YouTube Transcript:
Costanzo Physiology (Chapter 9B) Endocrine Physiology: Hypothalamus/Pituitary axis || Study This!

hello and welcome to the second part of
the endocrine physiology chapter of
costanzo's physiology textbook
in this video we are going to go over
the hypothalamic pituitary axis
which is essentially the mastermind
that's able to control the majority of
our endocrine systems
it consists of the hypothalamus which is
clearly up in the brain which we covered
in the neurology portion
and then also the pituitary gland that
kind of sits just underneath it
the pituitary gland is made up of two
separate glands
or two separate lobes the posterior lobe
which is called
also the neural hypothesis mainly
because it's made out of neuron cells
and secretes neuropeptides and then we
have the anterior lobe
which is also called the adeno
hypothesis which is actually made out of
endocrine cells
themselves so you can see it over here
figure 9.9 here
where we have the posterior lobe made
out of neurons and you can see that the
cell body
of the neuron is actually located within
the hypothalamus
and then also the anterior lobe made out
of endocrine cells
which is connected with the hypothalamus
with a bloodstream its own hypothalamic
hypophyseal portal vessels so this is
essentially the venous system
to the hypothalamus so then the anterior
lobe of the pituitary gland receives
high concentrations
of the hormones from the hypothalamus
that does not enter the systemic
circulation
and that directs which hormones should
be released from
the anterior pituitary gland once either
the posterior or anterior pituitary
gland is stimulated to release a certain
type of hormone
that just gets released into the
systemic circulation
now the posterior pituitary gland only
secretes
two neuropeptide hormones adh
and oxytocin adh is primarily associated
with the supraoptic nuclei within the
hypothalamus
whereas oxytocin is primarily associated
with the paraventricular nuclei in the
hypothalamus
so how this works is that the hormone is
actually synthesized in the cell body of
the neuron within the hypothalamus
and then actually gets transported to
then sit in vesicles
right at the end of the neuron and the
dendrites waiting to be stimulated to be
released when told so
by the hypothalamus whether that's adh
or oxytocin we'll go into more details
about those two different hormones
later on in this video and to start with
we'll talk about the
anterior pituitary gland hormones
because we have six
major hormones here and each are
secreted by their own
cell type ending in troph for example
we have thyroid stimulating hormone or
tsh released from
thyrotropes we have acth
released from corticotropes we've got
growth hormone released from
somatotropes
prolactin from the lactotrophs and then
lastly follicular stimulating hormone
and luteinizing hormone
fsh and lh secreted by gonadotrophs so
these
tropes a particular endocrine cells
within the anterior pituitary gland that
secretes its own endocrine hormone
when stimulated too from the release of
a releasing hormone from the
hypothalamus
so hypothalamus secretes a releasing
hormone in response to a stimuli that
releasing hormone
tells the stimulating hormones from the
pituitary gland to be released which
then get released into the systemic
circulation
and then these stimulating hormones go
to their target endocrine glands within
the body
to then stimulate the release of the
hormone that they want to release
so for instance when it comes to thyroid
hormone which we'll go in in another
video
the hypothalamus releases thyroid
releasing hormone which then tells the
anterior pituitary gland to release
thyroid stimulating hormone and the
thyroid stimulating hormone tells the
thyroid gland to release
thyroid hormone so that's the basics
behind the
hypothalamic territory axis so going
through
some of the particular hormones released
from the anterior pituitary gland
specifically now
just briefly tsh fsh and lh are all
glycoproteins it goes into a little bit
of detail about their actual molecular
structure which i don't think is as
important but essentially they are all a
similar type of protein a glycoprotein
tsh we will go into more details in the
thyroid hormone video which will be
coming up shortly
and then fsh and lh will be in the
reproductive tract is
acth or adrenocorticotrophy hormone
is released from the anterior pituitary
gland to
increase the secretion of our adrenal
cortical hormones from the adrenal gland
we will go into much more details about
that actually in the adrenal video
coming up i know
this seems ridiculous that we're going
to go over these in more detail later
but these are the major hormones that we
will be covering in much more detail
in a later video so acth is slightly
different to these other ones and how it
is formed within the anterior pituitary
gland you can see that
ac th actually comes from originally
this molecule called pomc
or pro opio melanocortin the main point
here
is that although we get acth getting
produced we do have these
other and the fragments of acth that can
also have a minor effect and more
importantly if we have a high production
of acth we will get increased of these
other fragments
and more important clinically is the
production of
the melanocytes stimulating hormones the
msh hormones
so these hormones will actually cause
skin pigmentation so then that will
cause
clinical signs in the presence of
excessive acth or end up with
increased skin pigmentation so we'll go
into growth hormone in more detail
now so growth hormone is also released
from the anterior pituitary remember
from the somatotropes
the growth hormone as the name implies
is important for growth
