Final Review Flashcards

1
Q

What are the biological effects and behavioural outcomes of leptin and ghrelin?

A

Leptin - produced by fat cells, influnecings neurons in hypothalamic regions to reduce blood intake and appetite, increase energy expenditure, inhibit reward-seeking behaviours (satiety)

Ghrelin - produced in gut and acts antagonistically to leptin by stimulating appetite, reducing energy expenditure, enhancing reward-seeking behaviours, and modulating stress responses (hunger)

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2
Q

What are the biological effects and behavioural outcomes of insulin?

A

Produced by beta cells in pancreas and is responsible for regulating fat and carb metabolism, gets glucose from blood not target cells stored as glycogen, interactions with immune functioning

In the brain, it simulates hormones that reduce food intake

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3
Q

What type of depression is most closely linked to inflammation?

A

Atypical depression - characterized by increasing eating, sleeping, and tendency towards persistent rejection sensitivity and mood reactivity

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4
Q

What is the biological and behavioural outcomes of testosterone and dehydroepiandrosterone (DHEA)

A

testosterone - produced in testes and of lesser extent in adrenal glands of males; involved in the sexual differentiation of brain and reproductive system, fundamental in secondary sexual features (muscle, body hair, bone mass), and associated with aggressive, dominant, and sexual behaviours

DHEA - produced in adrenals, gonads, and brain; acts as a anabolic steroid to affect muscle development; behaviourally acts like testosterone

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5
Q

What is the biological effect and behavioural outcomes of estrogens and progesterone?

A

Estrogen (estradiol) - produced in ovaries and regulates hypothalamic-pituitary-ovarian axis; involved in protein synthesis, GI functioning, coagulation, cholesterol levels and fat depositions, affects bone density; important for maternal behaviour, maintaining cognition, as well as anxiety and stress responses

Progesterone - formed in ovaries; involved in triggering menstruation and maintaining pregnancy; reduces uterine smooth muscle contraction; influences resilience of various tissues; affects maternal behaviours and has anti-anxiety actions

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6
Q

How does the menstruation cycle affect the stress response?

A

During ovulation women have a spike of hormones including follicle stimulating hormones, lutenziing hormone, and estradiol which promotes changes in both termpature and uterine status.

Following ovulation during the luteal phase there is a slow decrease in leninizeing hormone and an increase in progesterone (anti-anxiety) - also when cortisol levels are generally thought to be the highest

These changes can moderate how one reactions to stressors as well as contribute to their immune changes

  • estrogen can attenuate HPA activity and act as a protective factor until menopause
  • progesterone is anti-inflammatory
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7
Q

What is the biological effect and behavioural outcome of prolactin?

A

It is released from the pituitary and the primary function is milk production and maternal behaviours

However, it also has powerful immunomodulatory effects and might influence the development of autoimmune disorders that preferential occur in women or during pregancy

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8
Q

What are the biological effect and behavioural outcomes of brain-derived neurotropic factors (BDNF)?

A

Supports survival or neurons, encourages growth and differentiation of new neurons; and promote synaptic growth/plasticity

It also influences memory processes, stress responses, and mood states; disruption of neurotrophins can be implicated in a variety of psychological disorders

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9
Q

What are the biological effects of the following neurotropins:

Basic fibroblast growth factor (bFGF)
Nerve growth factor (NGF)

A

bFGF - formation of new blood vessels; protective actions in relation to heart injury essential for maintaining stem cell differentiation

NGF - contributes to cell survival; growth & differentiation of new neurons

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10
Q

Describe the function of macrophages

A

Monocytes leave the bloodstream and covert to macrophages which is a type of antigen presenting cell

It engulfs microorganisms of a foreign particle and presents in on the MHC-II complex to T cells

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11
Q

Describe what happens when we encounter a foreign particle

A

Our first life defence is our innate immunity - exposure causes rapid activation of NK cells and macrophages (APCs) will engulf the organisms and present them as an epitope

