stress Flashcards

Question

**Q: What is **epigenetics** (stress context)?**

Answer 1

**A:** * **Epigenetics** = changes in gene expression without changing DNA sequence. * Stress can cause: * DNA methylation * Histone modification * These changes alter how genes are turned on/off and can persist long-term.

Answer 2

**A:** * Stress hormones can modify genes regulating: * Cortisol receptors * Neurotransmitters * Synaptic proteins * Early stress can leave a biological “signature”.

Answer 3

**A:** * Mild stress may be adaptive (prepare for challenging environment, greater vigilance). * Severe/chronic stress increases psychiatric risk. * Exam pearl: effects depend on intensity and duration.

Answer 4

**A:** * Increased risk of: * Anxiety disorders * ADHD * Depression * Emotional dysregulation * Possibly psychosis (via stress sensitisation) * Risk ≠ destiny.

Answer 5

**A:** * Stress occurring: * During labour * Around delivery * Immediately after birth * Includes: * Hypoxia (low oxygen) * Birth trauma * Prematurity * Maternal separation (e.g. NICU admission) * Severe infection

Answer 6

**A:** * At birth: * Brain growth is extremely rapid * Synaptogenesis is active * Myelination is beginning * Glial cells are developing * Stress systems are coming “online” * Brain is in a high plasticity state (high adaptability but also high vulnerability).

Answer 7

**A:** * Brain needs oxygen for: * ATP production * Synaptic transmission * Myelination * Neuronal survival * Perinatal hypoxia can: * Damage vulnerable white matter * Disrupt oligodendrocyte development (cells that make myelin) * Alter connectivity patterns

Answer 8

**A:** * Myelination begins around birth * Oligodendrocytes are immature * White matter is metabolically sensitive * White matter damage can impair: * Fronto-striatal connectivity * Fronto-limbic regulation * Executive functioning later in life

Answer 9

**A:** * Premature infants: * Experience environmental stress earlier than expected * Have immature autonomic systems * Often experience separation from caregivers * May have repeated medical interventions * This alters: * Stress-system calibration * Sensory processing * Emotional regulation development

Answer 10

**A:** * Prolonged separation: * Social buffering is reduced * Cortisol levels remain elevated * Attachment circuits develop under stress * May lead to: * Heightened stress reactivity * Altered attachment formation * Emotional dysregulation vulnerability

Answer 11

**A:** * Altered myelination patterns * Impaired long-range connectivity * Dysregulated autonomic balance * Heightened HPA reactivity * Often reflects altered network maturation, not discrete lesions.

Answer 12

**A:** * Increased risk of: * ADHD * Emotional regulation difficulties * Anxiety * Neurodevelopmental disorders * Possibly schizophrenia vulnerability (via developmental sensitisation) * Risk is probabilistic, not deterministic.

Answer 13

**A:** * During infancy and childhood the brain is: * Rapidly forming synapses (synaptogenesis) * Overproducing connections * Undergoing pruning * Establishing long-range connectivity * Calibrating stress systems * Brain is deciding: * Which circuits to keep * Which circuits to eliminate * Stress influences those decisions.

Answer 14

**A:** * ↑ **Amygdala** growth & reactivity * ↓ **Hippocampal** neurogenesis * ↓ **Prefrontal** dendritic complexity * Impaired connectivity between PFC and limbic structures * Exam phrase: “Limbic dominance with reduced prefrontal regulation.”

Answer 15

**A:** * High density of glucocorticoid receptors * Ongoing neurogenesis (especially dentate gyrus) * Key role in HPA axis feedback

Answer 16

**A:** * ↓ Neurogenesis * ↓ Dendritic branching * Impaired synaptic plasticity * Reduced ability to shut off cortisol * Result: poor stress regulation + memory impairment * Clinical link: depression, PTSD

Answer 17

**A:** * ↑ Dendritic growth * ↑ Threat sensitivity * ↑ Fear conditioning * ↑ Emotional memory strength * Exam phrase: “Amygdala hyperreactivity following early-life stress.”

Answer 18

**A:** * ↓ Dendritic branching * ↓ Synaptic complexity * Impaired top-down control * Delayed maturation * Result: poor impulse control, emotional dysregulation, reduced executive function * Risk: ADHD symptoms, emotional instability, conduct problems

Answer 19

**A:** * Weakens: * PFC–amygdala inhibitory pathways * Hippocampus–PFC feedback loops * Long-range white matter tracts * Creates: a brain that reacts strongly but regulates poorly.

