Anxiety OCD

Study Notes

Sources: Kaplan & Sadock's Comprehensive Textbook of Psychiatry (10th ed.), Stahl's Essential Psychopharmacology (4th ed.), Oxford Textbook of Psychiatry, ICD-11 (2022), DSM-5-TR (2022)

TABLE OF CONTENTS

1. Generalized Anxiety Disorder (GAD)
2. Panic Disorder
3. Agoraphobia
4. Social Anxiety Disorder (SAD)
5. Specific Phobias
6. Obsessive-Compulsive Disorder (OCD)
7. Treatment-Resistant OCD
8. PTSD & Acute Stress Disorder
9. Adjustment Disorder
10. Separation Anxiety Disorder (Adults)
11. OCD Spectrum Disorders (Hoarding, BDD, Trichotillomania, Excoriation)
12. Anxiety in Medical Illness
13. Substance-Induced Anxiety

1. GENERALIZED ANXIETY DISORDER (GAD)

1.1 Diagnostic Criteria

DSM-5 Criteria (F41.1)

• A. Excessive anxiety and worry about multiple events/activities, occurring more days than not for ≥6 months
• B. Difficult to control the worry
• C. ≥3 of 6 symptoms (only 1 required in children):
• Restlessness/feeling keyed up/on edge
• Easily fatigued
• Difficulty concentrating / mind going blank
• Irritability
• Muscle tension
• Sleep disturbance (difficulty falling/staying asleep, restless unsatisfying sleep)
• D. Causes significant distress or functional impairment
• E. Not attributable to substances or medical condition
• F. Not better explained by another mental disorder

ICD-11 Criteria (6B00)

• Marked symptoms of anxiety manifesting as general apprehension ("free-floating anxiety") or worry about multiple domains
• Anxiety and worry accompanied by:
• Motor tension (trembling, twitching, muscle aches, restlessness)
• Autonomic hyperactivity (palpitations, sweating, cold/clammy hands, dry mouth, dizziness)
• Hypervigilance and scanning
• Concentration problems, irritability, sleep disturbance
• Symptoms persistent (more days than not, for several months)
• Not better explained by another condition

1.2 Epidemiology

1.3 Neurobiology

Amygdala-PFC Circuit (Fear Circuitry)

In GAD:

• Amygdala hyperreactivity, exaggerated threat detection
• Prefrontal cortex (vmPFC) hypoactivity, failure of top-down inhibition of amygdala
• Anterior cingulate cortex (ACC) dysfunction, impaired error monitoring and emotional regulation
• Bed nucleus of stria terminalis (BNST), mediates sustained anxiety states (vs amygdala's phasic fear response)

Neurotransmitter Systems

GABA:

• GABA is the primary inhibitory neurotransmitter in the CNS
• GABAergic interneurons normally inhibit amygdala hyperactivity
• In anxiety: reduced GABA-A receptor function or reduced GABA availability
• Benzodiazepines act on GABA-A receptor (allosteric modulator at Cl− channel, increase frequency of Cl− channel opening)
• Pregabalin binds α2δ subunit of voltage-gated Ca2+ channels → reduces presynaptic Ca2+ influx → reduces glutamate/norepinephrine release

Serotonin (5-HT):

• Dorsal raphe nucleus (DRN) → amygdala, hippocampus, prefrontal cortex
• 5-HT1A receptor: autoreceptor (somatodendritic), inhibits 5-HT firing; postsynaptic, anxiolytic
• 5-HT2A receptor: postsynaptic, anxiogenic (especially when stimulated)
• Buspirone: partial agonist at 5-HT1A → desensitizes presynaptic autoreceptor → increased 5-HT transmission chronically
• SSRIs initially increase 5-HT2A activation (may cause initial anxiety increase) → chronic desensitization → net anxiolytic

Norepinephrine (NE):

• Locus coeruleus (LC) → widespread cortical/limbic projections
• NE excess → hyperarousal, vigilance, somatic anxiety symptoms
• SNRIs reduce excessive NE via autoreceptor desensitization

Glutamate:

• Excessive NMDA activation in amygdala circuits → fear conditioning and anxiety
• mGluR2/3 presynaptic autoreceptors: novel targets for anxiolytics

CRF (Corticotropin-Releasing Factor):

• CRF1 receptor in amygdala/BNST: overactivation → anxiety, HPA axis dysregulation
• HPA axis: CRF → ACTH → cortisol (dysregulated in chronic anxiety)

1.4 Pharmacotherapy

First-Line Agents

Swipe to compare →

Second-Line Agents

Adjuncts / Short-term

Treatment Algorithm (GAD)

1.5 Psychotherapy for GAD

Cognitive-Behavioural Therapy (CBT)

• Gold standard for GAD (NNT comparable to pharmacotherapy)
• Components:
• Psychoeducation, nature of anxiety, worry
• Self-monitoring, worry diary, identifying triggers
• Cognitive restructuring, identifying catastrophizing, thought challenging, probability estimation
• Worry postponement/Stimulus control, scheduled worry time (15–30 min/day)
• Relaxation training, progressive muscle relaxation (PMR), diaphragmatic breathing
• Interoceptive exposure, for somatic symptoms
• Behavioural experiments, testing worry predictions
• Problem-solving therapy, for real-world stressors

Borkovec's Avoidance Model of Worry:

• Worry = cognitive avoidance of emotional processing of threatening images
• Suppresses somatic activation (paradoxically) → negatively reinforces worry
• CBT targets this cycle

Metacognitive Therapy (Wells):

• Targets beliefs about worry ("I must worry to cope") and beliefs about uncontrollability/danger of worry
• "Detached mindfulness" and attention training

Acceptance & Commitment Therapy (ACT)

• Defusion from anxious thoughts; valued living despite anxiety
• Evidence base growing; comparable to CBT in some trials

2. PANIC DISORDER

2.1 Diagnostic Criteria

DSM-5 Criteria (F41.0)

Panic Attack (not a diagnosis itself, a specifier):

13 symptoms, ≥4 required:

1. Palpitations / pounding heart / accelerated heart rate
2. Sweating
3. Trembling or shaking
4. Shortness of breath / smothering sensation
5. Feelings of choking
6. Chest pain / discomfort
7. Nausea / abdominal distress
8. Dizziness / unsteady / lightheaded / faint
9. Chills or hot flushes
10. Paresthesias (numbness/tingling)
11. Derealization / depersonalization
12. Fear of losing control / going crazy
13. Fear of dying

Panic attacks are abrupt surges reaching peak within minutes; can be expected (cued) or unexpected (uncued/spontaneous).

Panic Disorder requires:

• A. Recurrent unexpected panic attacks
• B. At least one attack followed by ≥1 month of:
• Persistent concern about additional attacks or consequences ("am I having a heart attack?")
• OR significant maladaptive change in behaviour (avoidance, safety behaviours)
• C. Not attributable to substances or medical condition
• D. Not better explained by another mental disorder

ICD-11 Criteria (6B01)

• Recurrent unexpected panic attacks
• At least one attack followed by at least one month of anxiety about recurrence OR maladaptive behaviour
• Key: unexpected = not triggered by identifiable feared object/situation

2.2 Epidemiology

2.3 Clark's Cognitive Model of Panic

Core premise: Panic attacks result from the catastrophic misinterpretation of bodily sensations.

Maintaining factors:

1. Selective attention / hypervigilance to bodily sensations
2. Safety behaviours (sitting down, calling ambulance), prevent disconfirmation
3. Avoidance of triggers, prevents learning
4. Anticipatory anxiety, increases physiological arousal before next attack

Treatment implications (Clark's model → CBT):

• Psychoeducation (corrects misinterpretation)
• Interoceptive exposure (induced sensations → learn they are not dangerous)
• Cognitive restructuring (challenging catastrophic thoughts)
• Behavioural experiments (drop safety behaviours, enter feared situations)

2.4 Neuroanatomy of Panic

Suffocation Alarm Theory (Klein, 1993)

• Proposes an evolved hypersensitive CO2/suffocation alarm system in the brainstem
• Panicogenic agents: CO2 inhalation, sodium lactate → trigger suffocation alarm
• Imipramine blocks false alarms (hence antidepressants prevent panic)
• Explains respiratory panic symptoms and response to respiratory hyperventilation

Key brain regions:

• Locus coeruleus (LC): noradrenergic nucleus in pons; hyperactivation → panic symptoms (yohimbine provokes panic by blocking α2 autoreceptors)
• Periaqueductal grey (PAG): mediates freezing and flight responses; dorsal PAG stimulation → panic-like responses
• Hypothalamus: HPA axis activation during panic
• Amygdala: fear conditioning; learned associations for expected panic attacks
• Hippocampus: contextual fear conditioning

Neurochemistry:

• NE excess (LC) → palpitations, sweating, tremor
• 5-HT dysregulation, SSRIs highly effective
• CCK-4 (cholecystokinin), exogenous injection provokes panic attacks
• GABA-A deficiency (parahippocampal region)

2.5 Pharmacotherapy

First-Line

Second-Line

Duration of treatment: Minimum 12 months after remission; 2+ years if recurrent.

2.6 CBT for Panic Disorder

Highly effective (60–80% response); may be superior to pharmacotherapy in long-term follow-up.

Components:

1. Psychoeducation, Clark's model, nature of panic/anxiety, fight-or-flight
2. Breathing retraining, diaphragmatic breathing (caution: may become safety behaviour)
3. Cognitive restructuring, challenging catastrophic misinterpretations
4. Interoceptive exposure, deliberately inducing feared sensations:
5. Spinning in chair (dizziness)
6. Running in place (palpitations, breathlessness)
7. Breathing through straw (choking sensation)
8. Staring at point on wall (derealization)
9. In vivo exposure, entering avoided situations (combined with situational exposure for agoraphobia)
10. Eliminating safety behaviours

3. AGORAPHOBIA

3.1 Diagnostic Criteria (DSM-5: F40.00)

• A. Marked fear/anxiety about ≥2 of:
• Using public transport
• Being in open spaces (parking lots, marketplaces, bridges)
• Being in enclosed places (shops, theatres, cinemas)
• Standing in line or being in a crowd
• Being outside of the home alone
• B. Person fears/avoids because of thoughts that escape might be difficult or help unavailable in event of panic-like symptoms
• C. Situations almost always provoke fear/anxiety
• D. Actively avoided, require companion, or endured with intense anxiety
• E. Fear disproportionate to actual danger
• F. Persistent (≥6 months)
• G. Significant distress/impairment
• H. Not attributable to another medical condition or substance

3.2 Management

• First-line: CBT (exposure therapy) ± SSRIs
• Graded exposure hierarchy (SUDS, subjective units of distress)
• Partner-assisted exposure when complete avoidance
• Goal: not to eliminate anxiety but to increase tolerance and reduce avoidance

4. SOCIAL ANXIETY DISORDER (SAD)

4.1 Diagnostic Criteria

DSM-5 (F40.10)

• A. Marked fear/anxiety about one or more social situations where exposed to scrutiny (conversation, performance, being observed eating/drinking)
• B. Fears acting/showing anxiety in humiliating/embarrassing way or provoking negative evaluation
• C. Social situations almost always provoke fear/anxiety
• D. Avoided or endured with intense anxiety
• E. Disproportionate to actual threat
• F. Persistent (≥6 months)
• G. Significant distress/impairment
• H. Not substance/medical
• I. Not better explained by another disorder (ASD, PTSD, BDD, etc.)

