0:00 hello and welcome to the review of the
0:01 next portion of the endocrine physiology
0:04 chapter in costanzo's physiology
0:06 textbook going over the adrenal medulla
0:08 and the cortex
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0:13 to the channel
0:14 if you are in need of the textbook there
0:15 is a link within the description
0:17 otherwise we're going to dive straight
0:18 into the adrenal gland with a bit of
0:20 anatomy first
0:21 starting off with the adrenal medulla
0:23 which is the central portion of the
0:25 adrenal gland which produces catechol
0:27 amines
0:28 a part of the sympathetic nervous system
0:30 obviously we're not going to talk about
0:31 that
0:31 in this chapter we're going to go over
0:33 the endocrine functions
0:35 via the cortex of the adrenal glands
0:38 so in the cortex we have these three
0:40 layers that produces
0:41 three types of hormones mineral
0:43 corticoids coming from the
0:45 outer layer for coming from the zona
0:47 glomerulosa
0:48 glucocorticoids which comes
0:50 predominantly from the middle layer a
0:52 little bit from the inner layer but
0:53 predominantly the middle layer from the
0:55 zona fasciculata
0:57 and then our androgens coming
0:59 predominantly from the innermost layer
1:01 the zona reticularis
1:03 so an easy way to think about this from
1:05 outside to in
1:06 is that we produce the hormones for salt
1:09 sugar
1:09 and sex so mineral corticoids control
1:12 salt regulation
1:13 glucocorticoids has glucose in the name
1:16 and controls our sugar regulation
1:18 and then androgens sexual hormones which
1:21 in the cortex has a pretty minor role
1:23 because we predominantly produce our sex
1:25 hormones from our reproductive system so
1:27 clearly the test is in the ovaries now
1:29 each of these adrenal cortical hormones
1:31 are steroids meaning that they are made
1:33 out of cholesterol
1:34 and they enter the cell where their
1:36 receptor is on the actual dna
1:39 to then synthesize new proteins so each
1:42 one of the steroids coming from
1:44 cholesterol
1:45 and you can see the pathway for
1:46 production over here in this pretty
1:48 confusing diagram of figure 9.23
1:52 just to orientate yourself you can see
1:54 cholesterol at the top that starts off
1:56 this entire process
1:58 via the cholesterol dismalase enzyme to
2:00 start the breakdown of cholesterol
2:03 so each layer has cholesterol within its
2:05 layers stored
2:07 ready to be processed into its
2:08 respective hormones
2:10 when stimulated by acth so acth starts
2:14 the breakdown of cholesterol
2:16 now where each layer is slightly
2:17 different is the enzymes present
2:20 for each pathway so you can see our
2:22 mineral corticoids over here on the left
2:24 side
2:24 where aldosterone is in order for
2:26 aldosterone to get produced we need
2:28 these hormones on the side here
2:30 which are going to convert progesterone
2:32 into aldosterone
2:34 predominantly also aldosterone synthase
2:36 which requires stimulation from a
2:38 completely different peptide and
2:40 angiotensin ii
2:42 so the zona golomarulosa is different to
2:45 the other layers because it contains for
2:47 instance
2:47 aldosterone synthesis to actually
2:50 produce aldosterone
2:51 it also lacks one of these enzymes 17
2:54 alpha hydroxylase
2:55 which is responsible for starting the
2:58 conversion into
2:59 these other hormones cortisol and
3:01 androgens
3:02 so the zona glomerulosa is incapable of
3:05 producing these other hormones just
3:06 because of the enzymes that's present
3:08 now another key point here is that once
3:10 again
3:10 androgens are predominantly produced in
3:13 our reproductive
3:14 organs so our adrenal cortex plays a
3:16 pretty minor role in the secretion of
3:18 androgens the reason why that's
3:20 important is because
3:22 if we have stimulation of acth secretion
3:25 from our anterior pituitary glands
3:28 the predominant effect is actually the
3:30 increased levels of
3:32 cortisol because aldosterone requires
