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Pain and Stress > Stress 2 > Flashcards

Stress 2 Flashcards

1
Q

What are the two kinds of receptors in the limbic system involved in cortisol feedback?

A

MR and GR

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2
Q

How do the receptors changed gene transcription. Name two ways.

A
  1. directly binding to recognition sites in the DNA

2. indirectly via interactions with other transcription factors

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3
Q

What effect does excess cortisol have on the hippocampus?

A

It will down regulate various cell signals including action of BDNF on synaptic integrity. A treaty for this problem will enhance BDNF and monoamine neuromodulation.

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4
Q

MR - high or low affinity for cortisol?

A

High!

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5
Q

Do MRs increase decrease of maintain excitability of the hippocampal neurons?

A

maintain

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6
Q

GR - high or low affinity for cortisol?

A

low

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7
Q

GR are only when?

A

with high levels of stress-related cortisol

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8
Q

As cortisol levels increase at later stages of stress, GR activity leads to inhibition or activation of stress response?

A

Inhibtion

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9
Q

MR - fast or slow response

A

fast

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10
Q

GR - fast or slow response

A

slow

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11
Q

What are the three phases of brain stress responses?

A

Stress, recovery, and adaptation

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12
Q

stress generates responses from where?

A

the limbic system

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13
Q

After a stress response is generate from the limbic system, where are they projected to?

A

The OVN in the hypothalamus and the HPA axis

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14
Q

After a stressor, when do cortisol levels peak?

A

30-45 minutes

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15
Q

In the Stress phase, increased cortisol levels bind to which type of receptors?

A

MR

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16
Q

The binding of cortisol to MRs has what response in the body?

A

Enhanced arousal, vigilance, alertness, and attention. (non-genomic action through MRs)

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17
Q

When do the recovery and adaption stages occur?

A

After 1-2 hours

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18
Q

In the recovery and adaption stages, cortisol decreases but there is still enough to suppress the stress response from the initial phase via which type of receptors? Is it a genomic or nongenomic response?

A

GR - genomic

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19
Q

What else occurs in the recovery and adaptation phases besides suppression?

A

consolidation and preservation of info about the stressful event. (Memory!!)

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20
Q

Cortisol facilitated memory and learning is dependent on what brain structure? What else is required for proper learning?

A

Hippocampus. - TIMING!

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21
Q

Stress within the context of learning release what three things? What do they facilitate with?

A

NA, CRH, and CORT - all of which facilitate the ongoing precesses of perception and attention in the initial phases of learning

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22
Q

cortisol also initiated a ________ pathways which facilitates consolidation of relevant info and temporarily ______ input of unrelated info.

A

gene-mediated; inhibits

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23
Q

If stress precede learning, when will the gene-mediates suppression of activity occur?

A

During the time when you want to learn the new task!

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24
Q

Cortisol feedback on the AMYGDALA: the amygdala stimulates or inhibits the HPA axis during stress?

A

stimulates

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25
Q

cortisol feedback increases or decreases amygdala’s responses to stress by facilitating its activation by ____(what neurotransmitter?)

A

increases; NE

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26
Q

NOTE how both _____ and _____ enhance amygdala activity in response to stress.

A

NE and cortisol…the two limbs of the stress response

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27
Q

Cortisol feedback on the PFC: in acute stress does cortisol activate or inhibits MPFC?

A

activates

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28
Q

What does activation of the mPFC do in acute stress? 2 things.

A

improves working memory and helps terminate HPA stress response

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29
Q

During Greater stress, high levels or cortisol do what to working memory?

A

disrupt it and cause distractibility!

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30
Q

In Chronic Stress are the glucocorticoid receptors down regulated or up regulated in the mPFC?

A

downregulated

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31
Q

What does down regulation of the glucocorticoid receptors in the mPFC during chronic stress or aging associated with?

A

impaired negative feedback regulation by cortisol AKA hypercortisolism

32
Q

Excess cortisol can lead to a reduction or increase in top-down regulation of the amygdala?

A

reduction

33
Q

Chronic stress leads to increased cortisol release because of up regulation of what two things?

A

VP and ACTH receptors

34
Q

How does up regulated VP lead to cortisol resistance?

A

VP is ledd inhibited by cortisol feedback compared to CRH leading to increased cortisol release

35
Q

What in the clinical presentation of someone with Melancholic depression?

A

insomnia, anorexia, motor agitation, over arousal

36
Q

What is the cause of melancholic depression?

A

HPA-axis hyperactivity and hypercortisolemia (higher CRH levels)

37
Q

What other conditions might someone with atypical drepression have?

A

Inflammatory and metabolic dysregulation: higher levels on inflammatory markers, BMI, waist circumference, and triglycerides. Lower HDL cholesterol.

38
Q

How would a patent with atypical depression present in the clinic?

A

hypersomnia, weight gain, lethargy,

39
Q

What do cortisol levels look like in a patient with atypical depression?

A

NORMAL!

40
Q

What is the switch hypothesis?

