lecture 11/13 - endocrine Flashcards

(167 cards)

1
Q

nervous vs endocrine

A

nervous
- NTs
- target cells are specific
- effect is brief
- act fact

endocrine
- hormones
- target cells broad
- longer lasting effects
- take longer to act

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2
Q

exocrine glands

A

secrete products into ducts

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3
Q

endocrine glands

A

secrete hormones into ISF

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4
Q

general functions of hormones

A

regulate
- chemical comp
- metabolism
- energy balance
- contraction of smooth/cardiac muscle
- gland function
- immune system
- circadian rhythms

growth
reprodcution

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5
Q

circulating hormones

A

secreted into ISF then absorbed into bloodstream

most hormones

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6
Q

autocrine hromones

A

local hormoens that act on the same cell that secreted them

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7
Q

paracrine hormones

A

local hormoens secreted into ISF anf act on nearby cells only

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8
Q

local hormones are inactivated _______ than circulating hormones

waht are they inactivated by?

A

quicker

inactivated by liver, excreted by kidneys

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9
Q

general mechanism of hormone action (2)

A
  1. hormone binds to receptor
  2. binding of hormone triggers a response in the target cell
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10
Q

example of responses in target cells

A

new molecule porduction
change of membrane permeability
stimulate transport
alter rate of metabilic reaction
cause contraction

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11
Q

classes of hormones (2)

A

lipid soluble
- hydrophibic
- usually bound to transport proteins for transport

water soluble
- hydrophilic
- circulate freely in plasma

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12
Q

why are hormone classes important

A

because chemical properties of the hormones determine where the bind to their receptors

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13
Q

lipid soluble hormones (examples)

A

steroids
thyroid hormones (t3/t4)
eicosanoidsw

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14
Q

waht do transport proteins do for lipid soluble hormones

A

increase hormone solubility in blood
increase molecule size
provide ready hormones in blood stream

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15
Q

action of lipid soluble hormones (4)

A
  1. free hormones (once released) diffuses thru phospholipid bilayer of target cell
  2. binds to receptor in cell
  3. new proteins are syntehsized
  4. cells activity changes due to new proteins
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16
Q

water soluble hormones (2)

A

amine hormones (modified amino acids)
- NE/E

peptide/protein hormones

hydrophilic

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17
Q

signalling cascade process (not steps, general)

A

process of the action of water soluble hormones

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18
Q

steps in a signalling cascade (7)

A
  1. hormone cannot diffuse across cell membrane
  2. hormone binds to membrane on a receptor
    - this activates a G protein, where the signalling cascade is triggered, which activates adenylyl cyclase (very similar to smell)
  3. in cytosol, adenylyl cyclase converts ATP to second messenger (can be cGMP/cAMP/IP3, etc)
  4. second messenger activates protein kinases
  5. Protein kinases activate proteins by phosphorylation
  6. modified proteins produce a physiological response
  7. phosphodiesterase inactivated cAMP (or second messenger)
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19
Q

non-covalent bonds between receptors and hormones are:

A

reversible

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20
Q

3 factors that determine the level of activation in a target cell

A
  1. hormone conc in blood
  2. number of receptors on the target
  3. influence of other hormones
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21
Q

influence of other hormones can be synergistic or antagonistic, what does htis mean

A

synergistic - both hormones wokr togehter
- eg. epinephrine and glucagon both stimualt glycogen breakdown

antagonistic - hromones work against each other
- eg. insulin stimulate glycogen synthesis, but glucagon = breakdown

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22
Q

most hormones are released in:

A

short bursts

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23
Q

regulation of hormone secretion at a cellular level (3)
(number, what is it, example)

A
  1. humoral stimuli: chemical changes in blood
    - hormone is released in response to changing blood chemicals
    eg. Ca in blood regulates parathyroid hormone
  2. neural stimuli: signals from nervous system
    - nerve impulses trigger release of hormones from certain glands
    eg. posterior pituitary
  3. hormonal stimuli: presence of other hormones
    - hormones can be released in response to other hormones
    eg. ACTH (adrenocorticotropic H) from anterior pituitary stimulates release of cortisol from suprarenal cortex
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24
Q

how many receptors are there on a target cell

A

2k-100k

higher number = cell is more sensitive

receptors are constantly being made and destroyed, so number can change based on feedback mechanisms