Answer 20

**A:** * Adolescence involves: * Major synaptic pruning * Dopamine system reorganisation * PFC maturation * Increased social salience * Stress during adolescence can: * Unmask earlier vulnerabilities * Alter reward processing * Increase risk for depression, psychosis, substance misuse

Answer 21

**A:** * Stress can: * Sensitise dopamine release * Alter salience processing * Increase reward-seeking or threat attribution * Links to: * Addiction vulnerability * Psychosis risk * Impulsivity

Answer 22

**A:** * Not necessarily permanent. * Many changes reflect: * Altered synaptic structure * Functional network changes * Can improve with: * Safe environments * Therapy * Social support * Reduced stress * Exam phrase: “Stress-induced alterations reflect maladaptive plasticity rather than irreversible neuronal loss.”

Answer 23

**A:** * Yes. * Adult brain can still: * Modify synapses * Change dendritic structure * Alter connectivity * Change gene expression * Remodel networks * Exam principle: adult brain remains capable of structural and functional plasticity.

Answer 24

**A:** * No. * Acute stress can: * Improve attention * Enhance emotional memory * Increase vigilance * Enhance learning short term * Moderate cortisol enhances amygdala–hippocampal interaction and facilitates encoding of salient events. * Exam phrase: “Moderate stress can enhance memory consolidation.”

Answer 25

**A:** * Reduced hippocampal volume (functional shrinkage) * Amygdala hyperreactivity * Reduced prefrontal cortical regulation * Impaired working memory * Impaired executive function * Same pattern as early stress, but typically less severe.

Answer 26

**A:** * Yes. * Chronic stress reduces: * Neurogenesis in the dentate gyrus * Dendritic branching * Synaptic plasticity * Contributes to memory problems, depression vulnerability, poor stress shut-off.

Answer 27

**A:** * Increase dendritic growth * Increase threat sensitivity * Strengthen fear learning * Result: hypervigilance & anxiety.

Answer 28

**A:** * Reduce dendritic complexity * Impair cognitive control * Reduce emotional regulation capacity * Produces impulsivity, emotional dysregulation, poor decision-making.

Answer 29

**A:** * Usually no. * Most adult stress effects reflect: * Dendritic retraction * Synaptic changes * Functional connectivity changes * Not widespread neuron death. * Exam phrase: “Stress effects represent altered plasticity rather than neurodegeneration.”

Answer 30

**A:** * Removal of chronic stressor * Antidepressant treatment * Psychotherapy * Physical exercise * Social support * Environmental enrichment * Can increase neurogenesis, restore dendritic complexity, improve PFC function, reduce amygdala hyperreactivity.

Answer 31

**A:** * Resilience depends on: * Genetics * Early-life experiences * Social support * Cognitive style * Baseline stress calibration * Resilient individuals show: * Efficient PFC–amygdala regulation * Faster cortisol recovery * Higher parasympathetic tone

Answer 32

**A:** * Brain does not develop all at once; different systems mature at different times. * Stress affects whatever system is developing at that moment. * Exam phrase: “Stress effects are developmentally stage-specific.”

Answer 33

**A:** * A developmental window when the brain is especially plastic and therefore especially vulnerable to environmental input. * Circuits are being formed; connections strengthened or pruned; regulatory systems calibrated.

Answer 34

**A:** * Critical period = development must occur then or it won’t occur properly (e.g. vision) * Sensitive period = development most easily influenced then, but not exclusively * In psychiatry, mostly talk about sensitive periods.

Answer 35

**A:** * Attachment systems * Stress regulation (HPA calibration) * Amygdala–PFC connectivity * Language circuits * Basic emotional processing * Stress during this period can bias threat processing, impair regulation development, alter internal working models.

Answer 36

**A:** * Early stress affects circuit formation, synaptic pruning, baseline stress calibration. * Adult stress modifies already-formed circuits. * Early stress shapes the blueprint; adult stress modifies the structure.

Answer 37

**A:** * Adolescence is when: * Dopamine systems reorganise * Salience attribution systems mature * Cortical thinning occurs * Stress can: * Sensitise dopamine release * Increase aberrant salience * Interact with earlier developmental vulnerabilities * Fits the two-hit model.

