lecture 11/13 - endocrine Flashcards
nervous vs endocrine
nervous
- NTs
- target cells are specific
- effect is brief
- act fact
endocrine
- hormones
- target cells broad
- longer lasting effects
- take longer to act
exocrine glands
secrete products into ducts
endocrine glands
secrete hormones into ISF
general functions of hormones
regulate
- chemical comp
- metabolism
- energy balance
- contraction of smooth/cardiac muscle
- gland function
- immune system
- circadian rhythms
growth
reprodcution
circulating hormones
secreted into ISF then absorbed into bloodstream
most hormones
autocrine hromones
local hormoens that act on the same cell that secreted them
paracrine hormones
local hormoens secreted into ISF anf act on nearby cells only
local hormones are inactivated _______ than circulating hormones
waht are they inactivated by?
quicker
inactivated by liver, excreted by kidneys
general mechanism of hormone action (2)
- hormone binds to receptor
- binding of hormone triggers a response in the target cell
example of responses in target cells
new molecule porduction
change of membrane permeability
stimulate transport
alter rate of metabilic reaction
cause contraction
classes of hormones (2)
lipid soluble
- hydrophibic
- usually bound to transport proteins for transport
water soluble
- hydrophilic
- circulate freely in plasma
why are hormone classes important
because chemical properties of the hormones determine where the bind to their receptors
lipid soluble hormones (examples)
steroids
thyroid hormones (t3/t4)
eicosanoidsw
waht do transport proteins do for lipid soluble hormones
increase hormone solubility in blood
increase molecule size
provide ready hormones in blood stream
action of lipid soluble hormones (4)
- free hormones (once released) diffuses thru phospholipid bilayer of target cell
- binds to receptor in cell
- new proteins are syntehsized
- cells activity changes due to new proteins
water soluble hormones (2)
amine hormones (modified amino acids)
- NE/E
peptide/protein hormones
hydrophilic
signalling cascade process (not steps, general)
process of the action of water soluble hormones
steps in a signalling cascade (7)
- hormone cannot diffuse across cell membrane
- 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) - in cytosol, adenylyl cyclase converts ATP to second messenger (can be cGMP/cAMP/IP3, etc)
- second messenger activates protein kinases
- Protein kinases activate proteins by phosphorylation
- modified proteins produce a physiological response
- phosphodiesterase inactivated cAMP (or second messenger)
non-covalent bonds between receptors and hormones are:
reversible
3 factors that determine the level of activation in a target cell
- hormone conc in blood
- number of receptors on the target
- influence of other hormones
influence of other hormones can be synergistic or antagonistic, what does htis mean
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
most hormones are released in:
short bursts
regulation of hormone secretion at a cellular level (3)
(number, what is it, example)
- humoral stimuli: chemical changes in blood
- hormone is released in response to changing blood chemicals
eg. Ca in blood regulates parathyroid hormone - neural stimuli: signals from nervous system
- nerve impulses trigger release of hormones from certain glands
eg. posterior pituitary - 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
how many receptors are there on a target cell
2k-100k
higher number = cell is more sensitive
receptors are constantly being made and destroyed, so number can change based on feedback mechanisms
receptor upregulation
start
- low receptor density
- weak response
end
- increase receptor density
- increased sensitivity
maintains homeostasis
receptor downregulation
start
- high receptor density
- strong response
end
- low receptor density
- weak response
maintains homeostasis
feedback loops contain: (5) (in endocrine case)
stimulus
endocrine cell
signalling hormone
target cell
response
hypothalamus endocrine function
regulated ANS, temp, thirst, hunger
serves as a link between nervous and endocrine systems
hypothalamus can make up to
9 hormones
pituitary gland anatomy
anterior
- 75%
- epitehlial tissue
posterior
- 25%
- neural tissue
hypophyseal portal system
where the hypothalamus secreted releasing and inhibiting hormones into to control secretion of anterior pituitary hormones
hypophyseal portal system controls:
anterior pituitary hormones
superior hypophyseal artery location
top left of diagram, leading onto infundibular stalk
connects to primary plexus at the top
hypophyseal portal veins location
two veins extending down from primary plexus of the portal system to the secondary plexus in anterior pituitary
primary plexus of hypophyseal portal system location
top of infundibular stalk
secondary plexus of hypophyseal portal system location
anterior pituitary
portal system circulation pathway
blood flows from one capillary network, thru portal vein, to another capillary network to heart
hypophyseal veins
lead out of anterior pituitary inferiorly
to take hormones to the heart and into circulation
control of anterior pituitary secretion (4)
- hormones produced by neurosecretory cells in hypothalamus reach axon terminal
- upon excitation of cells, hormones are released in vesicles and diffuse into blood via plexus of hypophyseal portal system
- 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
- anterior pituitary hormones drain into hypophyseal veins to join circulation
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
thyrotropin RH sitmulates
release of thyroid stimulating hormone from AP
corticotropin RH stimulates
release of adrenocorticotropic hormone from AP
gonadotropin RH stimulates (2)
release of LH and FSH from AP
cells of the anterior pituitary (5)
corticotrophic cells
prolactin cells
somatotrophic cells
thyrotrophic cells
gonadotrophic cells
corticotrophic cells secrete
adrenocorticotropic hormone
prolactin cells secrete
prolactin
somatotrophic cells of the AP secrete
grwoth hromone
thyrotrophic cells secertte
thyroid stimulating hormones
gonadotrophic cells secrete
FSH and LH
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
MSH`
melanocyte stimulating hormone
how are releasing and inhibiting hromones of the AP regulated?