A

As stesors becomes increased or sustained, CRH secretion decreases in the PVN, while AVP secretion increases.

41
Q

In CRH associate with chronic or acute stressors?

A

acute

42
Q

Is AVP associate with acute or chronic stessors?

A

chronic

43
Q

Brain exposure to what two things leads to experience of melancholic depression?

A

CRH and cortisol

44
Q

Brain exposure to what what results in symptoms seen in atypical depression?

A

Cortisol alone, or cortisol +AVP

45
Q

What happens to the circadian fluctuations of cortisol during chronic stress?

A

They are flattened

46
Q

Chronic stress with increase or reduce the CRH sensitivity to stressors?

A

reduce

47
Q

What will a flattened circadian flu cation in cortisol do to someones sleep?

A

Cause sleep disruption which will elevate evening cortisol and glucose levels…this could lead to insulin resistance

48
Q

Throughout the day, when does cortisol secretion peak?

A

About an hour or so after waking

49
Q

Throughout the day, when are cortisol levels at their minimum?

A

In the evening

50
Q

With chronic stress, what changes to the amount of cortisol secretion in the morning and in the evening?

A

lowers cortisol in the morning, increases cortisol in the evening

51
Q

What are the pulsatile secretions in the circadian flu cations necessary for?

A

Prevention of receptor desensitization. And it may also represent periods of enhances stress responsiveness.

52
Q

How does fasting effect cortisol levels?

A

enchances them

53
Q

How does fasting change cortisol secretions?

A

It delays maximal blood cortisol concentrations to the early afternoon

54
Q

What metabolic effects results from hypercortisolism?

A

Osteoporosis
Insulin resistence
vascular disease

55
Q

What affect does hypercortisolism have on the amygdala?

A

Can cause amygdala hypertrophy and hyperactivity -> increased emotion responsiveness

56
Q

What effect does hypercortisolism have on the PFCand hippocampus?

A

Reduction in synaptic contact and volume - disfunction in cognition, working memory, and memory consolidation

57
Q

How can the negative effect of hypercortisolism be revered in the hippocampus and PFC?

A

With lithium and antidepressants

58
Q

Why are woman twice as likely to develop major depressive disorder?

A

Estrogen is associated with greater stress-related dendritic remodeling in the nPFC

59
Q

How would an early life trauma effect your current stress levels?

A

They increase the number and sensitivity of CRH neurons

60
Q

What does early trauma do to epigenetics?

A

It causes epigenetic suppression of BDNF, a factor that is necessary to limit neural degeneration in hippocampus relate to stress

61
Q

In the absence of stress is the BDNF gene coiled or uncoiled?

A

coiled

62
Q

In chronic stress, does the demethylation of the BDNF gene open or close the gene?

A

close

63
Q

Does stress result in inhibition or release of pro-inflammatory cytokines?

A

release!

64
Q

How to cytokines disrupt the feedback control of cortisol?

A

They diminish central cortisol receptor sensitivity

65
Q

Inflammatory cytokine interfere with neuromodulation. specifically what neurotransmitters?

A

Dopamine (DA), Sertonin (5HT), and Norepinephrin (NE)

66
Q

In depression, disruption of seratonin, dopa, and NE transmission impairs what?

A

the regulatory feedback loops that turn of the stress response

67
Q

What causes neuropinflammation?

A

Classical factors: infection, autoimmunity, toxins

Factors that lead to enhanced neuronal activity :noxious stimuli, psychological stress and epileptic seizures

68
Q

In learning: circadian glucocorticoid peaks promote what?

A

Postsynaptic dendritic spine formation

69
Q

In learning: circadian glucocorticoid troughs promote what?

A

stabilization of newly formed spines that are important for long-term memory retention

70
Q

chronic and excessive exposure to stress eliminates what necessary steps to learning?

A
  1. learning associated new

2. it also disrupts acquired memories

71
Q

What causes Hypoadrenalism? (Addison’s disease)

A

Atrophy of tissue due to autoimmune, TB, or cancer

72
Q

What happen to cortisol levels in Addison’s disease?

A

decrease

73
Q

What are the symptoms of Addison’s disease?

A

Hypoglycemia between meals
Decreased gluconeogensis
Susceptible to Stress
Blotchy melanin pigmentation of mucous membrane and skin
Aldosterone decrease leads to excess excretion of sodium and water and excess reabsorption of potassium.

74
Q

What is Hyperadenalism calles?

A

Cushing’s syndrome

75
Q

What is Cushing’s syndrome caused by?

A

Excess cortisol due to any etiology
Hypersecretion of ACTH from a pituitary adenoma
Autoimmune hyperplasia of adrenal cortical cells

76
Q

What are the symptoms of Chushing’s syndrome?

A 
Buffalo Torso
Hyperglycemia (Insulin resistance)
Protein loss
Aldosterone excess: facial edema, hypertension, hypokalemia
DHEA excess, acne, hirsutism

Pain and Stress (3 decks)

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