-10 Classification (2 marks)
  • F64, Gender Identity Disorders under Mental and Behavioural Disorders; categories: transsexualism, dual-role transvestism, GID of childhood
ICD-11 Reclassification (3 marks)
  • Moved to "Conditions Related to Sexual Health", separate from mental disorders
  • Renamed: Gender incongruence of adolescence/adulthood (HA60), childhood (HA61)
  • Dual-role transvestism removed entirely
Rationale (3 marks)
  • Destigmatisation, evidence that distress is largely from social factors, not intrinsic
  • Retained in ICD for healthcare access (hormonal, surgical, psychological support)
  • Follows pattern of homosexuality removal from ICD-10 in 1990
Management principles (2 marks)
  • Affirmative approach, multidisciplinary care, WPATH SOC 8, Indian legal framework (TG Act 2019)
03
Cultural Psychiatry & Indian Syndromes
Dhat syndrome, possession states, cultural formulation, and adapting psychotherapy
Culture-Bound Syndromes & Cultural Formulation
Culture-Bound Syndromes: Key Entities
SyndromeRegionCore FeaturesClosest ICD-11 Category
Dhat syndromeSouth Asia (India, Pakistan, Nepal, Bangladesh)Preoccupation with semen loss via urine, nocturnal emissions, masturbation; somatic complaints (fatigue, weakness, anxiety)Bodily distress disorder / Hypochondriasis
KoroSoutheast Asia, China, India (sporadic)Acute anxiety that penis (or vulva/nipples) is retracting into body and will cause deathOther specified anxiety disorder
LatahMalaysia, IndonesiaExaggerated startle response → echolalia, echopraxia, automatic obedienceDissociative disorder / Tic disorder (context-dependent)
AmokMalaysia, PhilippinesSudden episode of indiscriminate violent attack, often preceded by brooding; followed by amnesia and exhaustionDissociative disorder / Intermittent explosive disorder
SustoLatin America"Soul loss" after frightening event; malaise, anorexia, insomnia, social withdrawalAdjustment disorder / Depressive episode
Possession statesIndia (widespread), sub-Saharan AfricaTrance with identity replacement by deity/spirit; may include glossolalia, altered voice, amnesiaDissociative trance disorder / Possession trance disorder
ICD-11 Approach to Cultural Formulation

ICD-11 does not use the term "culture-bound syndrome." Instead, it recognises that cultural factors shape the expression, interpretation, and help-seeking of all mental disorders. The approach involves:

  • Cultural identity, patient's ethnic, linguistic, religious identity; degree of acculturation
  • Cultural conceptualisation of distress, how the patient understands and labels their symptoms (e.g., "Dhat" rather than "anxiety")
  • Psychosocial stressors and cultural features of vulnerability, role of family, community, migration, discrimination
  • Cultural features of the relationship between patient and clinician, language barriers, trust, explanatory model mismatch
  • Overall cultural assessment for diagnosis and care, how cultural factors affect diagnosis, treatment planning, prognosis
Exam Pearl
ICD-11 replaced "culture-bound syndromes" with a dimensional, formulation-based approach to culture. The Cultural Formulation Interview (CFI) from DSM-5 is a useful structured tool, 16 questions covering 4 domains. ICD-11's approach is conceptually similar but less structured.
Possession States: Differential Diagnosis
DiagnosisKey Distinguishing Features
Normative possession tranceCulturally sanctioned (temple rituals, festivals); not associated with distress or impairment; community-endorsed
Dissociative trance disorderInvoluntary, distressing, causes impairment; identity disruption; occurs outside sanctioned contexts
Psychotic disorderPersistent delusions of being possessed (not episodic trance); auditory hallucinations (command type); deterioration in functioning; lack of episodic pattern
Temporal lobe epilepsyStereotyped episodes, aura, automatisms, post-ictal confusion; EEG abnormalities
MalingeringExternal incentive; inconsistent symptoms; symptom production under observation
Dhat Syndrome: Comprehensive Review
High-frequency PG exams topic: asked repeatedly in short notes and long answers
Definition

Dhat syndrome is a culture-bound condition prevalent in the Indian subcontinent, characterised by excessive preoccupation with semen loss and attribution of a wide range of somatic and psychological symptoms to this perceived loss.