so it does that by altering our protein
carbohydrate and fat metabolism
it gets stimulated to be released from
the anterior pituitary gland
due to growth hormone releasing hormone
from the
hypothalamus and that occurs in a
pulsatile way every
roughly two hours and also has some
other stimulatory
factors as well all noted in table 9.4
here
in addition to its inhibitory factors
the best way to think about this
is that anything that will be inhibiting
growth so let's say you don't have
enough nutrients
then your growth hormone will be
stimulated to increase those nutrients
in your body
so growth hormone is trying to provide
an environment for you to grow
so if you have decreased glucose
decreased free fatty acids
you're fasting or you're exercising
you're under stress then you're going to
release growth hormones to try and
provide an environment for you to
actually grow
obviously when you're going through
puberty you have higher growth hormone
during those times as well growth
hormone will then steadily decrease as
you get older now our inhibitory factors
are going to be the opposite of those so
if we have high glucose high free fatty
acids then we already
kind of have an environment for growth
so you don't need to release your growth
hormone
obesity reduces it some metastatin
remember that's our stop hormone from
our gi chapter somatostatin
also plays a role with inhibiting our
growth hormone effects as well
growth hormone itself actually inhibits
itself there are negative feedback
mechanism and then circling back to
somatostatin
this is an example of a gi protein
coupled receptor remember we talked
about the gs
protein receptors which cause an
increase in cyclic amp
gi proteins are inhibitory g proteins
they reduce the level of
cyclic amp by inhibiting the admiral
cyclase enzyme
so somatostatin the stopping hormone
which inhibits growth hormone does so
by interacting with a gi protein
as a receptor so figure 9.11 here
tells us how growth hormone has a
negative feedback on itself
the first thing to point out here is
that when growth hormone actually has
its effect on the target tissue
it gets broken down into these
somatometers or igf's
these igfs then actually have an
inhibitory role
on the release of further growth hormone
by having a direct effect on
inhibiting our anterior pituitary gland
but then also
by having a stimulatory effect on the
hypothalamus to release somatostatin
remember somatostatin our stopping
hormone inhibits also the anterior
pituitary gland
so that's one way the growth hormone has
negative feedback on itself
when it's broken down the byproducts
have an inhibitory effect growth hormone
itself
also has an inhibitory effect on itself
by
increasing the release of somatostatin
from the hypothalamus so
increased growth hormone will actually
self-regulate itself
and the last mechanism out of the three
is
growth hormone releasing hormone
actually having an inhibitory effect
on the hypothalamus itself so although
it's released from the hypothalamus as
soon as that increases in concentration
it's going to tell itself to stop
secreting itself
essentially so the growth hormone that
negative feedback mechanism has these
three different
feedback systems somatometers growth
hormone and growth hormone releasing
hormone
so how does growth hormone actually have
an effect
on the body we know it's used to promote
growth but what is it actually doing
well we have three main effects here to
remember number one
is being diabetogenic or having an
insulin resistant
effect it blocks the effects of insulin
which is trying to reduce your glucose
levels in your body or in your blood
so by blocking or making insulin
resistant you increase the amount of
glucose in your bloodstream
and then it also increases lipolysis and
adipose tissues
basically what this is doing is
increasing our energy stores and our
plasma
so then our body has a lot of energy to
be able to grow
so we're increasing energy availability
by antagonizing insulin in an effect for
an easy way to think about that first
effect our second effect
is increasing growth by stimulating
protein synthesis and organ growth so
we're increasing the uptake of amino
acids into
our cells and we're increasing the
stimulation of protein development this
will increase
lean body mass and organ size our third
effect
is an increased in linear growth so
before puberty before your growth
plates have used it will increase the
production of bone within your growth
plate so then you're able to grow you
know this is why during your growth
spurt your
high growth hormone but then if you're
already finished your growth it will
actually
increase our periosteal bone growth so
kind of the
edges of our bones so we have this
influence on bone growth
more dramatic obviously before puberty
that brings
us to when we have an issue with our
growth hormone
if we have deficiency then that's going
to lead into dwarfism which is treated
with
growth hormone with excess what you're
going to see depends on when this occurs
if it's before puberty
then you end up with gigantism because
you're actually
increasing your long bone growth after
puberty
when linear growth is complete then you
end up with just
larger features so larger facial
features larger hands
increased organ size insulin resistance
glucose intolerance etc from that
excessive growth hormone so that is
growth hormone in a nutshell
next up is prolactin now prolactin is
responsible for milk
production so producing milk not letting
it down that's oxytocin
but milk production and the development
of the breasts
so obviously we're going to have an
increased secretion of prolactin during
pregnancy and lactation
now the thing with prolactin secretion
from the anterior pituitary gland which