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25
receptor upregulation
start - low receptor density - weak response end - increase receptor density - increased sensitivity maintains homeostasis
26
receptor downregulation
start - high receptor density - strong response end - low receptor density - weak response maintains homeostasis
27
feedback loops contain: (5) (in endocrine case)
stimulus endocrine cell signalling hormone target cell response
28
hypothalamus endocrine function
regulated ANS, temp, thirst, hunger serves as a link between nervous and endocrine systems
29
hypothalamus can make up to
9 hormones
30
pituitary gland anatomy
anterior - 75% - epitehlial tissue posterior - 25% - neural tissue
31
hypophyseal portal system
where the hypothalamus secreted releasing and inhibiting hormones into to control secretion of anterior pituitary hormones
32
hypophyseal portal system controls:
anterior pituitary hormones
33
superior hypophyseal artery location
top left of diagram, leading onto infundibular stalk connects to primary plexus at the top
34
hypophyseal portal veins location
two veins extending down from primary plexus of the portal system to the secondary plexus in anterior pituitary
35
primary plexus of hypophyseal portal system location
top of infundibular stalk
36
secondary plexus of hypophyseal portal system location
anterior pituitary
37
portal system circulation pathway
blood flows from one capillary network, thru portal vein, to another capillary network to heart
38
hypophyseal veins
lead out of anterior pituitary inferiorly to take hormones to the heart and into circulation
39
control of anterior pituitary secretion (4)
1. hormones produced by neurosecretory cells in hypothalamus reach axon terminal 2. upon excitation of cells, hormones are released in vesicles and diffuse into blood via plexus of hypophyseal portal system 3. hormones enter portal veins and travel to secondary plexus in anterior pituitary. they diffuse into the blood stream, and stimulate specific hormones to be released 4. anterior pituitary hormones drain into hypophyseal veins to join circulation
40
hypothalamus hormones (5) + (2)
growth hormone RH thyrotropin RH corticotropin RH prolactin RH gonadotropin RH RH = releasing hormone growth hormone IH prolactin IH IH = inhibiting hormone all hormones go to anterior pituitary
41
thyrotropin RH sitmulates
release of thyroid stimulating hormone from AP
42
corticotropin RH stimulates
release of adrenocorticotropic hormone from AP
43
gonadotropin RH stimulates (2)
release of LH and FSH from AP
44
cells of the anterior pituitary (5)
corticotrophic cells prolactin cells somatotrophic cells thyrotrophic cells gonadotrophic cells
45
corticotrophic cells secrete
adrenocorticotropic hormone
46
prolactin cells secrete
prolactin
47
somatotrophic cells of the AP secrete
grwoth hromone
48
thyrotrophic cells secertte
thyroid stimulating hormones
49
gonadotrophic cells secrete
FSH and LH
50
hormones from AP and what cells secrete them (70
GH - somatotrophic cells TSH - thyrotrophic cells FSH/LH - gonadotrophic cells PRL - prolactin cells ACTH - corticotrophic cells MSH - corticotrophic cells
51
MSH`
melanocyte stimulating hormone
52
how are releasing and inhibiting hromones of the AP regulated?
by the hypothalamus
53
how are thyrotrophic, corticotrophic, and gonadotrophic hormones form the AP regulated?
by blood levels of the target gland hormones
54
growth hormone full chart
low glucose/stress stimulates: hypothalamus to release GHRH, this binds to somatotrophic cells in AP. growth hormone is released, and does 3 things: - produce isulin like growth factors (IGFs) - glycogenolysis/gluconeogenesis in liver cells - lipolysis in adipose cells IGFs support muscle growth, bone growth, development other two (lipolysis and glycogenolysis) increase blood glucose
55
main function of growth hormone
to produce insulin like growth factors that stimulate growth
56
IGFs functions
increase cell growth and division by: - increase amino acid uptake - increasing protein synthesis - stimulating glycogen breakdown to increase blood glucose