Our adaptive immunity (T cells and B cells) then uses the MHC complex to determine if the epitope is self or pathogen
- Th1 cells will recognize the antigen and inform T cytotoxic cells to begin multiplying - these pro-inflammatory cells bind to infected cells and make hole and inject enzymes that destroy the cell

  • Th2 cells work to modulate the effects of Th1 cells but also signal B cells which release antibodies (immunoglobulins) that marks foreign particles and signals complement factors to destroy them (humoral immunity)
  • Treg cells then suppress cytotoxic T cells and prevent immune over activation
  • T and B cells (and a lesser extent NK cells) develop memory for pathogen and are thus primed for a sensitized and proliferate immune response if there is a secondary exposure
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12
Q

What are cytokines?

A

They are immune messaging molecules that are released by immune cells and microglia to communicate with other immune cells

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13
Q

What is the relationship between cortisol and the immune system?

A

Cortisol is activated by inflammatory stimuli which can in turn dampen the inflammatory immune functioning

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14
Q

What is sterile inflammation?

A

An immune response that is promoted by non-infectious agents or events

When cells are stressed they release danger-associated molecular patterns (DAMPs) which stimulate pattern recognition receptors (PRRs) which effect immune and inflmmatory processes

PRRs can promote inflammation and encourage progression of disease

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15
Q

What happens to a babies microbiota who is born via caesarean delivery?

A

Since babies receive bacteria when passing through the vaginal canal sometimes babies who are born via cesarean lack the commensal bacteria making them more susceptible to illness from bacteria found in hospitals

Having a diverse microbiota is crucial for immunity as it increases the ability to fight off a greater variety of bad bacteria

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16
Q

How can people increase the diversity of their microbiota?

A
  • Fecal transplant
  • Vaginal Seeding
  • Diet
  • Probiotics and probiotics might be able to reduce chronic disorders of the gut
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17
Q

What is the difference between processor and systematic stressors?

A

Processive - involve cognitive processing and may be either psychogenic (psychological) or neurogenic (physical origin)

Systemic - lack of cognitive processing, something we are unaware of

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18
Q

Using primary and secondary appraisals discuss what occurs when someone encounters a potential stressor

A

Primar appraisal occurs when a person considerers whether the stressor is a risk or not, influenced by social heuristics and personal experiences

Secondary appraisals is when a person considers if they have the coping resources necessary to meet the demands of the stressor, influenced by social influences

If the person does not feel equip to deal with the stressor a stress response involving neurobiological, emotional, and behavioural coping responses will ensue, effects which can be dampened with a social buffer

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19
Q

Using priming and anchoring discuss how people make decisions

A

In a moment of immediate decision making we are primed to make decisions in a particular way based heuristics established from previous experiences - not always appropriate and can be impacted by your current mood (system 1 - fast thinking)

When making decisions about things wi lack information about we look for anchors - things we know that can help guide our behaviour

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20
Q

Discuss the following characteristics of stressors:

Controllability 
Unpredictability 
Uncertainty 
Ambiguity
Complexity 
Volatility
A

Controllability - uncontrollable stressors can favour development of the cognitive schema of helplessness which influences motivation/ability to handle future stress

Unpredictability - knowing the event will happen but unsure of when/severity/specific characteristics can make a stressor more aversive

Uncertainty - don’t know if the event will happen (can also be unpredible) will increase aversiveness due to lack of preparation allowed

Ambiguity - when the risk/info is unclear there is an increase in neuronal activity and people often adopt a representative heuristic in which they appraise the situation based on similar experience

Complexity - if a situation is too complex a person may resort to simplified coping/problem solving as it is too difficulty to work out all the possible responses

Volatility - stressors that change very quickly and may require us to adapt and change our coping strategies

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21
Q

What is stress sensitization?

