Anxiety and Stressor problems
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## CHAPTER 6 – ANXIETY DISORDERS (Complete)
### Section A: Specific Phobia
**Card 1 (Definition & Criteria)**
**Q:** Define specific phobia. What are the DSM-5 criteria?
**A:** Excessive, unreasonable, persistent fear triggered by a specific object/situation lasting ≥6 months.
Criteria:
1. Marked fear about specific object/situation
2. Almost always provokes immediate fear/anxiety
3. Actively avoided or endured with distress
4. Fear out of proportion to actual danger
5. Persistent ≥6 months
6. Causes significant distress/impairment
7. Not better explained by another disorder.
**Card 2 (Subtypes)**
**Q:** List the 5 DSM-5 subtypes of specific phobia with examples.
**A:** 1) Animal (spiders, snakes, dogs)
2) Natural environment (heights, storms, water)
3) Blood-injection-injury (needles, medical procedures) – causes fainting (biphasic response)
4) Situational (airplanes, elevators, enclosed spaces)
5) Other (choking, vomiting; children: loud sounds, costumed characters).
**Card 3 (Aetiology – Multiple Pathways)**
**Q:** Explain how different phobias have different causes.
**A:**
- Classical conditioning (dog, dental, choking, accident phobia) – Little Albert study
- Disgust-based/disease-avoidance model (animal phobias, BII) – Davey: animals signal contamination
- Panic-related (situational phobias: heights, claustrophobia, flying) – catastrophic misinterpretation of bodily sensations
- Nonassociative model (height, water) – innate fears that failed to habituate (Poulton & Menzies)
- Biological preparedness (Seligman) – evolutionary predisposition to fear ancient threats.
**Card 4 (Treatment)**
**Q:** How are specific phobias treated? Describe one-session treatment.
**A:** Exposure therapy (systematic desensitisation, flooding, counterconditioning).
One-session treatment (Öst, 1997): 3-hour session – graded exposure + modelling. Steps for spider phobia:
1. Catch spider in bowl
2. Touch spider
3. Hold spider in hand.
Also cognitive restructuring to challenge phobic beliefs (harm, unpredictability, response beliefs).
**Card 5 (Case Study Cues for Specific Phobia)**
**Q:** In a case study, what features tell you it's specific phobia?
**A:**
- Fear of a single object/situation (e.g., spiders, flying, needles)
- Avoidance of that specific trigger
- No fear of social evaluation (unlike SAD)
- No trauma required (unlike PTSD)
- No panic attacks outside the phobic situation (unlike panic disorder)
- Insight usually preserved (knows fear is excessive).
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### Section B: Social Anxiety Disorder (SAD)
**Card 6 (Definition & Criteria)**
**Q:** Define social anxiety disorder. List DSM-5 criteria.
**A:** Severe, persistent fear of social/performance situations where person fears negative evaluation, embarrassment, or offending others.
Criteria:
- Fear of scrutiny in social interactions, being observed, or performing
- Fears acting in a way that will be negatively evaluated
- Social situations almost always provoke fear
- Avoided or endured with distress
- Fear out of proportion to threat
- Persistent ≥6 months
- Causes impairment.
**Card 7 (Prevalence & Demographics)**
**Q:** What are the key prevalence and demographic features of SAD?
**A:**
- Lifetime prevalence ~4% (cross-national)
- Age of onset early to mid-teens (before 18)
- Lowest remission rate of all anxiety disorders (most persistent)
- More common in females, younger, unmarried, lower education/income.
**Card 8 (Differentiation from other disorders)**
**Q:** How do you differentiate SAD from specific phobia, agoraphobia, and panic disorder?
**A:**
- vs. Specific phobia: SAD fears evaluation by others; specific phobia fears object/situation itself.
- vs. Agoraphobia: SAD fears judgment; agoraphobia fears being trapped with no escape.
- vs. Panic disorder: SAD fears embarrassment; panic disorder fears bodily sensations/attacks.
**Card 9 (Aetiology – Genetic & Developmental)**
**Q:** What genetic and developmental factors contribute to SAD?
**A:**
- Genetic: heritability 13-76%; inherits general anxiety vulnerability; behavioural inhibition (BI) is a risk factor (heritability 50-70%) but not sufficient.
- Familial: parents exert more control, show less warmth, use shame as discipline; parents may model social avoidance.
**Card 10 (Aetiology – Cognitive Factors – Essay ready)**
**Q:** Explain the 4 cognitive biases that maintain SAD.
**A:**
1. Negative prediction bias – overestimate probability of negative social outcomes.
2. Critical self-evaluation – judge own performance more harshly than observers; ignore positive feedback.
3. Self-focused attention (Clark & Wells) – shift attention inward onto own anxiety responses; believe they look as anxious as they feel; prevents objective processing.