Specifier: "Performance only", if fear limited to public speaking/performing

Performance-only vs Generalized SAD

4.2 Assessment: Liebowitz Social Anxiety Scale (LSAS)

• 24 items: 13 performance situations + 11 social interaction situations
• Each rated for fear (0–3) and avoidance (0–3)
• Maximum score: 144
• Scoring: 55–65 = social phobia; 65–80 = marked; 80–95 = severe; >95 = very severe
• Widely used in clinical trials; sensitive to treatment change

4.3 Cognitive Model (Clark & Wells, 1995)

1. Social situation → perceived social threat
2. Self-focused attention (focuses on internal sensations/thoughts about performance)
3. Safety behaviours (avoiding eye contact, over-preparing, rehearsing)
4. Problematic processing before and after events
5. Negative self-image as a social object

4.4 Pharmacotherapy

4.5 Psychotherapy

CBT components:

• Clark & Wells model-based: attention training (external focus), video feedback, dropping safety behaviours
• Exposure therapy (social situations hierarchy)
• Cognitive restructuring

Social skills training: For those with genuine skills deficits (not just inhibition)

5. SPECIFIC PHOBIAS

5.1 Classification (DSM-5 Specifiers)

1. Animal type (spiders, insects, dogs, snakes)
2. Natural environment type (heights, storms, water)
3. Blood-injection-injury (BII) type, unique: vasovagal response (bradycardia, hypotension → fainting)
4. Situational type (airplanes, elevators, enclosed spaces)
5. Other type (vomiting, loud sounds, costumed characters)

5.2 Psychological Theories of Origin

1. Classical conditioning (Pavlovian), traumatic conditioning (dog bite → dog phobia)
2. Observational learning, watching others fear (vicarious conditioning)
3. Information transmission, told snakes are dangerous
4. Preparedness theory (Seligman), biologically prepared to fear evolutionarily dangerous stimuli (snakes, heights, spiders), these phobias are resistant to extinction

5.3 Treatment

Systematic Desensitization (Wolpe)

• Based on reciprocal inhibition (relaxation incompatible with anxiety)
• Three components:
• Relaxation training (PMR or hypnosis)
• Fear hierarchy construction (8–12 steps, anchored by SUDS 0–100)
• Graded exposure (starting from least anxiety-provoking, pairing with relaxation)
• Can be in vivo or imaginal
• Best for: specific phobias, simple situations

Flooding (Implosion Therapy)

• Prolonged, intensive exposure to feared stimulus without relaxation
• Maximal anxiety → habituation → extinction
• In vivo flooding = most effective; imaginal flooding (implosion) = less effective
• Contraindications: severe cardiac disease, psychosis, severe trauma history

Virtual Reality Exposure Therapy (VRET)

• Computer-generated phobic stimuli
• Evidence for: acrophobia, arachnophobia, aviophobia, claustrophobia, driving phobia
• Advantages: controllable, accessible, privacy, high-fidelity
• Comparable efficacy to in vivo exposure in meta-analyses

Pharmacotherapy (Limited Role)

• D-cycloserine (NMDA partial agonist), augments extinction learning; adjunct to exposure
• Benzodiazepines (short-term, not for long-term phobia treatment, may interfere with extinction)

6. OBSESSIVE-COMPULSIVE DISORDER (OCD)

6.1 Diagnostic Criteria

DSM-5 (F42)

• A. Presence of obsessions, compulsions, or both
• Obsessions: (1) recurrent intrusive thoughts/urges/images causing marked anxiety; (2) person attempts to ignore/suppress or neutralize with other thought/action
• Compulsions: (1) repetitive behaviours or mental acts driven by the obsession or rigid rules; (2) aimed at preventing/reducing distress or dreaded event, but are NOT realistically connected or are excessive
• B. Time-consuming (>1 hr/day) OR cause significant distress/impairment
• C. Not attributable to substances or medical condition
• D. Not better explained by another mental disorder

Insight specifiers:

• Good or fair insight
• Poor insight
• Absent insight/delusional beliefs

Tic-related specifier: if current or past history of tic disorder

ICD-11 (6B20)

• Same core features
• Classified under "Obsessive-Compulsive and Related Disorders" (separate chapter from anxiety disorders, same as DSM-5)

6.2 Common OCD Symptom Dimensions

6.3 Yale-Brown Obsessive Compulsive Scale (Y-BOCS)

Structure:

• 10 items: 5 for obsessions + 5 for compulsions
• Each item scored 0 (none) to 4 (extreme)
• Range: 0–40

Five dimensions per subscale (O = obsessions, C = compulsions):

1. Time occupied (O)/Time spent on (C)
2. Interference with functioning
3. Distress/anxiety caused
4. Resistance (degree of effort to resist)
5. Control (ability to control/stop)

Severity thresholds:

Response to treatment: ≥35% reduction in Y-BOCS score

Y-BOCS-II: Updated version with insight modifier; broader content coverage.

OCI-R (OCD Inventory Revised): 18-item self-report; 6 subscales; used in research and screening.

6.4 Neurobiology: CSTC Circuit

CSTC Circuit Architecture

In OCD (Saxena & Rauch model):

NET RESULT: Overactive OFC generates error signals → overactive direct pathway drives repetition → compulsions are the brain's failed attempt to resolve the "error signal."

Why SSRIs work: 5-HT modulates striatal and thalamic function; chronic SSRI use normalizes caudate hypermetabolism (seen on FDG-PET).

Neuroimaging Evidence

• FDG-PET: Hypermetabolism in OFC, caudate nucleus, thalamus at baseline; normalizes with successful treatment
• fMRI: Hyperactivation of OFC, ACC during symptom provocation
• Structural MRI: Decreased grey matter in OFC, ACC; increased in caudate

Serotonin Hypothesis

• OCD selectively responds to serotonin-specific agents (clomipramine > desipramine in Zohar's studies)
• 5-HT2C receptors: postsynaptic in striatum, modulate repetitive behaviour
• Augmenting agents (atypical APs) act on D2 in striatum, block dopamine hyperactivity in striato-thalamic loops

6.5 Pharmacotherapy

First-Line: SSRIs

All 5 SSRIs are FDA-approved for OCD. Fluvoxamine was first (1994).

Clomipramine

SSRIs vs Clomipramine: Key Comparison

Augmentation Strategies

6.6 Psychotherapy: Exposure and Response Prevention (ERP)

Principles of ERP

Theoretical basis:

• Inhibitory learning model (Craske): exposure creates new non-threatening associations, not erasure of old ones
• Habituation (older model): prolonged exposure → reduced anxiety response

Components:

1. Exposure: Contact with feared stimulus/situation (in vivo, imaginal, or interoceptive)
2. Response Prevention: Deliberately refraining from compulsions

Process:

• Construct hierarchy (SUDS 0–100)
• Start with moderate SUDS (40–50), not lowest
• Prolonged exposure (≥45 minutes per session) until SUDS reduces by 50%
• Gradual progression up hierarchy
• Therapist-assisted → self-directed

Critical rule: The anxiety WILL peak and then decrease. Compulsions terminate anxiety prematurely and reinforce the obsession-compulsion cycle.

Variants of ERP

• Intensive ERP: Daily sessions for 2–3 weeks; used for severe/refractory cases
• Family-based ERP: Involves family members (who may be accommodation providers)
• Imaginal ERP: For obsessions without behavioral rituals (harm obsessions, pure O)
• IOCDF protocol: International OCD Foundation standardized approach

Inference-Based CBT (I-CBT)

• For poor-insight OCD; targets "inferential confusion", treating imagined possibilities as actual reality
• "Case narrativization", understanding the obsessional story

ACT for OCD

• Defusion from obsessions; values-based action
• Does not require challenging obsessional content
• Useful for poor insight

6.7 Neuromodulation and Surgery

Neurosurgery for OCD

Indicated only for: severe, treatment-resistant OCD, failing ≥3 adequate SRI trials + adequate ERP, significant disability, Y-BOCS >30.

DBS targets for OCD:

• Primary: Anterior limb of internal capsule (ALIC) / Ventral striatum / Nucleus accumbens (NAcc)
• Alternative: Subthalamic nucleus (STN), also used in Parkinson's
• BNST (bed nucleus of stria terminalis)

Transcranial Magnetic Stimulation (TMS)

• Repetitive TMS (rTMS) to supplementary motor area (SMA), FDA cleared for OCD (2018)
• Less invasive neuromodulation option
• Deep TMS (dTMS), H7 coil targeting mPFC and anterior cingulate

7. TREATMENT-RESISTANT OCD

7.1 Definition

Treatment-resistant OCD = failure to achieve ≥35% Y-BOCS improvement after:

• 2–3 adequate SSRI trials (at maximum tolerated dose, ≥12 weeks each)
• 1 adequate clomipramine trial (≥250 mg or maximum tolerated)
• Adequate ERP (≥20 sessions by competent therapist)

7.2 Management Algorithm

7.3 IV Clomipramine

• Bypasses first-pass metabolism → higher peak plasma levels
• Protocol: 25–75 mg IV in dextrose over 45–90 minutes
• Used in centres with expertise; not widely available
• Evidence from Indian studies (Bhave & Bhave, 1986; Koran et al.)
• Response even in oral clomipramine failures

7.4 Other Strategies

• Glutamate-modulating agents: Riluzole, memantine, NAC (N-acetylcysteine), topiramate
• Ondansetron (5-HT3 antagonist): small studies showing benefit
• Tramadol (opioid + SRI): case reports of rapid response
• Ketamine: Emerging evidence for rapid but transient OCD reduction (NMDA antagonism)
• Psilocybin/MDMA: Under investigation; very preliminary

8. PTSD & ACUTE STRESS DISORDER

8.1 PTSD Diagnostic Criteria (DSM-5: F43.10)

Criterion A, Trauma exposure (at least one):

1. Directly experiencing traumatic event
2. Witnessing in person
3. Learning that close person experienced violent/accidental death/threatened death/sexual violence
4. Repeated/extreme indirect exposure (first responders, forensic workers), NOT media exposure

Qualifying traumatic events: actual or threatened death, serious injury, or sexual violence

Criterion B, Intrusion (≥1):

1. Intrusive distressing memories
2. Recurrent distressing dreams
3. Dissociative reactions (flashbacks), range from brief to complete loss of awareness
4. Intense/prolonged psychological distress at internal/external trauma cues
5. Marked physiological reactions to trauma cues

Criterion C, Avoidance (≥1):

1. Avoidance of distressing memories, thoughts, feelings
2. Avoidance of external reminders (people, places, situations, activities)

Criterion D, Negative alterations in cognition and mood (≥2):

1. Inability to remember important aspects (dissociative amnesia)
2. Persistent/exaggerated negative beliefs about self/world ("I am bad")
3. Persistent distorted blame of self/others
4. Persistent negative emotional state (fear, horror, anger, guilt, shame)
5. Diminished interest/participation in activities
6. Feelings of detachment or estrangement from others
7. Persistent inability to experience positive emotions (emotional numbing, anhedonia)

Criterion E, Alterations in arousal and reactivity (≥2):

1. Irritable behaviour and angry outbursts
2. Reckless or self-destructive behaviour
3. Hypervigilance
4. Exaggerated startle response
5. Concentration problems
6. Sleep disturbance

Criterion F: ≥1 month duration

Criterion G: Significant distress/functional impairment

Criterion H: Not substance/medical

Specifiers:

• With dissociative symptoms: depersonalization, derealization
• With delayed expression: full criteria not met until ≥6 months post-event

Complex PTSD (ICD-11: 6B41)

ICD-11 recognizes Complex PTSD as a distinct disorder (not in DSM-5):

• All PTSD features PLUS "disturbances in self-organization" (DSO):
• Affect dysregulation
• Negative self-concept (shame, guilt, worthlessness)
• Disturbances in relationships

Typically follows prolonged/repeated trauma (childhood abuse, domestic violence, trafficking, torture).

