Lecture 17 Flashcards

1
Q

activation of HPA axis =

A

increased glucocorticoids

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2
Q

activation of ANS =

A

increased catecholamines

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3
Q

activation of additional pathways in NS

A

motor responses (locomotion)

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4
Q

HPA starts in

A

CRH neurons of hypothalamus

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5
Q

HPA ends with

A

GC released from adrenal cortex

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6
Q

HPA pathway

A

CRH neurons in hypothalamus release CRH at median eminence, CRH stimulates release of ACTH from anterior pituitary, ACTH stimulates release of GC from adrenal cortext, GC mobilize energy, give negative feedback

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7
Q

ANS (sympathetic) in stress response

A

norepinephrine to target tissues
epinephrine widespread
- decreased digestion, saliva, increased heart rate, blood glucose levels, shunting of blood from gut, etc.

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8
Q

Sympathetic-AdenoMedullary (SAM)

A
  • adrenal medulla released epinephrine and norepinephrine
  • is the rapid response
  • works w/ HPA
  • both triggered by hypothalamus
  • rapid mobilization of metabolic resources
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9
Q

most important GC in humans

A

cortisol

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10
Q

HPA (differences from SAM)

A
  • adrenal cortex produces GC and MC
  • slower response
    -> changes gene expression
  • targets the brain
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11
Q

Mineralocorticoid receptors

A

Type 1, higher affinity
- get binded to first

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12
Q

Glucocorticoid receptors

A

Type 2, lower affinity
- get binded to after MR is saturated
- for responding to stressors

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13
Q

As a monomer, ____ can inhibit gene expression

A

GR

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14
Q

how do GR and MR stimulate gene expression

A

dimerization of the hormone/receptor complex recruits co-activators

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15
Q

how does CBG affect GC levels

A

it binds it, once bound GC is not free

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16
Q

GC binds receptors where?

A

in cytoplasm

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17
Q

How do MR/GRs affects the membranes conductance/excitability? Slow or fast? Short or long-lasting?

A

by regulating the transcription of genes control the properties of GPCRs, ion channels, ionotropic receptors, and ion pumps
- slow in onset, long-lasting

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18
Q

Catecholamines act fast or slow

A

fast

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19
Q

MR and GR actions affect

A

structural integrity and excitability

20
Q

limbic system + stress

A

adds emotional dimensions
- centered in hypothalamus
- interprets the stressfulness of a threat
- connected to organs of perception

21
Q

allostasis =

A

achieving stability by change via stress response

22
Q

hypothalamus

A

Secretes CRH, which causes AP to secrete ACTH, which stimulates the adrenal medulla to release epinephrine, and the adrenal cortex to release GC

23
Q

Do SAM and HPA involve our feelings?

24
Q

CRH released from

A

hypothalamus

25
ACTH released from
anterior pituitary
26
GC released from
Adrenal cortex
27
NE and EP released from
Adrenal medulla
28
gluconeogenesis (liver), protein catabolism (muscle), and lipolysis (adipose tissue) all increase ____________
energy available
29
goal of metabolic acute stress response
increase glucose levels in bloodstream
30
metabolic (acute stress response) : T3 and T4 affect
bind mitochondria, increase ATP, increase transcription of genes, increase metabolism of cell
31
beta cells in pancreas secrete _________ which _______ glucose
insulin, stores (it as glycogen)
32
alpha cells in pancreas secrete ________ which _______ glucose
glucagon, releases (hydrolyzes glycogen in liver)`
33
after a meal, ____ is secreted to _____ blood sugar
insulin, lower
34
several hours after a meal, ______ is secreted to ______ blood sugar levels
glucagon, raise
35
lipolysis, glucogenolysis, proteolysis, gluconeogenesis, all ______ blood glucose levels
increase, via epinephrine and norepinephrine, and more slowly by GC which increase gluconeogenesis
36
cardiovascular (acute stress response)
sympathetic ANS, norepinephrine mediates increase in breathing rate, heart rate, blood pressure, shunting of blood away from gut, etc
37
opiate dependant analgesia
endogenous opiates like enkephalins, beta-endorphin (released within brain)
38
opiate independent analgesia
other NTs like glutamate
39
_____ analgesia type occur during normal stress encounter
both
40
alterations in behaviour (acute stress response) caused by
CRH - increased vigilance, freezing, etc
41
why is the immune system inhibited by GC's during acute stress response
to protect it from becoming too active and attacking itself (autoimmune disease)
42
Th1 cells
immune response - type-1 pathway, cellular immunity, ex. bacteria, viruses - type 1 diabetes, multiple schlerosis, etc
43
Th2 cells
immune response - type 2 pathway, humoral immunity, ex. toxins, allergens - lupis, asthma, cancer
44
endorphin release =
reduced pain
45
effects of chronic stress
diabetes, obesity, coronary heart disease, gastric ulcers (reduction in thickening of stomach walls, prostaglandin aid here)