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Costanzo Physiology (Chapter 9D) Endocrine Physiology: Adrenal Gland || Study This!

hello and welcome to the review of the
next portion of the endocrine physiology
chapter in costanzo's physiology
textbook going over the adrenal medulla
and the cortex
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if you are in need of the textbook there
is a link within the description
otherwise we're going to dive straight
into the adrenal gland with a bit of
anatomy first
starting off with the adrenal medulla
which is the central portion of the
adrenal gland which produces catechol
amines
a part of the sympathetic nervous system
obviously we're not going to talk about
that
in this chapter we're going to go over
the endocrine functions
via the cortex of the adrenal glands
so in the cortex we have these three
layers that produces
three types of hormones mineral
corticoids coming from the
outer layer for coming from the zona
glomerulosa
glucocorticoids which comes
predominantly from the middle layer a
little bit from the inner layer but
predominantly the middle layer from the
zona fasciculata
and then our androgens coming
predominantly from the innermost layer
the zona reticularis
so an easy way to think about this from
outside to in
is that we produce the hormones for salt
sugar
and sex so mineral corticoids control
salt regulation
glucocorticoids has glucose in the name
and controls our sugar regulation
and then androgens sexual hormones which
in the cortex has a pretty minor role
because we predominantly produce our sex
hormones from our reproductive system so
clearly the test is in the ovaries now
each of these adrenal cortical hormones
are steroids meaning that they are made
out of cholesterol
and they enter the cell where their
receptor is on the actual dna
to then synthesize new proteins so each
one of the steroids coming from
cholesterol
and you can see the pathway for
production over here in this pretty
confusing diagram of figure 9.23
just to orientate yourself you can see
cholesterol at the top that starts off
this entire process
via the cholesterol dismalase enzyme to
start the breakdown of cholesterol
so each layer has cholesterol within its
layers stored
ready to be processed into its
respective hormones
when stimulated by acth so acth starts
the breakdown of cholesterol
now where each layer is slightly
different is the enzymes present
for each pathway so you can see our
mineral corticoids over here on the left
side
where aldosterone is in order for
aldosterone to get produced we need
these hormones on the side here
which are going to convert progesterone
into aldosterone
predominantly also aldosterone synthase
which requires stimulation from a
completely different peptide and
angiotensin ii
so the zona golomarulosa is different to
the other layers because it contains for
instance
aldosterone synthesis to actually
produce aldosterone
it also lacks one of these enzymes 17
alpha hydroxylase
which is responsible for starting the
conversion into
these other hormones cortisol and
androgens
so the zona glomerulosa is incapable of
producing these other hormones just
because of the enzymes that's present
now another key point here is that once
again
androgens are predominantly produced in
our reproductive
organs so our adrenal cortex plays a
pretty minor role in the secretion of
androgens the reason why that's
important is because
if we have stimulation of acth secretion
from our anterior pituitary glands
the predominant effect is actually the
increased levels of
cortisol because aldosterone requires
angiotensin
ii to stimulate its release and
androgens that have a pretty minor role
acth basically increases the production
of glucocorticoids
mainly now aldosterone does require
acth to start the process but you only
need a small amount
so when it comes to the actual increased
secretion of aldosterone that is where
we get the rest
system to increase angiotensin too so
it's a completely independent mechanism
to acth
and that will become important because
when we have acth secreting
tumors within the anterior pituitary
glands yeah we may get slightly
increased levels of these other hormones
but predominantly the influence is an
increase in cortisol so that is the main
point
there now when it comes to the
regulation of
the secretion of these steroids we're
going to dive into a little bit deeper
so we mentioned acth increases our
cortisol
from the adrenal cortex acth gets
stimulated to be released
from the anterior pituitary glands
because of the hypothalamus
releasing cortisol releasing hormone so
cortisol releasing hormone
then increases acth which then increases
cortisol
cortisol then has a negative feedback on
the anterior pituitary and hypothalamus
that leads us to how do you diagnose an
issue here
let's say you take a blood test and you
measure your cortisol levels and they
are high
they may be high because of stress from
