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Organ Systems 3 Exam 5 > Part 2 > Flashcards

Part 2 Flashcards

1
Q

What are the three stages of stress according to Hans Selye?

A 
Alarm stage (HPA, sympathetic activation, fight/flight)
Resistance stage (physiological arousal set point is higher)
Exhaustion stage (increased disease susceptibility)
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2
Q

What are the two primary hormones involved in the stress response?

A

adrenaline(NE/EPI) and cortisol

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3
Q

What does the adrenergic stress response system do?

A

sympathetic nervous system/adrenal medulla affects physiological alertness, increasing HR, BP, activates cerebral cortex, scans the environment

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4
Q

What does the cortisol stress response system do?

A

the HPA axis
enhances emotional arousal
promotes motivational, cognitive processes, aids memory, facilitates immune system readiness but can lead to allergy/autoimmune disorders is persistent
(permissive/suppressive effects)

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5
Q

how does the limbic system regulate the HPA axis?

A

via the PVN of the hypothalamus

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6
Q

What parts of the limbic system are involved in the stress response?

A

amygdala, hippocampus, limbic cortex

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7
Q

What is the pathway from external stimuli to the hypothalamus?

A

stimulus –>limbic system –>BNST which modulates amygdala–>hypothalamus

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8
Q

How does the BNST regulate the limbic cortex?

A

directly and via the PVN of the hypothalamus

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9
Q

cue threat processing is mediated by the ______, but sustained anxiety is mediated by _______ and ______.

A

cue threat –>amygdala

sustained –> tonic BNST engagement and ventral basal forebrain structure

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10
Q

The locus coeruleus projects NE caudally in order to _____ and rostrally in order to ______

A

caudal: activate sympathetic response, cause release of NE from adrenal medulla
rostral: neurofeedback to PFC, hippocampus and anygdala, to help reset limbic ANS controls

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11
Q

What are three responses to EPI and NE in the acute stress response?

A

increased muscle metabolism, EPI facilitates glucagon in releasing glucose from the liver, symp innervation of the heart, lungs, vessels and viscera

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12
Q

in non-stressed situations, moderate levels of NE engage ______receptors, strengthening _______functions and weakening responses from the ________ and ____________

A

in non-stressed situations, moderate levels of NE engage a2 receptors, strengthening PFC functions and weakening responses from the amygdala and hippocampus

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13
Q

in stressed situations, high levels of NE engage ______ receptors, weakening _____________functions and strengthening ________ and ____________ functions.

A

in stressed situations, high levels of NE engage B receptors, weakening PFC functions and strengthening amygdala and hippocampus functions.

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14
Q

high levels of NE cause what kinds of shifts in function of the PFC, amygdala and the hippocampus

A

PFC functions less in working memory, more in scanning, arousal and decision making
H and A enhance fear conditioning and memory consolidation

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15
Q

What is the pathway of the HPA axis?

A

hypothalamus releases corticotropin releasing hormone from the PVN.
CRH goes to the anterior pituitary, –> ACTH and B-endorphin released from the anterior pituitary.
–>adrenal gland

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16
Q

CRH release patterns are partly determined by ___________

A

early life events

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17
Q

Vasopressin is released from the _______ and does ______

A

released from the PVN and potentiates the ability of CRH to trigger ACTH release. (this effect is upregulated during chronic stress)

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18
Q

ACTH is derived from______ and triggers release of _______from _______

A

ACTH is derived from pro-opiomelanocortin protein and triggers the release of glucocorticoids from the adrenal cortex

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19
Q

Long term ACTH stimulation can cause ______ and ______ of the adrenal gland

A

hypertrophy and hyperplasia

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20
Q

cortisol binds to high affinity ______ and low affinity _____receptors

A

high affinity mineralocorticoid and low affinity glococorticoid receptors

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21
Q

The permissive actions of cortisol occur at ______ (low/high) levels of cortisol and bind _____receptors, causing an _________(inc/dec) in glucose levels

A

The permissive actions of cortisol occur at low levels or cortisol and bind MR receptors, causing an increase (inc/dec) in glucose levels

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22
Q

The suppressive actions of cortisol occur at __________(low/high) levels of cortisol and function through the binding of ________receptors

A

occur at high cortisol levels via binding of the GR receptor

23
Q

Is cortisol anabolic or catabolic?

A

catabolic

24
Q

What are three metabolic functions of cortisol at low levels?

A

gluconeogeneis, proteolysis, lipolysis

25
Q

What are four metabolic effects of excess cortisol?

A

high blood sugar, insulin resistance, protein loss (muscle wasting), fat accumulation

26
Q

What are two immune effects of excess cortisol?