57
abnormal secretion of growth hormone can lead to (hypo/hyper)
hyposecretion - pituitary dwarfism hypersecretion - gigantism - in adults, large extremities (acromegaly) - in kids, abnormally tall
58
excess growth hormone can lead to
hyperglycemia - increased blood glucoes pancreas constantly releasing insulin beta cell burnout - no insulin - can cause diabetes mellitus
59
what stimulates GH secretion (3)
low glucose levels, low blood fatty acids, high blood amino acids
60
thyrotropin releasing hormone stimulates
the release of thyroid stimulating hormone from thyrotrophic cells of the AP
61
TSH stimulates:
secretion of t3 and t4 (triiodothyronine, thyroxin) from thyroid gland
62
what inhibits thyrotropin RH and thyroid stimulating hormone?
high levels of t3/t4 in teh blood (negative feedback loop)
63
gonadotropin RH stimulates
release of FSH and LF from gonadotrophic cells of teh AP
64
functions of FSH in males/females
males - stimulates sperm production females - oocyte maturation - estrogen porduction
65
functions of LH in males/females
males - stimulates test production females - ovulation - formation of corpus luteum
66
what stimulates FSH and GnRH suppression
estrogen in females, test in males negative feedback loop
67
what does prolactin RH stimulate
release of prolactin from the prolactin cells of the AP
68
when is PRL released?
during pregnancy together with other hormones
69
functions of prolactin
controls milk production oxytocin controls ejection
70
hypersecretion of PRL can lead to (male/female)
female - galactorrhea (excessive lactation) - loss of menstruation males - erectile dysfunction
71
what does corticotropin RH stimulate
release of adrenocorticotropic from corticotrophic cells of AP release of melanocyte stimulating hormone from corticotrophic cells of AP
72
waht does ACTH stimulate
the suprarenal cortex to release glucocorticoids like cortisol
73
how is prolactin secretion stopped?
by prolactin inhibiting hormone from hypothalamus (aka dopamine)
74
CRH
corticotropin releasing hormone
75
how are CRH and ACTH inhibited?
by glucocorticoids in the blood (what ACTH stimulated release of) negative feeback
76
what inhibits MSH
dopamine
77
what inhibits hormones released form corticotropic cells of the AP
dopamine
78
MSH functions
increase skin pigmentation may playa roole in brain functions
79
negative feedback loops control the secretions of: (3)
thyrotropic cells gonadotrophic cells corticotrophic cells
80
hypothalamus releases inhibiting hormones to control the secretions of (2)
somatotrophic cells prolactinc cells
81
function of posterior pituitary
stored and release oxytocin and ADH does not synthesize hormones
82
pathway of posterior pituitary hormones (
1. synthesized in neurosecretory cells of hypothalamus 2. travel from hypothalamus-hypophyseal tract into posterior pituitary 3. exocytosis of hormones into capillaries of PP 4. travel out thru hypophyseal vein
83
neurosecretory cells of the hypothalamus function
synthesize oxytocin and antidiuretic hormone
84
ADH function
decrease water loss from the body
85
osmoreceptors in hypothalamus
monitor blood osmolarity
86
baroreceptors/atrial voluume receptors ( what do tehy detect)
blood volume
87
when is ADH secreted
when there is an increase in blood osmolarity or a decrease in blood volume
88
effects of ADH
decreased urine output vasoconstriction - increase BP
89
another name for ADH
vasopressin
90
where is ADH transported to? (2)
kidneys smooth muscle in arteriole walls
91
ADH flow chart of stuff it does
low blood vol/pressure/high osmolarity stimulates, neurosecretory cells in PP to make ADH. ADH binds to arteriole muscle/sweat glands/principal cells of nephron tubules in kidneys to: - arteriole - vasoconstrict - sweat glands - inhibit sweating - kidneys - increase water reabsorption all of these increase blood volume/pressure and maintian normal osmolarity
92
feedback loop for ADH