Answer 38

**A:** * Brain sets baseline stress reactivity based on early experience: * Safe → stress system calibrated low * Threatening → stress system calibrated high * Baseline can persist into adulthood.

Answer 39

**A:** * Both matter, but timing often more critical. * Severe stress in adulthood → often reversible * Moderate but chronic stress in early childhood → long-term bias * Exam phrase: “Early-life stress has disproportionate effects due to heightened plasticity.”

Answer 40

**A:** * Synaptic strength * Dendritic branching * Spine density * Neurogenesis * Myelination * Gene expression * Stress reshapes structure and wiring.

Answer 41

**A:** * Synaptic plasticity = change in the strength of a synapse. * **LTP** (Long-Term Potentiation) = strengthening * **LTD** (Long-Term Depression) = weakening * Cellular basis of learning.

Answer 42

**A:** * Acute stress: * Can enhance LTP in the amygdala * Enhances emotional memory encoding * Chronic stress: * Impairs LTP in the hippocampus * Reduces learning flexibility * Exam pattern: stress strengthens fear learning but impairs contextual learning.

Answer 43

**A:** * Dendrites are branching extensions of neurones that receive input. * More branches = more connections.

Answer 44

**A:** * Chronic stress: * **Hippocampus** → dendritic atrophy * **Prefrontal cortex** → reduced branching * **Amygdala** → increased dendritic branching * High-yield pattern: PFC ↓, hippocampus ↓, amygdala ↑

Answer 45

**A:** * Usually no. * Reflect retraction, not cell death; structural plasticity; can reverse with stress reduction.

Answer 46

**A:** * Spines are small protrusions where synapses form. * More spines = more excitatory connections.

Answer 47

**A:** * Chronic stress: * ↓ spine density in PFC * ↓ spine density in hippocampus * ↑ spine density in amygdala

Answer 48

**A:** * Primarily in the dentate gyrus of the **hippocampus**.

Answer 49

**A:** * Chronic stress: * Reduces hippocampal neurogenesis * Impairs mood regulation * Impairs memory * Antidepressants: * Increase neurogenesis * May restore plasticity * Exam link: reduced neurogenesis implicated in depression.

Answer 50

**A:** * Yes. * Stress can: * Alter oligodendrocyte function * Disrupt white matter integrity * Impair long-range connectivity * Especially important in perinatal stress and early developmental stress.

Answer 51

**A:** * Cortisol binds to glucocorticoid receptors (**GR**). * Complex enters nucleus and modifies transcription of stress-related genes, synaptic protein production, receptor density. * Produces long-term changes in circuit sensitivity.

Answer 52

**A:** * DNA methylation * Histone modification * Can reduce glucocorticoid receptor expression, prolong stress responses, increase vulnerability to psychiatric illness.

Answer 53

**A:** * Yes. * Chronic stress can: * Activate microglia * Increase inflammatory cytokines * Alter synaptic pruning * Neuroinflammation may link stress to depression and cognitive dysfunction.

Answer 54

**A:** * Repeated stress exposure makes the brain respond more strongly to future stress. * System becomes hyper-reactive; smaller stressors trigger bigger responses. * “The alarm becomes easier to set off.”

Answer 55

**A:** * Increase baseline cortisol levels * Increase cortisol response to minor stress * Reduce efficiency of negative feedback * Stress system becomes “primed”.

Answer 56

**A:** * Strengthens fear circuits * Enhances dendritic growth * Increases salience of threat * Neutral stimuli more likely interpreted as threatening.

Answer 57

**A:** * Weakens top-down control * Reduces regulatory capacity * Makes emotional reactions harder to inhibit

Answer 58

**A:** * Achieving stability through physiological change. * Body adjusts baseline under stress (e.g., increased baseline cortisol, elevated heart rate baseline, heightened vigilance).

Answer 59

**A:** * The cumulative “wear and tear” on the body and brain caused by repeated stress activation. * Reflects: * Chronic HPA activation * Persistent sympathetic activation * Ongoing inflammatory signalling * Damages regulation systems over time.

