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This deck focuses on 7a Biological Bases Psychological Disorders, giving you a quick way to review the definitions, rules, and examples that matter most for MCAT Psychological Social Foundations.
Study 7a Biological Bases Psychological Disorders in MCAT Psychological Social Foundations with focused flashcards that help you recognize the idea, recall the key rule, and apply it in practice-style prompts.
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Which option best matches the symptom type in schizophrenia: hallucinations and delusions are what type?
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Positive symptoms. Added experiences (hallucinations/delusions) beyond normal function.
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This deck focuses on 7a Biological Bases Psychological Disorders, giving you a quick way to review the definitions, rules, and examples that matter most for MCAT Psychological Social Foundations.
Work through these flashcards in short sessions. Try to answer each prompt before flipping the card, then revisit any cards you miss until the explanation feels automatic.
Answer: Positive symptoms. Added experiences (hallucinations/delusions) beyond normal function.
Answer: Disorder risk = predisposition plus environmental stressors. Combines genetic vulnerability with environmental triggers.
Answer: D2 receptor antagonism. Blocks dopamine D2 receptors to reduce positive symptoms but may cause extrapyramidal side effects.
Answer: Cortico-striato-thalamo-cortical (CSTC) loop. Dysfunction in this loop impairs inhibition of intrusive thoughts, central to OCD symptoms.
Answer: Proportion of trait variance due to genetic differences in a population. Measures genetic contribution to phenotypic variation in populations.
Answer: Environmental effects on disorder risk depend on genotype (and vice versa). It describes how genetic factors moderate environmental impacts on psychopathology, or vice versa, influencing disorder manifestation.
Answer: Inhibit serotonin reuptake (block SERT) to increase synaptic 5-HT. Blocking the serotonin transporter prolongs neurotransmitter presence in the synapse, alleviating depressive symptoms.
Answer: Cortisol. HPA activation culminates in glucocorticoid release, mediating stress effects on brain and behavior.
Answer: Dopamine (especially increased mesolimbic activity). Hyperactive dopamine pathways cause hallucinations and delusions.
Answer: Serotonin dysregulation. Altered serotonin signaling in frontostriatal circuits contributes to obsessive thoughts and compulsions.
Answer: Dopamine. Activates reward pathways; dysregulated in substance use disorders.
Answer: Increase GABA-A receptor activity (greater Cl⁻ influx). Enhances inhibitory signaling by opening chloride channels.
Answer: Decreased activity in prefrontal cortical regions. Hypoactivity impairs emotional regulation and executive function.
Answer: Tardive dyskinesia. Long-term D2 antagonism leads to involuntary movements due to dopamine receptor upregulation.
Answer: Increase GABAA receptor activity (increase inhibitory signaling). Enhances GABA's inhibitory effect, reducing neural excitation.
Answer: Substantia nigra pars compacta. Dopaminergic neurons die, causing movement disorders.
Answer: Serotonin (also norepinephrine). The hypothesis posits low monoamine levels cause depressive symptoms, with serotonin and norepinephrine deficits central.
Answer: Depression involves reduced 5-HT, NE, and/or DA signaling. Links depression to deficient serotonin, norepinephrine, or dopamine.
Answer: DNA methylation. Methyl groups on DNA compact chromatin and silence genes.
Answer: Twin studies comparing monozygotic versus dizygotic concordance. MZ twins share 100% DNA; DZ share 50%, allowing genetic effect isolation.
Answer: Increase GABAA receptor activity (increase Cl− channel opening frequency). Allosteric modulation enhances GABA binding, promoting inhibition to reduce anxiety symptoms.
Answer: Serotonin (5-HT). Low serotonin linked to depression; SSRIs block its reuptake.
Answer: Amygdala. Central to threat detection and fear response.
Answer: Twin study. MZ twins share 100% DNA; DZ twins share 50%, allowing genetic estimation.
Answer: Enlarged ventricles with reduced cortical gray matter. Brain tissue loss leads to fluid-filled space expansion.
Answer: GABA. Reduced GABAergic inhibition heightens neural excitability, contributing to anxiety; benzodiazepines enhance it.
Answer: Cortico-striato-thalamo-cortical (CSTC) loop dysfunction. Hyperactive loop creates repetitive thoughts and behaviors.