Etymology

"Dhat" derives from the Sanskrit dhatu (vital body fluid/essence). Rooted in Ayurvedic belief that semen is the most refined of the seven dhatus, and its loss leads to physical and mental deterioration.

Epidemiology
  • Predominantly affects young men (15–30 years), rural or semi-urban, lower socioeconomic status
  • Prevalence: accounts for 10–30% of male attendees at psychiatric outpatients in India (Bhatia & Malik, 1991)
  • Similar concepts: Shen-k'uei (China), Jiryan (Middle East), Prameha (Sri Lanka)
Aetiology: Biopsychosocial Model
DomainFactors
BiologicalComorbid depression, anxiety; prostatic/urethral pathology (rare); phosphaturia mistaken for semen
PsychologicalSexual guilt (often from religious/moral teachings about masturbation); performance anxiety; low sexual literacy; somatisation of distress
SocioculturalAyurvedic semen conservation belief; traditional healer reinforcement; family silence about sexuality; peer myths
Clinical Presentation
  • Core complaint: passage of "Dhat" in urine (whitish discolouration), nocturnal emissions, or semen loss during defecation
  • Somatic: fatigue, body aches, weakness, weight loss, palpitations, poor appetite
  • Psychological: anxiety, depressed mood, guilt, poor concentration, irritability
  • Sexual: premature ejaculation, erectile dysfunction, loss of libido
  • Patients often first consult traditional healers or quacks, may have received harmful "treatments"
Management: Stepped Approach
  1. Therapeutic alliance, take the complaint seriously; do not dismiss or ridicule; validate the distress
  2. Psychoeducation, explain semen physiology (continuous production, not a finite resource); normalise nocturnal emissions; address myths about masturbation
  3. Cognitive restructuring, challenge catastrophic beliefs about semen loss; graduated exposure to anxiety-provoking situations
  4. Treat comorbidities, SSRIs for comorbid depression/anxiety; PE can be treated with dapoxetine or low-dose SSRI
  5. Cultural sensitivity, use patient's explanatory model as a bridge; involve family if appropriate; consider referencing Ayurvedic framework in psychoeducation
  6. Address sexual knowledge gaps, basic sex education, dispel myths, address performance anxiety
Mnemonic, Dhat Management: SACRED
SACRED

Sympathetic listening · Assess comorbidities · Cognitive restructuring · Reassurance with education · Explanatory model bridging · Drug therapy if needed

Model Answer Outline, "Write a short note on Dhat syndrome with management" (10 marks)
Definition & Etymology (1.5 marks)
  • Define Dhat syndrome; mention dhatu concept, cultural context in Indian subcontinent
Epidemiology (1 mark)
  • Young men, rural, lower SES; 10–30% of male OPD; cross-cultural parallels
Aetiology (2 marks)
  • Biopsychosocial: Ayurvedic beliefs, sexual guilt, somatisation, comorbid depression/anxiety
Clinical Features (2 marks)
  • Core complaint of semen loss + somatic symptoms + psychological symptoms + sexual dysfunction
Management (3 marks)
  • Psychoeducation (semen physiology, nocturnal emission normalisation)
  • CBT, cognitive restructuring of catastrophic beliefs
  • Pharmacotherapy for comorbidities (SSRIs)
  • Cultural sensitivity, use explanatory model as bridge, involve family
Prognosis (0.5 marks)
  • Good with psychoeducation and treatment of comorbidities; refractory cases often have untreated depression
Cultural Adaptation of Psychotherapy in India
Why Cultural Adaptation Matters

Evidence-based therapies (CBT, IPT, DBT) were developed in Western, educated, industrialised contexts. Direct application in Indian settings faces barriers:

