A patient reports no subjective feelings of sadness, but has completely lost interest in activities they previously enjoyed, has significant sleep and appetite changes, difficulty concentrating, and fatigue — all present for three weeks. The correct diagnosis is:
ANot MDD — depressed mood is required as the primary gatekeeper criterion
BAdjustment disorder — the patient lacks the emotional component of depression
CMDD — anhedonia is a sufficient gatekeeper criterion, and the full symptom cluster meets diagnostic threshold
DPersistent depressive disorder — the absence of sadness indicates a milder, chronic form
MDD requires either depressed mood OR anhedonia — not both — as the gatekeeper criterion, plus at least four additional symptoms from the remaining list, lasting at least two weeks. This patient has anhedonia plus sleep changes, appetite changes, fatigue, and concentration difficulties — five symptoms total, exceeding threshold, well over two weeks. Option A is the most common misconception: students assume sadness is mandatory. Anhedonia (loss of interest/pleasure) is equally valid as the anchor symptom, and many MDD patients present primarily with emotional blunting and loss of motivation rather than explicit sadness.
Question 2 Multiple Choice
The kindling hypothesis explains a well-documented pattern in MDD. Which of the following best describes what it predicts?
AEach successive depressive episode is more severe than the previous one, leading to permanent worsening
BLater depressive episodes tend to emerge with less environmental provocation than earlier ones, as if the threshold for triggering an episode has been lowered by prior episodes
CGenetic vulnerability accounts for the full recurrence risk — environment becomes irrelevant after the first episode
DThe first depressive episode is always the most severe, with subsequent episodes gradually diminishing
The kindling hypothesis holds that each depressive episode sensitizes the neural systems involved, lowering the threshold for subsequent episodes. Early episodes typically follow identifiable stressors; later ones can emerge with minimal or no clear provocation. This has direct clinical implications: it supports maintenance treatment (ongoing medication or therapy) even after remission, because preventing the next 'kindling event' is more important than waiting for symptoms to return. Option A confuses severity with threshold — the hypothesis is specifically about provocation threshold, not symptom intensity.
Question 3 True / False
MDD is best understood as an extreme form of normal sadness — it differs from ordinary unhappiness primarily in degree rather than kind.
TTrue
FFalse
Answer: False
MDD is a distinct clinical syndrome, not amplified sadness. Its defining features — neurovegetative symptoms (disrupted sleep, appetite, energy), psychomotor changes, and cognitive impairments (concentration, worthlessness, death ideation) — reflect specific neurobiological dysregulation: HPA axis dysregulation, amygdala hyperreactivity, hippocampal atrophy, and disrupted prefrontal-subcortical circuits. Normal sadness does not produce these neurovegetative and cognitive features. The syndrome's coherence (why these specific symptoms cluster together) is explained by shared biological mechanisms, not by a quantitative amplification of normal emotional responses.
Question 4 True / False
Chronic elevation of cortisol in MDD can cause structural hippocampal volume reduction, contributing to the memory and concentration impairments seen in the disorder.
TTrue
FFalse
Answer: True
HPA axis dysregulation in MDD produces sustained cortisol elevation. At high prolonged concentrations, glucocorticoids are neurotoxic to hippocampal neurons — they suppress neurogenesis, impair dendritic branching, and can cause cell death. Neuroimaging studies consistently show hippocampal volume reduction in chronic MDD, and the extent of reduction correlates with cumulative episode duration. This structural change likely contributes to the episodic memory deficits and impaired contextual regulation of emotion seen in MDD, and is one reason early and effective treatment matters — each episode may cause progressive hippocampal changes.
Question 5 Short Answer
How does the diathesis-stress model of MDD integrate genetic vulnerability, developmental history, and current stressors, and what does it imply for treatment?
Think about your answer, then reveal below.
Model answer: The diathesis-stress model holds that MDD results from the interaction of a diathesis (vulnerability) and stress (environmental triggers). Diatheses include genetic polymorphisms affecting serotonin signaling and HPA reactivity, childhood adversity that calibrates the stress response toward hyperreactivity, and cognitive styles like rumination. These vulnerabilities lower the threshold at which stressors tip the system into a depressive episode. The model implies that treatment can target either side: medications targeting monoamine or HPA function address the diathesis directly; psychotherapies like CBT target maladaptive stress responses and cognitive patterns. Prevention and early intervention are also supported — reducing cumulative stress load or building resilience can raise the threshold and delay or prevent recurrence.
The diathesis-stress framework is clinically powerful because it explains why some people develop MDD under moderate stress (high diathesis) while others require severe stress (low diathesis), and why identical stressors produce different outcomes. It also explains the kindling pattern: repeated episodes strengthen the diathesis, progressively lowering the stress threshold. Treatment implications are bidirectional — you can modify the neurobiology (medication), the stress response (therapy), or the environment (social support, lifestyle) — and combination approaches targeting multiple levels simultaneously are generally more effective than single-modality treatments.