3:34 angiotensin
3:35 ii to stimulate its release and
3:38 androgens that have a pretty minor role
3:40 acth basically increases the production
3:44 of glucocorticoids
3:45 mainly now aldosterone does require
3:48 acth to start the process but you only
3:51 need a small amount
3:52 so when it comes to the actual increased
3:54 secretion of aldosterone that is where
3:56 we get the rest
3:58 system to increase angiotensin too so
4:00 it's a completely independent mechanism
4:02 to acth
4:03 and that will become important because
4:05 when we have acth secreting
4:07 tumors within the anterior pituitary
4:09 glands yeah we may get slightly
4:11 increased levels of these other hormones
4:13 but predominantly the influence is an
4:15 increase in cortisol so that is the main
4:18 point
4:19 there now when it comes to the
4:21 regulation of
4:22 the secretion of these steroids we're
4:24 going to dive into a little bit deeper
4:26 so we mentioned acth increases our
4:28 cortisol
4:29 from the adrenal cortex acth gets
4:32 stimulated to be released
4:33 from the anterior pituitary glands
4:35 because of the hypothalamus
4:37 releasing cortisol releasing hormone so
4:40 cortisol releasing hormone
4:42 then increases acth which then increases
4:45 cortisol
4:46 cortisol then has a negative feedback on
4:48 the anterior pituitary and hypothalamus
4:51 that leads us to how do you diagnose an
4:53 issue here
4:53 let's say you take a blood test and you
4:56 measure your cortisol levels and they
4:58 are high
4:58 they may be high because of stress from
5:01 purely the blood draw so
5:03 maybe that's why the cortisol is high or
5:05 it could indicate that you may have an
5:07 adrenal tumor producing cortisol
5:09 or an anterior pituitary gland tumor
5:11 secreting acth
5:13 which is increasing your cortisol
5:15 release so how are you going to tell the
5:16 difference
5:17 that's where the dexamethasone
5:19 suppression test comes in
5:20 this involves injecting the molecule of
5:23 dexamethasone
5:24 which essentially acts as cortisol to
5:27 have a negative feedback
5:28 influence on your anterior pituitary
5:30 gland so if you give dexamethasone
5:33 a normal patient who is just stressed we
5:36 will have a reduction in our icth
5:38 production and a reduction in our
5:39 cortisol
5:40 so your cortisol level will drop after
5:43 giving dexamethasone
5:44 if you have a tumor in the anterior
5:46 pituitary gland or your cortex
5:48 then you may not have that reduction in
5:50 cortisol if you have an anterior
5:52 pituitary gland
5:54 tumor then low those dexamethasone may
5:56 only temporarily reduce your acth but
5:59 then it overcomes it and you produce
6:01 even more icth so your cortisol remains
6:03 high over time
6:04 so you may require a high dose of
6:06 dexamethasone to actually suppress your
6:08 acth secretion if it is an adrenal
6:11 cortex tumor secreting cortisol then it
6:14 is not dependent on acth altogether and
6:16 in fact your acth levels are already low
6:19 because that increased cortisol level is
6:21 already
6:22 inhibiting the anterior pituitary gland
6:24 regardless you may give low or high dose
6:26 dexamethasone
6:27 and there is no influence on cortisol
6:29 release so cortisol remains high despite
6:32 giving dexmethazone so that is one of
6:34 the
6:35 diagnostic tests for hypercorticalism or
6:38 hyperadrenal corticalism
6:39 now in the normal person you will
6:41 secrete cortisol
6:43 in a pulsatile nature and then also
6:45 diurnally as well
6:46 predominantly increasing your cortisol
6:48 release just after you wake up
6:50 to kind of help stimulate the waking up
6:53 process
6:53 now when it comes to the regulation of
6:55 aldosterone secretion we already talked
6:57 about how a cth only plays a minor role
6:59 with the predominant influence for
7:01 increasing aldosterone secretion
7:03 being a change in your extracellular
7:05 fluid volume so hypotension
7:08 which stimulates the rest system the
7:10 renin angiotensin aldosterone system