  • Collectivistic vs individualistic values, Indian families often make treatment decisions jointly; "autonomy" is relational, not individual
  • Explanatory models, karma, fate, divine punishment, evil eye, humoral imbalance (vata-pitta-kapha) coexist with biomedical understanding
  • Stigma, "psychiatry = pagal" remains pervasive; somatisation is a preferred idiom of distress
  • Therapist shortage, task-shifting to community health workers requires simplified, manualised protocols
Bernal's Ecological Validity Framework: 8 Dimensions of Adaptation
DimensionApplication in Indian Context
LanguageUse local language; translate idioms accurately (not literally); use Hindi/regional metaphors for cognitive concepts
PersonsMatch therapist-patient on language/culture where possible; use lay counsellors (MANAS trial model)
MetaphorsUse culturally resonant stories (e.g., Panchatantra, religious parables) to explain cognitive distortions
ContentAddress culturally relevant stressors, dowry, in-law conflict, arranged marriage adjustment, caste-based discrimination
ConceptsFrame "thoughts-feelings-behaviour" triangle in local terms; use "man ki baat" (mind's talk) for automatic thoughts
GoalsInclude family-level goals, not just individual; acceptance of family involvement in goal-setting
MethodsActivity scheduling can include temple visits, community events; behavioural activation can leverage joint family support
ContextDeliver in primary care (PHC/CHC), community settings, or via telehealth; address migration, urbanisation stress
Indian Evidence for Culturally Adapted Interventions
  • MANAS trial (Patel et al., 2010, Lancet): Collaborative stepped-care with lay counsellors in Goa PHCs, reduced depression and anxiety prevalence by 30–40% compared to enhanced usual care
  • PREMIUM (Patel et al., 2017, Lancet): Healthy Activity Program (HAP), culturally adapted behavioural activation for depression; Counselling for Alcohol Problems (CAP), MI-based, lay counsellor-delivered
  • Thinking Healthy Programme (WHO, Rahman et al., 2008, Lancet): CBT-based, pictorial aids, delivered by Lady Health Workers for perinatal depression in Pakistan, adapted and tested in India
Exam Pearl
When writing about cultural adaptation, always cite the MANAS trial (Goa, Patel et al., Lancet 2010), it is the landmark Indian RCT for task-shifting in mental healthcare and is frequently examined. Also mention the District Mental Health Programme (DMHP) under NMHP as the national framework for community mental health.
04
Grief, Bereavement & Adjustment Disorders
Prolonged Grief Disorder, Worden's tasks, dual process model, and adjustment disorders
Normal Grief vs Prolonged Grief Disorder
Normal Grief: Features

Grief is a universal, adaptive response to bereavement. It is NOT a disorder. Normal grief includes:

  • Emotional: Sadness, yearning, anger, guilt, anxiety, loneliness
  • Cognitive: Disbelief, preoccupation with the deceased, confusion, intrusive memories
  • Behavioural: Crying, social withdrawal, restlessness, searching behaviour, visiting grave/memorials
  • Physical: Fatigue, insomnia, appetite changes, somatic complaints (tightness in chest, hollow stomach)
  • Timeline: Intensity typically peaks in first 6 months; gradual adaptation over 12 months; grief "pangs" may persist but decrease in frequency and intensity
Prolonged Grief Disorder (PGD): NEW in ICD-11 and DSM-5-TR

PGD is a newly codified diagnostic entity in both ICD-11 (6B42) and DSM-5-TR (added 2022). It represents grief that is persistent, pervasive, and functionally impairing beyond what is expected.