4. Post-event rumination – excessive critical reappraisal after social events; maintains negative appraisals over time.
**Card 11 (Treatment – CBT vs Medication)**
**Q:** Describe the treatment of SAD. Compare CBT and medication.
**A:**
- CBT: exposure therapy + social skills training + cognitive restructuring (challenge biases, reduce self-focused attention).
- Medication: SSRIs, SNRIs (first-line).
- Comparison: Drugs work faster; CBT provides better long-term maintenance. Combination may be best.
- Clark & Wells cognitive therapy: 6 steps – psychoeducation, drop safety behaviours, external attention shift, video feedback, behavioural experiments, modify post-event processing.
**Card 12 (Case Study Cues for SAD)**
**Q:** In a case study, what features indicate SAD?
**A:**
- Fear of public speaking, eating in front of others, using public restrooms
- Avoidance of social situations or enduring with extreme distress
- Belief that others notice their trembling, blushing, sweating
- Physical symptoms: palpitations, tremors, blushing, GI distress
- Post-event rumination: replaying conversations critically
- Onset in early teens, persistent for years.
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### Section C: Panic Disorder & Agoraphobia
**Card 13 (Panic Attack vs. Panic Disorder)**
**Q:** Distinguish a panic attack from panic disorder.
**A:**
Panic attack = abrupt surge of intense fear with ≥4 symptoms (palpitations, sweating, trembling, SOB, choking, chest pain, nausea, dizziness, fear of dying, depersonalisation).
Panic disorder = recurrent unexpected panic attacks + at least 1 month of persistent worry about future attacks OR maladaptive behaviour change to avoid attacks.
**Card 14 (Agoraphobia Definition & Criteria)**
**Q:** Define agoraphobia. What are DSM-5 criteria?
**A:** Fear/anxiety about ≥2 situations where escape might be difficult or help unavailable:
1. Public transport
2. Open spaces (parking lots, bridges)
3. Enclosed spaces (shops, theatres)
4. Standing in line/crowds
5. Being outside home alone.
Duration ≥6 months. Fear is out of proportion.
**Card 15 (Panic-Agoraphobia Relationship)**
**Q:** What is the relationship between panic disorder and agoraphobia?
**A:**
- ~1/3 of panic disorder patients have agoraphobia.
- Of those with agoraphobia, ~50% have regular panic attacks.
- For most, agoraphobia develops within 1 year of first panic attack (fear of having panic in public).
- But agoraphobia can occur without panic attacks (fear of what might happen if other anxiety symptoms develop).
**Card 16 (Aetiology – Biological)**
**Q:** What biological factors are involved in panic disorder?
**A:**
- Locus coeruleus (brain stem) – main source of norepinephrine; PD patients show greater sensitivity.
- Hyperventilation – common feature; biological challenge tests (CO₂) induce panic only in those with PD history.
- Suffocation alarm theory (Klein) – oversensitive CO₂ detection.
- Low cortisol post-trauma (but more relevant to PTSD).
- Smaller hippocampus (risk factor, but also PTSD).
**Card 17 (Aetiology – Psychological – Anxiety Sensitivity)**
**Q:** What is anxiety sensitivity? How does it relate to panic disorder?
**A:** Anxiety sensitivity = fear of anxiety symptoms based on belief they have harmful consequences (e.g., rapid heartbeat = heart attack). Measured by Anxiety Sensitivity Index (ASI). PD patients score higher. High ASI predicts future panic attacks. Heritability up to 61%. Stressors (health events, family discord) increase ASI.
**Card 18 (Aetiology – Catastrophic Misinterpretation – Clark's model)**
**Q:** Explain Clark's (1986) catastrophic misinterpretation model of panic disorder. Include the vicious cycle.
**A:** Bodily sensations are ambiguous. PD patients have a cognitive bias toward threatening interpretations.
Vicious cycle:
Trigger (internal/external) → perception of threat → apprehension → bodily sensations → catastrophic misinterpretation ("I'm having a heart attack") → more anxiety → more sensations → full panic attack.
Evidence: PD patients attend to bodily sensations more; expectancy alone triggers panic (compressed air told as CO₂).
**Card 19 (Treatment of Panic Disorder)**
**Q:** How is panic disorder treated? What are the most effective components?
**A:**
- CBT: education + breathing training + cognitive restructuring + interoceptive exposure + prevent safety behaviours.
- Most effective ingredients (Pompoli et al., 2018): interoceptive exposure and cognitive restructuring.
- Medication: SSRIs, tricyclic antidepressants.
- Comparison: CBT ≥ medication long-term; combined best for severe cases.
**Card 20 (Case Study Cues for Panic Disorder & Agoraphobia)**
**Q:** In a case study, how do you identify panic disorder vs. agoraphobia?
**A:**
Panic disorder: recurrent unexpected panic attacks (dizziness, palpitations, fear of dying) + ≥1 month worry about next attack.
