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Station 1: Definition and Diagnosis
Examiner: Define panic disorder and distinguish it from a panic attack, GAD and agoraphobia.
Expected answer: A panic attack is an abrupt surge of intense fear peaking within minutes, with at least 4 of 13 symptoms (palpitations, sweating, trembling, dyspnoea, choking, chest pain, nausea, dizziness, chills/flushes, paraesthesia, derealisation, fear of losing control, fear of dying). It is a specifier, not a diagnosis — it can occur in any disorder, in medical illness, and in substance intoxication or withdrawal.
Panic disorder = recurrent, unexpected panic attacks (at least one out of the blue) plus at least 1 month of at least one of: persistent concern about further attacks, worry about their consequences (going crazy, dying), or maladaptive behaviour change (avoidance, agoraphobia, repeated ED attendance, pulse-checking).
Generalised anxiety disorder (GAD) is excessive, difficult-to-control worry about multiple topics, more days than not for at least 6 months, plus at least 3 of 6 somatic/cognitive symptoms (restlessness, fatigue, concentration, irritability, muscle tension, sleep). The worry is pervasive and chronic — distinct from the episodic fear of panic.
Agoraphobia (DSM-5) = marked fear of at least 2 of 5 situations (public transport, open spaces, enclosed places, crowds/queues, being outside alone) where escape might be difficult or help unavailable, persistent at least 6 months. DSM-5 de-coupled agoraphobia from panic disorder — it is now a standalone diagnosis, although panic disorder and agoraphobia frequently co-occur.
Station 2: Pathophysiology
Examiner: Describe the neurobiological basis of panic disorder.
Expected answer: Three converging models, all relevant:
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Amygdala–prefrontal circuit dysregulation (Etkin 2007 meta-analysis) — the basolateral amygdala (threat detection) is hyperactive, and the medial prefrontal cortex and ventromedial PFC (top-down inhibition, extinction learning) are hypoactive. The insula (interoception) is also hyperactive — patients are hypersensitive to bodily sensations. Successful SSRI or CBT normalises these patterns.
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False Suffocation Alarm theory (Donald Klein, 1993) — a phylogenetically ancient brain-stem suffocation detector fires a false alarm, generating overwhelming breathlessness, choking and chest tightness even with normal blood gases. Patients with panic disorder reliably panic in response to 5 to 35% CO2 inhalation, sodium lactate infusion, doxapram, bicarbonate and caffeine — agents that increase brain-stem pH sensing or ventilatory drive — while healthy controls do not. This CO2 hypersensitivity is the most reproducible biological marker of panic disorder. The amygdala, BNST and retrotrapezoid nucleus are now implicated.
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Modern learning theory (Bouton, Mineka, Barlow 2001) — the first panic attack is initially triggered by an internal bodily sensation (exercise-induced tachycardia, hypoglycaemia, caffeine). Through interoceptive conditioning, the patient learns to fear these bodily sensations themselves. Anticipatory anxiety and phobic avoidance then develop through negative reinforcement, culminating in agoraphobia. This model is the basis of interoceptive exposure in CBT.
Neurochemistry: noradrenaline excess (locus coeruleus — yohimbine provokes panic); serotonin dysregulation (basis for SSRI; 5-HT1A receptor down-regulated); GABA deficiency (basis for benzodiazepines). HPA axis activation is phasic during the attack, normalising between attacks. Genetics: heritable 30 to 40%, polygenic (no single gene of large effect).
Station 3: Pharmacotherapy
Examiner: Outline the pharmacological management of panic disorder. Why must SSRIs be started at low dose?
Expected answer:
- First-line: SSRI. Sertraline 25 mg OD for week 1, then 50 mg OD, titrate weekly to 100 to 200 mg OD (max 200 mg); alternatives — escitalopram 5 to 20 mg OD, paroxetine 10 to 40 mg OD (worst discontinuation; avoid in under-25s), citalopram 10 to 40 mg OD (QT; 20 mg max in over-65s), fluoxetine 10 to 60 mg OD (least discontinuation syndrome).
- Start LOW and titrate slowly: patients with panic disorder are highly sensitive to the activating effect of SSRIs; the first 1 to 2 weeks can paradoxically increase anxiety, jitteriness and insomnia ("jitteriness syndrome"). Starting at half the depression dose reduces this risk.