ICD-11 Diagnostic Criteria (6B42)
  1. Death of a close person (partner, parent, child, or other person close to the bereaved)
  2. Persistent and pervasive longing for OR persistent and pervasive preoccupation with the deceased
  3. Accompanied by intense emotional pain (sadness, guilt, anger, denial, blame, difficulty accepting death, feeling part of self has died, inability to experience positive mood, emotional numbness, difficulty engaging in social/other activities)
  4. Duration: persists for an abnormally long period after the loss, at least 6 months (minimum); longer periods may be appropriate depending on cultural/contextual norms
  5. The disturbance clearly exceeds expected social, cultural, or religious norms
  6. Causes significant impairment in personal, family, social, educational, occupational, or other important areas
Key Distinction: Normal Grief vs PGD
FeatureNormal GriefProlonged Grief Disorder
YearningPresent, diminishes over monthsPersistent, pervasive, does not diminish
DurationMonths, with gradual adaptation≥6 months (ICD-11) / ≥12 months adults, ≥6 months children (DSM-5-TR)
Functional impactTemporary disruption, gradual returnSignificant, persistent impairment across domains
IdentitySense of self preserved"Part of me died"; identity confusion; difficulty imagining future
Social engagementGradually resumesPersistent avoidance or inability to re-engage
Positive emotionsCan experience moments of joyEmotional numbness; anhedonia specific to post-loss life
Cultural normsWithin expected rangeExceeds cultural/religious expectations for mourning
Exam Pearl
PGD is NOT the same as depression. In PGD, the yearning is focused on the deceased and the lost relationship. In depression, the low mood and anhedonia are pervasive and not specifically tied to the loss. Comorbidity is common (~30–50%), but they are distinct entities requiring different treatments.
Bereavement Counselling & Adjustment Disorders
Bereavement Counselling Models
Worden's Four Tasks of Mourning
TaskDescriptionTherapeutic Approach
1. Accept the reality of the lossMoving from denial to cognitive and emotional acknowledgment that the person is dead and will not returnGently revisit the circumstances of death; use the deceased's name; avoid euphemisms
2. Process the pain of griefExperience and work through the full range of grief emotions without avoidanceNormalise emotions; create safe space for expression; identify suppressed affect
3. Adjust to a world without the deceasedExternal adjustments (new roles, practical tasks), internal adjustments (identity, self-concept), spiritual adjustments (meaning-making)Problem-solving for practical challenges; identity work; meaning-making
4. Find a way to maintain connection while embarking on a new lifeEstablish a continuing bond with the deceased while re-engaging with lifeRituals, legacy projects, permission to form new relationships
Stroebe & Schut's Dual Process Model (DPM)

The DPM proposes that healthy grieving involves oscillation between two orientations:

  • Loss-oriented coping: Processing the loss itself, crying, yearning, reminiscing, confronting the reality of death
  • Restoration-oriented coping: Attending to life changes, learning new skills, developing new identity, forming new relationships, distraction from grief
  • Oscillation between these two is normal and adaptive; getting "stuck" in either orientation is problematic
Clinical Anchor
Evidence-based treatment for PGD: Complicated Grief Treatment (CGT; Shear et al., 2005), a 16-session protocol combining elements of IPT and CBT with exposure (revisiting the death story) and restoration work. RCT evidence shows CGT superior to IPT alone for PGD.
Risk Factors for Complicated Grief
  • Relationship: Loss of child > spouse > parent; dependent or ambivalent relationship; caregiving burden
  • Circumstances: Sudden/violent death, suicide, uncertain death (missing persons), multiple losses
  • Personal: Pre-existing depression/anxiety, insecure attachment style, prior losses, social isolation
  • Social: Disenfranchised grief (loss not socially recognised, e.g., extramarital partner, pet, perinatal loss), lack of social support
Adjustment Disorders: ICD-11
Definition

Maladaptive reaction to an identifiable psychosocial stressor, characterised by preoccupation with the stressor and failure to adapt, leading to functional impairment.