8.2 Acute Stress Disorder (ASD: F43.0)

Duration: 3 days to 1 month post-trauma (PTSD requires >1 month)

DSM-5 criteria:

• Trauma exposure (same as PTSD Criterion A)
• ≥9 of 14 symptoms across 5 categories: intrusion, negative mood, dissociation, avoidance, arousal
• Functional impairment
• Duration: 3 days to 1 month

8.3 Ehlers & Clark Cognitive Model of PTSD (2000)

Two core processes generate persistent PTSD:

1. Appraisal of the traumatic event and/or its sequelae as a current serious threat:
2. "I am permanently changed/damaged"
3. "Nowhere is safe"
4. "I am going mad" (about PTSD symptoms themselves)

1. Nature of the trauma memory, autobiographical memory characteristics:
2. Poor contextual embedding (trauma memory lacks time/place context)
3. Strong associative triggering (sensory cues trigger intrusions without conscious recall)
4. "Data-driven processing" during trauma (sensory focus, not conceptual) → weak elaboration

Maintaining behaviours:

• Thought suppression → paradoxically increases intrusions
• Rumination (about causes, consequences) → increases distress without processing
• Safety behaviours (staying indoors, never being alone) → prevent disconfirmation
• Cognitive avoidance, prevents memory elaboration

Treatment (CT-PTSD, Ehlers & Clark):

1. Identify and modify appraisals ("update" threat appraisals)
2. Trauma memory elaboration (write/revisit in detail → add context/meaning)
3. Drop safety behaviours
4. Address triggers/discriminating stimuli

8.4 Pharmacotherapy for PTSD

First-Line

Second-Line / Adjuncts

8.5 Psychotherapy for PTSD

Trauma-Focused CBT (TF-CBT) / CPT / PE

These are first-line psychological treatments:

1. Cognitive Processing Therapy (CPT, Resick):

• 12 sessions; individual or group
• Identifies and challenges "stuck points", distorted beliefs about trauma/its consequences
• Written trauma account; Socratic questioning of maladaptive appraisals
• 5 themes: safety, trust, power/control, esteem, intimacy
• Evidence: Large VA trials; guideline-recommended (NICE, VA/DoD, ISTSS)

2. Prolonged Exposure (PE, Foa):

• 8–15 sessions
• Two core components:
• Imaginal exposure: Repeated revisiting of trauma narrative in session + processing
• In vivo exposure: Gradual approach to avoided (safe) reminders
• Based on emotional processing theory (fear network activation → modification)

3. Cognitive Therapy for PTSD (CT-PTSD, Ehlers & Clark):

• Based on their 2000 model (see 8.3)
• Memory elaboration and contextualisation
• Identifying and modifying trauma-related appraisals
• Behavioural experiments to drop safety behaviours

4. Eye Movement Desensitisation and Reprocessing (EMDR):

• Developed by Francine Shapiro (1987)
• 8-phase protocol:
• History-taking and treatment planning
• Preparation
• Assessment (target memory, negative cognition, emotion, SUDS)
• Desensitisation (bilateral stimulation while focusing on memory)
• Installation (positive cognition)
• Body scan
• Closure
• Re-evaluation
• Works via: dual attention (present safety + past trauma); bilateral stimulation may tax working memory; adaptive information processing (AIP) model
• Evidence: Comparable to TF-CBT; may be faster

9. ADJUSTMENT DISORDER (F43.2)

9.1 Diagnostic Criteria (DSM-5)

• A. Emotional or behavioural symptoms developing in response to identifiable stressor(s) within 3 months of onset
• B. Clinically significant:
• Marked distress out of proportion to severity of stressor (cultural/contextual factors considered)
• OR significant functional impairment
• C. Not criteria for another disorder; not exacerbation of existing disorder
• D. Does not represent normal bereavement
• E. Once stressor (or consequences) terminates, symptoms do not persist for >6 months

Subtypes:

• With depressed mood
• With anxiety
• With mixed anxiety and depressed mood
• With disturbance of conduct
• With mixed disturbance of emotions and conduct
• Unspecified

9.2 ICD-11 Adjustment Disorder (6B43)

• More specific: requires preoccupation with the stressor and failure to adapt
• Duration: variable; specify if acute (<6 months) or prolonged (>6 months when stressor persists)

9.3 Key Distinctions

9.4 Treatment

• Psychotherapy first-line: supportive therapy, brief CBT, problem-solving
• Pharmacotherapy: adjunctive; treat specific symptoms (sleep, anxiety)
• Time-limited; good prognosis if stressor resolves

10. SEPARATION ANXIETY DISORDER IN ADULTS (F93.0)

10.1 Key Points

• DSM-5 now includes adult onset (previously childhood only)
• Fear of separation from attachment figures (not just children to parents)
• Adults: fear of separation from romantic partners, children, parents
• >6 months duration in adults
• Distinguish from: panic disorder (which may involve fears of being alone), dependent PD, agoraphobia

10.2 Treatment

• Cognitive-behavioural approaches
• Attachment-informed therapy
• SSRIs for pharmacological management

11. OCD SPECTRUM DISORDERS

11.1 Overview

DSM-5 groups these under "Obsessive-Compulsive and Related Disorders" (OCRD):

11.2 Hoarding Disorder (F42.3)

Diagnostic criteria (DSM-5):

• Persistent difficulty discarding or parting with possessions regardless of actual value
• Due to perceived need to save and distress associated with discarding
• Accumulation resulting in clutter that precludes use of living spaces
• Causes significant distress/impairment
• Not secondary to another mental disorder or medical condition

Specifiers:

• With excessive acquisition
• With good/fair/poor/absent insight

Neurobiology:

• ACC and insula hyperactivity when discarding owned items
• Not CSTC circuit, this is why SSRIs less effective

Treatment:

• CBT for Hoarding (CBT-H): Steketee & Frost protocol
• Motivational enhancement
• Categorization and decision-making skills training
• Sorting and discarding practice (not just exposure)
• Addressing acquisition
• Cognitive restructuring (beliefs about possessions, memory deficits concerns)
• SSRIs: Less effective than in OCD; paroxetine has best evidence
• Home visits essential for severe cases

11.3 Body Dysmorphic Disorder (BDD: F45.22)

Diagnostic criteria (DSM-5):

• Preoccupation with one or more perceived defects/flaws in physical appearance that are unnoticeable or appear slight to others
• Has performed repetitive behaviours (mirror checking, skin picking, excessive grooming, reassurance-seeking) OR mental acts (comparing to others)
• Causes significant distress/impairment
• Not better explained by eating disorder

Specifiers:

• With muscle dysmorphia (primarily in men; preoccupation with not being muscular/lean enough)
• With good/fair/poor/absent insight

Common preoccupations: Skin, nose, hair, eyes, chin, lips (face most common); any body part possible

Key features:

• Camouflaging (makeup, clothing, posture)
• Mirror checking/avoidance, both occur
• Referential thinking, believes others notice/stare
• Insight often poor to absent; may have delusional intensity
• Suicide risk high: lifetime ideation ~80%; attempts ~25%
• Patients seek cosmetic procedures, provide NO relief; often worsens BDD

Pharmacotherapy:

• High-dose SSRIs (same as OCD): fluvoxamine, fluoxetine best evidence
• Clomipramine
• Augmentation with antipsychotics if delusional features prominent
• Pimozide NOT recommended (historically used; not superior)

Psychotherapy:

• CBT for BDD (Veale protocol): exposure + response prevention, attentional training (from self-focused to environment), cognitive restructuring, mirror-based ERP
• Perceptual mirror retraining

11.4 Trichotillomania (Hair-Pulling Disorder: F63.3)

DSM-5 criteria:

• Recurrent pulling out of one's hair
• Repeated attempts to decrease or stop
• Causes significant distress/impairment
• Not attributable to another medical condition (dermatological) or mental disorder

Sites: Scalp (most common), eyebrows, eyelashes, pubic hair, axillary hair

Phenomenology:

• Focused (tension → pull → relief) vs automatic (not consciously aware)
• Can be triggered by emotional states, boredom

Treatment:

• HRT (Habit Reversal Training): First-line psychological treatment
• Awareness training
• Competing response training (clenching fist instead of pulling)
• Social support + motivation
• CBT with ACT components
• N-acetylcysteine (NAC): Best pharmacological evidence (glutamate modulation); 1200–2400 mg/day
• Clomipramine: Some evidence; olanzapine shows benefit in trials
• SSRIs: inconsistent evidence (unlike OCD, SSRIs don't work as reliably)

11.5 Excoriation Disorder (Skin-Picking: F42.4)

DSM-5 criteria:

• Recurrent skin picking resulting in skin lesions
• Repeated attempts to decrease/stop
• Significant distress/impairment
• Not attributable to substance or medical condition
• Not better explained by stereotypies or NSSI in another disorder

Treatment: Same as trichotillomania, HRT is first-line; NAC; clomipramine

12. ANXIETY IN MEDICAL ILLNESS

12.1 Overview

12.2 Medical Conditions Causing Anxiety

Key investigations to rule out medical causes:

• TFTs (hyperthyroidism critical to exclude)
• Urinary catecholamines/metanephrines (pheochromocytoma)
• ECG, Holter monitor (arrhythmias)
• Blood glucose (hypoglycemia)
• CBC, electrolytes, renal function
• EEG (if seizure suspected)

12.3 Cancer and Anxiety

• Anxiety is most prevalent in cancer (40–50% of patients have significant anxiety)
• Highest: lung, pancreatic, brain tumors
• Reactive anxiety + adjustment disorder + pharmacological causes
• Treatment: SSRIs, short-course benzodiazepines, CBT, supportive therapy, mindfulness

12.4 Pheochromocytoma: The Great Mimicker

• Episodic hypertension (may be paroxysmal)
• Triad: headache, sweating, palpitations
• Mimic panic attacks
• Screening: 24-hour urinary metanephrines/catecholamines, plasma free metanephrines
• CT/MRI adrenal glands once biochemistry positive
• Treatment: surgical excision; alpha-blockers first (phenoxybenzamine), then beta-blockers

13. SUBSTANCE-INDUCED ANXIETY

13.1 DSM-5 Criteria

• Panic attacks or anxiety that is prominent
• Evidence from history, examination, or laboratory that the disturbance developed during or soon after substance intoxication or withdrawal, or after exposure to medication
• Not better explained by independent anxiety disorder

13.2 Common Substances

QUICK REFERENCE TABLES

Pharmacotherapy Summary Table

Psychotherapy Summary Table

Study Notes compiled for PG exams MD Psychiatry exit examination. Sources: Kaplan & Sadock (10th ed.), Stahl's Essential Psychopharmacology (4th ed.), Oxford Textbook of Psychiatry, DSM-5-TR, ICD-11.