negative stim - low BP/vol/high osmo receptor - baro/osmo receptors control centre - hypothalamus effector - principal cells of kidney/sweat glands/arterioles response - raise in BP/vol/lower osmo
93
diabetes insipidus
passing a lot of dilute urine caused by hyposecretion of ADH can be neuro or nephrogenic urine output increases rapidly due to no water retention cuz no ADH treated with synthetic ADH
94
oxytocin functions (during/after delivery)
targets smooth muscle in uterus and breasts during - muscle contraction of uterus after - expulsion of placenta stimualtes ejection of milk from breasts socail bonding and sexual activties in both sexes can enhance brain function in children with autism
95
thyroid gland produces:
t3/t4 and calcitonin triiodothyronine thyroxine
96
what connects teh thyroid gland
isthmus
97
thyroid follicle
a circle of T thyrocytes with some C thyrocytes on the outside of it. lumen filled with thyroglobulin
98
thyroglobulin
sac of stored proteins
99
follicular cells
in thyroid gland these cells use thyroglobulin from thyroid follicles to produce t3/t4 along with tyrosine and iodine
100
C thyrocytes produce / are located
produce calcitonin located on the outside of thyroid follicles
101
calcitonin function
lowers blood Ca
102
TRH/TSH/Thyroid hormone flow chart
low blood glucose stimulates hypothalamus to release TRH (thyrotropin releasing hormone) whihc bind to thyrotrophic cells in AP that will then secrete TSH. TSH binds to follicular cells in the thyroid gland and produce thyroid hrmones (t3/4)
103
synthesis and secretion of thyroid hormones in 8 steps
1. iodide trapping - iodide is transported into T thyrocytes 2. synthesis of thyroglobulin (TGB) - TGB is release into lumen of follicle 3. oxidation of iodide - this is required for iodide to bind to tyrosine 4. iodination of tyrosine to form colloid - this step makes T1/T2 5. coupling of T1/T2 - this step makes T3/T4 (2+2=4) 6. pinocytosis and digestion of colloid - this releases t3 and t4 molecules 7. secretion of thyroid hormones - into capillaries 8. transport in blood by thyroxine binding globulin (transport protein)
104
t3/t3 flow chart when binded to body cells
binds to body cells: increases BMR, glucose metabolism, lipolysis, protein metabolism all this leads to increased ATP production and increased body temperature
105
t3/t4 flow chart when binded to muscle cells in blood vessels/heart
binds to muscle in vessels/heart: increases muscle contraction, vasoconstriction, BP, increase effects of NE/E all this leads to enhancee delivery of fuel to cell with hihg metabolic need
106
what controls secretion of t3/t4?
hypothalamus regulates release by releasing thyrotropin RH. this cause AP to release thyroid stimulating hormone from thyrotrophic cells. this stimulates release/production of T3/T4 in follicular cells of thyroid. elevated levels of T3 inhibit TRH and TSH release (negative feedback)
107
affects of thyroid hormones (T3/4)
affects almost all body cells increased BMR - protein syntheis - more ATP produced work with growth hormone and IGF to accelerate body growth
108
calcitonin flow chart
high Ca in blood stimulates parafollicular cells (C thyrocytes) to secrete calcitonin. this stimulates osteoblasts (and inhibits osteoclasts) to take up more Ca in blood and deposit into bone matrix this lowers blood Ca controlled by negative feedback loop
109
hypothyroidism can result in
dwarfism and severe mental disability in adults: sensitivity to cold, weight gain, edema
110
hyperthyroidism can lead to
graves disease - autoimmune disease that causes production of antibodies that mimic TSH - causes weight loss, anxiety, edema behind eyes goiter - enlarged thyroid gland
111
parathyroid glands
two in each lobe of thyroid has dense principal parathyroid cells that produce parathyroid hormone
112
parathyriod hormone flowchart
decrease in Ca in blood stimulates principal cells of parathyroid gland to secrete parathyroid hormone. this stimulates: - osteoclasts to: increase number and activity - kindeys: slow Ca and Mg loss in urine these lead to an increase of blood Ca and Mg