ICD-11 Key Changes
  • ICD-11 introduces a core symptom: preoccupation with the stressor (recurrent distressing thoughts, constant worry, rumination about the stressor or its consequences)
  • No subtypes in ICD-11 (unlike DSM-5 which retains subtypes: with depressed mood, with anxiety, with mixed anxiety and depressed mood, with disturbance of conduct, unspecified)
  • Duration: symptoms arise within 1 month of stressor; resolve within 6 months of stressor cessation
  • If symptoms meet criteria for another disorder (MDD, GAD), that diagnosis takes precedence
Model Answer Outline, "Distinguish between normal grief and prolonged grief disorder" (10 marks)
Normal Grief (3 marks)
  • Adaptive response; emotional, cognitive, behavioural, somatic features
  • Peaks in first 6 months; gradual adaptation; moments of positive emotion preserved
  • Within cultural norms; functional recovery over time
Prolonged Grief Disorder (4 marks)
  • New in ICD-11 (6B42) and DSM-5-TR, define with diagnostic criteria
  • Persistent yearning/preoccupation + intense emotional pain ≥6 months
  • Exceeds cultural norms; significant functional impairment
  • Distinguish from depression (grief is relationship-focused, depression is pervasive)
Risk Factors for PGD (1.5 marks)
  • Nature of relationship, circumstances of death, personal vulnerability, disenfranchised grief
Management (1.5 marks)
  • CGT (Shear et al.), 16 sessions, exposure + restoration; Worden's tasks; Dual Process Model; SSRIs for comorbid depression
05
Somatic Symptom & Related Disorders
Bodily Distress Disorder, FNSD, factitious disorder, and stepped-care management
ICD-11 Reclassification: Somatic Symptom Disorders
The Paradigm Shift

ICD-11 made fundamental changes to the classification of somatic symptom disorders, moving away from the mind-body dualism that plagued ICD-10:

  • ICD-10: "Somatoform disorders" (F45), defined by absence of organic pathology (diagnosis by exclusion)
  • ICD-11: Focuses on positive psychological and behavioural features, excessive health-related cognitions/behaviours, regardless of whether a medical condition is present
ICD-11 Classification
Bodily Distress Disorder (BDD: 6C20)

Replaces most of ICD-10's somatoform categories (somatisation disorder, undifferentiated somatoform disorder, somatoform autonomic dysfunction).

  • Bodily symptoms that are distressing and result in excessive attention directed towards the symptoms (repeated contact with health services, avoidance behaviours, constant symptom checking)
  • Symptoms may or may not be attributable to a medical condition, the diagnosis does not require absence of organic pathology
  • Severity qualifiers: Mild (one body system, intermittent) or Moderate to severe (multiple systems, persistent, significantly impairing)
Comparison: ICD-10 → ICD-11
ICD-10ICD-11Key Change
Somatisation disorder (F45.0)Bodily Distress Disorder (6C20)Unified under one category; no arbitrary symptom counts; positive criteria instead of exclusion-based
Undifferentiated somatoform disorder (F45.1)
Somatoform autonomic dysfunction (F45.3)
Hypochondriacal disorder (F45.2)Hypochondriasis (6B23), under OCD-related disordersMoved to OCD spectrum; reconceptualised as health anxiety
Dissociative (conversion) disorders (F44)Dissociative Neurological Symptom Disorder (6B60)Now in dissociative disorders chapter; standalone entity
Pain disorder (F45.4)Chronic primary pain (MG30.0)Moved to pain chapter, no longer a "psychiatric" diagnosis
Somatic Symptom Disorder (DSM-5) vs Bodily Distress Disorder (ICD-11)
FeatureSSD (DSM-5)BDD (ICD-11)
NameSomatic Symptom DisorderBodily Distress Disorder
FocusDisproportionate thoughts, feelings, behaviours about somatic symptomsExcessive attention to bodily symptoms
Requires organic exclusion?NoNo
SeverityMild, moderate, severe (specifier)Mild vs moderate-to-severe
Duration≥6 monthsSeveral months
Body system specificationNot requiredYes (gastrointestinal, cardiopulmonary, etc.)
Exam Pearl
The single most important change: both ICD-11 and DSM-5 abandoned the requirement to prove absence of organic pathology. A patient with diabetes AND excessive health-related distress can receive a diagnosis of BDD/SSD. The diagnosis rests on positive psychological criteria, not negative medical workup.
FNSD, Factitious Disorder & Management
Functional Neurological Symptom Disorder (FNSD) / Conversion Disorder

ICD-11 renames this as Dissociative Neurological Symptom Disorder (6B60) and places it under the dissociative disorders chapter, a significant reclassification.