Answer 60

**A:** * Reduced hippocampal function * Impaired executive function * Increased anxiety * Increased depression risk * Increased physical illness risk

Answer 61

**A:** * Early stress: * Calibrates HPA axis high * Strengthens amygdala circuits * Weakens PFC regulation * Later stress acts on an already vulnerable system. * Biological basis of the two-hit model.

Answer 62

**A:** * Chronic stress can: * Sensitise mesolimbic dopamine pathways * Increase salience attribution * Increase vulnerability to psychosis * Increase addiction risk * Stress makes dopamine system more reactive to stimuli.

Answer 63

**A:** * After repeated depressive episodes: * Smaller stressors can trigger relapse * Stress response becomes easier to activate * This is called episode sensitisation.

Answer 64

**A:** * Stress alters neuroplasticity via HPA-axis and autonomic mechanisms, producing timing-dependent changes in synapses, dendrites, neurogenesis, connectivity and gene expression, which can increase psychiatric vulnerability through stress sensitisation and allostatic load.

Answer 65

**A:** * Stress always causes neuron death * Cortisol is purely toxic * Early adversity = inevitable disorder * Brain changes are irreversible * Correct understanding: * Stress modifies plasticity * Effects depend on timing and duration * Recovery is possible * Vulnerability ≠ destiny

Answer 66

**A:** * **Cortisol** → **HPA axis** * **Fear learning** → **amygdala + noradrenaline** * **Chronic stress** → **↓ hippocampus + ↓ PFC + ↑ amygdala** * **Hypervigilance** → **sympathetic overactivation**

Answer 67

**A:** * **HPA = Hormones change Architecture** * **ANS = Immediate Alarm System**

Answer 68

**A:** * Placental enzyme: **11β-HSD2** (inactivates some cortisol) * **High/chronic maternal stress** can **overwhelm** this buffer → more cortisol reaches fetus

Answer 69

**A:** * “Maternal stress during pregnancy” → **fetal programming** * “Epigenetic modification of glucocorticoid receptors” → **stress calibration** * “Increased amygdala reactivity in childhood” → **prenatal stress effects**

Answer 70

**A:** * Prenatal stress = **“Programming the alarm system before birth.”**

Answer 71

**A:** * **Prenatal = programming** * **Perinatal = wiring** * **Postnatal = pruning**

Answer 72

**A:** * “Prematurity” → **white matter vulnerability** * “Perinatal hypoxia” → **connectivity disruption** * “NICU separation” → **reduced social buffering + stress calibration** * “Altered myelination” → **early-life stress effect on white matter**

Answer 73

**A:** * Chronic early stress: **↓ hippocampus**, **↓ PFC**, **↑ amygdala** * Shorthand: **Emotion > Regulation**

Answer 74

**A:** * **“Fast to fear, slow to calm.”**

Answer 75

**A:** * Chronic adult stress: **↓ hippocampus**, **↓ PFC**, **↑ amygdala** * Key nuance: often **reversible** (plastic change, not neuron death)

Answer 76

**A:** * Adult stress = **“Plastic strain, not permanent brain loss.”**

Answer 77

**A:** * Stress impacts the system **developing at that time**: * **Prenatal** → HPA programming * **Perinatal** → connectivity/myelination * **Early childhood** → attachment + regulation circuits * **Adolescence** → dopamine + pruning + executive control * **Adulthood** → synapses + functional networks

Answer 78

**A:** * “Sensitive period” → **high plasticity + vulnerability** * “Calibration” → **HPA axis set-point** * “Adolescent stress” → **dopamine reorganisation** * “Two-hit model” → **early vulnerability + later trigger**

Answer 79

**A:** * **Building vs renovating**: * Early stress = alters **construction** * Adult stress = rearranges **furniture**

Answer 80

**A:** * Chronic stress → **↓ PFC structure**, **↓ hippocampal neurogenesis**, **↑ amygdala growth**, **altered gene expression**, **reduced synaptic flexibility** * Result: **emotional bias + impaired regulation + sensitisation**

Answer 81

**A:** * “Reduced hippocampal volume” → **↓ neurogenesis + dendritic atrophy** * “Amygdala enlargement” → **chronic stress exposure** * “Impaired executive function under stress” → **PFC dendritic/spine loss** * “Epigenetic GR changes” → **prolonged HPA activation**