purely the blood draw so
maybe that's why the cortisol is high or
it could indicate that you may have an
adrenal tumor producing cortisol
or an anterior pituitary gland tumor
secreting acth
which is increasing your cortisol
release so how are you going to tell the
difference
that's where the dexamethasone
suppression test comes in
this involves injecting the molecule of
dexamethasone
which essentially acts as cortisol to
have a negative feedback
influence on your anterior pituitary
gland so if you give dexamethasone
a normal patient who is just stressed we
will have a reduction in our icth
production and a reduction in our
cortisol
so your cortisol level will drop after
giving dexamethasone
if you have a tumor in the anterior
pituitary gland or your cortex
then you may not have that reduction in
cortisol if you have an anterior
pituitary gland
tumor then low those dexamethasone may
only temporarily reduce your acth but
then it overcomes it and you produce
even more icth so your cortisol remains
high over time
so you may require a high dose of
dexamethasone to actually suppress your
acth secretion if it is an adrenal
cortex tumor secreting cortisol then it
is not dependent on acth altogether and
in fact your acth levels are already low
because that increased cortisol level is
already
inhibiting the anterior pituitary gland
regardless you may give low or high dose
dexamethasone
and there is no influence on cortisol
release so cortisol remains high despite
giving dexmethazone so that is one of
the
diagnostic tests for hypercorticalism or
hyperadrenal corticalism
now in the normal person you will
secrete cortisol
in a pulsatile nature and then also
diurnally as well
predominantly increasing your cortisol
release just after you wake up
to kind of help stimulate the waking up
process
now when it comes to the regulation of
aldosterone secretion we already talked
about how a cth only plays a minor role
with the predominant influence for
increasing aldosterone secretion
being a change in your extracellular
fluid volume so hypotension
which stimulates the rest system the
renin angiotensin aldosterone system
because remember the hypotension gets
sensed by the kidneys
specifically the juxtaglomerular cells
that secrete
renin the enzyme to convert
angiotensinogen to angiotensin one
that gets converted to angiotensin ii by
ace
angiotensin ii then once again
influences the adrenal cortex and zona
glomerulosa
to stimulate aldosterone release
aldosterone then goes to the kidneys and
tells it to hold on to more sodium
and also secrete potassium so since it
also tells the kidneys to secrete
potassium
high serum potassium levels will also
stimulate the release of aldosterone to
help to release and secrete more
potassium into the urine
now aldosterone also has an influence of
increasing hydrogen secretion so if you
have
excessively high aldosterone then you
will have an
increased extracellular fluid volume
because of sodium retention
and increased potassium secretion so
hypokalemia in your plasma
and then a metabolic alkalosis because
you're releasing a lot of hydrogen ions
so those are the actions of mineral
corticoids which we also covered in the
renal chapter
what are the actions of our
glucocorticoids well the glucocorticoids
is our stress hormone cortisol is our
stress hormone so it's involved
with the fight or flight so what would
the body want to do
to prepare itself for fight or flight
responses or stress responses
the main thing is making energy readily
available in the body to be able to
perform an action
so having a lot of energy available
which would include having glucose very
available in the bloodstream so
increasing gluconeogenesis
increasing proteolysis of breaking down
your proteins so then amino acids can be
converted to glucose
and then also breaking down our fats as
well by lipolysis to make them
available for energy utilization as well
not only that but we need to block the
actions of insulin which is trying to do
the opposite effects of storing our
energy away
so blocking insulin allows glucose to be
readily available
for our energy use now this is all very
similar to
growth hormone as we touched on earlier
the main difference is that growth
hormones trying to make energy available
to then increase our growth as the name
implies
so that will increase protein synthesis
and increase growth in that way
whereas steroids is actually breaking
down proteins to make them available for
glucose so then we're available
just for immediate action so growth
hormone is increasing
energy utilization for growth
glucocorticoids
are increasing energy availability in
order for us to have
a fight or flight response
glucocorticoids also inhibit our
inflammatory response and suppress our
immune system
in addition to enhancing our vascular
responsiveness
to catecholamines basically making our
vasculature
easier to control so we're able to