Key Clinical Features
  • Motor symptoms: weakness/paralysis, abnormal movements (tremor, dystonia, myoclonus), gait disorder, aphonia
  • Sensory symptoms: anaesthesia, blindness, deafness
  • Seizure-like episodes: Psychogenic Non-Epileptic Seizures (PNES), most common FNSD presentation in referral centres
  • Positive clinical signs (demonstrate inconsistency, NOT absence of pathology):
SignTestInterpretation
Hoover's signInvoluntary hip extension of "weak" leg when flexing contralateral leg against resistancePositive = functional weakness
Drift without pronationArm drifts downward without pronation (organic UMN lesion → drift WITH pronation)Functional weakness
Give-way weaknessInitial resistance followed by sudden collapse of effortFunctional (but not specific)
Tubular visual fieldsVisual field testing at different distances, field stays same size (should expand with distance)Functional blindness
PNES featuresAsynchronous limb movements, eye closure during episode, prolonged duration, no post-ictal confusion, preserved corneal reflexPsychogenic seizure (gold standard = video EEG)
Factitious Disorder vs Malingering
FeatureFactitious DisorderMalingering
MotivationAssume the sick role (internal psychological need)External incentive (compensation, avoiding duty, legal advantage)
Symptom productionDeliberate fabrication or induction of symptomsDeliberate fabrication or exaggeration
AwarenessAware of producing symptoms; may not understand whyFully aware and goal-directed
Diagnosis in ICD-11Yes, Factitious Disorder (6D50)Not a diagnosis, coded as Z-code (reason for encounter)
Munchausen'sSevere form, peregrinating, dramatic presentations, pathological lying (pseudologia fantastica)N/A
By proxyFactitious disorder imposed on another (Munchausen by proxy), child abuseN/A
Management: Stepped Care for Somatic Symptom Disorders
  1. Step 1, Primary care management: Regular scheduled appointments (not symptom-driven), single treating physician, limit investigations, validate distress, physical activity prescription
  2. Step 2, Low-intensity psychological: Psychoeducation, graded exercise therapy, guided self-help, relaxation training
  3. Step 3, Specialist psychological: CBT (most evidence, addresses catastrophic cognitions, safety behaviours, attention to symptoms); ACT; brief psychodynamic therapy
  4. Step 4, Pharmacological: SSRIs/SNRIs (for comorbid depression/anxiety and direct analgesic effects); low-dose TCAs for pain; avoid opioids and benzodiazepines
Model Answer Outline, "Discuss the ICD-11 approach to somatic symptom disorders" (10 marks)
ICD-10 Limitations (2 marks)
  • Mind-body dualism; diagnosis by exclusion of organic pathology; arbitrary symptom counts; poorly reliable categories
ICD-11 Reclassification (4 marks)
  • Bodily Distress Disorder, positive criteria (excessive attention to symptoms), severity-based, body system specification
  • Hypochondriasis → OCD spectrum
  • FNSD → Dissociative Neurological Symptom Disorder in dissociative disorders chapter
  • Pain disorder → Chronic primary pain in pain chapter
Advantages of ICD-11 Approach (2 marks)
  • No exclusion-of-organic-pathology requirement, reduces iatrogenic harm from excessive investigation
  • Positive diagnostic criteria improve reliability and reduce stigma
  • Can coexist with medical conditions, more clinically realistic
Management (2 marks)
  • Stepped care: scheduled appointments → psychoeducation/graded exercise → CBT → SSRIs. Emphasise therapeutic alliance, limit investigations, single physician model.
06
Adolescent Psychiatry (Extended)
Early-onset psychosis, conduct disorder, tics, adolescent substance use, and safety planning
Early-Onset Psychosis & Conduct Disorder
Early-Onset Psychosis (EOP) vs Childhood-Onset Schizophrenia (COS)
FeatureEarly-Onset Psychosis (EOP)Childhood-Onset Schizophrenia (COS)
Age of onset13–17 years<13 years (very rare: 1 in 10,000–30,000)
Prevalence~1–2% of all schizophrenia<0.01% of children
Premorbid functioningVariableOften impaired: language delays, motor delays, social difficulties, ADHD-like features
HallucinationsPredominantly auditoryAuditory + visual hallucinations more common than in adult-onset
Thought disorderPresentMarked formal thought disorder; may be mistaken for developmental language disorder
Negative symptomsVariableProminent and early; flat affect, avolition, social withdrawal
PrognosisIntermediateWorse than adult-onset; progressive grey matter loss on serial MRI; poor functional outcome
Differential Diagnosis: Key Considerations
  • Autism spectrum disorder, social withdrawal and odd behaviour may mimic negative symptoms; ASD does not have true hallucinations or delusions (distinguish from fantasy play)
  • Bipolar disorder with psychotic features, episodic course, mood congruence, grandiosity
  • PTSD with dissociation, flashbacks may be mistaken for hallucinations; trauma history crucial
  • Substance-induced psychosis, cannabis, synthetic cannabinoids, stimulants; urine drug screen mandatory
  • Anti-NMDA receptor encephalitis, young females, psychiatric symptoms preceding neurological; test for anti-NMDAR antibodies
  • 22q11.2 deletion syndrome (DiGeorge), 25% develop psychosis; congenital cardiac anomalies, palatal abnormalities, learning difficulties
Exam Pearl
Always mention anti-NMDA receptor encephalitis in the differential of first-episode psychosis in young people, it is potentially reversible and increasingly tested in exam vivas. Also mention 22q11.2 deletion syndrome as the strongest genetic risk factor for schizophrenia.
Conduct Disorder
ICD-11 Classification