Model Answers

Format: Each answer is structured for a 10-mark long essay. Target: 3–4 A4 pages of handwriting (~800–1000 words in exam). Write: introduction → body (structured with subheadings) → conclusion.

Q1. Discuss the management of Obsessive-Compulsive Disorder. [10 marks]

Answer:

Introduction

OCD is a chronic neuropsychiatric disorder characterised by obsessions (recurrent intrusive thoughts/images/urges) and/or compulsions (repetitive behaviours or mental acts). It affects 2–3% of the population, causes marked functional impairment, and ranks among the top 10 most disabling conditions (WHO). Management requires a biopsychosocial approach combining pharmacotherapy, psychotherapy, and, in refractory cases, neuromodulation.

Assessment

Before initiating treatment, a thorough assessment is essential:

• Diagnostic confirmation, meet DSM-5/ICD-11 criteria; rule out OCD spectrum disorders
• Severity rating, Yale-Brown Obsessive Compulsive Scale (Y-BOCS): 0–40; moderate = 16–23; severe = 24–31
• Insight assessment, good/fair/poor/absent (impacts treatment strategy)
• Comorbidity screening, depression (in ~50%), other anxiety disorders, tic disorders
• OCD symptom dimensions, contamination, harm, symmetry, forbidden thoughts, hoarding (guides ERP hierarchy)

Pharmacotherapy

Step 1, First-line: SSRIs

All five SSRIs are FDA-approved for OCD:

Key principles:

• Use higher doses than for depression
• Minimum trial: 10–12 weeks (longer onset than depression)
• Gradual titration; start low to avoid early activation

Step 2, If SSRI inadequate: Switch or add clomipramine

Clomipramine (75–250 mg/day): most efficacious agent (effect size ~1.0 vs SSRIs ~0.5–0.7). Limitations: anticholinergic side effects, QTc prolongation, seizures at high doses, overdose risk. Monitor ECG and plasma levels.

Step 3, Augmentation (if partial response)

Low-dose antipsychotics added to SRI:

• Risperidone 0.5–2 mg/day, best RCT evidence
• Aripiprazole 5–15 mg/day, well-tolerated
• Haloperidol 2–10 mg/day, especially with comorbid tic disorder

Psychotherapy: Exposure and Response Prevention (ERP)

ERP is the gold-standard psychological treatment (effect size 1.0–1.5).

Principles:

1. Construct anxiety hierarchy (SUDS 0–100 scale)
2. Planned exposure to feared stimuli/situations
3. Response prevention, deliberately withhold compulsive ritual
4. Prolonged exposure (~45 min/session) until SUDS reduces 50%
5. Begin at moderate SUDS (40–50), not lowest

Mechanism: Inhibitory learning, new non-threatening associations form; anxiety peaks then habituates without performing compulsion.

CBT additions: Cognitive restructuring of overestimated threat/responsibility; psychoeducation; relapse prevention.

Intensive ERP: Daily sessions (2–3 weeks) for severe/refractory cases.

Combined Treatment

Meta-analyses demonstrate that SSRI + ERP is superior to either alone. Combination is recommended for moderate-severe OCD.

Treatment-Resistant OCD

Defined as failure of ≥2 SSRI trials + 1 clomipramine trial + adequate ERP. Options:

• IV clomipramine
• Transcranial magnetic stimulation (TMS), rTMS to supplementary motor area; FDA-cleared
• Deep Brain Stimulation (DBS), targets anterior limb of internal capsule (ALIC)/nucleus accumbens; FDA Humanitarian Device Exemption (2009)
• Stereotactic ablative surgery, anterior capsulotomy, anterior cingulotomy
• Gamma Knife radiosurgery, bilateral ALIC capsulotomy (non-invasive, delayed 6–12 months)

Duration and Maintenance

• Continue treatment for 1–2 years after remission
• Taper slowly (25% dose reduction every 1–2 months)
• Relapse risk ~50% on discontinuation; higher if inadequate ERP
• Booster ERP sessions reduce relapse

Conclusion

OCD management follows a stepped approach: SSRI + ERP as foundation, augmentation for partial response, neuromodulation for refractory cases. The combination of pharmacotherapy and ERP delivers the best outcomes. Long-term maintenance is essential given the chronic course of OCD.

Q2. Compare SSRIs and clomipramine in the treatment of OCD. [10 marks]

Answer:

Introduction

OCD is treated with serotonin reuptake inhibitors (SRIs). Both SSRIs and clomipramine (a tricyclic with potent SRI activity) are effective, but they differ in efficacy, tolerability, safety, and clinical application.

Pharmacological Mechanisms

Swipe to compare →

Efficacy

Tolerability and Side Effects

Safety in Overdose

Drug Interactions

Monitoring Requirements

Special Populations

Guidelines Recommendation

• First-line: SSRIs (all 5 FDA-approved)
• Second-line: Clomipramine (or when SSRIs fail)
• Combination: Low-dose clomipramine can augment SSRI (careful monitoring required, elevated clomipramine levels)

Conclusion

Clomipramine is more efficacious but SSRIs are better tolerated and safer. Current guidelines recommend SSRIs as first-line due to the tolerability advantage, reserving clomipramine for SSRI failures or severe refractory cases. The ideal pharmacological approach may be to start with an SSRI, then use clomipramine augmentation or substitution in partial responders.

Q3. Discuss evidence-based treatments for PTSD. [10 marks]

Answer:

Introduction

Post-traumatic stress disorder (PTSD) is a potentially chronic condition arising after exposure to actual/threatened death, serious injury, or sexual violence. It affects ~8% of trauma-exposed individuals and features intrusion, avoidance, negative cognitions/mood, and hyperarousal. Evidence-based treatments include trauma-focused psychotherapies and pharmacotherapy.

Assessment Framework

• Diagnostic criteria: DSM-5, 4 symptom clusters (B: intrusion, C: avoidance, D: negative cognitions/mood, E: arousal), ≥1 month duration
• Severity measures: PTSD Checklist-Civilian version (PCL-5), Clinician-Administered PTSD Scale (CAPS-5)
• Risk assessment: Suicidal ideation, comorbid depression/substance use

Trauma-Focused Psychotherapies (First-Line)

1. Prolonged Exposure (PE, Foa et al.)

• Duration: 8–15 weekly sessions
• Components:
• Imaginal exposure: Repeated verbal retelling of trauma narrative in session
• In vivo exposure: Gradual approach to avoided safe situations
• Psychoeducation: Rationale for exposure
• Mechanism: Emotional processing theory, activation and modification of the fear network
• Evidence: Multiple RCTs; ~65–70% response; comparable to CPT

2. Cognitive Processing Therapy (CPT, Resick et al.)

• Duration: 12 sessions (individual or group)
• Components:
• Written trauma account (clarifies appraisals)
• Socratic questioning of "stuck points", maladaptive beliefs
• Challenging across 5 domains: safety, trust, power/control, esteem, intimacy
• Mechanism: Targets distorted cognitions about trauma and its consequences
• Evidence: Large VA/DoD trials; guideline-endorsed by NICE, VA/DoD, ISTSS

3. Cognitive Therapy for PTSD (CT-PTSD, Ehlers & Clark)

• Based on Ehlers & Clark's (2000) cognitive model
• Identifies: (a) appraisals that generate current threat; (b) characteristics of trauma memory (poorly contextualised, easily triggered)
• Techniques: Trauma memory elaboration, updating problematic meanings, dropping safety behaviours, site visits
• Evidence: Multiple UK RCTs; recommended by NICE

4. Eye Movement Desensitisation and Reprocessing (EMDR, Shapiro)

• Duration: 8–12 sessions
• 8-phase protocol: History-taking → Preparation → Assessment (negative/positive cognitions, SUDS) → Desensitisation (bilateral stimulation) → Installation → Body scan → Closure → Re-evaluation
• Bilateral stimulation: Eye movements, taps, auditory tones
• Mechanism: Working memory taxation model, concurrent attention reduces vividness/emotionality; Adaptive Information Processing (AIP) model
• Evidence: Non-inferior to TF-CBT; possibly faster; endorsed by WHO, NICE, APA, VA/DoD
• Note: The eye movement component is debated; meta-analyses suggest bilateral stimulation adds benefit

Comparative efficacy:

All four therapies are equivalent in systematic reviews; choice based on patient preference, therapist training, comorbidities.

What Does NOT Work

• Psychological debriefing (Critical Incident Stress Debriefing, CISD): Single-session debrief immediately post-trauma, NOT effective; may be harmful by interfering with natural recovery
• Benzodiazepines: Contraindicated in PTSD, no evidence for PTSD symptoms; interfere with extinction; increase dependence risk
• Non-trauma-focused therapies (supportive counselling, relaxation alone): Less effective than TF-CBT

Pharmacotherapy

First-line (FDA-approved):

• Sertraline (50–200 mg/day), largest evidence base
• Paroxetine (20–60 mg/day), FDA-approved

Evidence-based (not FDA-approved):

• Venlafaxine XR (75–300 mg/day), strong evidence; comparable to SSRIs

Adjuncts:

• Prazosin (1–15 mg at night), alpha-1 antagonist; reduces nightmares and sleep disturbance (Raskind VA trials)
• Mirtazapine (15–45 mg), sleep, nightmares, comorbid depression
• Quetiapine (25–300 mg), augmentation, comorbid insomnia/MDD

Duration: Minimum 12 months; 2+ years if recurrent/severe.

Emerging Treatments

• MDMA-assisted psychotherapy: Phase 3 trials (MAPS); 67–71% no longer meet PTSD criteria post-treatment; breakthrough therapy designation
• Ketamine infusions: Rapid but transient PTSD symptom reduction (2–3 weeks); under investigation
• Cannabis-based therapy: Preliminary; insufficient evidence

Special Considerations

• Complex PTSD (ICD-11): TF-CBT requires modification, phase-based approach (stabilisation → trauma processing → integration); DBT skills training first
• Military/veteran PTSD: PE and CPT most evidence-based in VA settings; moral injury-focused approaches emerging
• Children: TF-CBT (Cohen et al.), involves caregivers; strong evidence

Conclusion

Trauma-focused psychotherapies (PE, CPT, CT-PTSD, EMDR) are the cornerstone of PTSD treatment. Pharmacotherapy (SSRIs, venlafaxine) is adjunctive or for those who decline/cannot access psychotherapy. Prazosin specifically addresses nightmares. The combination of trauma-focused therapy + SSRI is recommended for severe/chronic cases.

Q4. Describe the cognitive model of panic disorder and its therapeutic implications. [10 marks]

Answer:

Introduction

Panic disorder is characterised by recurrent unexpected panic attacks followed by persistent concern about future attacks or maladaptive behavioural changes. David Clark's (1986) cognitive model provides the most influential theoretical account of how panic attacks are generated and maintained, and directly informs cognitive-behavioural treatment.

Clark's Cognitive Model: Core Proposition

Catastrophic misinterpretation of bodily sensations is the central mechanism. Normal bodily sensations (palpitations, breathlessness, dizziness) are misinterpreted as evidence of imminent catastrophe (heart attack, going mad, losing control).