A

Stressful experiences can impact how we respond to future stressors by priming or sensitizing our biological systems and influencing how we appraise situations having a more dramatic response to subsequent stressors

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22
Q

Describe allostatic and allostatic overload

A

When an individual encounters an acute stressor there are biological changes to deal with that stressor such as an increase in synthesis and thus production of NTs to maintain a balance, known as allostatisis

When a stressor is severe or experienced for a prolonged time the biological systems cannot keep up and can become overly taxed, known as allostatic overload, increasing sucesebility to negative consequences and illness

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23
Q

Describe stress proliferation

A

When someone is experiencing significant stress it can give rise to more stressors in their life due to behaviour change, lack of resources, lack of social support, etc.

If someone is ill they may not be able to work which decreases their financial stability, influences their patenting abilities as they don’t feel well, causes a change in behaviour which may push their social support circle away, etc.

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24
Q

How are telomeres impacted by stress?

A

Telomeres are at the end of chromosome that protect from breaking or fusing with others

Stressful experiences reduce telomere length and can act as a marker of both aging and cumulative stressor experiences

25
Q

Describe the following coping processes. Which is the best one?

Problem-solving 
Avoidant/disengagement 
Emotion-focused 
Religion
Social support
A

Problem-solving - includes finding methods to deter/decrease impact of stressor, cognitive restructuring/positive reframing, or benefit finding

Avoidant/disengagement - includes active or distraction, denial, humour, drugs,

Emotion-focused - emotional expression, blaming self or others, wishful thinking (thinking about happier times), and passive resignation (it is what it is)

Religion - internal (belief in god to deal with event) or external (social competent with likeminded individuals)

Social support - informative, instrumental, or emotional support

*Although problem solving is typically thought of as superior it is import important to be skilled at using a broad range of coping skills as each can have a positive impact depending on the stressor

26
Q

What are some of the benefits of social support & connectedness?

A
  • Lower levels of stress
  • Better health outcomes
  • Reduced anxiety/depression and lower depressive relapse rates
  • Married may have fewer health problems and longevity
  • Reduced inflammaiton
27
Q

How does unsupportive reactions influence a persons stress response?

A

Blaming, bumbling, minimizing, or distancing can be more damaging then simply having no support at all

Research found that it can elicit negative rumination, alter mood, elevate cortisol, and can overlap with physical pain as it activates the dorsal anterior cingulate cortex

28
Q

How may being born and raised in poverty influence your life trajectory?

A

Adverse prenatal experiences (lack of prenatal care, environmental toxicants, poor diet, lack of diverse microbiota) can all potentially influence inflammatory factors and may cause biological sensitization or epigenetic changes that disrupt neurological development

ACEs/prenatal experiences can have enduring effects on BDNF & FGF-2 (growth factors) which can disturb functioning and impact neuroplacticity

This disruption can impair immune, social, emotional, and cognitive development causing someone to adopt more riskier health behaviours, favouring development of psychopathology or illness and potentially lead to early mortality

Although early life events have significant implications of the future, trajectories are not set in stone

29
Q

What does a dose-response relationship in relation to adverse childhood experiences mean?

A

The more ACEs experiences, the greater risk for negative health and well-being

They alter stress-regulating pathways underling emotional functions and endocrine responses, resulting in a long-lasting altered stress responsitivty

30
Q

What is the difference between tolerable or toxic challenges?

A

Tolerable - mild/moderate stressors that can be covercome with effective supports and can help facility learning effective appraisal and coping strategies

Toxic - poverty, abuse, neglect, etc. that are all more closely aligned with later pathology (chronic and severe)

31
Q

Describe intergenerational trauma and the idea that trauma is cumulative

A

When looking at the offspring of survivors of residential schools it was found that the higher the family link to residential schools (the more generations attended) the more psychological distress and suicidal ideation of the child

This may be due to prenatal stress/epigenetic changes, stress proliferation, stress sensitization, discrimination, communication about trauma/re-traumatization, lack of support/loss of protective factors (language, culture)

32
Q

Describe stress adaption

A

When a stressor is chronic your body will adapt to keep the balance of NT synthesis and utilization by up or down regulating monoamine receptors

but will eventually reach allostatic overload as it cannot maintain this balance forever as critical systems are overloaded which can have secondary negative outcomes (ex. hippocampal loss)

Allostatic overload is more likely to occur when stressors are intermittent, unpredictable, uncontrollable, and ambiguous

33
Q

How is glutamate and GABA influenced by stress?

