Psychological Disorders

Diagnostic Concepts

The DSM-5 (Diagnostic and Statistical Manual of Mental Disorders, 5th edition) is the standard classification system used by mental health professionals in the United States. It defines disorders by clusters of symptoms, duration, functional impairment, and exclusion of other causes. The biopsychosocial approach integrates biological factors (genetics, neurotransmitter function, brain structure), psychological factors (cognitive patterns, learning history, coping styles), and social factors (socioeconomic status, culture, family dynamics) into a comprehensive model of disorder etiology. The diathesis-stress model proposes that disorders emerge when a pre-existing vulnerability (diathesis) interacts with environmental stressors. Key diagnostic concepts include the distinction between incidence (new cases in a time period) and prevalence (total existing cases), and between positive symptoms (excess or distortion of normal function, e.g., hallucinations) and negative symptoms (diminution or loss of normal function, e.g., flat affect). The Rosenhan study (1973) demonstrated labeling effects: pseudopatients feigning auditory hallucinations were admitted and then behaved normally, yet all were diagnosed with schizophrenia, illustrating how diagnostic labels can bias perception of behavior.

Anxiety Disorders

Anxiety disorders involve excessive fear, worry, and related behavioral disturbances disproportionate to actual threat. Generalized anxiety disorder (GAD) features persistent, uncontrollable worry across multiple domains lasting at least six months, accompanied by restlessness, fatigue, difficulty concentrating, irritability, muscle tension, and sleep disturbance. Panic disorder is characterized by recurrent, unexpected panic attacks (sudden surges of intense fear peaking within minutes) with persistent concern about future attacks or maladaptive behavioral changes. Specific phobias involve marked fear or anxiety about a particular object or situation (e.g., heights, animals, blood-injection-injury), leading to active avoidance. Social anxiety disorder centers on fear of negative evaluation in social or performance situations. Agoraphobia is fear of situations where escape might be difficult or help unavailable. Neurotransmitter correlates include dysregulation of GABA (reduced inhibitory signaling), serotonin, and norepinephrine. The amygdala and prefrontal cortex show hyperactivity in anxiety states. Behavioral explanations (classical conditioning of fear responses, operant maintenance through avoidance) and cognitive explanations (catastrophic misinterpretation of bodily sensations, attentional bias toward threat) are complementary, not competing, accounts. CBT and SSRIs are first-line treatments.

Mood Disorders

Mood disorders are characterized by disturbances in emotional state severe enough to impair functioning. Major depressive disorder (MDD) requires at least five symptoms present during the same two-week period, including at least one of: depressed mood or anhedonia (loss of interest/pleasure). Additional symptoms include significant weight change, insomnia or hypersomnia, psychomotor agitation or retardation, fatigue, feelings of worthlessness or guilt, diminished concentration, and recurrent thoughts of death or suicidal ideation. Persistent depressive disorder (dysthymia) is a chronic, lower-grade depression lasting at least two years. Bipolar I disorder requires at least one manic episode (elevated, expansive, or irritable mood with increased goal-directed activity lasting at least one week), often with major depressive episodes. Bipolar II involves hypomanic episodes (less severe than mania, no marked impairment) plus major depressive episodes. Cyclothymic disorder features chronic fluctuating hypomanic and depressive symptoms that do not meet full episode criteria. Biologically, MDD is associated with reduced monoamine neurotransmission (serotonin, norepinephrine, dopamine), hypothalamic-pituitary-adrenal (HPA) axis hyperactivity (elevated cortisol), reduced hippocampal volume, and altered prefrontal cortex activity. The learned helplessness model (Seligman) explains depression as the result of repeated exposure to uncontrollable aversive events, generating a cognitive style of pessimistic explanatory attributions (internal, stable, global).

Schizophrenia Spectrum

Schizophrenia is a severe chronic disorder involving disturbances in thought, perception, emotion, and behavior lasting at least six months with at least one month of active-phase symptoms. Positive symptoms are excesses or distortions: hallucinations (perception-like experiences without external stimulus, most commonly auditory), delusions (fixed false beliefs resistant to contrary evidence, e.g., persecutory, grandiose, referential), disorganized speech (derailment, tangentiality, word salad), and grossly disorganized or catatonic behavior. Negative symptoms are diminutions: diminished emotional expression (flat affect), avolition (decreased motivated self-initiated activities), alogia (poverty of speech), anhedonia, and asociality. The dopamine hypothesis posits that positive symptoms arise from excess striatal dopamine D2 receptor activity, evidenced by the fact that D2 antagonists (typical antipsychotics) reduce positive symptoms and that dopamine agonists (amphetamines) can induce psychotic symptoms. Negative and cognitive symptoms are linked to reduced prefrontal dopamine and glutamate NMDA receptor hypofunction. Structural brain abnormalities include enlarged ventricles and reduced gray matter volume. The course typically begins in late adolescence or early adulthood. Schizoaffective disorder combines schizophrenia symptoms with a concurrent major mood episode. Brief psychotic disorder lasts less than one month with full return to premorbid functioning.