113
parathyroid hormone is the main regulator of
HPO4 levels in blood
114
parathyroid hormone function
acts to increse Ca and Mg and decrease phosphate in blood
115
what does parathyroid hormone do to achieve its goal of raising Ca and Mg in blood
increase osteoclast activity increase reabsorption of Ca and Mg and excretion of phosphate by kindeys promotes formation of calcitriol by kidneys whihc enhances Ca and MG absorption in intestinal cells
116
what opposes parathyroid hormone?
calcitonin this decreases blood calcium by inhibiting osteoclasts
117
hypoparathyroidism can lead to
low levels of Ca/Mg in blood can result in muscle spasms, or tetanus
118
hyperparathyroidism can result in
high Ca in blood promote kidney stones excessive bone resorption causes osteoporosis
119
suprarenal glands
two portions (medulla and cortex)
120
suprarenal cortex produces
steroid hormones
121
suprarenal medulla produces
E and NE
122
zones of suprarenal glands form super to deep and what they secrete
zona glomerulosa - secretes mineralocortiocids (aldosterone) zona fasciculata - secretes glucocorticoids (cortisol) zona reticularis - secretes androgens (dehydroepiandrosterone)
123
cortisol function
provide stress resistance - promote fat and protein breakdown to make ATP - gluconeogenisis - convert AAs into glucose for ATP - enhance vasoconstriction anti inflammatory and immune effects - decrease capillary permeability - delay tissue repair - used in organ transplants
124
ACTH and corticol flow chart
low blood glucose stimulates: corticotrophic cells in AP to relase ACTH. ACTH bind to cells in zona fasciculata of suprarenal cortex to produce cortisol. cortisol does 3 things - glycogenolysis/gluconeogenesis to liver cells - lipolysis - protein breakdown in muscle cells all of these options lead to gluconeogenesis which increases glucose levels
125
gluconeogenesis
process of glucose being made
126
glycogenolysis
process that breaks down glycogen to make glucose
127
cushings syndrome
high levels of circulating cortisol (hypersecretion) hyperglycemia poor wound healing infection susceptibility fat redistribution
128
what stimulates the release of glucocorticoids
low blood levels of it
129
how does cortisol get released (whole loop)
stim - low blood levels of cortisol receptors - neurosecretory cells of hypothalamus - release corticotropin RH control centre - AP - releases ACTH effectors - suprarenal cortex - zona fasciculata releases cortisol
130
aldosterone functions
acts mainly on nephrons promotes Na and K reabsorption in kidneys helps regulate BP and Blood vol by water reabsorption promotes excretion of H in urine to prevent acidosis
131
Renin-angiotensin-aldosterone pathway flowchart
dehydration/Na deficiency/hemorrhages causes a decrease in blood Vol and therefore BP. this causes juxtaglomerular cells of kidney to make renin. renin converts angiotensin to angiotensin 1. angiotensin 1 travels to the lungs to be converted into angiotensin 2 by ACE (converting enzyme) this causes 2 things: - vasoconstriction of arterioles - increase aldosterone secretion, which causes increased Na and water reabsorption, while increased excretion of K and H in urine both of these things eventually lead to rising BP until normal
132
RAA pathway steps (16)
1. RAA is initiated (dehydration, low NA, hemorrhage) 2. decreases blood vol 5. decreased BP 4. low BP stimulates renin release from kidneys 5. renin blood level increases 6. renin converts liver made angiotensin to angiotensin 1 7. AG 1 levels in blood rise 8. Angiotensin converting enzyme converts AG 1 into AG2 9. AG 2 levels in blood rise 10. Ag 2 stimulates aldosterone secretion from suprarenal cortex 11. aldosterone travels to kidneys 12. aldosterone increases Na reabsorption which causes water reabsorption by osmosis, and K and H secretion in urine 13. water reabsorption = higher blood vol 14. higher blood vol = BP returns to normal 15. AG 2 stimulates constriction in arterioles to raise BP
133