- Onset 4 to 6 weeks; full effect 8 to 12 weeks. Counsel the patient; do not stop early.
- Continue at least 12 months after remission to prevent relapse.
- Withdraw gradually over at least 4 weeks to avoid discontinuation syndrome (flu-like symptoms, dizziness, "brain zaps", anxiety rebound).
Second-line / alternatives: SNRIs (venlafaxine XR 75 to 225 mg OD; duloxetine 30 to 120 mg OD); pregabalin 150 to 600 mg/day (binds α2δ calcium-channel subunit; useful for GAD and as adjunct for panic); TCAs (clomipramine, imipramine — reserve for treatment resistance; ECG; overdose toxicity).
Benzodiazepines — strictly short-term (2 to 4 weeks max): lorazepam 0.5 to 1 mg, diazepam 2 to 5 mg, alprazolam 0.25 to 0.5 mg for acute rescue or while waiting for SSRI onset. Dependence develops within 4 to 6 weeks of regular use; abrupt withdrawal can cause seizures.
Station 4: Psychological Treatment
Examiner: Describe the cognitive-behavioural model of panic disorder and the CBT components.
Expected answer: The Clark cognitive model proposes that panic arises from a catastrophic misinterpretation of bodily sensations — a slight increase in heart rate is interpreted as "I'm having a heart attack"; the resulting fear increases sympathetic output, which increases heart rate further, completing a vicious cycle that culminates in panic.
CBT has three components (12 to 15 weekly sessions, 60 minutes each):
- Psychoeducation — explain the model and the benign nature of the sensations.
- Cognitive restructuring — challenge the catastrophic cognitions, examine the evidence ("Have you ever actually had a heart attack? What is the alternative explanation?").
- Exposure — both interoceptive exposure (deliberately inducing the feared sensations by spinning, hyperventilating, breathing through a straw — and staying with the sensations without escaping) and in-vivo exposure (graded return to avoided situations using a hierarchy).
Efficacy: response rate 60 to 80%; effect size g about 0.73 versus placebo (Carpenter 2018 meta-analysis). CBT prevents relapse after discontinuation — a major advantage over drugs. Combination of CBT plus SSRI is superior to either alone in moderate-to-severe cases.
Station 5: Special Populations and Red Flags
Examiner: How would you manage anxiety in pregnancy, and what organic causes must you exclude in any first panic attack?
Expected answer: Anxiety in pregnancy is common and undertreated. Untreated maternal anxiety predicts preterm delivery, low birth weight, postnatal anxiety and depression in the mother, and adverse neurodevelopmental outcomes in the child. CBT is first-line. If medication is needed, sertraline is the SSRI of choice (lowest milk transfer, largest safety database; safe in pregnancy and breastfeeding). Avoid benzodiazepines (neonatal withdrawal / floppy baby syndrome, preterm delivery). Avoid paroxetine in the first trimester (small absolute increase in cardiac defects). The postpartum period is a high-risk window for relapse — restart SSRI if previously effective.
Organic causes to exclude in any first panic attack (especially with chest pain, syncope, abnormal vitals, age over 40):
- Cardiac — ACS, arrhythmia, MVP, HOCM: ECG, troponin.
- Hyperthyroidism — weight loss, heat intolerance, goitre: TSH, free T4.
- Phaeochromocytoma — episodic headache, sweating, hypertension: 24-hour urine fractionated metanephrines.
- Hypoglycaemia — fasting episodes, Whipple's triad: capillary glucose.
- Pulmonary embolism — sudden dyspnoea, hypoxia, risk factors: D-dimer, CTPA.
- Substance-induced / withdrawal — caffeine, cannabis, cocaine; alcohol or benzodiazepine withdrawal (onset 6 to 72 h after last dose): urine drug screen, CIWA-Ar.
- Temporal lobe epilepsy — ictal fear, postictal confusion, EEG.
Red flags that demand investigation before labelling "anxiety": abnormal vitals, syncope, focal neurology, late onset (over 45), episodic severe hypertension, hypoxia, weight loss. About 25 to 60% of ED chest-pain attendees with normal troponins turn out to have panic disorder — but this is a diagnosis of exclusion.