The Panic Attack Cycle

Maintaining Factors

1. Selective attention/hypervigilance to bodily sensations

Once in the cycle, attention narrows onto the body, this amplifies perceived sensation intensity.

2. Safety behaviours

Actions taken to prevent the feared catastrophe:

• Sitting down when dizzy (prevents "confirming" collapse is not from cardiac cause)
• Calling ambulance
• Escaping the situation
• Gripping walls/surfaces

Safety behaviours MAINTAIN the disorder, they prevent disconfirmation of catastrophic beliefs and prevent learning.

3. Avoidance

Avoiding panic-provoking situations (shopping centres, exercise, caffeinated drinks) prevents exposure to disconfirming information. Leads to secondary agoraphobia.

4. Anticipatory anxiety

Fear of the next panic attack → increased physiological arousal → lower threshold for triggering next attack.

5. Interoceptive conditioning

Internal sensations become conditioned stimuli that trigger anxiety, even before reaching conscious awareness.

Neurobiological Complement: Suffocation Alarm Theory (Klein)

Klein proposed a hypersensitive CO2/suffocation alarm, panicogenic agents (CO2 inhalation, sodium lactate) trigger panic via this brainstem alarm, independent of cognitive appraisal. Explains why antidepressants (imipramine) prevent panic even before subjective beliefs change.

Therapeutic Implications: CBT for Panic Disorder

Clark's model maps directly onto treatment:

Interoceptive exposure exercises:

Key CBT components:

1. Psychoeducation (fight-or-flight response, anxiety is not dangerous)
2. Breathing retraining (caution: can become safety behaviour)
3. Cognitive restructuring (alternative explanations for sensations)
4. Interoceptive exposure
5. In vivo exposure (± situational exposure for agoraphobia)
6. Safety behaviour elimination
7. Relapse prevention

Efficacy

CBT for panic disorder: response rate 60–80%; may be superior to pharmacotherapy in long-term follow-up (lower relapse). NICE recommends CBT as first-line.

Conclusion

Clark's cognitive model identifies catastrophic misinterpretation as the engine of panic disorder. It generates a clear, testable, and therapeutically actionable formulation. CBT derived from this model, particularly interoceptive exposure and safety behaviour elimination, is highly effective and represents the gold standard psychological treatment for panic disorder.

Q5. Discuss the pharmacotherapy of Generalised Anxiety Disorder (GAD). [10 marks]

Answer:

Introduction

GAD is characterised by excessive, uncontrollable worry about multiple domains for ≥6 months, with somatic symptoms (muscle tension, fatigue, poor sleep, difficulty concentrating, irritability, restlessness). Pharmacotherapy is effective and often combined with psychotherapy. Treatment should follow a stepped approach.

Neuropharmacological Rationale

GAD involves dysregulation of three key systems:

• Serotonergic: dorsal raphe → amygdala/PFC; SSRIs/SNRIs restore balance
• Noradrenergic: locus coeruleus hyperactivity → somatic symptoms; SNRIs/buspirone reduce this
• GABAergic: reduced GABA-A function → benzodiazepines augment; pregabalin modulates voltage-gated calcium channels

First-Line Agents

SSRIs:

Key principles:

• Start LOW (may worsen anxiety initially, initial 5-HT2A activation)
• Allow 4–6 weeks at therapeutic dose before judging response
• Full effect at 8–12 weeks
• Taper slowly on discontinuation (discontinuation syndrome, especially paroxetine)

SNRIs:

SNRIs provide dual action on serotonin and norepinephrine, helpful when somatic symptoms dominate (muscle pain, fatigue).

Second-Line Agents

Buspirone:

• 5-HT1A partial agonist (desensitises somatodendritic autoreceptors → increases 5-HT tone chronically)
• Dose: 15–60 mg/day in 2–3 divided doses
• Onset: 2–4 weeks (no acute effect, major disadvantage)
• Advantages: No dependence, no cognitive impairment, safe in elderly
• Limitations: No effect in BZD-naive patients only works if BZD-free; must taper BZDs before switching
• Contraindicated in: Acute anxiety requiring rapid relief; prior long-term BZD users

Pregabalin:

• α2δ subunit voltage-gated Ca2+ channel ligand → reduces presynaptic neurotransmitter release (glutamate, norepinephrine)
• Dose: 150–600 mg/day (divided doses)
• Onset: Faster than SSRIs (~1 week)
• Evidence: Multiple RCTs; approved by EMA for GAD; FDA Schedule V (moderate abuse potential)
• Side effects: Sedation, dizziness, weight gain, dependence risk (less than BZDs)
• Advantages: Faster onset; helpful for somatic symptoms, comorbid neuropathic pain

TCAs (imipramine):

• Effective but side effect burden; second/third-line
• Useful when comorbid depression/pain is prominent

Short-Term / Adjunctive Agents

Benzodiazepines:

• Allosteric potentiators of GABA-A (increase frequency of Cl− channel opening)
• Rapid onset (30 minutes to hours), value for acute symptom relief
• Preferred agents: clonazepam (long t1⁄2, less euphoric), lorazepam
• Limitations: Tolerance, dependence, cognitive impairment (especially elderly), falls, risk in substance misuse
• Role: Short-term bridging while awaiting SSRI/SNRI response; acute exacerbations; avoid >4 weeks
• Tapering protocol: Reduce by 5–10% every 1–2 weeks

Hydroxyzine:

• H1 antihistamine; anxiolytic without dependence
• Dose: 25–50 mg TID or PRN
• Useful as benzodiazepine alternative; rapidly absorbed

Atypical antipsychotics:

• Quetiapine (25–150 mg/day): Evidence for GAD; especially with comorbid insomnia/MDD; metabolic side effects
• Olanzapine: Limited evidence; weight gain concern

Treatment Algorithm

Special Considerations

Duration of Treatment

• Minimum 12 months after remission (GAD is chronic; relapse rate high)
• If >2 episodes: consider indefinite maintenance
• Taper over 4–8 weeks when discontinuing

Conclusion

SSRIs and SNRIs are first-line pharmacotherapy for GAD, combined with psychotherapy (CBT) for optimal outcomes. Buspirone and pregabalin are useful alternatives. Benzodiazepines should be reserved for acute/short-term use. The chronic nature of GAD means long-term maintenance therapy is often required.

Q6. Describe the neurobiology of anxiety. [10 marks]

Answer:

Introduction

Anxiety is a normal adaptive response to perceived threat. Pathological anxiety involves dysregulation of threat detection, appraisal, and extinction circuits. The neurobiology involves multiple interacting systems: limbic structures, monoaminergic pathways, GABAergic circuits, neuropeptides, and the HPA axis.

Key Brain Structures

Amygdala:

• Central hub for fear processing
• Basolateral amygdala (BLA), receives sensory input, evaluates threat
• Central nucleus (CeA), output: drives autonomic/neuroendocrine/behavioural responses
• Two routes from thalamus:
• Short route (thalamo-amygdala): Fast, automatic, rough threat detection (milliseconds)
• Long route (thalamo-cortical-amygdala): Slower, refined, contextual appraisal (seconds)
• In anxiety disorders: amygdala hyperreactivity to threat cues

Prefrontal Cortex (PFC):

• Ventromedial PFC (vmPFC): Extinction memory storage; inhibits amygdala fear response; reduced activity in PTSD/anxiety
• Dorsolateral PFC (dlPFC): Working memory; cognitive control; relevant for worry in GAD
• Orbitofrontal Cortex (OFC): Error signalling; OCD, hyperactive OFC drives "something is wrong" loop

Anterior Cingulate Cortex (ACC):

• Error monitoring, conflict resolution
• OCD: hyperactive → compulsive checking
• PTSD: hyperactive → hypervigilance

Hippocampus:

• Contextual fear conditioning
• Inhibits amygdala in safe contexts
• Reduced hippocampal volume in PTSD, GAD (stress-related neurogenesis reduction)

Bed Nucleus of Stria Terminalis (BNST):

• Sustained, diffuse, non-specific anxiety (vs amygdala's phasic, stimulus-specific fear)
• Mediates "state anxiety" and sustained vigilance
• GAD involves BNST more than amygdala

Locus Coeruleus (LC):

• Primary NE nucleus; bilateral, pontine
• Hyperactivation → sympathetic arousal (palpitations, sweating, tremor)
• Panic disorder: LC hyperactivity (yohimbine provokes panic by blocking α2 autoreceptors)

Periaqueductal Grey (PAG):

• Freezing (dorsal PAG) and flight (ventral PAG) responses
• Panic attacks involve PAG activation

Neurotransmitter Systems

Serotonin (5-HT):

• Dorsal raphe nucleus (DRN) → amygdala, hippocampus, PFC
• 5-HT1A autoreceptors (somatodendritic): inhibit DRN firing → SSRIs initially reduce 5-HT
• Chronic SSRI: autoreceptor desensitisation → increased 5-HT transmission → anxiolytic effect
• 5-HT2C: in striatum; modulates repetitive behaviour (OCD relevant)
• 5-HT3: in limbic system; ondansetron (3 antagonist), some anxiolytic evidence

GABA:

• Primary inhibitory neurotransmitter
• GABA-A receptors: ionotropic (Cl− channel); benzodiazepines → allosteric potentiation → increased frequency of Cl− opening
• GABA-B receptors: metabotropic; baclofen effects
• GABAergic interneurons suppress amygdala hyperactivity
• Reduced GABA-A function in anxiety disorders

Norepinephrine:

• LC → widespread cortical/limbic
• Excessive NE: hyperarousal, somatic anxiety
• Alpha-2 agonists (clonidine, guanfacine) → reduce LC firing → anxiolytic
• Propranolol: peripheral beta-blockade → reduces somatic anxiety feedback loop

Glutamate:

• NMDA receptor in amygdala: fear conditioning and memory
• D-cycloserine (partial NMDA agonist) enhances extinction learning
• mGluR2/3 presynaptic autoreceptors: reduce glutamate release → anxiolytic target
• Ketamine (NMDA antagonist) → rapid anxiolytic/antidepressant effects

Dopamine:

• Mesolimbic system: reward, salience, dysregulated in substance-induced anxiety
• D2 receptors in striatum: OCD, antipsychotic augmentation
• VTA → NAcc: prediction error signalling; threat salience

CRF/Neuropeptides:

• CRF1 receptor (amygdala, BNST): overactivation → anxiety; CRF1 antagonists, clinical trials
• Neuropeptide Y (NPY): anxiolytic; reduced in PTSD
• Substance P (NK1 receptor): anxiety, pain; NK1 antagonists, limited evidence

HPA Axis

• Acute cortisol: adaptive (mobilises energy, enhances fear memory)
• Chronic excess: hippocampal neuronal damage (glucocorticoid toxicity) → impaired contextual fear inhibition
• PTSD: dysregulated HPA (often hypocortisolaemia, not hypercortisolaemia, due to enhanced negative feedback)

CSTC Circuit (OCD-specific)

• Cortico-Striato-Thalamo-Cortical loop
• OFC hyperactivity → excessive "error signals"
• Striatal dysfunction (direct/indirect pathway imbalance) → thalamic disinhibition → repetitive motor output
• Normalised by SSRIs and ERP on FDG-PET

Summary Table

Conclusion

Anxiety disorders involve dysregulation of interconnected neural circuits spanning brainstem (LC, PAG), limbic (amygdala, hippocampus, BNST), and cortical (PFC, OFC, ACC) structures, modulated by serotonin, norepinephrine, GABA, and glutamate systems. Understanding this neurobiology explains both the phenomenology of anxiety disorders and the mechanism of effective treatments.