by the hypothalamus
how are thyrotrophic, corticotrophic, and gonadotrophic hormones form the AP regulated?
by blood levels of the target gland hormones
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
main function of growth hormone
to produce insulin like growth factors that stimulate growth
IGFs functions
increase cell growth and division by:
- increase amino acid uptake
- increasing protein synthesis
- stimulating glycogen breakdown to increase blood glucose
abnormal secretion of growth hormone can lead to (hypo/hyper)
hyposecretion
- pituitary dwarfism
hypersecretion
- gigantism
- in adults, large extremities (acromegaly)
- in kids, abnormally tall
excess growth hormone can lead to
hyperglycemia - increased blood glucoes
pancreas constantly releasing insulin
beta cell burnout - no insulin
- can cause diabetes mellitus
what stimulates GH secretion (3)
low glucose levels, low blood fatty acids, high blood amino acids
thyrotropin releasing hormone stimulates
the release of thyroid stimulating hormone from thyrotrophic cells of the AP
TSH stimulates:
secretion of t3 and t4 (triiodothyronine, thyroxin) from thyroid gland
what inhibits thyrotropin RH and thyroid stimulating hormone?
high levels of t3/t4 in teh blood (negative feedback loop)
gonadotropin RH stimulates
release of FSH and LF from gonadotrophic cells of teh AP
functions of FSH in males/females
males
- stimulates sperm production
females
- oocyte maturation
- estrogen porduction
functions of LH in males/females
males
- stimulates test production
females
- ovulation
- formation of corpus luteum
what stimulates FSH and GnRH suppression
estrogen in females, test in males
negative feedback loop
what does prolactin RH stimulate
release of prolactin from the prolactin cells of the AP
when is PRL released?
during pregnancy together with other hormones
functions of prolactin
controls milk production
oxytocin controls ejection
hypersecretion of PRL can lead to (male/female)
female
- galactorrhea (excessive lactation)
- loss of menstruation
males
- erectile dysfunction
what does corticotropin RH stimulate
release of adrenocorticotropic from corticotrophic cells of AP
release of melanocyte stimulating hormone from corticotrophic cells of AP
waht does ACTH stimulate
the suprarenal cortex to release glucocorticoids like cortisol
how is prolactin secretion stopped?
by prolactin inhibiting hormone from hypothalamus (aka dopamine)
CRH
corticotropin releasing hormone
how are CRH and ACTH inhibited?
by glucocorticoids in the blood (what ACTH stimulated release of)
negative feeback
what inhibits MSH
dopamine
what inhibits hormones released form corticotropic cells of the AP
dopamine
MSH functions
increase skin pigmentation
may playa roole in brain functions
negative feedback loops control the secretions of: (3)
thyrotropic cells
gonadotrophic cells
corticotrophic cells
hypothalamus releases inhibiting hormones to control the secretions of (2)
somatotrophic cells
prolactinc cells
function of posterior pituitary
stored and release oxytocin and ADH
does not synthesize hormones
pathway of posterior pituitary hormones (
- synthesized in neurosecretory cells of hypothalamus
- travel from hypothalamus-hypophyseal tract into posterior pituitary
- exocytosis of hormones into capillaries of PP
- travel out thru hypophyseal vein
neurosecretory cells of the hypothalamus function
synthesize oxytocin and antidiuretic hormone
ADH function
decrease water loss from the body
osmoreceptors in hypothalamus
monitor blood osmolarity
baroreceptors/atrial voluume receptors ( what do tehy detect)
blood volume
when is ADH secreted
when there is an increase in blood osmolarity or a decrease in blood volume
effects of ADH
decreased urine output
vasoconstriction - increase BP
another name for ADH
vasopressin
where is ADH transported to? (2)
kidneys
smooth muscle in arteriole walls
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
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
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
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
thyroid gland produces:
t3/t4 and calcitonin
triiodothyronine
thyroxine
what connects teh thyroid gland
isthmus
thyroid follicle
a circle of T thyrocytes with some C thyrocytes on the outside of it. lumen filled with thyroglobulin
thyroglobulin
sac of stored proteins
follicular cells
in thyroid gland
these cells use thyroglobulin from thyroid follicles to produce t3/t4 along with tyrosine and iodine
C thyrocytes produce / are located
produce calcitonin
located on the outside of thyroid follicles
calcitonin function
lowers blood Ca
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)
synthesis and secretion of thyroid hormones in 8 steps
- iodide trapping
- iodide is transported into T thyrocytes - synthesis of thyroglobulin (TGB)
- TGB is release into lumen of follicle - oxidation of iodide
- this is required for iodide to bind to tyrosine - iodination of tyrosine to form colloid
- this step makes T1/T2 - coupling of T1/T2
- this step makes T3/T4 (2+2=4) - pinocytosis and digestion of colloid
- this releases t3 and t4 molecules - secretion of thyroid hormones
- into capillaries - transport in blood by thyroxine binding globulin (transport protein)
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
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
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)
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
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
hypothyroidism can result in
dwarfism and severe mental disability
in adults: sensitivity to cold, weight gain, edema
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
parathyroid glands
two in each lobe of thyroid
has dense principal parathyroid cells that produce parathyroid hormone
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
parathyroid hormone is the main regulator of
HPO4 levels in blood
parathyroid hormone function
acts to increse Ca and Mg and decrease phosphate in blood
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
what opposes parathyroid hormone?