Answer 82

**A:** * **Fear circuits grow. Control circuits shrink. Memory circuits weaken.**

Answer 83

**A:** * **Stress sensitisation** = future responses become **bigger** (lower threshold; “alarm easier to trigger”) * **Allostatic load** = cumulative **wear and tear** from repeated activation

Answer 84

**A:** * Sensitisation = **alarm gets louder + easier to trigger** * Allostatic load = **system wears out**

Answer 85

**A:** 1) **Timing** matters 2) **Acute vs chronic** matters 3) Plasticity ≠ **neurodegeneration** 4) **Limbic–prefrontal balance** 5) **Stress sensitisation** 6) **Developmental programming**

Answer 86

**A:** * **Fetal programming** * **HPA calibration** * **Epigenetic modification** * **Amygdala sensitisation**

Answer 87

**A:** * **White matter vulnerability** * **Myelination disruption** * **Connectivity alteration**

Answer 88

**A:** * **↓ hippocampal neurogenesis** * **↓ PFC regulation** * **↑ amygdala reactivity** * **Stress sensitisation**

Answer 89

**A:** * **Dopamine reorganisation** * **Synaptic pruning** * **Increased psychosis risk**

Answer 90

**A:** * **Reversible dendritic remodeling** * **HPA dysregulation** * **Limbic dominance**

Answer 91

**A:** * Chronic stress: **↓ PFC**, **↓ hippocampus**, **↑ amygdala** * Shorthand: **Emotion > Regulation**

Answer 92

**A:** * **Acute** stress: can **enhance** emotional memory/learning short-term * **Chronic** stress: **impairs** hippocampal LTP + neurogenesis; **weakens** PFC control

Answer 93

**A:** * **Early stress**: alters **developmental blueprint** + HPA baseline; harder to reverse * **Adult stress**: modifies existing circuits; often **reversible**

Answer 94

**A:** * **Depression**: HPA hyperactivity + ↓ hippocampal neurogenesis * **Anxiety**: ↑ amygdala + sympathetic overactivation * **PTSD**: impaired fear extinction + hippocampal context dysfunction * **Psychosis**: dopamine sensitisation + aberrant salience * **Addiction**: dopamine sensitisation

Answer 95

**A:** 1) Early stress → **HPA calibration** 2) **Amygdala–PFC** connectivity altered 3) **↓ hippocampal** neurogenesis / context control 4) **Sensitisation** + **allostatic load** 5) ↑ vulnerability to later stressors

Answer 96

**A:** * **HPA axis dysregulation** * **Glucocorticoid receptor (GR) modulation** * **Stress sensitisation** * **Allostatic load** * **Sensitive period** * **Epigenetic modification** * **Limbic–prefrontal imbalance** * **Experience-dependent plasticity**

Answer 97

**A:** * Stress effects depend on: * **When** (developmental stage) * **How long** (acute vs chronic) * **How intense** * **Whether buffered** * Outcomes depend on: * **Plasticity**, regulation systems, dopamine salience, cumulative load

Answer 98

**A:** * **Early stress builds the blueprint.** * **Adolescent stress reshapes control.** * **Adult stress strains circuits.** * **Repeated stress lowers the alarm threshold.**

Answer 99

Stress is the brain’s response to a perceived threat to **homeostasis**, involving activation of **neuroendocrine** and **autonomic** systems.

Answer 100

Maintenance of stable internal physiological conditions (e.g. **glucose**, **temperature**, **safety**, **predictability**).

Answer 101

A **stressor** is the external/internal event. **Stress** is the biological response.

Answer 102

**Acute, moderate** stress enhances **vigilance**, **energy mobilisation**, and **memory encoding**.

Answer 103

When it is **chronic**, **severe**, or occurs during **sensitive developmental periods**.

Answer 104

Because stress hormones alter **synaptic strength**, **dendritic structure**, **neurogenesis**, **connectivity**, and **gene expression**.

Answer 105

**HPA axis** (hormonal) and **autonomic nervous system (ANS)** (neural).

Answer 106

**Hypothalamic–Pituitary–Adrenal** axis.

Answer 107

Hypothalamus releases **CRH** → Pituitary releases **ACTH** → Adrenal cortex releases **cortisol**.

Answer 108

It crosses the **blood–brain barrier**, binds **glucocorticoid receptors**, and alters **gene transcription**.