Q7. What is Y-BOCS? Describe its structure and clinical utility. [10 marks]

Answer:

Introduction

The Yale-Brown Obsessive Compulsive Scale (Y-BOCS) is the gold-standard clinician-administered instrument for assessing OCD severity. Developed by Goodman et al. (1989), it evaluates the severity of obsessions and compulsions independently of their content, making it sensitive to treatment change and useful across OCD symptom dimensions.

Development and Rationale

Prior to Y-BOCS, rating scales conflated symptom content with severity. Y-BOCS solved this by:

• Rating severity regardless of the type of obsession/compulsion
• Using a semi-structured interview format
• Providing independent subscales for obsessions and compulsions

Structure

Format: Semi-structured clinician-administered interview

Total items: 10 (5 for obsessions, 5 for compulsions)

Scoring: Each item 0 (none) to 4 (extreme) → total range 0–40

Five dimensions (same for both subscales):

Severity Classification

Y-BOCS Symptom Checklist

The Y-BOCS is administered with a symptom checklist (separate from the severity scale) that identifies which obsessions and compulsions are present across all dimensions:

• Contamination obsessions/washing compulsions
• Harm obsessions/checking compulsions
• Symmetry obsessions/ordering compulsions
• Forbidden thoughts (sexual, religious, aggressive)/mental neutralising
• Hoarding obsessions/collecting compulsions
• Somatic obsessions/body-checking compulsions

Response Criteria

Insight Assessment (Part of Administration)

Before completing the scale, clinician rates insight:

• Good insight: recognises obsessions as definitely/probably not true
• Fair insight: thinks they may be true
• Poor insight: thinks they are probably true
• Absent insight/delusional beliefs: completely convinced

Updated Versions

Y-BOCS-II (2010):

• Revised to avoid problems with resistance item interpretation
• Added insight item to severity scale
• Broader content coverage; better psychometrics

CY-BOCS: Children's version (Scahill et al.), validated for ages 6–17

Other OCD Scales

Clinical Utility

1. Baseline assessment: Establish severity before starting treatment

2. Treatment monitoring: Administer every 4–6 weeks during treatment; Y-BOCS guides decisions:

• <25% reduction at 8 weeks → consider dose increase or augmentation
• ≥35% reduction = treatment response

3. Research: Standard outcome measure in all OCD clinical trials

4. Communicating with patients: Numeric score helps patients track progress concretely

5. Disability assessment: Supports documentation for leave, accommodation, treatment funding

6. Predicting prognosis: Higher baseline Y-BOCS, poorer insight, and washing/contamination dimension predict poorer pharmacotherapy response

Limitations

• No self-report version (clinician-administered; requires training)
• Resistance item counterintuitive (lower = better)
• Does not assess functional impairment comprehensively
• Not sensitive to rapid changes (designed for 4–6 week intervals)
• Symptom checklist takes additional time

Conclusion

Y-BOCS remains the definitive instrument for OCD severity assessment in both clinical and research settings. It provides a reliable, valid, and content-independent measure of obsession and compulsion severity, guides treatment decisions, and defines response and remission. Every clinician managing OCD should be proficient in its administration.

Q8. Discuss the management of treatment-resistant OCD. [10 marks]

Answer:

Introduction

Treatment-resistant OCD is defined as failure to achieve a clinically significant response (≥35% Y-BOCS reduction) despite adequate trials of at least 2–3 SSRIs at maximum tolerated doses for ≥12 weeks each, one clomipramine trial, and adequate exposure and response prevention (ERP) therapy. It affects approximately 40–60% of OCD patients and represents a significant clinical challenge.

Assessment of "True" Resistance

Before labelling a case resistant, confirm:

• Adequate dose (SSRIs at high-end: fluoxetine 80 mg, fluvoxamine 300 mg, etc.)
• Adequate duration (≥12 weeks at therapeutic dose, longer than for depression)
• Adherence (plasma level confirmation if needed)
• Adequate ERP (≥20 sessions by trained therapist; patient cooperation)
• Comorbidities identified (depression, ADHD, autism, personality disorder) and treated
• Insight level (poor insight predicts poorer response)

Step-by-Step Management

Step 1: Optimise existing treatment

• Ensure SSRI at maximum dose; consider augmenting with clomipramine
• Caution: fluvoxamine inhibits CYP1A2 → raises clomipramine to toxic levels (max clomipramine 75–100 mg if combining with SSRIs)
• Reinforce ERP adherence; consider intensive ERP (daily sessions)

Step 2: Switch SRI

• If SSRI failed: try second SSRI (different CYP profile)
• If 2 SSRIs failed: clomipramine (monotherapy or low-dose augmentation)
• Effect size of clomipramine > all SSRIs; may work when SSRIs fail

Step 3: Antipsychotic augmentation

Mechanism: D2 blockade in striatum augments SRI-mediated 5-HT effects on CSTC circuit.

Step 4: Glutamate modulators

• Riluzole (50–100 mg/day): Reduces glutamate release; several open-label studies positive
• Memantine (10–20 mg/day): NMDA antagonist; case series and small RCTs
• N-acetylcysteine (NAC) (2400 mg/day): Cystine/glutamate antiporter modulation; positive RCTs in augmentation
• Topiramate (25–200 mg/day): Glutamate reduction; some evidence

Step 5: IV clomipramine

• Bypasses first-pass metabolism → higher peak plasma concentrations
• Protocol: 25–75 mg IV in dextrose over 45–90 minutes, 2–3 times per week
• Evidence: Koran et al. studies; Indian data (Bhave & Bhave 1986); responds even when oral fails
• Availability: Limited to centres with expertise

Step 6: Neuromodulation

TMS (Transcranial Magnetic Stimulation):

• rTMS to supplementary motor area (SMA) or dorsal medial PFC
• FDA 510(k) cleared (2018) via Brainsway deep TMS (dTMS, H7 coil)
• Sessions: 20 sessions over 4 weeks (response rate ~40%)
• Non-invasive; minimal side effects; no anaesthesia

Step 7: Neurosurgery (Last Resort)

Criteria for neurosurgical referral:

• Severe OCD (Y-BOCS ≥30)
• Failed ≥3 adequate SRI trials + adequate ERP
• Significant disability (unable to work/live independently)
• Multidisciplinary consensus
• Full informed consent; ethics review

DBS details:

• FDA Humanitarian Device Exemption (2009), not full approval
• Reversible, adjustable (stimulation parameters)
• Requires multidisciplinary team: neurosurgeon, psychiatrist, neurologist, psychologist, ethics board
• Targets: ALIC (most used), ventral striatum, NAcc, BNST, STN (bilateral)
• Complications: infection, haemorrhage (~1–2%), mood changes, hypomania

Emerging Strategies

• Ketamine infusions: Rapid but transient; NMDA mechanism; under investigation
• Psilocybin: Very preliminary; theoretical (5-HT2A agonism); case reports only
• MDMA-assisted therapy: Not specifically for OCD; very early data

Conclusion

Treatment-resistant OCD requires systematic escalation through optimised SRI therapy, antipsychotic augmentation, glutamate modulators, IV clomipramine, neuromodulation, and finally neurosurgery for the most severe cases. Ongoing ERP throughout all pharmacological steps is essential. Multidisciplinary care with realistic goal-setting is paramount.

Q9. Discuss Body Dysmorphic Disorder: clinical features, assessment, and management. [10 marks]

Answer:

Introduction

Body Dysmorphic Disorder (BDD) is classified in DSM-5 under Obsessive-Compulsive and Related Disorders. It involves preoccupation with perceived defects in physical appearance that are unnoticeable or appear slight to others, causing significant distress and functional impairment. It is underdiagnosed because patients seek cosmetic treatment, not psychiatric care.

Epidemiology

• Prevalence: 1.7–2.4% in general population
• Higher in dermatology (9–12%), plastic surgery (6–15%) settings
• Sex: Approximately equal; men more commonly have muscle dysmorphia
• Onset: Typically adolescence (mean 16–17 years)
• Course: Chronic; mean duration before treatment 9–10 years

Clinical Features

Core symptom: Preoccupation with ≥1 perceived appearance flaw, perceived as visible and significant, but objectively absent or minimal.

Common preoccupation sites: Skin (acne, scarring, texture) most common; nose, hair, eyes, lips, chin, face overall; any body part possible.

Muscle dysmorphia (bigorexia):

• Primarily males (but not exclusively)
• Preoccupation with not being muscular/lean enough despite large musculature
• Exercise obsessions, steroid misuse, dietary restriction/supplements

Repetitive behaviours (98% of patients):

• Mirror checking or deliberate mirror avoidance
• Skin picking (camouflage disguised)
• Excessive grooming (hair combing, styling)
• Excessive make-up/camouflage clothing
• Reassurance-seeking from others
• Comparing own appearance to others
• Internet photo searching for comparisons

Cognitive features:

• Overvalued or delusional ideation about defect
• Referential thinking: believes others stare at/mock the perceived defect
• Self-referential cognitive bias: interprets neutral/positive feedback as confirmation of ugliness

Insight spectrum:

• Good/fair insight: knows the belief may be irrational
• Poor insight: belief is probably true
• Delusional beliefs: complete certainty, historically "delusional disorder, somatic type"
• DSM-5 combined BDD with delusional form; now a single spectrum with insight specifier

Suicide risk: HIGH

• Lifetime suicidal ideation: ~80%
• Suicide attempts: ~25–30%
• Rates higher than MDD, bipolar disorder
• Risk factors: delusional insight, comorbid MDD, prior attempts, substance misuse

Differential Diagnosis

Assessment

• BDD-YBOCS: Yale-Brown Obsessive Compulsive Scale modified for BDD; 12 items; same 5-domain structure; severity thresholds parallel to OCD
• BDD-Q (questionnaire): Screening tool
• Full suicide risk assessment (essential given high risk)
• Ask explicitly, patients rarely volunteer appearance concerns without direct inquiry

Management

Pharmacotherapy:

Key points:

• Use high doses (same principle as OCD)
• Allow 12 weeks minimum trial
• SSRIs effective regardless of insight level (even delusional BDD)
• Do NOT use antipsychotics alone for delusional BDD, SSRIs are still required
• Antipsychotic augmentation: consider if delusional features prominent
• Do NOT prescribe pimozide (historical use; not superior; harms outweigh benefits)

Psychotherapy, CBT for BDD (Veale protocol):

Components:

1. Psychoeducation, BDD model; how attention and safety behaviours maintain disorder
2. Attention retraining: From self-focused internal (bodily sensations, imagined defect) to external (surroundings, other people)
3. Exposure and Response Prevention (ERP):
4. Exposure to avoided social situations
5. Mirror ERP: structured mirror use (holistic, not zoomed in; with guidance)
6. Drop safety behaviours (camouflage, reassurance-seeking, checking)
7. Cognitive restructuring: Challenge "appearance assumptions" and self-referential beliefs
8. Behavioural experiments: Test predictions about others' reactions
9. Imagery rescripting: For early-life experiences that shaped appearance-related beliefs

What NOT to do:

• Cosmetic procedures / dermatological treatments: Should NOT be provided
• Provide no lasting relief in BDD (>80% remain preoccupied or find new concerns)
• May worsen BDD by reinforcing the belief that the defect is real
• Surgeons/dermatologists are encouraged to screen for BDD before any procedure

Conclusion

BDD is a serious, often underdiagnosed condition with high suicide risk. It requires high-dose SSRIs and BDD-specific CBT. Cosmetic procedures are contraindicated. Early recognition in dermatology and plastic surgery settings is essential.