A

inhibition of inflammation and immune response (impaired reactions to trauma or foreign substances)

27
Q

What type of immune reaction does the body have to low levels of cortisol?

A

permissive effect on inflammation and immunity

28
Q

What areas of the cortex regulate the hypothalamus? What type of regulation is it? (inhibitory/excitatory)?

A

PFC, hippocampus, amygdala regulate the PVN (via the BNST). largely inhibitory (GABA), but certain PFC areas can enhance HPA activity

29
Q

stress activates CRH neurons in the PFC for:

A

aniticpation/cognition (mPFC specifically, recieves salient information related to the stressor from the hippocampus, amygdala eg. memories of past experience)

30
Q

CRH acting on the mPFC causes:

A

excitatory influence on the HPA axis

31
Q

stress activates CRH neurons in the amygdala and BNST for:

A

emotional aspects of responses and memory

32
Q

stress activates CRH neurons in the hypothalamus for:

A

descending pain control plus motivation and drive

33
Q

stress activates CRH neurons in the PAG, raphe nucleus and locus coeruleus to:

A

mediate behavioral, adrenergic and serotonergic components of stress response

34
Q

What are some reactive responses to stress and what system regulates this?

A

changes in cardivascular tone, respiratory distress, visceral/somatic pain, inflammation, infection
mediated by the HPA axis

35
Q

What is an anticipatory reaction? what is it dependent on?

A

a physiological reaction that occurs in the absence of a physiological stimuli. functions via the HPA axis, but dependent on limbic conditioning (motivational loop)

36
Q

What causes the termination of HPA axis activation?

A

cortisol feedback (but changes to limbic (psychogenic) and BNST (systemic) during chronic stress causes chronic stress states)

37
Q

Cortisol binds to GR receptors in the _______ and ______ to inhibit ACTH and cortisol release following a bout of acute stress (rapid cortisol feedback)

A

in the PVN and pituitary

38
Q

How does cortisol resistance occur?

A

increased chronic levels of cortisol cause a decreased number of GR receptors to be expressed, leading to decreased cortisol feedback to the PVN and pituitary

39
Q

What is hypercortisolism and what conditions is it seen in (3)?

A

increased ACTH and cortisol production after GR downregulation and cortisol resistance. occurs in: chronic pain, depression, anorexia

40
Q

What is hypocortisolism and what conditions is it seen in (3)?

A

supersensitivity of GR that enhances cortisol feedback and decreased the amount of cortisol. occurs in: PTSD, chronic fatigue syndrome, fibromyalgia

41
Q

What type of receptors are MR and GR receptors?

A

ligand-driven transcription factors that bind DNA directly

42
Q

In the kidney, MR binds mainly _______. In the brain MR only binds _______.

A

aldosterone, cortisol

43
Q

What is the fast response to cortisol?

A

cortisol binds MR first, increasing excitability of the hippocampus to sensory information. this maintains the basal activity of the HPA axis

44
Q

What is the slow response to cortisol?

A

as cortisol rises, it binds GR. GR activity leads to inhibition of the stress response (feedback) (unless chronic)

45
Q

When in the stress response does memory formation occur?

A

the third phase (recovery/adaptation), when cortisol binds GR

46
Q

How can cortisol facilitate learning?

A

stress within the learning context leads to release of NA, CRH and CORT, which facilitate perception and attention. thus consolidation of learning can occur while the input of unrelated information is inhibited

47
Q

How can cortisol impair learning?

A

If stress precedes learning, gene-mediated suppression of activity impair learning

48
Q

Does cortisol inhibit or help in memory recall?

A

inhibits recall

49
Q

How does cortisol feedback affect the amygdala?

A

in increases the amygdalas response to NE, producing stress related fight/flight/risk assessment behavior and learning

50
Q

How does cortisol affect the PFC during acute stress?

A

cortisol activates the mPFC to improve working memory and terminate HPA stress responses

51
Q

How does cortisol affect the PFC during greater stress?

A

working memory is disrupted creating distractability

52
Q

How does cortisol affect the PFC during chronic stress?

A

GR downregulated, impaired negative feedback, enhanced HPA activity (hypercortisolism)

53
Q

What is an effect of excess cortisol on top-down/bottom-up regulation of the amygdala?

A

reduced top-down regulation of the amygdala by the PFC

54
Q

What is the extrahypothalamic CRF stress system?

A

cortisol actually increases synthesis of CRF in the BNST and the amygdala, providing means to extend the stress response to allostasis

Organ Systems 3 Exam 5 (2 decks)

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