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Endocrinology & Reproduction > HPA axis and stress > Flashcards

HPA axis and stress Flashcards

1
Q

HPA axis

A

hypothalamic-pituitary-adrenal axis

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2
Q

examples of experimental stressors

A

toxic injection, trauma, infection, cold environment, swimming to exhaustion

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3
Q

examples of experimental responses to stress

A

adrenal hyperplasia, atrophy of immune system organs, peptic ulcers

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4
Q

what do stressors increase

A

secretion of glucocorticoid

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5
Q

when is secretion of glucocorticoid increased

A

in response to stressors

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6
Q

what is the stress hormone

A

cortisol

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7
Q

what is cortisol

A

glucocorticoid steroid hormone

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8
Q

physiological stress

A

any event that elecits increased secretion of the glucocorticoid steroid hormone cortisol

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9
Q

GAS

A

general adaptation syndrom

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10
Q

3 parts of GAS

A

alarm - fight or flight, short term adrenaline
resistance to stress - chronic cortisol levels x 10
exhaustion - immune suppresion, illness or death

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11
Q

how many adrenal glands

A

2, left and right

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12
Q

what is a plastic organ & example

A

can get bigger and smaller. If one adrenal gland is removed, the other will increase in size to compensate

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13
Q

where are steroid hormones made

A

the cortex of the adrenal glands

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14
Q

how many zones does the adrenal cortex have

A

3

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15
Q

zona glomerulosa makes

A

aldosterone

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16
Q

zona fasciculata & reticularis make

A

cortisol & androgens

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17
Q

medulla makes

A

adrenaline and noradrenaline

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18
Q

what is the outer zone of adrenal called

A

cortex

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19
Q

what is the inner zone of the adrenal called

A

medulla

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20
Q

what part of the adrenal has the slow response

A

outer cells; where steroid hormones are made

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21
Q

what part of the adrenal has the immediate response

A

the medulla; where adrenaline is released

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22
Q

describe steroid hormones

A

lipid like becuase they’re maed from cholesterol

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23
Q

what are steroid hormones made from

A

cholesterol

made from lipid droplets in the outermembrane of the mitochondria

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24
Q

specifically where are steroid hormones amde

A

outermembrane of the mitochondria

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25
Q

what do sterois hormone make cells have lots of

A

mitochondira, lipid droplets and SER

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26
Q

what happens to steroids once made

A

they diffuse out of cell into blood circualtion. they are not stored

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27
Q

steroid release is

A

slow

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28
Q

what is the meduall made up of

A

modified nerve cells

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29
Q

what happens to adrenaline once made

A

stored in vesicles

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30
Q

how does adrenaline enter circulation

A

stored in secretory vesicles then released rapidly by exocytosis

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31
Q

half life of adrenaline

A

3-4 minutes

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32
Q

what is adrenaline synthesised from

A

tyrosine AA

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33
Q

where are steroid hormone receptors found

A

intracellular, becsuse steroids can diffuse plasma membrane

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34
Q

how do steroid hormone receptors work

A 
bind to hormone 
translocate to nucleus
bind to specific DNA sequence
influce gene expression
= relatiely long term effects
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35
Q

example of transmembrane receptor

A

catecholamine

36
Q

where is catecholamine receptor found

A

transmembrane

37
Q

where does hormone bind to catecholamine receptor

A

will bind in the extracellular domain of this transmembrane receptor because cant cross plasma membrane

38
Q

how does catecholamine receptor work

A

receptor transmits signal to intracellular domain via GTP binding prodtein
this activates 2nd messenger e.g cyclic AMP, DAG Ca2+
= rapid reversible response, short term effects

39
Q

examples of 2nd messenegers

A

cyclic AMP, DAG, Ca 2+

40
Q

Endocrine response to stress

A

fight or flight = noradrenaline and adrenaline as a short term rapid response

41
Q

short term response to stress

A

adrenaline / noradrenaline

42
Q

what does increased noradrenaline and adrenaline do to the body

A
  • increases glycogenolysis in liver and muscle
  • increases lipolysis in fat
  • increases Cardiac output
  • diverts blood flow from viscera to skeletal muscle
  • increases ventialation to increase VO2
43
Q

resistance to stress

A

occurs with chronically elevated cortisol leels

44
Q

what regulates levels of cortisol

A

anterior pituiatry

45
Q

what regulates the anterior pituiatry

A

hypothalamus

46
Q

what does the HPA axis regulate

A

endorcrine and neurocrine system

47
Q

how does the HPA axis work

A
  • neurones in the hypothalamus send axons to the medien eminence
  • CRH is released at the medien eminence and enters blood with ease
  • CRH controls the release of ACTH from the anterior pituiatry
  • ACTH is relreased and enters venous drainage to be transported to adrenals
48
Q

where is CRH released from

A

medien eminence

49
Q

how does CRH enter blood stream

A

with ease at the medien eminence becuase there is no BBB

50
Q

what does CRH control

A

the release of ACTH from the anterior pituitary

51
Q

where is ACTH released

A

anterior pituitary

52
Q

where does ATCH go

A

from anterior piuitary, enters venous drainage to travel in blood to the adrenals

