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According to DSM-5-TR, what defines a mental disorder?
A syndrome causing significant disturbances in cognition, emotional regulation, or behavior, reflecting dysfunction in psychological/biological/developmental processes.
When is a reaction NOT considered a mental disorder?
If it’s a normal or culturally approved response to loss or stress.
What are psychotherapies designed to address?
A person’s thoughts, behaviors, emotions, and relationships by building insight and changing cognition/behavior.
What do pharmacotherapies usually target?
Specific symptoms, not diagnoses.
What are somatic therapies?
Direct stimulation of neural circuits, e.g., ECT, TMS, DBS, vagal nerve stimulation.
What are DSM-5-TR criteria for MDE?
≥5 symptoms in 2 weeks, must include either:
Depressed mood*
Anhedonia*
Plus 3+ of:
Appetite/weight changes
Sleep issues
Psychomotor changes
Fatigue
Guilt/worthlessness
Poor concentration
Suicidal ideation
What must be considered when diagnosing MDE?
Symptoms must impair function, occur most days, and not be due to substances or other disorders.
What is the average age of onset for MDD?
25–30 years old.
What is the lifetime prevalence of MDD?
~17%. Women: 10–20%, Men: 5–10%.
How does recurrence risk change with more episodes?
1 episode → 50% risk of second
2 episodes → 80% risk of third
What increases risk of chronicity in MDD?
: Delayed treatment.
How much does family history increase MDD risk?
Risk ↑ 2–3x with first-degree relatives.
What do twin/adoption studies suggest about MDD?
There's a strong genetic component, but environment also plays a role.
What are Adverse Childhood Experiences (ACEs)?
Early negative life events linked to long-term health & mental health risks. Protective factors can buffer the harmful effects
What outcomes are associated with high ACEs?
MDD
Substance use
Chronic illness
Lower education/work outcomes
What brain changes are seen in MDD?
Reduced brain volume, especially in:
Medial prefrontal cortex
Hippocampus
Hypothalamus
HPA axis
How does chronic stress impact neurogenesis?
↑ cortisol impairs feedback and neurogenesis, making MDD harder to treat.
What is the Biogenic Amine Hypothesis?
Depression = ↓ norepinephrine (NA) and/or serotonin (5-HT) at synapses.
Why is the monoamine hypothesis considered oversimplified?
Depression involves more than NA/5HT — also dopamine, acetylcholine, GABA, glutamate, inflammation, neurogenesis, etc.
What is the average response and remission rate for antidepressants?
Response: 60–80% | Remission: 30–40%. Antidepresants should be continues atleasy 1 year AFTER remission
What risk arises after starting antidepressants?
Possible increased suicidality due to energy increase before mood improves.
How do MAO inhibitors work?
Inhibit monoamine oxidase, preventing breakdown of NA and 5-HT → ↑ NT levels.
How do TCAs (Tricyclic Antidepressants) work?
Block reuptake of NA and 5-HT → more NT at synapses.
How do SSRIs work?
Block reuptake of 5-HT only.
How do SNRIs work?
Block reuptake of both 5-HT and NA.
When is Electroconvulsive Therapy (ECT) used?
For severe, treatment-resistant depression or psychotic depression; mechanism unknown.
When does anxiety become a disorder?
When it causes functional impairment and significant distress.
What is the 12-month prevalence of anxiety disorders?
Around 18%.
What neurochemical systems are involved in anxiety?
Mainly serotonin (5-HT) and noradrenaline (NA).
What brain structures are key in anxiety response?
Thalamus: processes sensory input
Amygdala: triggers fear
Locus ceruleus: spreads fear via NA
Hypothalamus: initiates hormonal response
Hippocampus: stores emotional memories
What is panic disorder?
Recurrent, unexpected panic attacks with tachycardia, sweating, fear, trembling, etc.
What is social anxiety disorder?
Persistent fear of social situations, leading to avoidance or anxiety attacks.
What are specific phobias?
Clinically significant anxiety in response to specific objects/situations, often with avoidance behavior.
What is Generalized Anxiety Disorder (GAD)?
Excessive worry >6 months with motor tension, autonomic hyperactivity, and hypervigilance.
What are the primary treatments for anxiety disorders?
CBT (Cognitive Behavioral Therapy)
Antidepressants
Benzodiazepines
Beta-blockers
How do benzodiazepines work?
Bind to GABA-A receptors, enhance GABA → ↑ Cl⁻ flow = calming effect. ~25% risk of psychological dependence.