Conduct-dissocial disorder (6C91), a pattern of repetitive and persistent behaviour that violates the basic rights of others or major age-appropriate societal norms.

Core Behaviours (4 Clusters)
  1. Aggression to people and animals, bullying, fighting, use of weapons, physical cruelty, robbery
  2. Destruction of property, fire-setting, deliberate vandalism
  3. Deceitfulness or theft, lying, shoplifting, breaking into others' property
  4. Serious rule violations, truancy, running away, staying out at night despite parental prohibition
Callous-Unemotional (CU) Traits: ICD-11 Specifier

ICD-11 includes a "with limited prosocial emotions" specifier (equivalent to DSM-5's CU specifier). Features:

  • Lack of remorse or guilt
  • Callous, lack of empathy; unconcerned about others' feelings
  • Unconcerned about performance, not bothered by poor schoolwork or disappointing authority figures
  • Shallow or deficient affect, emotions appear insincere, used to manipulate
Exam Strategy
CU traits are the most important prognostic marker in conduct disorder. They predict: (1) more severe and stable antisocial behaviour, (2) poorer treatment response to standard behavioural interventions, (3) higher risk of adult antisocial personality disorder. Always mention CU traits when discussing conduct disorder aetiology or prognosis.
Conduct Disorder Management, Tic Disorders & Adolescent Substance Use
Conduct Disorder: Management
Psychosocial Interventions (First-Line)
InterventionTarget AgeDescriptionEvidence Level
Parent Management Training (PMT)3–12 yearsTeaching parents consistent discipline, positive reinforcement, effective commands, time-out techniquesStrong RCT evidence
Multisystemic Therapy (MST)12–17 yearsIntensive family- and community-based; addresses family, peer, school, and neighbourhood factors simultaneouslyStrong; reduces incarceration
Functional Family Therapy (FFT)11–18 yearsBrief (8–12 sessions); targets family interaction patterns that maintain problem behaviourModerate-strong
Problem-Solving Skills Training (PSST)7–14 yearsCBT-based; teaches cognitive steps for interpersonal problem-solving; reduces hostile attribution biasModerate
Incredible Years Programme3–8 yearsGroup-based parent training + child social skills; video-modelling of parenting techniquesStrong
Pharmacological (Adjunctive Only: No Drug is First-Line for Conduct Disorder)
  • Risperidone (0.25–1.5 mg), for severe aggression unresponsive to psychosocial interventions; short-term use; monitor metabolic effects
  • Methylphenidate, when comorbid ADHD is present (treating ADHD reduces ODD/CD severity by 30–50%)
  • Mood stabilisers (lithium, valproate), for explosive aggression, limited evidence in children
  • No evidence for SSRIs in conduct disorder without comorbid depression/anxiety
Tic Disorders & Tourette Syndrome
Classification
DiagnosisCriteriaDuration
Provisional tic disorderMotor and/or vocal tics<1 year