Answer: Glutamate. NMDA receptor hypofunction may contribute to psychotic symptoms.
Answer: Increased cortisol secretion. HPA axis hyperactivity releases excess stress hormone.
Answer: Disorder risk = predisposition (diathesis) + environmental stressors. Vulnerability plus stress triggers disorder onset.
Answer: Depression relates to reduced monoamine signaling (5-HT, NE, DA). Deficient serotonin/norepinephrine/dopamine causes depressive symptoms.
Answer: Environment-driven changes in gene expression without DNA change. Heritable changes in gene activity without altering DNA sequence.
Answer: Amygdala. Fear center shows increased activity during threat processing.
Answer: Shortened REM latency (earlier onset of REM sleep). REM occurs sooner after sleep onset in depressed patients.
Answer: Hippocampus. Stress hormones can damage this memory-forming structure.
Answer: Autosomal dominant CAG trinucleotide repeat expansion. HTT gene mutation; >40 repeats causes disease.
Answer: Increased dopaminergic signaling (especially mesolimbic). Excess dopamine activity linked to positive symptoms.
Answer: D2 receptor antagonism (dopamine blockade). Blocks dopamine receptors, reducing positive symptoms.
Answer: Hyperactive HPA axis with elevated cortisol. Chronic stress causes persistent cortisol elevation.
Answer: Norepinephrine. Part of fight-or-flight response; elevated in anxiety states.
Answer: Dopamine. Hyperactivity causes hallucinations; hypoactivity causes anhedonia.
Answer: Serotonin. Low levels linked to depression; SSRIs block its reuptake.
Answer: Population variance fraction attributable to genetic differences. Measures genetic contribution to trait variation in a population.
Answer: Disorder risk = predisposition (diathesis) + environmental stress. This model explains how genetic vulnerabilities interact with stressors to precipitate disorders, emphasizing multifactorial causation.
Answer: Dopamine. Excess dopamine activity in certain pathways contributes to hallucinations and delusions in schizophrenia.
Answer: Beta-amyloid plaques and hyperphosphorylated tau tangles. Plaques form between neurons; tangles form inside neurons.
Answer: Decreased GABA (and decreased acetylcholine) in the striatum. Loss of inhibitory control causes involuntary movements.
Answer: Environment-driven changes in gene expression without DNA sequence change. Modifies gene activity through mechanisms like methylation, linking early life stress to long-term disorder susceptibility without altering DNA.
Answer: Major depressive disorder. Low serotonin impairs mood regulation, while HPA hyperactivity elevates stress hormones, exacerbating symptoms.
Answer: Hippocampus. Chronic cortisol exposure can cause hippocampal atrophy.
Answer: Genetic factors contribute to the disorder. MZ twins share more genes, so higher concordance suggests genetic influence.
Answer: Inhibit reuptake of serotonin and norepinephrine (block SERT and NET). Dual inhibition elevates both neurotransmitters in synapses, effective for depression resistant to SSRIs.
Answer: GABA. Reduces neural excitability; enhanced by anti-anxiety drugs.
Answer: Mesocortical pathway. Underactivity in this prefrontal pathway contributes to cognitive deficits and emotional blunting in schizophrenia.
Answer: Decreased serotonin (often with decreased norepinephrine). Monoamine hypothesis: low 5-HT (and NE) causes depressive symptoms.
Answer: GABA. Primary inhibitory neurotransmitter; benzodiazepines enhance GABA.
Answer: They do not predict an individual's risk; they apply to populations. Heritability describes population variance, not individual genetic risk.
Answer: Decreased dopamine in the nigrostriatal pathway. Loss of DA neurons causes motor symptoms (tremor, rigidity).
Answer: Increase GABAA receptor activity (positive allosteric modulators). Enhance GABA's inhibitory effects at receptors.
Answer: Serotonin dysregulation (often conceptualized as decreased 5-HT). SSRIs treat OCD by increasing serotonin availability.
Answer: Mesolimbic pathway. Overactivity in this reward-related pathway underlies positive symptoms like paranoia and auditory hallucinations.
Answer: Decreased acetylcholine (cholinergic deficit). ACh-producing neurons degenerate, especially in the basal forebrain.
Answer: Cortisol. Primary stress hormone released by adrenal cortex.