works on the breasts
is that on the day-to-day it's getting
inhibited from dopamine release from the
hypothalamus
up until pregnancy or lactation that's
when that gets overridden and we
start to increase trh release trh
stimulates the release of prolactin and
prolactin nature has an
inhibitory effect on itself for its own
negative feedback by increasing the
level of dopamine
so the stimuli for prolactin release
is suckling that's the main stimulation
so
obviously that's a need for lactation
after pregnancy
then you're going to increase milk
production there is also another time
for
prolactin release which is that puberty
for breast development but otherwise
it only gets released during lactation
in order to produce milk for the baby
any pathophysiology of prolactin
includes deficiency where obviously you
fail to lactate and then
excess which can occur due to some kind
of prolactin producing tumor which can
lead to infertility because prolactin
does inhibit ovulation and also
galactoria or excessive milk production
so moving on to
our posterior lobe hormones now remember
we talked about adhd and oxytocin
as our two posterior pituitary gland
hormones produced
and synthesized by the cells within the
hypothalamus in the neuron
but then that neuron extends all the way
down into that posterior pituitary gland
where it sits waiting to be
stimulated to be released so adh
is the first one that we'll focus on
here this gets secreted
whenever we have a depolarization of
that nerve
that the adh is sitting in that
stimulates calcium and to enter the
terminal and causes exocytosis
of the adh and also the oxytocin when we
get to talking about oxytocin
now we've already talked about adh in
our renal chapter remember adh is
involved with controlling our oils
predominantly and then also an influence
on controlling our blood pressure
now our hypothalamus will sense if our
osmolarity will change
if there is an increase in osmolarity
then that stimulates increased
adh secretion adh goes to the kidneys
and then tells the kidneys to increase
the reabsorption of water
it's able to do that by actually
interacting with a v2 receptor which is
a gs
protein to increase cyclic amp in the
principal cell of the
late distal tubule and cortical tubules
that will ultimately end up with the
phosphorylation of
aquaporin two proteins that insert
themselves into the membranes
aquaporin ii results in increased
permeability of those principal cells to
water so now that terminal nephron can
actually absorb water when it was
previously impermeable
so the absorbing of water from the
nephron reduces the osmolarity in our
plasma
and helps to restore our osmolarity now
if we also need to increase the water
reabsorption from our kidneys because of
hypotension
then that will occur because our dairy
receptors within our carotid artery and
aortic arch
will sense a low blood pressure that
will transmit a signal via the vagus
nerve to the hypothalamus
and then that will tell the hypothalamus
to stimulate the release of adh to
increase water reabsorption to help to
increase our blood volume again
and blood pressure now adh also has
another influence to help with blood
pressure
through contraction of our vascular
smooth muscle via the v1 receptor so v1
for vascular smooth muscle contraction
v2 for aquaporin 2
and increasing water reabsorption from
the kidneys
now interestingly the v1 receptor for
the vascular smooth muscle
actually utilizes the ip3 calcium
secondary messenger system
versus the v2 receptor which utilizes
the cyclic amp
secondary messenger system so when it
comes to disorders of
adh we have central diabetes insipidus
and nephrogenic diabetes
insipidus diabetes insipidus just means
very watery urine or very dilute urine
now
that occurs because we have an
inappropriate response to adh either
because we don't have
enough adh such as in central diabetes
insipidus where there is no secretion of
adh
from the posterior pituitary gland at
all which needs to be treated by
giving an adh analogue like ddavp or
nephrogenic diabetes insipidus where the
principal cells are actually
unresponsive to adh altogether
now these will not respond to adh
analogues and will actually require a
different type of treatment like
thiazide diuretics to help to reduce our
sodium reabsorption to increase our
osmolarity of our urine and also reduce
the gfr to reduce the amount of water
that's getting excreted so diabetes
insipidus means dilute
urine due to inappropriate adh either
due to
reduced secretion and low levels in
central
or not responding to adh in the kidneys
which is nephrogenic
diabetes insipidus we do have syndrome
of inappropriate adh
siadh which means adh is getting
secreted from an anomalous site
like a cancer within the lungs this will
dilute our body fluids by
actually hyper concentrating our urine
because now adh is sucking all the water
out of our nephrons and that gets
treated by an
adh antagonist the last hormone we'll
talk about coming from the posterior
pituitary gland
is oxytocin which is the milk let down
hormone so prolactin
stimulates milk production oxytocin then
tells that milk to be let down or
ejected
so the stimulus for that is obviously
going to be suckling or we do have some
other stimulatory factors like the sight
sound or smell of an infant
and it is also released with dilation of
the cervix during pregnancy it actually
helps with uterine contractions this is
one of those positive feedback
mechanisms during pregnancy
it is inhibited from opioids but other
than that that'll conclude
our video for today in the next video
we'll go over
our thyroid hormones in our thyroid
gland feel free to drop a comment
otherwise we'll see in the next video