Chronic motor tic disorderMotor tics only (no vocal)≥1 year
Chronic vocal tic disorderVocal tics only (no motor)≥1 year
Tourette syndromeMultiple motor + ≥1 vocal tic (not necessarily concurrent)≥1 year; onset <18 years
Management: Stepped Approach
  1. Psychoeducation and watchful waiting, many tics improve by late adolescence; explain waxing-waning course
  2. CBIT (Comprehensive Behavioural Intervention for Tics), first-line therapy; includes habit reversal training (awareness training + competing response training) + functional intervention; NNT ~3
  3. Pharmacological (moderate-severe): Alpha-2 agonists (clonidine 0.05–0.3 mg, guanfacine) → atypical antipsychotics (aripiprazole first choice, risperidone) → fluphenazine, pimozide (second-line, QTc monitoring)
Adolescent Substance Use: Screening & Brief Intervention
CRAFFT Screening Tool (for ages 12–21)
Mnemonic, CRAFFT
CRAFFT

Car, Have you ridden in a CAR driven by someone (including yourself) who was high?
Relax, Do you use alcohol/drugs to RELAX, feel better, or fit in?
Alone, Do you ever use alcohol/drugs while you are ALONE?
Forget, Do you ever FORGET things you did while using?
Friends, Do FRIENDS or family tell you to cut down?
Trouble, Have you gotten into TROUBLE while using?

Scoring: ≥2 positive = significant problem; sensitivity 76%, specificity 94%

Adolescent-Specific Safety Planning
  • Screen every adolescent presenting with substance use for suicidal ideation (ASQ or Columbia Protocol)
  • Involve parents/guardians unless safety concern (balance confidentiality with duty to protect)
  • Safety plan components: warning signs, internal coping, social supports, adult contacts, restricting means, emergency numbers
  • Means restriction, remove/lock medications, restrict access to lethal means (particularly relevant for pesticide ingestion in rural India)
Model Answer Outline, "Discuss the management of conduct disorder in adolescents" (10 marks)
Definition & Epidemiology (1.5 marks)
  • Define CD; prevalence 2–10%; male predominance; childhood-onset vs adolescent-onset
Assessment (1.5 marks)
  • Multidomain: family (parenting style, conflict, abuse), peer (deviant peer group), school (academic failure), individual (CU traits, comorbid ADHD, substance use); functional assessment of aggression triggers
Psychosocial Interventions (4 marks)
  • PMT for younger children (3–12), consistent discipline, positive reinforcement
  • MST for adolescents, intensive, community-based, addresses all ecological systems
  • FFT, brief, targets family interaction patterns
  • PSST / CBT, reduces hostile attribution bias, problem-solving skills
Pharmacological (2 marks)
  • Not first-line; risperidone for severe aggression (short-term); methylphenidate when comorbid ADHD
  • No evidence for SSRIs in CD without depression
Prognosis (1 mark)
  • CU traits predict worse outcome; childhood-onset worse than adolescent-onset; 40% develop ASPD in adulthood
← All study guides