OCD

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Last updated 12:57 PM on 6/28/26
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26 Terms

1
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What is OCD?

A chronic psychiatric disorder with recurrent obsessions (intrusive, ego-dystonic thoughts/images/urges) and/or compulsions (repetitive behaviours to neutralise anxiety), time-consuming >1 hr/day, causing significant distress or functional impairment.

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What does ego-dystonic mean in OCD?

The patient recognises their thoughts as irrational/excessive but cannot stop them. Insight is usually preserved — this distinguishes OCD from psychosis.

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What is a compulsion?

A repetitive behaviour or mental act performed to reduce the anxiety caused by an obsession. Compulsions are negatively reinforced — they provide short-term relief, creating a habit loop.

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What is the lifetime prevalence of OCD?

~2-3%. Bimodal onset: early (10-12 yrs) and late adolescence/early adulthood (~20-25 yrs). Males have earlier onset (often with tics); females have slightly higher overall adult prevalence.

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What are the 4 OCD symptom dimensions?

  1. Contamination / Washing 2. Symmetry / Ordering 3. Forbidden Thoughts / Checking 4. Hoarding
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Name 5 common types of compulsions.

  1. Washing/Cleaning rituals 2. Checking (locks, stove) 3. Counting/Repeating a fixed number of times 4. Ordering/Arranging until 'feels right' 5. Mental compulsions (silent praying, neutralising bad thoughts)
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What are the 3 DSM-5 insight specifiers for OCD?

Good/fair insight: recognises beliefs are probably not true. Poor insight: thinks beliefs are probably true. Absent insight/delusional: completely convinced. WARNING: Absent insight does NOT mean psychosis.

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What neurotransmitter is most implicated in OCD, and what is the evidence?

Serotonin — strongest evidence: SSRIs and clomipramine (potent serotonin reuptake inhibitors) are effective; weak/non-serotonergic antidepressants are not. Also implicated: Dopamine (tic-related OCD) and Glutamate (CSTC circuit).

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Explain the CSTC circuit in OCD.

Cortico-Striato-Thalamo-Cortical circuit hyperactivity. Normally: OFC/ACC send 'something is wrong' signal; caudate filters unnecessary worry before reaching thalamus/cortex. In OCD: this gating FAILS; loop keeps re-firing; anxiety signal never switches off. This is WHY checking/reassurance doesn't help — the loop resets, not the worry.

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What are the genetic findings in OCD?

MZ twin concordance ~0.65 vs DZ ~0.15. First-degree relatives have 4-8x increased risk. Associated with SLC1A1 (glutamate transporter gene) — recent research focus.

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What is PANDAS?

Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections. Abrupt-onset OCD in children following strep infection — autoantibodies cross-react with basal ganglia. Needs paediatric/immunology referral.

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What does Mowrer's two-factor theory say about OCD?

Factor 1 (Classical conditioning): Neutral stimulus becomes associated with fear. Factor 2 (Operant conditioning): Compulsion is negatively reinforced by anxiety relief. This is the behavioural basis for ERP therapy.

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What are the DSM-5-TR criteria for OCD? (mnemonic)

Mnemonic: TIME. T = Time-consuming (>1 hr/day). I = Intrusive thoughts/images/urges. M = Marked distress or impairment. E = Ego-dystonic. Also: not due to substances/medical condition; not better explained by another mental disorder.

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How does DSM-5 classify OCD vs prior classification?

OCD was MOVED OUT of anxiety disorders in DSM-5 — now in its own chapter: 'Obsessive-Compulsive and Related Disorders'. Both DSM-5 and ICD-11 agree OCD is NOT an anxiety disorder — it has its own CSTC circuit-based neurobiological identity.

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How do you distinguish OCD from GAD?

GAD: Worries about real-life concerns (finances, health, relationships) — realistic, not senseless. OCD: Obsessions are intrusive, senseless, ego-dystonic — the person recognises them as irrational.

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How do you distinguish OCD from psychosis?

OCD: Obsessions are ego-dystonic with PRESERVED INSIGHT — patient knows thoughts are irrational. Psychosis: Delusions = fixed false beliefs with NO insight. WARNING: OCD with absent insight does NOT equal psychosis — don't give antipsychotic monotherapy.

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How do you distinguish OCD from Autism Spectrum Disorder?

OCD rituals are ego-DYSTONIC — distressing, unwanted by the patient. ASD rituals are ego-SYNTONIC — comforting, desired by the patient.

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What is the gold standard rating scale for OCD severity?

Y-BOCS (Yale-Brown Obsessive Compulsive Scale). Used for severity assessment and monitoring treatment response. Neuroimaging (fMRI/PET) shows CSTC hyperactivity but is a research tool only — not routine clinical use.

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What is first-line treatment for OCD?

Pharmacotherapy: SSRI at HIGH dose (Fluoxetine, Fluvoxamine, Sertraline, Paroxetine, Escitalopram). Psychotherapy: CBT with ERP (Exposure and Response Prevention). Combined SSRI + CBT = best outcome, especially in severe cases. KEY: OCD needs higher doses and longer duration (10-12 weeks) than depression.

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What is ERP and why does it work?

Exposure and Response Prevention. Exposure: Gradual, planned exposure to feared stimulus (e.g. touching 'contaminated' object). Response Prevention: Not performing the compulsion (e.g. not washing hands after). Rationale: Anxiety naturally decreases over time with prolonged exposure (habituation) — breaks the negative reinforcement cycle.

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What is second-line pharmacotherapy for OCD?

Clomipramine (TCA — potent serotonergic agent). Effective but more side effects: anticholinergic effects, cardiotoxicity in overdose. Used when SSRIs fail.

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How is treatment-resistant OCD managed?

  1. Augment SSRI with low-dose atypical antipsychotic (Risperidone, Aripiprazole) — especially if poor insight or comorbid tics. 2. Switch to Clomipramine. 3. rTMS (repetitive Transcranial Magnetic Stimulation) — FDA approved, targets SMA/OFC. 4. Deep Brain Stimulation (DBS) — targets anterior limb of internal capsule / nucleus accumbens.
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What is the role of the family in OCD management?

Family must NOT participate in rituals or provide reassurance — this is called 'family accommodation' and it WORSENS OCD. Family psychoeducation is essential.

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What are good prognostic factors in OCD?

Later age of onset. Good insight. Short duration before treatment. Good initial treatment response. Mild symptoms, good premorbid functioning.

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What are poor prognostic factors in OCD?

Early/childhood onset. Poor insight or delusional beliefs. Hoarding symptoms (most resistant to treatment). Comorbid tic disorder / Tourette's. Comorbid personality disorder. Long duration of untreated illness. Course: Often chronic, waxing/waning.

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What are the recent advances in OCD treatment?

Glutamate hypothesis: new targets — Memantine, N-acetylcysteine (under research). Ketamine: rapid but short-lived anti-obsessional effect (under research). rTMS: now FDA-approved for resistant OCD. DBS: established for severe refractory OCD. SLC1A1 gene / GWAS studies ongoing. PANDAS/PANS: growing recognition of autoimmune OCD in children.