Agoraphobia: avoids ≥2 situations (crowds, public transport, open spaces) for fear of being unable to escape during panic-like symptoms.
Combined: panic disorder with agoraphobia – both criteria met.
Key differentiator: agoraphobia without panic disorder – no history of panic attacks, fears other anxiety symptoms.
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### Section D: Generalized Anxiety Disorder (GAD)
**Card 21 (Definition & Cardinal Feature)**
**Q:** What is the cardinal feature of GAD? How is worrying different from normal worry?
**A:** Cardinal feature = chronic, uncontrollable worrying.
Three disabling features:
1. Chronic and pervasive (major life issues AND minor day-to-day hassles)
2. Perceived as uncontrollable (cannot stop)
3. Catastrophising (worry worsens the problem, anxiety increases).
**Card 22 (DSM-5 Criteria for GAD)**
**Q:** List DSM-5 criteria for GAD.
**A:**
- Excessive anxiety/worry about ≥2 domains (finances, health, family, work)
- Occurs more days than not for ≥3 months
- Associated with restlessness, muscle tension (physical) OR avoidance, procrastination, reassurance seeking (behavioural)
- Causes distress/impairment.
**Card 23 (Differentiation: GAD vs. Panic vs. OCD vs. MDD)**
**Q:** How do you differentiate GAD from panic disorder, OCD, and major depression?
**A:**
- vs. Panic: GAD = chronic worry about many things; panic disorder = discrete panic attacks + fear of attacks.
- vs. OCD: GAD = worry about real-life events (ego-syntonic); OCD = obsessions often unrealistic (ego-dystonic) + compulsions.
- vs. MDD: GAD = anxiety/future-focused; MDD = sad mood/past-focused (but highly comorbid).
**Card 24 (Aetiology – Biological & Cognitive Biases)**
**Q:** What biological and cognitive factors cause GAD?
**A:**
Biological: heritability ~30% (vulnerability to anxiety generally); decreased amygdala-PFC connectivity (poor emotion regulation).
Cognitive biases: attentional bias to threat, threat-interpretation bias (resolve ambiguity as threatening), expectancy bias, reasoning bias. These biases maintain hypervigilance and may actually cause anxiety.
**Card 25 (Aetiology – Metacognitive Theory – Wells)**
**Q:** Explain Wells' metacognitive theory of GAD.
**A:** Individuals hold two sets of beliefs about worry:
- Positive metacognitive beliefs: "worrying helps solve/avoid problems" or "keeps me alert to threats"
- Negative metacognitive beliefs: "worrying is uncontrollable" or "harmful"
The contradiction between positive and negative beliefs causes worry-related distress. Metacognitive therapy challenges these beliefs.
**Card 26 (Aetiology – Mood-as-Input Hypothesis)**
**Q:** What is the mood-as-input hypothesis? How does it explain perseverative worrying?
**A:** People use their concurrent mood as information about whether they have successfully completed a task. In GAD, negative mood is interpreted as "not satisfied with my worrying" → continue worrying → makes worry seem uncontrollable. Also, worriers have intolerance of uncertainty, perfectionism, poor problem-solving confidence.
**Card 27 (Treatment of GAD – Psychological)**
**Q:** What psychological treatments are effective for GAD? Describe stimulus control.
**A:**
- Stimulus control: restrict worrying to specific 30-minute time/place each day (conditioning principle).
- CBT: self-monitoring, relaxation training (progressive muscular relaxation), cognitive restructuring, behavioural rehearsal.
- Metacognitive therapy: challenge positive/negative beliefs about worry.
CBT effective long-term, but significant percentage still have residual symptoms ("The Lost 40%").
**Card 28 (Treatment of GAD – Medication)**
**Q:** What medications are used for GAD?
**A:**
- SSRIs/SNRIs: received by ≥50% of GAD patients; first-line; better tolerated than benzodiazepines; also treat comorbid depression.
- Benzodiazepines: <35% receive these; effective but risk of dependence.
Problem: at least 1 in 4 do not respond to most effective medications.
**Card 29 (Case Study Cues for GAD)**
**Q:** In a case study, what features suggest GAD?
**A:**
- Chronic worry about multiple domains (health, finances, family, work)
- Worry feels uncontrollable – "I can't stop thinking about it"
- Catastrophic chains: "If I fail this exam, I'll lose my job, then my house, then my family will leave me"
- Physical symptoms: muscle tension, fatigue, restlessness
- Behaviours: reassurance seeking, procrastination, excessive preparation
- Duration ≥3 months
- No panic attacks (differentiates from PD), no compulsions (differentiates from OCD).
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**End of Chapter 6 flashcards.**
Say **"next"** for **Chapter 13 – Somatic Symptom Disorders** (or jump to another chapter if you prefer). I will produce them in the same comprehensive, essay/case-study ready format.