Q10. Discuss agoraphobia: clinical features and management. [10 marks]

Answer:

Introduction

Agoraphobia is an anxiety disorder characterised by marked fear or anxiety about situations from which escape might be difficult or help unavailable in the event of a panic attack or panic-like symptoms. DSM-5 made agoraphobia an independent diagnosis (no longer requiring co-occurring panic disorder).

Diagnostic Criteria (DSM-5: F40.00)

Fear/anxiety related to ≥2 of:

1. Using public transport (buses, trains, ships, planes)
2. Being in open spaces (car parks, marketplaces, bridges)
3. Being in enclosed spaces (shops, theatres, cinemas)
4. Standing in line or being in a crowd
5. Being outside of home alone

Situations feared because escape might be difficult or help unavailable if panic/panic-like symptoms develop.

Additional criteria: almost always provokes fear; actively avoided or endured with distress; disproportionate to actual danger; persistent (≥6 months); significant impairment.

Clinical Features

• Cognitive: "I will collapse/faint/lose control and nobody will help me"; "I cannot escape"; "I will be humiliated"
• Avoidance: Homebound in severe cases; requires companion to travel; restricts radius of independent activity
• Safety behaviours: Carrying phone, staying near exits, having medication, travelling at quiet times
• Comorbidity: Panic disorder (30–50%); major depression (common); GAD, social anxiety

Relationship to Panic Disorder

Management

Assessment:

• Identify agoraphobic situations (hierarchy of feared places)
• Rate fear and avoidance (0–10 scale)
• Assess safety behaviours and companions
• Screen for panic disorder, depression, substance use

Psychotherapy, First Line:

Graded Exposure Therapy:

• Based on habituation and inhibitory learning
• Steps:
• Psychoeducation (anxiety is not dangerous; avoidance maintains fear)
• Fear hierarchy construction (8–12 items; SUDS 0–100)
• Graded exposure (start ~40–50 SUDS; progress up hierarchy)
• Therapist-accompanied initially → partner-assisted → independent
• Drop safety behaviours gradually
• Relapse prevention

Example hierarchy:

Partner-assisted exposure: If homebound; family members trained to support exposure without accommodation.

Internet-delivered CBT: For those unable to attend; some evidence base.

Pharmacotherapy:

• SSRIs/SNRIs: First-line if panic disorder comorbid; helpful for overall anxiety reduction enabling exposure
• Sertraline, escitalopram, venlafaxine XR
• Benzodiazepines: Short-term acute relief; avoid long-term (may interfere with habituation during exposure)
• Combination (SSRI + CBT): Superior to either alone for severe agoraphobia with panic

Key principle: Pharmacotherapy WITHOUT exposure therapy has high relapse. Exposure is the active ingredient.

Prognosis

• Moderate with treatment: 60–70% improvement in avoidance
• Poorer prognosis: longer duration, comorbid depression, housebound status, poor social support
• Without treatment: progressive worsening; risk of permanent housebound status

Conclusion

Agoraphobia causes severe functional impairment through avoidance. Graded exposure therapy is the cornerstone of treatment; pharmacotherapy (SSRIs) supports exposure work. Full independence is achievable with adequate treatment, though severe cases require prolonged, intensive work.

Model Answers compiled for PG exams MD Psychiatry exit examination. All clinical vignettes are fictitious. Sources: Kaplan & Sadock (10th ed.), Stahl's Essential Psychopharmacology (4th ed.), Oxford Textbook of Psychiatry, DSM-5-TR, ICD-11, NICE Guidelines.

Mnemonics & Memory Tricks

How to use this file: Read each mnemonic actively, cover the expansion and attempt to recall before checking. Spaced repetition: review on Day 1, Day 3, Day 7, Day 14.

SECTION A: DIAGNOSTIC CRITERIA

1. GAD: The 6 Somatic Symptoms (DSM-5)

Usage: GAD needs ≥3 of 6 (adults); ≥1 of 6 (children). Duration: 6 months. Plus: excessive worry + difficulty controlling it.

2. Panic Attack: 13 Symptoms

Shortcut: ≥4 symptoms, abrupt onset, peaks within minutes. Unexpected = panic disorder.

3. OCD Neurocircuitry: CSTC Components

Broken down:

• Caudate nucleus (striatum), gates repetitive behaviour
• OFC (orbitofrontal cortex), error signal generator ("something is wrong")
• Striatum (caudate + putamen), direct and indirect pathways
• Thalamus, disinhibited in OCD → drives cortex
• Thalamo → back to cortex (loop closes)
• ACC (anterior cingulate cortex), conflict/error monitoring

Direct pathway (GO): Striatum → inhibits GPi → releases thalamus → drives cortex

Indirect pathway (STOP): Striatum → GPe → STN → GPi → inhibits thalamus

In OCD:

• OFC fires excessive "error signals"
• Caudate fails to gate the signal
• Thalamus disinhibited → keeps looping → compulsions

4. PTSD: 4 Symptom Clusters (DSM-5)

Swipe to compare →

Duration: ≥1 month. Stressor: Criterion A (traumatic event, actual/threatened death, serious injury, sexual violence).

5. PTSD Symptom Cluster D: Negative Cognitions (7 items)

6. Y-BOCS: 5 Severity Domains

Each scored 0–4, × 2 subscales (O + C) = 0–40 total.

7. OCD Insight Specifiers: 4 Levels

• Good insight, knows obsessions probably not true
• Fair insight, thinks they may be true
• Poor insight, thinks they are probably true
• Absent/delusional, completely convinced (delusional intensity)

SECTION B: PHARMACOLOGY

8. SSRIs Approved for OCD: 5 Drugs

Note: Officially, 5 SSRIs approved by FDA: Fluoxetine, Fluvoxamine, Paroxetine, Sertraline + Clomipramine (TCA). Escitalopram is used at high doses off-label.

9. Clomipramine Side Effects

10. PTSD First-Line Pharmacotherapy

• Sertraline, FDA-approved, first-line
• Paroxetine, FDA-approved, first-line
• Venlafaxine XR, strong evidence, not FDA-approved but widely used
• Prazosin, nightmares specifically (alpha-1 antagonist)

11. Augmentation Options for OCD (Antipsychotics)

Simpler version: "RHAOOQ" → Risperidone, Haloperidol, Aripiprazole, Olanzapine, Quetiapine

12. Drugs Contraindicated / Not Recommended in PTSD

SECTION C: THERAPY CONCEPTS

13. ERP Principles: Key Rules

14. Clark's Panic Model: 4 Key Maintaining Factors

15. Specific Phobia Types: DSM-5 Classification

16. OCD Spectrum Disorders: DSM-5 OCRD Chapter

17. EMDR: 8 Phases

18. Cognitive Processing Therapy (CPT): 5 Stuck-Point Themes

Official 5 themes: Safety, Trust, Power/Control, Esteem, Intimacy

19. Neurobiology of Anxiety: Key Structures

20. Hoarding Disorder: Key Distinguishing Features from OCD

SECTION D: QUICK-FIRE RECALL

Rapid-Fire Card 1: Duration Criteria

Rapid-Fire Card 2: Neurobiology One-Liners

Rapid-Fire Card 3: Y-BOCS Severity Thresholds

Rapid-Fire Card 4: First-Line Psychological Treatments

Rapid-Fire Card 5: Surgical Targets for OCD

Mnemonics file compiled for PG exams MD Psychiatry exit examination. Sources: Kaplan & Sadock (10th ed.), Stahl's Essential Psychopharmacology (4th ed.), DSM-5-TR, ICD-11.

High-Yield Comparisons

How to use: Each table is a potential short-answer or part of a long essay. Test yourself by covering one column and recalling the other.

Table 1: GAD vs Panic Disorder vs Social Anxiety Disorder

Swipe to compare →

Table 2: OCD vs OCPD (Obsessive-Compulsive Personality Disorder)

Table 3: PTSD vs Acute Stress Disorder vs Adjustment Disorder

Table 4: Clomipramine vs SSRIs for OCD

Table 5: CBT vs Pharmacotherapy in Anxiety Disorders

Table 6: Fear vs Anxiety: Neurobiological Distinction

Table 7: OCD vs Delusional Disorder (Somatic Type): Overvalued Ideas Spectrum

Table 8: Flooding vs Systematic Desensitisation

Table 9: Benzodiazepines: Role Across Anxiety Disorders

Table 10: Pharmacotherapy Comparison Across Anxiety Disorders: At a Glance

Comparisons file compiled for PG exams MD Psychiatry exit examination. Sources: Kaplan & Sadock (10th ed.), Stahl's Essential Psychopharmacology (4th ed.), Oxford Textbook of Psychiatry, DSM-5-TR, ICD-11, NICE Guidelines.

PYQ Frequency Analysis

Scope: PG exams MD Psychiatry Paper II, compiled from available question bank data (17+ years). Frequency ratings reflect estimated appearance across exam cycles. Use this to prioritise revision time.

SECTION 1: FREQUENCY HEAT MAP

Overall Topic Frequency (Anxiety & OCD)

Swipe to compare →

SECTION 2: QUESTION-TYPE ANALYSIS

Long Essay (10 marks): High Frequency Topics

Short Essay / Short Notes (5 marks): High Frequency

SECTION 3: TOPIC-BY-TOPIC PYQ BREAKDOWN

OCD: Most Tested Topic in This Chapter

Long essay patterns observed:

• "Discuss the management of Obsessive-Compulsive Disorder", comprehensive management question; appears every 1–2 years
• "Discuss the pharmacological treatment of OCD with emphasis on the role of clomipramine"
• "Compare the efficacy of SSRIs and clomipramine in the treatment of OCD"
• "Describe the neurobiology of OCD and its therapeutic implications"
• "Discuss treatment-resistant OCD, definition, evaluation, and management options"
• "Describe the role of neuromodulation in treatment-resistant OCD"

Short note patterns:

• "Y-BOCS", appears very frequently; know all 10 items, 5 domains, scoring, severity thresholds
• "ERP in OCD", mechanism, procedure, evidence
• "DBS in OCD", targets, evidence, FDA status
• "Augmentation strategies in OCD"
• "CSTC circuit in OCD"

PTSD: Second Most Tested

Long essay patterns:

• "Discuss the evidence-based psychological treatments for PTSD"
• "Describe PTSD, diagnostic criteria, neurobiology, and management"
• "Discuss EMDR, describe the technique, mechanism, and evidence base"
• "Describe the Ehlers and Clark cognitive model of PTSD"
• "Discuss pharmacological management of PTSD"

Short note patterns:

• "EMDR"
• "Prolonged Exposure therapy"
• "Cognitive Processing Therapy (CPT)"
• "Prazosin in PTSD nightmares"
• "Differences between PTSD and Acute Stress Disorder"
• "Complex PTSD (ICD-11)"

Panic Disorder

Long essay patterns:

• "Describe Clark's cognitive model of panic disorder and its therapeutic implications"
• "Discuss the management of panic disorder"
• "Describe the neuroanatomy of panic attacks"

Short note patterns:

• "Clark's cognitive model of panic"
• "Interoceptive exposure"
• "Suffocation alarm theory (Klein)"
• "Locus coeruleus and panic"
• "Agoraphobia, management"

GAD

Long essay patterns:

• "Discuss the pharmacotherapy of Generalised Anxiety Disorder"
• "Describe GAD, diagnostic criteria, neurobiology, and management"

Short note patterns:

• "Buspirone in GAD"
• "Pregabalin in GAD"
• "Borkovec's avoidance model of worry"
• "Metacognitive therapy in GAD"

Neurobiology of Anxiety

Patterns observed:

• "Describe the neurobiology of anxiety disorders"
• "Discuss the role of amygdala in anxiety"
• "Describe the role of serotonin in anxiety"
• "Discuss the neurobiology of OCD"

Key content tested:

• Amygdala fear circuit (fast vs slow routes from thalamus)
• BNST, sustained anxiety (GAD)
• Locus coeruleus, NE (panic)
• CSTC, OCD
• GABA-A, benzodiazepine mechanism
• 5-HT1A, buspirone; SSRIs mechanism
• HPA axis, chronic anxiety, PTSD

Systematic Desensitisation / Behaviour Therapy

Patterns observed:

• "Describe systematic desensitisation, principles and procedure"
• "Compare flooding and systematic desensitisation"
• "Describe behaviour therapy techniques in anxiety disorders"
• "What is VRET? Describe its applications in psychiatry"

SECTION 4: PREDICTED HIGH-YIELD QUESTIONS (Sep 2026 Exit Exam)

Based on frequency analysis and recency patterns, the following are highest-probability questions:

Tier 1: Almost Certain to Appear (in some form)

1. OCD management (full algorithm or treatment-resistant focus)
2. PTSD, evidence-based treatments OR EMDR specifically
3. Y-BOCS, structure, scoring, clinical use
4. Neurobiology of anxiety / OCD neurocircuitry (CSTC)
5. Clark's cognitive model of panic + therapeutic implications

Tier 2: Very Likely

1. Clomipramine vs SSRIs in OCD
2. GAD pharmacotherapy
3. BDD, clinical features and management
4. Exposure and Response Prevention, principles and procedure
5. Systematic desensitisation (short note)

Tier 3: Probable

1. DBS in OCD (short note or part of treatment-resistant OCD)
2. Prazosin in PTSD nightmares
3. Hoarding Disorder (short note)
4. Prolonged Exposure therapy / CPT
5. Ehlers & Clark cognitive model of PTSD

Tier 4: Possible

1. Social Anxiety Disorder
2. Flooding vs systematic desensitisation
3. Agoraphobia
4. Suffocation alarm theory
5. VRET

SECTION 5: COMMON EXAMINER TRAPS & FREQUENTLY MISSED POINTS

SECTION 6: MARKS ALLOCATION STRATEGY

10-Mark Long Essay: Time Budget (30 minutes)

5-Mark Short Essay: Time Budget (10–12 minutes)

SECTION 7: INTER-TOPIC LINKAGES (Exam Connections)

These topics frequently appear together or reference each other:

PYQ Analysis compiled for PG exams MD Psychiatry exit examination (September 2026). Frequency estimates based on 17+ years of available question bank data. All predictions are probabilistic, not guaranteed.

Quick Review

Instructions: Read each vignette carefully. Answer all three questions before checking the answers. Focus on: diagnosis → management algorithm → specific clinical reasoning. All patient names are fictitious.

VIGNETTE 1: OCD with Poor Insight

Clinical presentation:

Arjun, 28-year-old male software engineer, is brought by his wife to the outpatient clinic. She reports that for the past 2 years, he spends 4–5 hours daily washing his hands, sometimes until they bleed. He believes that unless he washes 27 times in a specific sequence, his mother will develop cancer. When his wife tries to interrupt the ritual, he becomes extremely distressed. When asked about this in clinic, Arjun states: "I know it sounds strange, but I am 80–90% sure that my rituals protect my mother. I'm not ready to stop." He has stopped attending social events and was recently placed on probation at work due to lateness.

His MSE: alert, oriented; affect anxious; thought content, ideas of reference to cleansing rituals; no hallucinations; insight: partial, acknowledges beliefs "may seem strange" but maintains strong conviction in their protective function. He is not actively suicidal.

Q1. What is the diagnosis? Identify the key diagnostic features and insight specifier. [3 marks]

Q2. How does poor insight affect management? Outline the treatment plan. [4 marks]

Q3. Arjun's wife asks: "Should we just do what he wants and let him wash, it calms him down?" How do you counsel her? [3 marks]

VIGNETTE 2: Panic Disorder with Agoraphobia

Clinical presentation:

Priya, 32-year-old bank teller, presents with a 6-month history of sudden attacks lasting 10–15 minutes. During these attacks she experiences heart pounding, breathlessness, dizziness, tingling in her hands, and an overwhelming fear that she is having a heart attack. Three cardiac workups (ECG, echo, Holter) were normal. She now refuses to take public transport, avoids shopping malls and cinemas, and travels only when accompanied by her husband. She has taken medical leave for 3 months. She carries her phone and a bottle of water everywhere and always sits near an exit.

Q1. Diagnose and formulate the case using Clark's cognitive model. [4 marks]

Q2. Outline a pharmacological and psychological treatment plan. [4 marks]

Q3. What is the role of benzodiazepines in this case? Are there any concerns? [2 marks]

VIGNETTE 3: PTSD: Complex Presentation

Clinical presentation:

Meena, 38-year-old nurse, was sexually assaulted by a colleague 8 months ago. She did not report the incident. Over the past 6 months she has had recurrent vivid nightmares of the assault, waking 3–4 times per week. During the day she experiences intrusive images when she passes the ward where it happened. She avoids that ward entirely (has requested a transfer), avoids male colleagues, and no longer meets friends. She feels "numb" most of the time, cannot feel joy, and believes "I should have fought back, it's my fault." She is hypervigilant at work and startles easily. She reports poor concentration and has made three medication errors in the past month. She denies suicidal ideation but says "I don't care if I live or die." She drinks 2–3 units of alcohol nightly to help sleep.

Q1. Diagnose fully. Are there any comorbidities to screen for? [3 marks]

Q2. Outline a comprehensive management plan, including safety, pharmacotherapy, and psychotherapy. [5 marks]

Q3. Meena asks: "Why can't you just give me something to forget it all?" How do you respond, and what does this reflect clinically? [2 marks]

VIGNETTE 4: GAD: Diagnostic Challenge

Clinical presentation:

Rajan, 45-year-old teacher, presents to a general psychiatry clinic with a 2-year history of "constant worry." He worries about his children's academic performance, his wife's health, his own finances, and his job security, even though objectively there are no major problems in any of these areas. He finds it impossible to stop worrying once it starts. He has muscle aches in his shoulders and neck, wakes at 2 AM and cannot return to sleep, and feels "on edge" throughout the day. He says his mind is "always running." He is exhausted by 3 PM. He denies panic attacks, obsessions, or social fears. He has no medical history. TSH, FBC, renal, and liver function tests, all normal.

Q1. Diagnose and justify. What is the key differential? [3 marks]

Q2. Design a complete treatment plan combining pharmacotherapy and CBT. [4 marks]

Q3. What is Borkovec's avoidance model of worry, and why is it clinically relevant? [3 marks]

VIGNETTE 5: Social Anxiety Disorder

Clinical presentation:

Deepa, 26-year-old medical intern, presents with a 10-year history of fear of speaking in public, attending ward rounds, and presenting cases. She becomes intensely anxious when expected to speak in group settings, heart pounding, flushing, voice trembling, sweating, and fears others will notice and think she is incompetent. She over-prepares excessively (4–5 hours for a 5-minute case presentation). She does not fear one-to-one conversations. She has declined a research conference invitation, turned down a teaching post, and avoids socialising with senior colleagues. LSAS total score: 72.

Q1. Diagnose, differentiate performance-only vs generalised SAD, and justify your classification here. [3 marks]

Q2. Outline the pharmacological and psychological management. [4 marks]

Q3. Deepa asks: "Propranolol, can I just take it before every presentation forever?" Advise her. [3 marks]

VIGNETTE 6: BDD: Cosmetic Surgery Clinic Referral

Clinical presentation:

Vikram, 24-year-old male, is referred from a plastic surgery clinic. He has requested rhinoplasty three times in 18 months. The first surgeon performed the procedure, and Vikram was distressed with the result within 4 weeks ("it's still crooked"). A second and third surgeon declined, noting that his nose appeared normal. He currently spends 3–4 hours daily examining his nose in mirrors from different angles, comparing photographs, and seeking reassurance from family. He has dropped out of college and does not leave home. PHQ-9 = 19 (severe depression). On questioning, he rates his conviction that his nose is disfigured at "99%." He denies suicidal ideation currently but mentions he "understands why people with this feeling might not want to live."

Q1. Diagnose, classify insight level, and assess risk. [3 marks]

Q2. What is your management plan? Address the surgical requests specifically. [4 marks]

Q3. How do you explain BDD to Vikram in a way he can accept? [3 marks]

VIGNETTE 7: Treatment-Resistant OCD

Clinical presentation:

Sunita, 35-year-old homemaker, has had OCD since age 16. She has checking and contamination obsessions. She has tried fluoxetine (80 mg × 14 weeks, partial response, Y-BOCS reduced from 34 to 27), then sertraline (200 mg × 12 weeks, no further benefit, Y-BOCS 28), then paroxetine (60 mg × 12 weeks, intolerance due to weight gain and sexual dysfunction, discontinued at 8 weeks). She had 20 sessions of ERP with a trained psychologist, Y-BOCS reached 24 at end, but has since risen back to 31. She is currently on escitalopram 20 mg. She is severely functionally impaired, cannot cook, manage finances, or leave the house unaccompanied.

Q1. Does Sunita meet criteria for treatment-resistant OCD? Justify. [2 marks]

Q2. What is the next step? Outline a management plan for treatment-resistant OCD. [5 marks]

Q3. Sunita's husband asks: "Is there any surgery that can cure her?" How do you counsel him? [3 marks]

VIGNETTE 8: Specific Phobia: Blood Injection Injury Type

Clinical presentation:

Rahul, 22-year-old medical student, faints when he has blood drawn for his own medical tests. He has also fainted while observing venepuncture procedures in clinical postings and once while suturing a laceration. He dreads clinical postings involving blood or injections, avoids them when possible, and plans to limit his career to "anything without blood." His heart races briefly when he anticipates these situations, but he then feels lightheaded and loses consciousness. He recovers within minutes. He has no cardiac history. ECG is normal.

Q1. Diagnose and explain the unique physiology. [3 marks]

Q2. What is the specific treatment? Why is it different from other phobias? [4 marks]

Q3. How does this case affect Rahul's medical career? How would you advise him? [3 marks]

Clinical Vignettes compiled for PG exams MD Psychiatry exit examination. All patient details are entirely fictitious. Sources: Kaplan & Sadock (10th ed.), Stahl's Essential Psychopharmacology (4th ed.), Oxford Textbook of Psychiatry, DSM-5-TR, ICD-11, NICE Guidelines.