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Genes 3670 > Lecture 17 > Flashcards

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?

A

yes

24
Q

CRH released from

A

hypothalamus

25
Q

ACTH released from

A

anterior pituitary

26
Q

GC released from

A

Adrenal cortex

27
Q

NE and EP released from

A

Adrenal medulla

28
Q

gluconeogenesis (liver), protein catabolism (muscle), and lipolysis (adipose tissue) all increase ____________

A

energy available

29
Q

goal of metabolic acute stress response

A

increase glucose levels in bloodstream

30
Q

metabolic (acute stress response) : T3 and T4 affect

A

bind mitochondria, increase ATP, increase transcription of genes, increase metabolism of cell

31
Q

beta cells in pancreas secrete _________ which _______ glucose

A

insulin, stores (it as glycogen)

32
Q

alpha cells in pancreas secrete ________ which _______ glucose

A

glucagon, releases (hydrolyzes glycogen in liver)`

33
Q

after a meal, ____ is secreted to _____ blood sugar

A

insulin, lower

34
Q

several hours after a meal, ______ is secreted to ______ blood sugar levels

A

glucagon, raise

35
Q

lipolysis, glucogenolysis, proteolysis, gluconeogenesis, all ______ blood glucose levels

A

increase, via epinephrine and norepinephrine, and more slowly by GC which increase gluconeogenesis

36
Q

cardiovascular (acute stress response)

A

sympathetic ANS, norepinephrine mediates increase in breathing rate, heart rate, blood pressure, shunting of blood away from gut, etc

37
Q

opiate dependant analgesia

A

endogenous opiates like enkephalins, beta-endorphin (released within brain)

38
Q

opiate independent analgesia

A

other NTs like glutamate

39
Q

_____ analgesia type occur during normal stress encounter

A

both

40
Q

alterations in behaviour (acute stress response) caused by

A

CRH
- increased vigilance, freezing, etc

41
Q

why is the immune system inhibited by GC’s during acute stress response

A

to protect it from becoming too active and attacking itself (autoimmune disease)

42
Q

Th1 cells

A

immune response
- type-1 pathway, cellular immunity, ex. bacteria, viruses
- type 1 diabetes, multiple schlerosis, etc

43
Q

Th2 cells

A

immune response
- type 2 pathway, humoral immunity, ex. toxins, allergens
- lupis, asthma, cancer

44
Q

endorphin release =

A

reduced pain

45
Q

effects of chronic stress

A

diabetes, obesity, coronary heart disease, gastric ulcers (reduction in thickening of stomach walls, prostaglandin aid here)

Genes 3670 (13 decks)

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