6.1 Psychiatric Disorders & Diagnostic Patterns

Mood Disorders: MDD and Bipolar Spectrum

Major depressive disorder (MDD) is defined by a discrete episode of depressed mood and/or anhedonia lasting at least two weeks, accompanied by neurovegetative and cognitive changes (sleep, appetite/weight, energy, concentration, psychomotor change, guilt/worthlessness, suicidal ideation). On CBSE, the mechanism frame is monoaminergic: reduced synaptic serotonin (5-HT), norepinephrine (NE), and dopamine (DA) signaling in limbic and prefrontal circuits, plus HPA-axis hyperactivity with elevated cortisol and impaired hippocampal feedback. Inflammatory cytokines and reduced BDNF/neuroplasticity appear in research vignettes as downstream correlates, not as alternate primary diagnoses.

Atypical depression features mood reactivity, hypersomnia, hyperphagia, leaden paralysis, and rejection sensitivity—still monoamine-linked, but often highlighted when MAOIs or SNRIs are discussed later. Melancholic features emphasize anhedonia, morning worsening, early awakening, and marked anorexia. Psychotic depression adds mood-congruent delusions or hallucinations and requires thinking about combined antidepressant plus antipsychotic strategies in the clinical layer, while the basic-science layer still centers monoamine and stress-axis pathology.

Bipolar I disorder requires at least one manic episode: persistently elevated, expansive, or irritable mood and abnormally increased energy/activity lasting ≥1 week (or any duration if hospitalization is required), with inflated self-esteem/grandiosity, decreased need for sleep, pressured speech, flight of ideas, distractibility, increased goal-directed activity or psychomotor agitation, and risky behavior. Hypomania is similar but less severe and without marked functional impairment or psychosis. Bipolar II pairs hypomania with major depression and never full mania. Mechanistically, mania is framed as excess catecholaminergic drive and circadian disruption; sleep deprivation is both a trigger and a reinforcing loop.

Suicide risk assessment is high-yield: prior attempt is the strongest historical predictor; active plan and means, severe hopelessness, agitation, substance intoxication, and social isolation raise acuity. Protective factors (social support, future orientation, religious prohibition) can appear as distractors that do not erase high-risk features.

Anxiety Disorders: Shared Arousal Circuits

Anxiety disorders share hyperactive fear circuitry—amygdala over-responsiveness with inadequate prefrontal top-down control—and noradrenergic hyperarousal via the locus coeruleus. Generalized anxiety disorder presents with excessive worry across domains for ≥6 months plus restlessness, muscle tension, irritability, sleep disturbance, and concentration difficulty. Panic disorder features recurrent unexpected panic attacks (abrupt surge of fear with autonomic and cognitive symptoms peaking within minutes) and persistent concern about additional attacks or maladaptive avoidance. Social anxiety disorder is fear of scrutiny in social/performance situations. Specific phobias are cue-bound and often maintained by avoidance that prevents extinction learning.

Obsessive-compulsive disorder (OCD) is no longer grouped under anxiety in modern nosology but remains adjacent on exams: intrusive ego-dystonic obsessions and neutralizing compulsions, with cortico-striato-thalamo-cortical (CSTC) circuit hyperactivity and serotonergic treatment responsiveness. Differentiate from obsessive-compulsive personality disorder (ego-syntonic perfectionism and control without true obsessions/compulsions).

Schizophrenia: Positive vs Negative Symptoms and Dopamine Hypotheses

Schizophrenia is a chronic psychotic disorder with continuous signs for ≥6 months and active-phase symptoms (delusions, hallucinations, disorganized speech/behavior, negative symptoms). Positive symptoms (delusions, hallucinations—classically auditory, disorganization) are linked to mesolimbic dopamine hyperactivity (ventral tegmental area → nucleus accumbens). Negative symptoms (flat affect, alogia, avolition, anhedonia, asociality) and cognitive deficits map more to mesocortical dopamine hypoactivity and broader glutamatergic (NMDA) hypofunction models. The classic dopamine hypothesis is therefore pathway-specific, not a single global “too much dopamine” claim.

Prodrome, young-adult onset, and family history are epidemiologic anchors. Rule out secondary psychosis (substances, medical illness, mood disorder with psychosis) when the vignette supplies fever, focal neuro findings, or exclusively mood-congruent content with a primary mood episode.

