Lecture 12: Stress & Anxiety Flashcards

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1
Q

adaptive stress and anxiety

A

contribute to our survival

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2
Q

maladaptive stress and anxiety

A

can cause deterioration of the body, which, if prolonged, can lead to harmful changes in physiology

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3
Q

physiological changes caused by stress

A

the heart beats faster, blood pressure increases, and stress hormones (including cortisol) are released

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4
Q

stressor

A

something that produces stress at any time

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5
Q

Hans Selye definition of stress

A

“the non-specific response of the body to any stressor”

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6
Q

general adaptation syndrome

A

a three stage process
- the general alarm response occurs in the first 6-48 hours and is characterized by numerous physiological changes (fight/flight physiology)
- resistance (coping with stressors) occurs from about 48 hours after the stressor
- exhaustion (if stress persists) and therefore the initial stress response is evident (leads to stress as a pathological state with continuation of this phase)

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7
Q

Kim and Diamond three-point definition of stress

A
  • stress requires increased irritability or excitement
  • stress must also be experienced as negative (excitement can increase under both pleasurable and negative conditions)
  • manageability
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8
Q

the reactivity hypothesis

A

originally proposed that physiological responses to stress, if frequent and intense, could cause physical harm
- has been criticized for failing to account for the prolonged physiological effects of stress, which often extend beyond the immediate stressful event

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9
Q

prolonged activation model

A

suggests that physiological responses to stress become harmful when they persist long after the stressor has ended, or when the body’s physiological activity is triggered by anticipation of the stressor before it occurs
- can persist during periods of worry, rumination, and anticipatory anxiety
- introduced to address the limitations of the reactivity hypothesis

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10
Q

perseverative cognition hypothesis

A
  • the autonomic nervous system (ANS) recovers much more quickly from physical stressors (e.g. running up a flight of stairs) than from psychological stressors (e.g. worry or rumination)
  • humans have the unique ability to mentally stimulate future events or reflect on past experiences, thereby prolonging the stress response
  • this ability allows us to anticipate future stressors or dwell on past ones, which can prolong physiological responses long before or after the stressful event, a phenomenon known as perseverative cognition
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11
Q

physiological profile of perseverative cognition

A

includes decreased heart rate variability, increased blood pressure, and prolonged cortisol responsiveness (reflecting a sustained state of physiological arousal
- additionally decreased activity in the prefrontal cortex and increased activity in the amygdala

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12
Q

psychological profile of perseverative cognition

A

characterized by increased anxiety, depression, neuroticism, impaired cognitive functions such as decision making and inhibitory control

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13
Q

complex network of signalling systems

A

the central nervous system (CNS), endocrine system, and immune system all interact with the body’s response to stress

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14
Q

hypothalamic-pituitary-adrenal (HPA) axis

A

when a stressor is detected, the CNS, particularly the hypothalamus, activates the HPA axis resulting in the release of stress hormones such as cortisol

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15
Q

central nervous system (CNS)

A

serves as the control center for processing and integrating sensory information about stressors and initiating the the physiological stress response

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16
Q

endocrine system (including HPA axis)

A

releases corticotropin-releasing hormone (CHRI), which stimulates the pituitary gland to release adrenocorticotropic hormone (ACTH)
- ACTH then stimulates the adrenal glands to secrete cortisol

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17
Q

immune system

A

also involved as cortisol affects immune functioning by regulating inflammatory responses and promoting lymphocyte maturation
- chronic stress and prolonged cortisol secretion can suppress the immune system resulting in poor immune function

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18
Q

the body’s stress response

A

begins with the detection of a stressor
- sensory pathways send information about the stressor to the CNS
- CNS processes input and initiates fight-or-flight response
- HPA axis becomes activated and the paraventricular nucleus of the hypothalamus releases CRH, stimulating the pituitary gland to release ACTH
- ACTH stimulates the adrenal glands to produce glucocorticoids including cortisol
- these hormones prepare the body to cope with the stressor by increasing energy availability, suppressing non-essential functions such as digestion and reproduction, and enhancing memory/sensory functions

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19
Q

acute stressors effects on the immune system

A

can enhance natural immunity by preparing the body to respond to immediate threats

20
Q

chronic stressors effects on the immune system

A

suppresses both the general and specific immune systems, making the body more susceptible to disease and impairing functions such as wound healing

21
Q

Marucha et al. (1998)

A

showed that stress during exam periods can slow wound healing compared to stress-free periods such as summer vacations

22
Q

role of sympathetic nervous system (part of the CNS) in response to stress

A

triggers rapid physical changes (increased heart rate and blood pressure)

23
Q

cortisol

A

the primary stress hormone produced by the HPA axis
- critical for regulating various functions during stress
- increases glucose availability, modulates immune function, and adjusts physiological properties such as suppressing reproduction and digestion
- follows a circadian rhythm

