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Pain and Stress > Stress 1 > Flashcards

Stress 1 Flashcards

1
Q

When the body is challenged by almost anything that happens to us, from getting out of bed in the morning or
running up a flight of stairs or having to stand up and give a talk, the brain activates two primary types of
hormones. what are they?

A

adrenergic (NE, EPI) and cortisol

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2
Q

Which Axis is produces adrenergic hormones?

A

SYMPATHOADRENAL AXIS

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3
Q

which axis produces cortisol

A

HYPOTHALAMIC-PITUITARY-ADRENAL AXIS (HPA)

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4
Q

Is the limbic system involved in stress?

A

yes, it regulates HPA axis via PVN of hypothalamus

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5
Q

SYMPATHOADRENAL AXIS generates a short or long latency?

A

short

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6
Q

SYMPATHOADRENAL AXIS is involved in the initial or latter part of the stress response?

A

initial

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7
Q

In the SYMPATHOADRENAL AXIS the Limbic system (PFC, amygdala, hippocampus) interprets threatening or intense environmental stimuli as stressful and projects this to what?

A

BNST!!! (bed nucleus of striaterminalis) - located just above the preopticnucleus of hypothalamus

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8
Q

The BNST mediate threatening info from ______ to ______ (two brain structures)

A

amygdala; hypothalamus

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9
Q

What two structures modulate reposes to threat?

A

PFC and hippocampus

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10
Q

BNST regulates ____ directly or via ______

A

LC; PVN of hypothalamus

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11
Q

what is the the largest NE pathway?

A

LOCUS COERULEUS (LC),

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12
Q 
LOCUS COERULEUS (LC), the largest NE pathway, generates
peripheral & central stress responses by projecting caudally or rostrally?
A

Both caudally and rostrally

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13
Q

Peripheral responses to acute stress involve which pathway?

A

sympathoadrenal axis

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14
Q

PERIPHERAL RESPONSE TO ACUTE STRESS includes Systemic responses due to endocrines (EPI & NE) released from what organ?

A

adrenal medulla

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15
Q

what two major systemic reposes occur in acute stress as a result of EPI and NE?

A
  • Increase muscle metabolism

* Epinephrine facilitates glucagon in releasing glucose from the liver

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16
Q

rostral projection of LC go where to provide feedback resetting control of ANS?

A

PFC, hippocampus, amygdala

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17
Q

central responses to acute stress are determines by the type of ___ receptor activates by the ___

A

NE; LC

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18
Q

In non-stress situation, LC produces _______ levels of NE that engage high-affinity ___receptors in PFC, hippocampus and amygdala

A

moderate; α2

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19
Q

What does NE on α2 receptors receptors do?

A

strengthens PFC functions (attentionalselectivity) and weakens those of the amygdala and hippocampus.

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20
Q

acute stress leads to increased or decreased LC activity?

A

increased

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21
Q

In acute stress, high levels of NE engage lower affinity_______, which weaken ___ but strengthen _______ and _______function.

A

βreceptors; PFC; amygdala; hippocampal

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22
Q

Higher NE levels shift PFC from working memory and attentional selectivity to what?

A

more arousal, scanning of the environment and decision making (PFC)

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23
Q

Higher levels of NE shift the hippocampus and amygdala to what?

A

enhanced memory consolidation and fear conditioning

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24
Q

The HPA produces short or long term stress reposes?

A

both short and long!

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25
Q

The HPA’s responds to stress using what?

A

cortisol!

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26
Q

What is CRH

A

corticotrophin releasing hormone/factor

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27
Q

What structure is CRH released from?

A

PVN (paraventricular hypothalamic nucleus)

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28
Q

CRH transport down what to the anterior pituitary?

A

portal vessel

29
Q

CRH transports down the portal vessel to what structure?

A

anterior pituitary

30
Q

CRH stimulates the release of what two things from anterior pituitary cells?

A

ACTH and beta-endorphin

31
Q

What is core leased with CRH from the PVN?

A

Vasopressin (VP)

32
Q

What strengthens CRH’s ability to trigger release of ACTH from anterior pituitary?

A

VP!

33
Q

VP is up-regulated or down-regulated with chronic stress?

A

up-regulated

34
Q

What does ACTH (adrenocorticotropic hormone) do?

A

triggers release of glucocorticoids from adrenal cortex

35
Q

what is cortisol?

A

human glucocorticoid stress hormone

36
Q

what is cortisol derived from?

A

cholesterol

37
Q

long term ACTH stimulation can have what effect on the adrenal cortex?

A

Causes upregulation, hyperplasia, and hypertrophy of the gland to produce more cortisol.

38
Q

In general, what does cortisol do for you?

A

It prepares your limbic system for stressful situations and helps your body
maintain metabolic energy

39
Q

Why does cortisol need to be restricted to times of need?

A

because excess cortisol can lead to tissue destruction

40
Q

cortisol binds to what two corticoid receptors?