Trauma-Related and Dissociative Disorders

Trauma- and stressor-related disorders are conditions in which exposure to a traumatic or stressful event is listed explicitly as a diagnostic criterion. Posttraumatic stress disorder (PTSD) requires exposure to actual or threatened death, serious injury, or sexual violence, followed by four symptom clusters: intrusion (involuntary memories, flashbacks, nightmares), avoidance (of trauma-related stimuli), negative alterations in cognition and mood (dissociative amnesia, persistent negative beliefs, diminished interest), and alterations in arousal and reactivity (hypervigilance, exaggerated startle, sleep disturbance). Symptoms must persist for more than one month. Acute stress disorder has similar criteria but lasts three days to one month after trauma. The amygdala is hyperactive in PTSD, while the prefrontal cortex (which normally inhibits the amygdala) is hypoactive, producing exaggerated fear responses. The hippocampus shows reduced volume, consistent with memory fragmentation. Dissociative disorders involve disruption in the normal integration of consciousness, memory, identity, emotion, perception, body representation, and behavior. Dissociative identity disorder (DID) features two or more distinct personality states with discontinuity in sense of self and agency, accompanied by recurrent gaps in recall of everyday events. Dissociative amnesia is an inability to recall important autobiographical information, usually of a traumatic or stressful nature. Depersonalization/derealization disorder involves persistent experiences of unreality or detachment from one's own mind, self, or body (depersonalization) or from the surroundings (derealization).

Somatic Symptom and Related Disorders

Somatic symptom disorders involve prominent somatic (bodily) symptoms associated with significant distress and impairment. Crucially, these are not intentionally produced or feigned: patients experience genuine distress even when medical findings are absent or inconsistent. Somatic symptom disorder features one or more somatic symptoms that are distressing or disruptive, with excessive thoughts, feelings, or behaviors related to the symptoms (disproportionate and persistent anxiety about the seriousness of symptoms). Illness anxiety disorder (formerly hypochondriasis) is preoccupation with having or acquiring a serious illness despite minimal or absent somatic symptoms; the individual performs excessive health-related behaviors (checking for signs of illness, seeking reassurance) or exhibits maladaptive avoidance (avoiding doctor visits). Conversion disorder (functional neurological symptom disorder) involves one or more symptoms of altered voluntary motor or sensory function incompatible with recognized neurological conditions (e.g., paralysis, blindness, non-epileptic seizures, gait disturbance), often following acute stress or trauma. The key MCAT distinction is between conversion disorder (genuine neurological symptoms without medical explanation, not consciously feigned) and malingering (intentional production of symptoms for external gain) or factitious disorder (intentional production of symptoms to assume the sick role, even without external reward).

Personality Disorders

Personality disorders are enduring patterns of inner experience and behavior that deviate markedly from cultural expectations, are pervasive and inflexible, onset in adolescence or early adulthood, and lead to distress or impairment. They are organized into three clusters in DSM-5. Cluster A (odd/eccentric) includes paranoid (pervasive distrust and suspiciousness), schizoid (detachment from social relationships, restricted emotional expression), and schizotypal (eccentricities in cognition, perception, appearance, and behavior, along with acute discomfort in close relationships). Cluster B (dramatic/erratic) includes antisocial (disregard for and violation of others' rights, preceded by conduct disorder before age 15), borderline (instability in interpersonal relationships, self-image, and affect, with marked impulsivity, frantic efforts to avoid abandonment, and recurrent self-harm), histrionic (excessive emotionality and attention seeking), and narcissistic (grandiosity, need for admiration, lack of empathy). Cluster C (anxious/fearful) includes avoidant (social inhibition, feelings of inadequacy, hypersensitivity to negative evaluation), dependent (excessive need to be taken care of, submissive and clinging behavior), and obsessive-compulsive (preoccupation with orderliness, perfectionism, and control). Note the critical MCAT distinction: obsessive-compulsive personality disorder (OCPD) is a personality pattern of rigidity and perfectionism (ego-syntonic), while obsessive-compulsive disorder (OCD) is an anxiety-related disorder characterized by intrusive obsessions and compulsive rituals (ego-dystonic). The biopsychosocial model integrates heritability (behavioral genetics studies show moderate heritability for Cluster B traits), adverse childhood experiences (trauma, neglect), and maladaptive cognitive schemas.