PTSD and Trauma-Related Patterns

Post-traumatic stress disorder follows exposure to actual or threatened death, serious injury, or sexual violence and includes intrusion (flashbacks, nightmares), avoidance, negative alterations in cognition/mood, and hyperarousal lasting >1 month. Mechanistically, exaggerated amygdala fear responses, reduced medial prefrontal regulation, and hippocampal contextual memory deficits explain re-experiencing and overgeneralized threat. Noradrenergic hyperreactivity drives startle and insomnia. Distinguish from acute stress disorder (<1 month) and from adjustment disorder (stressor without full PTSD criteria).

Somatic Symptom, Factitious, and Malingering Patterns

The official outline lists somatic symptoms and related disorders and factitious disorders as separate behavioral-health categories, and the exam almost always tests them as a discrimination problem: identical physical complaint, different underlying process. Sort every such vignette with two questions — is the symptom consciously produced? and what is the motivation?

Mechanistic framing the exam rewards. Conversion is not feigning. Functional-imaging work shows altered coupling between limbic/emotional processing and motor output, which is why the deficit is real to the patient yet does not respect peripheral nerve, root, or tract anatomy. That anatomic mismatch is the single most testable finding: a positive Hoover sign (the "paralyzed" leg extends involuntarily when the good leg flexes against resistance), hemianesthesia stopping exactly at the midline, or non-epileptic seizures with preserved awareness, closed eyes, and a normal postictal prolactin.

Traps. Malingering is not a psychiatric disorder — it is a condition of clinical attention, so it never belongs in an answer choice framed as "which psychiatric diagnosis." Factitious disorder is a psychiatric diagnosis. And the tested management stance for somatic symptom disorder is deliberately restrained: one consistent primary clinician, regularly scheduled (not symptom-triggered) visits, treatment of comorbid depression or anxiety, and CBT — not escalating imaging or invasive workup to "rule out" the complaint.

Personality Disorders: Clusters A, B, and C

Personality disorders are enduring, inflexible patterns of inner experience and behavior beginning by early adulthood and causing distress or impairment. Exams emphasize cluster prototypes:

Borderline and antisocial vignettes dominate Cluster B items. Schizotypal oddness without frank psychosis anchors Cluster A. OCPD versus OCD is a classic Cluster C contrast.

Eating Disorders: Medical Complications by Mechanism

Anorexia nervosa features restriction leading to significantly low weight, intense fear of weight gain, and body image distortion (restricting or binge-eating/purging type). Starvation physiology produces sinus bradycardia, hypotension, hypothermia, lanugo, amenorrhea (low GnRH → low LH/FSH → low estrogen), osteoporosis, and bone marrow hypoplasia. Refeeding syndrome is driven by insulin surge that shifts phosphate, potassium, and magnesium intracellularly—hypophosphatemia is the classic life-threatening marker.

Bulimia nervosa involves recurrent binge eating with compensatory behaviors (vomiting, laxatives, diuretics, excess exercise) at normal or above-normal weight. Self-induced vomiting causes metabolic alkalosis, hypokalemia, hypochloremia, dental enamel erosion, and parotid hypertrophy; Russell sign (dorsal hand calluses) may appear. Binge-eating disorder has binges without regular purging and links to obesity-related metabolic disease.

Child Psychiatry: ADHD and Autism—Basic Science Framing

ADHD is a neurodevelopmental disorder of inattention and/or hyperactivity-impulsivity beginning in childhood, with impairment in multiple settings. Circuit framing emphasizes frontostriatal networks and catecholamine (DA/NE) signaling in prefrontal cortex; stimulants increase synaptic DA/NE and improve signal-to-noise in those circuits. Distinguish from pure anxiety, sleep deprivation, or learning disorders that can mimic inattention.

Autism spectrum disorder (ASD) presents with persistent deficits in social communication/interaction plus restricted, repetitive behaviors/interests, with symptoms present in early development. Basic-science framing stresses early brain connectivity differences rather than a single neurotransmitter lesion. Comorbid intellectual disability, epilepsy, and genetic syndromes (e.g., fragile X, tuberous sclerosis associations in vignettes) may appear as integrated items. Language regression and hearing loss remain important differentials when “social delay” is the chief concern.

CBSE success in this section comes from linking each syndrome to a circuit or monoamine story, recognizing classic vignette fingerprints, and separating look-alikes (OCD vs OCPD; schizophrenia negative symptoms vs depression; mania vs ADHD-like distractibility in adults with decreased need for sleep and grandiosity).