A

MR (mineralocorticoid) and GR (glucocorticoid)

41
Q

What is cortisol’s permissive action?

A

at initially low levels, cortisol amplifies NE-glucagon pathway via MR to increase glucose levels

42
Q

What is cortisol’s suppressive action?

A

Later, at high levels (via GR), cortisol is suppressive

43
Q

metabolic actions: cortisol converts protons and lipids in glucose via what three biochemical processes?

A
  • Gluconeogenesis in liver
  • Proteolysis in muscle, lymphoid, skin & CT
  • Lipolysis of adipose
44
Q

Excess cortisol causes:

A

•High blood sugar
•Insulin resistance in fat & muscle (→NIDDM)
•Protein loss; wasting of muscle, bone matrix, & lymphoid tissues.
•Fat accumulation in
Abdomen (visceral and upper body fat)
Base of the neck (buffalo hump)
Face (moon face)

45
Q

longterm stress resets what levels?

A

homeostatic levels of cortisol and its action?

46
Q

Immune actions of cortisol: low cortisol has a permissive or inhibitory affect on inflammation and immunity?

A

permissive

47
Q

How do higher levels of cortisol limit inflammation?

A

By reducing release of histamine, bradykinin, PGE & leukotrienes to reduce swelling, vasodilation & phagocytosis

48
Q

How does high cortisol limit immunity?

A

By reducing cytokine release, antibody formation, cellular immunity and fever

49
Q

What three structures regulate the PVN?

A

PFC, hippocampus, and amygdala

50
Q

PFC, hippocampus, and amygdala regulate PVN via what?

A

BNST

51
Q

CRH does other things in addition to ACTH release. In the prefrontal cortex, stress activates CRH neurons for:

A

Anticipation and cognition:
•mPFCreceives cognitive and emotionally salient information related to the stressor from hippocampus & amygdala, eg. memories related to past stress experiences
•CRH acting in the mPFCexerts an excitatory influence on HPA responses to acute and repeated stress via the amygdala

52
Q

CRH does other things in addition to ACTH release. In the amygdala and BNST, stress activates CRH neurons for:

A

emotional aspects of responses (fear and anxiety) and memory

53
Q

CRH does other things in addition to ACTH release. In the hypothalamus, stress activates CRH neurons for

A

descending pain control plus motivation and drive

54
Q

CRH does other things in addition to ACTH release. In the PAG, rap he nucleus, and LC stress activates CRH neurons

A

to mediate the behavioral, adrenergic and serotonergic components of the stress response.

55
Q

Physiological stressors representing homeostatic challenges, conveyed by sensory pathways, generate reactivestress responses through the what structure(s)?

A

The hypothalamus and pituitary, NOT the limbic system.
Eg. changes in cardiovascular tone, respiratory distress, visceral or somatic pain, and factors in inflammation/infection

56
Q

which axis alters cognitive and emotional precesses relevant for behavioral adaptation?

A

HPA

57
Q

Anticipatory HPA réponses are generated by what?

A

Limbic dependent conditioning (memory) or by innate predispositions (e.g.. recognition of danger of heights, predators). AKA they occur in absence of physiological challenges.

58
Q

In anticipatory reactions, what riggers the release of cortisol?

A

Hypothalamic activation. This release of cortisol acts on target organs and also feeds back onto HPA and limbic structures

59
Q

What is cortisol feedback important for?

A

It is essential to limit the duration of cortisol secretion and for prevention of deleterious effects of persistently elevated levels of cortisol on cardiovascular, immune, metabolic, and neural systems.

60
Q

Normal levels of cortisol will simply inhibit HPA activity. What will persistent high levels of cortisol do instead?

A

Alter the functions of the limbic and HPA structures.

61
Q

What structures in the HPA does cortisol feed back on?

A

PVN, pituitary, hippocampus, amygdala, and mPFC

62
Q

Is cortisol feedback on the hypothalamus and pituitary rapid or slow? What does it consist of?

A

Rapid feedback: Cortisol binding to GR in PVN & pituitary cells inhibits ACTH & cortisol release following a bout of acute stress

63
Q

Cortisol resistance is due to the down regulation of what kind of receptor?

A

GR receptors

64
Q

The decrease in GR receptors seen in cortisol resistance leads to a decrease or increase in negative feedback?

A

decrease

65
Q

The decrease of the negative feedback seen in cortisol resistance leads to an increased or decrease in ACTH & cortisol production?

A

increase

66
Q

Hpercortisolism in seen in people with what three conditions?

A

chronic pain, depression, and anorexia

67
Q

Supersensitivity or GR (unclear cause) _______ cortisol feedback, ______ HPA activity.

A

enhancing; inhibiting

68
Q

What trigger hypocortisolism?

A

super sensitivity of GR

69
Q

Where is hypocortisolism seen?

A

PTSD, Chronic fatigue syndrome, fibromyalgia

Pain and Stress (3 decks)

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