Answer 109

**Hippocampus**, **amygdala**, **prefrontal cortex (PFC)**.

Answer 110

Increases **heart rate**, **blood pressure**, **vigilance**, and releases **adrenaline/noradrenaline**.

Answer 111

Promotes **calming**, **recovery**, and **emotional regulation**.

Answer 112

Long-term biological **calibration** of systems based on **prenatal environmental signals**.

Answer 113

Elevated maternal **cortisol** crosses the **placenta** and influences **fetal brain development**.

Answer 114

Setting of baseline **HPA reactivity** based on **early experience**.

Answer 115

Can increase baseline **reactivity** and impair stress **shut-off**.

Answer 116

Increases **threat sensitivity** and **reactivity**.

Answer 117

May impair **regulatory development** and **connectivity**.

Answer 118

**DNA methylation** and **histone modification** alter gene expression of **stress-related genes**.

Answer 119

Stress occurring during **labour**, **delivery**, or **immediately after birth**.

Answer 120

Ongoing **myelination** and immature **oligodendrocytes** are sensitive to **hypoxia** and stress.

Answer 121

Alters stress **calibration**, **autonomic balance**, and **connectivity** development.

Answer 122

Reduces **social buffering**, leading to prolonged **cortisol** activation.

Answer 123

↓ **Hippocampus**, ↓ **PFC**, ↑ **Amygdala**.

Answer 124

Reduces **neurogenesis** and impairs **stress feedback**.

Answer 125

Increases **dendritic growth** and **fear conditioning**.

Answer 126

Reduces **dendritic complexity** and **regulatory capacity**.

Answer 127

**Synaptic pruning**, **dopamine reorganisation**, and **PFC maturation** occur.

Answer 128

Through **dopamine sensitisation** and **aberrant salience** processing.

Answer 129

Yes — though less than in childhood (**adult neuroplasticity** persists).

Answer 130

Enhances **emotional memory** and **vigilance**.

Answer 131

Impairs **hippocampal** and **PFC** structure and increases **amygdala reactivity**.

Answer 132

No — often **reversible plastic changes**.

Answer 133

**Antidepressants**, **psychotherapy**, **exercise**, **social support**, **stress reduction**.

Answer 134

**Acute** stress enhances **amygdala LTP**; **chronic** stress impairs **hippocampal LTP**.

Answer 135

**Shrinking** in **hippocampus/PFC**; **growth** in **amygdala**.

Answer 136

Decreases in **PFC/hippocampus**; increases in **amygdala**.

Answer 137

**Dentate gyrus** of **hippocampus**.

Answer 138

Reduces it (↓ **hippocampal neurogenesis**).

Answer 139

Binds **glucocorticoid receptors**, altering transcription of **stress-related genes**.

Answer 140

Activates **microglia** and increases **inflammatory cytokines**.

Answer 141

Increased **reactivity** to future stress after **repeated exposure**.

Answer 142

Achieving stability through **physiological change**.

Answer 143

Cumulative **wear and tear** from chronic stress activation.

Answer 144

Smaller stressors can trigger new **episodes** over time (**episode sensitisation**).

Answer 145

Increases **mesolimbic dopamine** reactivity and **salience attribution**.

Answer 146

**HPA hyperactivity** + reduced **hippocampal neurogenesis**.

Answer 147

**Amygdala hyperreactivity** + impaired **fear extinction**.

Answer 148

Impaired **fear extinction** + **hippocampal dysfunction** + **amygdala sensitisation**.

Answer 149

**Dopamine sensitisation** + **stress–salience** interaction.

Answer 150

**Dopamine system sensitisation** increases **reward seeking**.

Answer 151

No — usually alters **plasticity** (not inevitable neurodegeneration).

Answer 152

No — **adaptive short-term**, harmful if **chronic**.

Answer 153

No — it increases **vulnerability**, not inevitability.

Answer 154

↓ **PFC**, ↓ **Hippocampus**, ↑ **Amygdala**.

Answer 155

Stress activates **HPA** and **autonomic** systems, altering **synaptic plasticity**, **dendritic structure**, **neurogenesis**, **myelination** and **gene expression** in a timing-dependent manner. Early-life stress calibrates stress systems and increases vulnerability via **stress sensitisation** and **allostatic load**, shifting toward **limbic dominance** and impaired **prefrontal regulation**.

stress Flashcards

(182 cards)