Answer: Hyperactive HPA axis with elevated cortisol. Chronic stress dysregulates hypothalamic-pituitary-adrenal feedback.
Answer: Inhibit serotonin and norepinephrine reuptake. Dual action blocks both SERT and NET transporters.
Answer: Serotonin (5-HT). SSRIs block reuptake, increasing synaptic serotonin levels.
Answer: Disorder risk = predisposition (diathesis) + environmental stressors. Combines genetic vulnerability with life stress to explain disorder onset.
Answer: Delirium is acute and fluctuating; dementia is chronic and progressive. Delirium develops rapidly with attention deficits; dementia develops slowly with memory loss.
Answer: Amygdala. Processes emotional threats, with hyperactivity leading to exaggerated fear responses in anxiety.
Answer: Environmental effects on gene expression without changing DNA sequence. Modifies gene activity via methylation/histones, not mutations.
Answer: Prefrontal cortex. Regulates attention, planning, and impulse control.
Answer: Posttraumatic stress disorder (PTSD). Chronic stress in PTSD atrophies the hippocampus, impairing memory consolidation and fear extinction.
Answer: Environment-driven changes in gene expression without DNA sequence change. Stress/trauma can alter gene activity via methylation/histones.
Answer: Adoption study (biological vs adoptive relatives). Compares adoptee traits to biological vs adoptive parents.
Answer: Inhibit serotonin reuptake, increasing synaptic 5-HT. Blocks SERT transporter, keeping serotonin in synapse longer.
Answer: Twin study (MZ vs DZ concordance comparison). MZ twins share 100% genes; DZ share 50%, revealing genetic effects.
Answer: Hippocampus. Stress and depression cause hippocampal atrophy.
Answer: Proportion of trait variance in a population due to genetic variation. It quantifies the genetic contribution to phenotypic differences, estimated via twin and adoption studies.
Answer: Cortisol. Primary stress hormone; chronically elevated in depression.
Answer: Prefrontal cortex. Top-down control center for planning and inhibiting behaviors.
Answer: D2 receptor antagonism (dopamine blockade). Blocks dopamine receptors to reduce positive symptoms.
Answer: Genetic risk alters sensitivity to environmental stressors. Genes modify how individuals respond to environmental factors.
Answer: GABA. Primary inhibitory NT; benzos enhance its calming effects.
Answer: Proportion of trait variance in a population due to genetic differences. Measures genetic contribution to population variation, not individual traits.
Answer: Amygdala. Processes threat detection and emotional salience.
Answer: Hippocampus. Stress hormones damage hippocampal neurons over time.
Answer: Prefrontal cortex. Reduced activity impairs planning, focus, and emotional regulation.
Answer: Glutamate. Primary excitatory NT; hypofunction may contribute to psychosis.
Answer: Proportion of trait variance in a population due to genetic variation. Measures how much genes (vs environment) contribute to individual differences.
Answer: HPA axis (hypothalamic-pituitary-adrenal axis). Overactive in depression, causing elevated cortisol levels.
Answer: Mesolimbic pathway hyperactivity. Overactive reward pathway causes hallucinations and delusions.
Answer: Amygdala. Processes emotional salience and triggers fear responses.
Answer: Inhibit serotonin reuptake, increasing synaptic 5-HT. Blocks SERT transporter, prolonging serotonin's synaptic action.
Answer: Equal environments assumption may be violated. MZ twins may be treated more similarly than DZ twins.
Answer: Mood stabilizer that modulates intracellular signaling (e.g., second messengers). Affects multiple pathways including GSK-3 and inositol systems.
Answer: Inhibit monoamine oxidase, decreasing breakdown of 5-HT, NE, and DA. Prevents enzymatic degradation of monoamines, increasing their availability for mood regulation.
Answer: Increased dopamine signaling (especially mesolimbic pathway). Dopamine hypothesis: excess DA activity causes psychotic symptoms.
Answer: GABA (reduced inhibitory signaling is associated with anxiety). Primary inhibitory neurotransmitter; deficiency increases anxiety.
Answer: Probability both twins show the same trait or disorder. If one twin has disorder, concordance = chance the other does too.
Answer: Norepinephrine. Low NE linked to mood/energy; SNRIs block its reuptake.