Neurodevelopmental Disorders

Neurodevelopmental disorders manifest early in development and produce impairments in personal, social, academic, or occupational functioning. Autism spectrum disorder (ASD) involves persistent deficits in social communication and social interaction across multiple contexts (deficits in social-emotional reciprocity, nonverbal communicative behaviors, and developing/maintaining relationships), plus restricted, repetitive patterns of behavior, interests, or activities (stereotyped movements, insistence on sameness, highly restricted fixated interests, hyper- or hyporeactivity to sensory input). Severity is specified by level of support needed. Attention-deficit/hyperactivity disorder (ADHD) involves a persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development. Inattention symptoms include difficulty sustaining attention, not following through on instructions, and being easily distracted. Hyperactivity-impulsivity includes fidgeting, difficulty remaining seated, excessive talking, and interrupting others. Symptoms must be present before age 12 and in at least two settings. ADHD is associated with reduced prefrontal cortex activity and dysregulation of dopamine and norepinephrine, consistent with the efficacy of stimulant medications (methylphenidate, amphetamines) that increase catecholamine availability. Intellectual disability involves deficits in intellectual functions (reasoning, problem solving, abstract thinking) confirmed by clinical assessment and individualized standardized intelligence testing, plus deficits in adaptive functioning that result in failure to meet developmental and sociocultural standards for personal independence and social responsibility, with onset during the developmental period.

Biopsychosocial Model

The biopsychosocial model (Engel, 1977) is the dominant framework for understanding psychological disorders, integrating three interacting levels of analysis. The biological level encompasses genetics (heritability estimates from twin and family studies, specific gene polymorphisms associated with disorder risk), neuroanatomy (structural brain differences, e.g., reduced hippocampal volume in depression, enlarged ventricles in schizophrenia), neurotransmitter systems (dopamine, serotonin, norepinephrine, GABA, glutamate), and neuroendocrine function (HPA axis dysregulation, cortisol abnormalities). The psychological level includes cognitive patterns (dysfunctional beliefs, attributional style, attentional biases), learning history (classical and operant conditioning of maladaptive responses), emotion regulation capacity, coping strategies, and personality traits. The social level incorporates socioeconomic status, culture (cultural concepts of distress, culture-bound syndromes), social support, family dynamics, adverse childhood experiences, discrimination, and stigma. The model's clinical power is demonstrated by treatment approaches targeting different levels: pharmacotherapy addresses biological factors, psychotherapy targets psychological patterns, and social interventions (family therapy, community support) address the social context. The MCAT tests the biopsychosocial model by presenting research scenarios where you must identify which level a finding operates at, or explain how an intervention at one level might produce changes at another (e.g., how CBT, a psychological intervention, produces measurable changes in prefrontal cortex activity, a biological outcome). The Rosenhan study underscores the social dimension: how diagnostic labels and institutional contexts shape the perception and treatment of mental illness.

How it works

Psychological disorders arise from interactions among biological vulnerabilities, psychological patterns, and social contexts: the biopsychosocial model. At the biological level, neurotransmitter dysregulation (dopamine in schizophrenia, serotonin/norepinephrine in mood and anxiety disorders), structural brain changes, and genetic predisposition create vulnerability. At the psychological level, maladaptive cognitive schemas, learned avoidance, and emotion regulation deficits maintain symptoms. At the social level, stress, trauma, socioeconomic disadvantage, and stigma amplify risk. The diathesis-stress model captures this interaction: a diathesis (biological or psychological predisposition) remains latent until activated by stressors. The DSM-5 organizes disorders by symptom clusters and course, using diagnostic criteria as heuristic guides, not exhaustive descriptions. MCAT passages test this framework by describing a clinical case and asking you to identify the most likely diagnosis, the level of the biopsychosocial model a finding supports, or the mechanism of a treatment.

How it works

Psychological disorders arise from interactions among biological vulnerabilities, psychological patterns, and social contexts: the biopsychosocial model. At the biological level, neurotransmitter dysregulation (dopamine in schizophrenia, serotonin/norepinephrine in mood and anxiety disorders), structural brain changes, and genetic predisposition create vulnerability. At the psychological level, maladaptive cognitive schemas, learned avoidance, and emotion regulation deficits maintain symptoms. At the social level, stress, trauma, socioeconomic disadvantage, and stigma amplify risk. The diathesis-stress model captures this interaction: a diathesis (biological or psychological predisposition) remains latent until activated by stressors. The DSM-5 organizes disorders by symptom clusters and course, using diagnostic criteria as heuristic guides, not exhaustive descriptions. MCAT passages test this framework by describing a clinical case and asking you to identify the most likely diagnosis, the level of the biopsychosocial model a finding supports, or the mechanism of a treatment.