divert blood to where we need it to go
it also inhibits bone formation the way
to think about that is that we don't
need to
form our bones at this moment because
we're about to do a fight or flight
response
it increases gfr and decreases rem sleep
as well
so our glucocorticoids are essential for
being
able to handle any stresses it may sound
like a bad thing
but it's actually a good thing you know
we need that energy available
so we can respond appropriately now when
it comes to the actions of adrenal
androgens
once again the cortex has a very minor
role in the production of these
adrenal androgens so those will be
covered more in the reproductive chapter
so how about when there's an issue with
our adrenal cortex and we have
too much hormones being produced well
the main thing to do is actually just to
understand
the pathways so understanding acth
stimulating cortisol release
the rare system stimulating aldosterone
release
and then also understanding what those
hormones do so
understanding what cortisol does
understanding what aldosterone does
and then you can kind of work your way
through it and thinking if we have a
tumor in our anterior pituitary
gland then that's going to produce acth
which is going to then
increase our cortisol release and if we
have excessive cortisol then we're going
to have
increased blood glucose we're going to
have muscle wasting as all the proteins
get degradated we're going to have
osteoporosis or weak bones we're going
to have immunocompromised and more
likely to have infections
etc so it's kind of just working through
it systematically
knowing each disease states by name will
just come with time because there are a
few names here you know we have
cushing's disease
for what we're talking about with the
anterior pituitary glands tumor
excessive acth and then cushing's
syndrome which is
an actual adrenal mass producing
cortisol so
cushing's results in increased cortisol
we have
addison's disease which is when we
actually destruction of the entire
cortex
of the adrenal gland so we have a
reduction in both else cortisol our
stress hormone
so you cannot respond to stress and also
a reduction
in your mineral corticoids so you have
low extracellular fluid volume and
hypotension
in addition to hyperkalemia or high
potassium because you're not
excreting your potassium so that can
actually end up
with an addisonian crisis because you
end up in a shock state
because your body cannot respond to a
stress and it also has low extracellular
fluid volume
so you end up in a shocky state another
characteristic of this disease is
increased pigmentation of the skin
because of increased acth levels because
there is low cortisol
from that destruction of the adrenal
cortex so there's a lack of the
inhibition on the
anterior pituitary gland so acth
increases
and we have these acth byproducts as a
side effect you know these
fragments which include melanocyte
stimulating hormone that increases
pigmentation of the skin so those are
some of the main diseases the other main
one is
con syndrome which is an aldosterone
secreting tumor
instead of cortisol so aldosterone will
increase reabsorption of sodium from the
kidneys
and without water so you end up with
hypertension from a high extracellular
fluid volume
you also end up with excessive excretion
of potassium
so you have hypokalemia and then also
excessive
excretion of acid so you end up with
metabolic alkalosis
so those are your main disease states
when it comes to the adrenal cortex it
does go into a little bit more detail
here of say cushing's syndrome
how you can diagnose it with the
dexamethasone suppression test
we've already touched on that you give
dexamethasone which should
inhibit the release of acth and cortisol
but if you have a
cushing's disease state or cushing's
syndrome
then you will still have the release of
cortisol even though you're giving
dexamethasone because those tumors are
overriding that negative feedback
response for the treatment clearly
you're just going to give something
that's going to block steroid hormone
synthesis
con syndrome you're going to treat by
giving an aldosterone receptor
antagonist and
spironolactone so you're just inhibiting
the effects of aldosterone on the body
and then there's two other more rare
types of disease include a deficiency in
21 beta hydroxylase which is one of
those
enzymes that's involved in synthesizing
both mineral corticoids and
glucocorticoids so you end up with
addison's disease
or the deficiency in 17 alpha
hydroxylase
which is only involved in really the
production of glucocorticoids
or androgens so you still have normal
mineral corticoids so you end up with
something called
atypical addison's because you have
normal mineral corticoids but you have a
lack of cortisol
and that will end the chapter for today
join us
in the next video where we're going to
go over the endocrine pancreas
otherwise feel free to drop a comment
and we'll see on the next one