7:13 because remember the hypotension gets
7:15 sensed by the kidneys
7:17 specifically the juxtaglomerular cells
7:19 that secrete
7:20 renin the enzyme to convert
7:21 angiotensinogen to angiotensin one
7:24 that gets converted to angiotensin ii by
7:26 ace
7:27 angiotensin ii then once again
7:29 influences the adrenal cortex and zona
7:31 glomerulosa
7:32 to stimulate aldosterone release
7:35 aldosterone then goes to the kidneys and
7:36 tells it to hold on to more sodium
7:38 and also secrete potassium so since it
7:41 also tells the kidneys to secrete
7:43 potassium
7:44 high serum potassium levels will also
7:46 stimulate the release of aldosterone to
7:48 help to release and secrete more
7:50 potassium into the urine
7:52 now aldosterone also has an influence of
7:54 increasing hydrogen secretion so if you
7:56 have
7:57 excessively high aldosterone then you
7:59 will have an
8:00 increased extracellular fluid volume
8:02 because of sodium retention
8:04 and increased potassium secretion so
8:06 hypokalemia in your plasma
8:08 and then a metabolic alkalosis because
8:10 you're releasing a lot of hydrogen ions
8:12 so those are the actions of mineral
8:14 corticoids which we also covered in the
8:16 renal chapter
8:17 what are the actions of our
8:18 glucocorticoids well the glucocorticoids
8:21 is our stress hormone cortisol is our
8:24 stress hormone so it's involved
8:25 with the fight or flight so what would
8:27 the body want to do
8:29 to prepare itself for fight or flight
8:31 responses or stress responses
8:33 the main thing is making energy readily
8:35 available in the body to be able to
8:37 perform an action
8:38 so having a lot of energy available
8:40 which would include having glucose very
8:43 available in the bloodstream so
8:44 increasing gluconeogenesis
8:46 increasing proteolysis of breaking down
8:49 your proteins so then amino acids can be
8:51 converted to glucose
8:52 and then also breaking down our fats as
8:55 well by lipolysis to make them
8:57 available for energy utilization as well
8:59 not only that but we need to block the
9:01 actions of insulin which is trying to do
9:03 the opposite effects of storing our
9:05 energy away
9:06 so blocking insulin allows glucose to be
9:08 readily available
9:10 for our energy use now this is all very
9:13 similar to
9:14 growth hormone as we touched on earlier
9:16 the main difference is that growth
9:18 hormones trying to make energy available
9:20 to then increase our growth as the name
9:23 implies
9:24 so that will increase protein synthesis
9:26 and increase growth in that way
9:28 whereas steroids is actually breaking
9:30 down proteins to make them available for
9:32 glucose so then we're available
9:34 just for immediate action so growth
9:36 hormone is increasing
9:37 energy utilization for growth
9:39 glucocorticoids
9:40 are increasing energy availability in
9:43 order for us to have
9:44 a fight or flight response
9:46 glucocorticoids also inhibit our
9:48 inflammatory response and suppress our
9:50 immune system
9:51 in addition to enhancing our vascular
9:53 responsiveness
9:54 to catecholamines basically making our
9:56 vasculature
9:58 easier to control so we're able to
10:00 divert blood to where we need it to go
10:02 it also inhibits bone formation the way
10:04 to think about that is that we don't
10:06 need to
10:07 form our bones at this moment because
10:08 we're about to do a fight or flight
10:10 response
10:11 it increases gfr and decreases rem sleep
10:13 as well
10:14 so our glucocorticoids are essential for
10:17 being
10:18 able to handle any stresses it may sound
10:20 like a bad thing
10:21 but it's actually a good thing you know
10:23 we need that energy available
10:25 so we can respond appropriately now when
10:27 it comes to the actions of adrenal
10:28 androgens
10:29 once again the cortex has a very minor
10:32 role in the production of these
10:33 adrenal androgens so those will be
10:35 covered more in the reproductive chapter
10:37 so how about when there's an issue with