Comparisons

• Biology (Neuroscience): Dopamine hypothesis of schizophrenia (excess striatal D2 activity for positive symptoms; reduced prefrontal dopamine for negative/cognitive symptoms). Monoamine hypothesis of depression (reduced serotonin, norepinephrine). NMDA receptor hypofunction in schizophrenia. GABA dysfunction in anxiety disorders.
• Biology (Brain structures): Enlarged ventricles in schizophrenia; reduced hippocampal volume in depression and PTSD; amygdala hyperactivity in anxiety disorders and PTSD; prefrontal cortex hypoactivity in ADHD and depression.
• Research Methods: The Rosenhan study (1973) demonstrates labeling effects and the limitations of diagnostic reliability. Twin and adoption studies establish heritability estimates. fMRI studies reveal neural correlates of disorders.
• Psychology (Learning): Classical conditioning of phobias (Little Albert), operant maintenance of avoidance (negative reinforcement), learned helplessness (Seligman) as a model of depression.
• Sociology: Stigma and labeling theory (Rosenhan), social determinants of mental health (SES, discrimination), cultural differences in symptom expression and diagnostic thresholds, medicalization of deviance.

Common confusions

• Confusing positive and negative symptoms of schizophrenia. Positive = added (hallucinations, delusions, disorganized speech). Negative = removed (flat affect, avolition, alogia, anhedonia). The MCAT will describe a patient and ask which symptom type is illustrated.
• Conflating bipolar I and bipolar II. Bipolar I requires at least one full manic episode (severe, often with psychotic features, marked impairment). Bipolar II involves hypomanic episodes (less severe, no marked impairment) plus major depressive episodes. If the question says 'manic episode,' the answer is bipolar I, not II.
• Mixing up OCD and OCPD. OCD involves intrusive obsessions and compulsive rituals that the person recognizes as excessive: it is ego-dystonic (distressing to the self). OCPD is a personality disorder involving rigidity, perfectionism, and orderliness that the person sees as correct: it is ego-syntonic (consistent with self-image).
• Assuming somatic symptom disorders are faked. Conversion disorder, somatic symptom disorder, and illness anxiety disorder all involve genuine distress and are not consciously feigned (that would be malingering or factitious disorder). Patients experience real symptoms even when no medical cause is found.
• Misapplying the diathesis-stress model. A diathesis alone does not cause a disorder; it requires an environmental stressor to activate. If a study finds a gene associated with depression only in people who experienced childhood trauma, this supports the diathesis-stress model.
• Overlooking the diagnostic hierarchy. If symptoms are better explained by another disorder, that diagnosis takes precedence. Substance-induced disorders and medical conditions must be ruled out before a primary psychiatric diagnosis can be made. The MCAT tests this by presenting cases where symptoms could fit multiple categories; the most specific diagnosis consistent with the full duration and impairment criteria is correct.

Quick review

• DSM-5 organizes disorders by symptom clusters, duration, and functional impairment. Biopsychosocial model integrates biological, psychological, and social levels. Diathesis-stress: predisposition + stressor yields disorder.
• Anxiety disorders: GAD (chronic worry, 6+ months), panic disorder (unexpected attacks + fear of recurrence), specific phobia, social anxiety, agoraphobia. GABA, serotonin, amygdala hyperactivity. Avoidance is negative reinforcement.
• Mood disorders: MDD (5+ symptoms, 2+ weeks, must include depressed mood or anhedonia). Bipolar I (mania, may include depression). Bipolar II (hypomania + MDD). Monoamine hypothesis, HPA axis hyperactivity, learned helplessness.
• Schizophrenia: positive symptoms (hallucinations, delusions, disorganized speech) vs. negative symptoms (flat affect, avolition, alogia). Dopamine hypothesis: excess striatal D2 yields positive symptoms; reduced prefrontal dopamine yields negative symptoms. 6+ months total, 1+ month active.
• Trauma-related: PTSD (intrusion, avoidance, negative cognition/mood, arousal: 1+ month). Acute stress disorder (3 days to 1 month). Dissociative: DID, dissociative amnesia, depersonalization/derealization. Somatic: somatic symptom, illness anxiety, conversion disorders.
• Personality disorders: Cluster A (paranoid, schizoid, schizotypal: odd/eccentric), Cluster B (antisocial, borderline, histrionic, narcissistic: dramatic/erratic), Cluster C (avoidant, dependent, OCPD: anxious/fearful). OCPD vs. OCD: ego-syntonic vs. ego-dystonic.
• Neurodevelopmental: ASD (social communication deficits + restricted/repetitive behaviors). ADHD (inattention and/or hyperactivity-impulsivity, pre-age-12 onset, two+ settings). Intellectual disability (intellectual + adaptive functioning deficits).
• Rosenhan (1973): pseudopatients admitted with schizophrenia label; normal behavior interpreted as pathological. Demonstrates labeling effects and diagnostic confirmation bias.