calcitonin
this decreases blood calcium by inhibiting osteoclasts
hypoparathyroidism can lead to
low levels of Ca/Mg in blood
can result in muscle spasms, or tetanus
hyperparathyroidism can result in
high Ca in blood
promote kidney stones
excessive bone resorption causes osteoporosis
suprarenal glands
two portions (medulla and cortex)
suprarenal cortex produces
steroid hormones
suprarenal medulla produces
E and NE
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)
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
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
gluconeogenesis
process of glucose being made
glycogenolysis
process that breaks down glycogen to make glucose
cushings syndrome
high levels of circulating cortisol (hypersecretion)
hyperglycemia
poor wound healing
infection susceptibility
fat redistribution
what stimulates the release of glucocorticoids
low blood levels of it
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
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
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
RAA pathway steps (16)
- RAA is initiated (dehydration, low NA, hemorrhage)
- decreases blood vol
- decreased BP
- low BP stimulates renin release from kidneys
- renin blood level increases
- renin converts liver made angiotensin to angiotensin 1
- AG 1 levels in blood rise
- Angiotensin converting enzyme converts AG 1 into AG2
- AG 2 levels in blood rise
- Ag 2 stimulates aldosterone secretion from suprarenal cortex
- aldosterone travels to kidneys
- aldosterone increases Na reabsorption which causes water reabsorption by osmosis, and K and H secretion in urine
- water reabsorption = higher blood vol
- higher blood vol = BP returns to normal
- AG 2 stimulates constriction in arterioles to raise BP
what stimulates aldosterone secretion
angiotensin 2 (technically)
increase K in blood
low BP
dehydration
does high or low Na promote aldosterone secretion
low
main androgen
dehydroepiandrosterone
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)
waht causes chromaffin cells to release hormones
NTs from preganglionic neurons (ACh)
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
pancreas
both and endocrine and exocrine gland
99% of cells are acini (for digestion)
1-2% are islets (endocrine cells)
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
pancreatic islet anatomy
alpha - purple
beta - orange (lots)
delta - violet
Pancreatic polypeptide - yellow on border
hyperglaecemia
low blood glucose
stimuli of glucagon release
hypoglaecemia
what will the release of glucagon increase (3)
glycogenolysis
gluconeogenesis
lipolysis
what is the sitmulus for insulin release
hyperglyaecemia
what will the release of insulin cause (4)
decrease in gluconeogenesis
increase glycogenesis
(NOT glycogenolysis)
increase lipogenesis
the level of blood glucose controls:
secretion of glucagon and insulin via negative feedback
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
ovaries hormones
two estrogens (estradiol/estrone)
progesterone
inhibin
relaxin
inhibin
inhibits FSH secretion
estrogens and progesterone functions
regulate reproductive cycle, pregnanacy maintenance, prepare mammary glands for lactation, maintain female sex traits
relaxin
helps dilate cervix during labour, increases pubic symphysis flexibility
testes hormones
testosterone and inhibin
testosterone functions
regulate sperm production, maintain male sex traits
pineal gland
pinealocytes secretes melatonin which is involved in circadian rhythm
located in epithalamus
thymus hormones
thymosin
thymic factor
thymic humoral factor
thymopoietin
thymic hormones functions
maturation of t lymphocytes
the heart secretes ______. what does it do
atrial natruiretic peptide in response ot high BP
acts on nephons to increase Na and water secretion
kidneys release: what does it do
erythropoietin in response to hypoxia
stimulates RBC production in red marrow
stress response ( types of stress0
eustress
- helpful, everyday stress that prepares us for challenges
distress
- harmful stress
stressor
stimulus that produces a stress response
key regulator of stress reponse
hypothalamus
3 stages of a stress response
fight or flight
resistance reaction
exhaustion
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
resistance reaction stage of stress response
stage 2
-involves CRH, GHRH, TRH
- lasts longer than fight/flight
- increases glucose and ATP to active cells
exhaustion stage of stress response
stage 3
- resistance stage fails
- prolonged exposure to hormones
- suppression immune system
- muscle wasting
the stress response is a:
neural and hormonal response