24
Q

homeostasis vs allostasis

A

homeostasis
- refers to the maintenance of physiological balance or equilibrium in response to stressors
allostasis
- the process by which the body achieves stability through physiological or behavioral changes

when stress persists over time, the body moves from homeostasis to allostasis, where set points for balance are adjusted to meet long-term demands

25
Q

allostatic load

A

refers to the cumulative wear and tear on the body when systems are over-activated in response to chronic stress
- prolonged activation of physiological systems due to stress can lead to pathology, which affects health by causing conditions such as weakened immune function, delayed wound healing, and chronic disease

26
Q

allostatic load effects on the immune system

A
  • acute stress boosts natural immunity by increasing neutrophils and NK cells to prepare the body for injury or infection
  • chronic stress suppresses both innate and specific immunicty, making the body more susceptible to disease
27
Q

effect of positive psychological factors

A

positive psychological factors such as social support and optimism can protect health

28
Q

neurobiology of anxiety

A

involves several neurotransmitter systems, with a focus on gamma-aminobutyric acid (GABA), norepinephrine, and serotonin
- help regulate the activity in the brain associated with fear and anxiety
- GABA is particularly important as it plays a key role in inhibiting overactivity in the brain regions associated with anxiety

29
Q

GABA

A

an inhibitory neurotransmitter that reduces neuronal excitability by making the cell membrane more negative (hyperpolarized)
- reduces likelihood of an action potential, effectively calming the brain and reducing anxiety
- GABA-A receptor received most attention due to it being the target of several anxiolytic drugs such as benzodiazepines

30
Q

norepinephrine (adrenaline)

A

primarily in the locus coeruleus, and is involved in arousal and the body’s stress response
- dysregulation of the system is associated with increased anxiety

31
Q

serotonin

A

located primarily in the amygdala and dorsal raphe nuclei, serotonin plays a role in mood regulation and emotional responses
- low serotonin levels associated with anxiety disorders

32
Q

how GABA functions

A

reduces anxiety by transporting chloride (Cl-) ions into the cell
- hyperpolarizes the neuron, making it less likely to fire an action potential

33
Q

benzodiazepines

A

drugs commonly used to reduce anxiety by enhancing the inhibitory effect of GABA
- act as positive allosteric modulators by binding to the benzodiazepine site on the GABA-A receptor
- allows for a greater influx of Cl- ions into the cell

34
Q

barbiturates

A

originally developed for their sedative and hypnotic effects
- classified as CNS depressants (e.g. diethylbarbituric acid (barbital) and phenobarbital)
- can induce sleep and have anxiolytic properties at moderate doses
- mimick GABA even in the absence of GABA by increasing Cl- conductance
- highly addictive with many risks (respiratory/cardiovascular depression, coma, and death)
- rarely used

35
Q

flumazenil

A

acts as an antagonist at the benzodiazepine binding site on the GABA-A receptor
- prevents benzodiazepines from potentiating the GABAergic effect
- GABA can still bind to its receptor, but the influx of Cl- ions is significantly less than in the presence of benzodiazepines
- used to counteract benzodiazepine overdose

36
Q

inverse agonists

A

binds to the benzodiazepine site but has the opposite effect of benzodiazepines
- decrease the flow of Cl- ions into the cell
- depolarizes neuron, increasing the likelihood of an action potential and leading to more neuronal activity
- anxiogenic (cause anxiety by reducing the inhibitory effects of GABA

37
Q

full agonists

A

such as benzodiazepines, fully activate the GABA-A receptor, resulting in maximum Cl- ion influx and complete inhibition of neural activity

38
Q

partial agonists

A

do not fully activate the receptor and therefore produce a weaker response
- induce less Cl- influx and provide less inhibition

39
Q

alpha-2-adrenoceptors

A

receptors in the locus coeruleus, which when blocked increases the release of noradrenaline and decreases the release of noradrenaline when stimulated

40
Q

clonidine

A

an antihypertensive drug that has been used to treat panic attacks and suppress symptoms of anxiety during nicotine withdrawal

41
Q

beta-adrenoceptors

A

postsynaptic receptors in which blockade is anxiolytic
- effects appear to be mediated by peripheral receptors

42
Q

propranolol

A

a beta-adrenoceptor antagonist that can treat some of the symptoms of anxiety
- particularly autonomic symptoms such as sweating, tremors, and tachycardia

43
Q

beta-adrenergic receptor antagonists

A

able to block the peripheral effects of anxiety
- do not block the conscious experience of anxiety

44
Q

low serotonin with high norepinephrine

A

produces anxiety

45
Q

enhancement vs reduction of serotonergic neurotransmission

A

enhancement increases anxiety, while reduction reduces anxiety
- opposite for depression (low serotonin, higher depression)