A

Glutamate (excitatory) release may be increased by stressors which contributes to establishment and retention of fear responses

GABA (inhibitory) increase accompanies anxiety-provoking situation and has been found to be dysregulated in people who die by suicide

34
Q

Describe cortisol adaption in the face of chronic stress and childhood trauma

A

Cortisol responses can be less pronounced due to a down-regulation in response to chronic stressors or trauma

However, this adaption is event specific as if a new stressor was to emerge there would be a sensitized response as is needed for the fight-or-flight reaction to deal with a stressor

This blunted cortisol is adaptive as prolonged elevated cortisol can result in dysfunctional HPA funcitoning but is not cross-desensitized as this would be harmful

35
Q

How does CRH influence stress?

A

Stress provoked CRH release in PFC and hippocampus can continue to appraisals, decision making, and memory

It can affect locus coeruleus activity which is involved in vigilance

It can also be released from amygdala and influence feat responses and processing of threats

CRH release due to acute stress (not severe) can promote DA activation within nucleus accumbens, making rewards more salient, driving eating behaviours

36
Q

Why do people prefer high caloric foods when stressed?

A

Increased cortisol levels in the presence of insulin enhances preference for high calorie foods and salience of pleasurable activities is increased as insulin excites DA neurons within the brain regions involved in reward processing

Leptin and ghrelin levels also increase - ghrlein stimulates DA release as well

37
Q

What are the effects of chronic stress of BDNF levels?

A

Has differential changes based on specific brain regions

  • reduced in hippocampus (memory of negative events)
  • increased in PFC (stronger cognitive response)
38
Q

Explain during acute or short term stress the two possible scenarios that can occur in terms of the immune response end-effect

A
  1. Acute stress can increase immunoprotection, activating pro inflammatory cytokines so the immune system to deal with a threat
  2. Acute stress can suppress immune system increase proinflmmatory and autoimmune diseases, leading to immunopathology
39
Q

Explain during chronic stress the two possible scenarios that can occur in terms of the immune response end-effect

A
  1. Chronic stress increases cytokine-meidated immune response, resulting in high levels of pro-inflmamiton, cortisol would likely be down regulated, allowing for the immune system to operate without being attenuated by cortisol allowing for a pro-inflammatory state to emerge increasing risk of pathology and autoimmune disorders
  2. The immune system may become suppressed in which glucocorticoid activity would not be down regulated so cortisol can attenuate the immune system resulting in a suppression which would reduce efficacy of healing and resistance to infection
40
Q

How can adverse childhood events impact cytokines?

A

It can result in a dysregulaiton or imbalance of pro and anti-inflammatory cytokines

41
Q

What are some of the effects of loneliness?

A
  • increased proinflammatory cytokines
  • increased depression
  • early mortality
  • increased risk of stroke/heart disease
42
Q

INF-a is a proinflammatory cytokine - how does it influence depression?

A

IFN-α, simulates an enzyme, indoleamine-2, 3-dioxygenase (IDO), that indirectly influences the production of serotonin; and

IFN-α produces metabolites (3-hydroxy-kynurenine and quinolinic acid) that has neuro-destructive effects (cell death of neurons).

IFN-a also has a more profound effect is the individual was moderately stressed prior to treatment which is the case as this is used as a treatment for hep-C and cancer

43
Q

What is the endophenotypic approach to treatment?

A

Illnesses need to be deconstructed and decomposed to identify ‘measurable’ aspects that link genetic factors to disease

By breaking it down you can focus on targeted treatments that are morst effective to specific symptoms and genetic profiles

44
Q

What is the genomic divide?