what stimulates aldosterone secretion
angiotensin 2 (technically) increase K in blood low BP dehydration
134
does high or low Na promote aldosterone secretion
low
135
main androgen
dehydroepiandrosterone
136
androgens effects (beofre/after puberty)
before - growth in both sexes after - insignificant in males - libido in girls, converted to estrogens (sole source of estrogens after menopause)
137
waht causes chromaffin cells to release hormones
NTs from preganglionic neurons (ACh)
138
E and NE flow chart (first on is release, second is effects)
increased sympathetic response stimulates chromaffin cells in suprarenal medulla to release NE and E NE and E bind to 3 things: liver cell - glycogenolysis - increase glucose cardiac muscle - increase contraction, HR, CO, BP smooth muscle of vessels - increase blood flow into vitals organs, decrease thru parasymapthetic stuff like repoductive organs
139
pancreas
both and endocrine and exocrine gland 99% of cells are acini (for digestion) 1-2% are islets (endocrine cells)
140
pancreatic islets subtypes and what they produce
alpha cells - glucagon - raise blood glucose beta cells - insulin - blood glucose delta cells - somatostatin - inhibits insulin/glucagon/hGH pancreatic polypeptide cells - pancreatic polypeptide - inhibits somatostatin secretion
141
pancreatic islet anatomy
alpha - purple beta - orange (lots) delta - violet Pancreatic polypeptide - yellow on border
142
hyperglaecemia
low blood glucose
143
stimuli of glucagon release
hypoglaecemia
144
what will the release of glucagon increase (3)
glycogenolysis gluconeogenesis lipolysis
145
what is the sitmulus for insulin release
hyperglyaecemia
146
what will the release of insulin cause (4)
decrease in gluconeogenesis increase glycogenesis (NOT glycogenolysis) increase lipogenesis
147
the level of blood glucose controls:
secretion of glucagon and insulin via negative feedback
148
diabetes mellitus
inability to produce insulin two types 1 - cause by absolute defiencey of insulin 2 - caused by decreased sensitivity to insulin characterized by hyperglycemia (high blood glucose) can lead to excess urination and thirst, excessive eating
149
ovaries hormones
two estrogens (estradiol/estrone) progesterone inhibin relaxin
150
inhibin
inhibits FSH secretion
151
estrogens and progesterone functions
regulate reproductive cycle, pregnanacy maintenance, prepare mammary glands for lactation, maintain female sex traits
152
relaxin
helps dilate cervix during labour, increases pubic symphysis flexibility
153
testes hormones
testosterone and inhibin
154
testosterone functions
regulate sperm production, maintain male sex traits
155
pineal gland
pinealocytes secretes melatonin which is involved in circadian rhythm located in epithalamus
156
thymus hormones
thymosin thymic factor thymic humoral factor thymopoietin
157
thymic hormones functions
maturation of t lymphocytes
158
the heart secretes ______. what does it do
atrial natruiretic peptide in response ot high BP acts on nephons to increase Na and water secretion
159
kidneys release: what does it do
erythropoietin in response to hypoxia stimulates RBC production in red marrow
160
stress response ( types of stress0
eustress - helpful, everyday stress that prepares us for challenges distress - harmful stress
161
stressor
stimulus that produces a stress response
161
key regulator of stress reponse
hypothalamus
162
3 stages of a stress response
fight or flight resistance reaction exhaustion
162
fight or flight stage of stress response
stage 1 - hypothalamus stimulates bodys resources for immediate activity - sympathetic NS kicks in - glucose supply to organs - RAA pathway active to retain water and BP
163
resistance reaction stage of stress response
stage 2 -involves CRH, GHRH, TRH - lasts longer than fight/flight - increases glucose and ATP to active cells
164
exhaustion stage of stress response
stage 3 - resistance stage fails - prolonged exposure to hormones - suppression immune system - muscle wasting
165
the stress response is a:
neural and hormonal response