53
Q

which has a long jourrney and which has a short journey

  • CRH
  • ACTH
A 
CRH = SHORT
ACTH = LONG
54
Q

HPA axis regulates the endorcrine and autonomic system by

A

negative feedback

55
Q

when does cortisol peak

A

in the morning to prepare you for th day

56
Q

what does a peak in cortisol do

A

increases vasucular tone BP
increases awareness CNS
mobilises fuel sotres and energy

57
Q

wha disturbs cortisol peak

A

disturbance of circadian rhythm

58
Q

what happens to cortisol secretion in response to stress

A

will peak in the fight or flight response then return to normal

59
Q

chronic stress

A

cortisol levels remain high after morning peak

60
Q

what is the effect of cortisol release in reponse to stress

A
  • has catabolic effects and opposes the effects of insulin
    maintains enzyme expression
  • enhances CV reactivity to catecholamines
  • inhibits inflammatory and immune response
  • inhibits non-essential function
61
Q

how does cortisol have catabolic effects

A

it maintains the expression of metabolic enzymes

62
Q

symptom of continued protein synthesis in chronic stress

A

muscle wastage and bone weakening

63
Q

symptom of continued hepatic gluconeogenesis inchronic stress

A

bruising

64
Q

how does chronic stress affect diabetics

A

alters their insulin requirements bc cortisol opposes the effects of insulin

65
Q

what does enhances CV reactivity to catecholamines mean

A

adrenaline and noradrenaline will cause vasoconstriction to increase BP

66
Q

what effect does high cortisol have on the heart

A

hypertension leading to stroke or heart disease

67
Q

what does low crotisol do to the heart

A

hypotension

68
Q

what are the metabolic processes stimulated by cortisol

A
  • stimulates protein breakdown
  • stimulates hepatic gluconeogenosis
  • stimulates lipolysis
69
Q

how does cortisol inhibit inflammatory and immune response

A
  • inhibits TG and LT production
  • inflammatory cytokines stimulate ACTH and hence cortisol secretion in a negative feedback loop to down regualte inflammatory response
70
Q

how does cortisol inhibit non-essesntial function & what

A

reproduction and growth
reduces bone density, skin thickness and muscle mass becuase of catabolic processes
growth retardation
reduced fertility & wound healing

71
Q

disease of cortisol deficiency

A

Addison’s disease

72
Q

how is cortisol deficieny caused in Addison’s

A

adrenal cortex is damaged by TB or by autoimmune destruction in over 80%

73
Q

adrenal insufficiency causes

A
  • hypotension, hypoglycemia, hyperpigmentaton, tiredness, weakness, anorexia, vomitting, depression
74
Q

what does addisons often get misdiagnosed as and why

A

chronic fatigue becuase Addisons is a progressive disease

75
Q

Addisonian crisis

A

inabilty to respond to stress

fatal if untreated

76
Q

treatment of Addison’s

A

oral sterid replacement therapies

77
Q

pathology of addisons

A
  • no negative feedback from cortisol
  • continued CRH secrtetion
  • continued ACTH secretio
  • very high plasma ACTH
78
Q

what does high plasma ACTH cause

A

hyperpigmentation

ACTH in high levels will act on melanocytes to generate melanin

79
Q

what normally acts on melanocytes to generate melanine

A

alpha MSH

80
Q

why can ACTH act on melanocytes

A

there is a alpha MSH sequence in ACTH which also triggers MCR

81
Q

cushing’s syndrome

A

inapproprite secretion of cotisol when not stressed

82
Q

what causes cushing’s syndrom

A
  • adrenal cortex tumours causing increased cortisol secretion
  • pituitary adenomas causing increased ACTH secretion (70%)
83
Q

most common form of endocrine cancer

A

pituitary adenoma causin excess ACTH = cushings

84
Q

net effects of cushings are similar to

A

chronic stress

85
Q

net effects of cushings

A
  • increase catabolic effects
  • increased vasoconstriction
  • suppressed immune response
86
Q

bone catabolism, hirsuitism (hair growth), skin thinning and bruising, muscle wastage and buffalo hump are signs of

A

cushing’s syndrome. Excess cortisol

Endocrinology & Reproduction (15 decks)

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