A

Health gaps that exist that may be in part due to the lack of represeation in genetic and genomic research

45
Q

Why can’t we use the end-phenotypic approach in psychiatric illnesses?

A

Significant comorbity

Heterogeneity - many variations and research groups them together to find one size fits all treatments

46
Q

What two factors are important in screening for illness?

A

High Sensitivity - true positives
High specificity - true negatives

However, screening is not 100% accurate and early detection does not always lead to a better prognosis

47
Q

Describe the following biases regarding screening:

Lead-time bias
Length-bias
Screening bias

A

Lead-time bias - misled by statistics (early diagnosis didn’t cause a person to live longer they just knew they were sick longer)

Length-bias - concerns how quickly an illness progresses (individual lived longer because of slow developing disease not because early detection)

Screening bias - the people who get routinely screened tend to be more educated, better off financially, and more likely to engage in positive health behaviour and thus live longer

48
Q

What is the difference between a hazard and a risk?

A

A hazard is the possibility of something causing harm

A risk is the probability of harm occurring when something actually does something that can create problems

49
Q

What are the 6 clusters that can influence probability of mortality ?

A
Childhood adversity
Adulthood adverse experiences 
Socioeconomic status 
psychological characteristics 
Social connections 
Health behaviours
49
Q

What are the 6 clusters that can influence probability of mortality ?

A
Childhood adversity
Adulthood adverse experiences 
Socioeconomic status 
psychological characteristics 
Social connections 
Health behaviours
50
Q

How does cultural and ethnic differences influence illness?

A
  • Diet and lifestyle differences
  • Genetic differences
  • Environmental (climate, poverty, etc) differences
  • Differences in help-seeking behaviour or perspectives/understanding of health

These can all influence vulnerability to illness and also impact treatment effectiveness as treatments are rarely culturally specific

51
Q

What are the best practices to promote behavioural change?

A

Focus on the determinant of illness and focus on prevention
Enagagement of education, support, laws, incentives, etc.
Include multiple levels of influences (families, communities, nations)
Consider unique needs of target groups
Engagement of multiple societal levels

52
Q

What is the framing effect?

A

People decide on options based on whether the options are presented with positive or negative connotations - they tend to avoid risk when a positive frame is presented by seeks risk when a negative frame is presented

Effective messaging entails information rather than persuasion, offer balance, disclose uncertainties, state evidence equality, and debunk against misinformation

53
Q

Describe the health belief model

A

This model considerers two fundamental elements that affect health motivation:

  • Perceived susceptibility/severity
  • Perceived benefits/barriers

Two additional elements were subsequently added that include health action:

  • Cues to action – the specific triggers that cause a health action to be endorsed, including internal or external cues
  • Self-efficacy – the persons confidence or belief they can successfully engage and succeed in certain behaviours
54
Q

Define the law of effect

A

Classical conditioning - reward of a behaviour will increase likelihood and punishment will decrease likelihood

55
Q

What are some clinically proven ways to alter health behaviours?

A
Classical conditioning/law of effect 
ABA 
CBT - learning cognitive restructuring 
Mindfullness - redirect thoughts toward moment-to-monent internal processes to have more appropriate appraisals and coping strategies 
Having a positive social identity
56
Q

What are positive effects of exercise?

A
  • Engage in larger variety of health behaviours
  • Decrease anxiety and depression
  • Improvement in attention, processing speed, executive funcitoning, and memory
  • Enhances neuroplasticity (enhances BDNF)
  • Limits inflammatory processes (decreases proinflammatory choices)
  • Promotes microbial diversity
  • Increases T-cell proliferation and phagocyte activity and increased surveillance of NK cells
57
Q

How does stress impact the microbiota?

A

It can influence the diversity and abundance of microbiota, potentially leading to diysbiosis

It can cause release of hormones, influence release of NTs and send signs via the vagus nerve which can influence the brain causing inflammation and depression