10:40 our adrenal cortex and we have
10:42 too much hormones being produced well
10:44 the main thing to do is actually just to
10:47 understand
10:48 the pathways so understanding acth
10:51 stimulating cortisol release
10:53 the rare system stimulating aldosterone
10:55 release
10:56 and then also understanding what those
10:58 hormones do so
11:00 understanding what cortisol does
11:01 understanding what aldosterone does
11:04 and then you can kind of work your way
11:05 through it and thinking if we have a
11:07 tumor in our anterior pituitary
11:08 gland then that's going to produce acth
11:11 which is going to then
11:12 increase our cortisol release and if we
11:15 have excessive cortisol then we're going
11:17 to have
11:17 increased blood glucose we're going to
11:20 have muscle wasting as all the proteins
11:22 get degradated we're going to have
11:24 osteoporosis or weak bones we're going
11:26 to have immunocompromised and more
11:28 likely to have infections
11:30 etc so it's kind of just working through
11:32 it systematically
11:33 knowing each disease states by name will
11:36 just come with time because there are a
11:38 few names here you know we have
11:39 cushing's disease
11:40 for what we're talking about with the
11:42 anterior pituitary glands tumor
11:44 excessive acth and then cushing's
11:47 syndrome which is
11:48 an actual adrenal mass producing
11:51 cortisol so
11:52 cushing's results in increased cortisol
11:54 we have
11:55 addison's disease which is when we
11:57 actually destruction of the entire
11:59 cortex
12:00 of the adrenal gland so we have a
12:01 reduction in both else cortisol our
12:04 stress hormone
12:05 so you cannot respond to stress and also
12:07 a reduction
12:08 in your mineral corticoids so you have
12:10 low extracellular fluid volume and
12:12 hypotension
12:13 in addition to hyperkalemia or high
12:16 potassium because you're not
12:17 excreting your potassium so that can
12:19 actually end up
12:20 with an addisonian crisis because you
12:23 end up in a shock state
12:25 because your body cannot respond to a
12:27 stress and it also has low extracellular
12:29 fluid volume
12:30 so you end up in a shocky state another
12:33 characteristic of this disease is
12:35 increased pigmentation of the skin
12:37 because of increased acth levels because
12:40 there is low cortisol
12:41 from that destruction of the adrenal
12:43 cortex so there's a lack of the
12:45 inhibition on the
12:46 anterior pituitary gland so acth
12:49 increases
12:50 and we have these acth byproducts as a
12:53 side effect you know these
12:54 fragments which include melanocyte
12:56 stimulating hormone that increases
12:58 pigmentation of the skin so those are
13:00 some of the main diseases the other main
13:02 one is
13:02 con syndrome which is an aldosterone
13:05 secreting tumor
13:06 instead of cortisol so aldosterone will
13:08 increase reabsorption of sodium from the
13:10 kidneys
13:11 and without water so you end up with
13:13 hypertension from a high extracellular
13:15 fluid volume
13:16 you also end up with excessive excretion
13:19 of potassium
13:20 so you have hypokalemia and then also
13:22 excessive
13:23 excretion of acid so you end up with
13:25 metabolic alkalosis
13:26 so those are your main disease states
13:29 when it comes to the adrenal cortex it
13:31 does go into a little bit more detail
13:33 here of say cushing's syndrome
13:35 how you can diagnose it with the
13:36 dexamethasone suppression test
13:39 we've already touched on that you give
13:41 dexamethasone which should
13:42 inhibit the release of acth and cortisol
13:45 but if you have a
13:46 cushing's disease state or cushing's
13:48 syndrome
13:49 then you will still have the release of
13:51 cortisol even though you're giving
13:53 dexamethasone because those tumors are
13:54 overriding that negative feedback
13:56 response for the treatment clearly
13:58 you're just going to give something
13:59 that's going to block steroid hormone
14:01 synthesis
14:02 con syndrome you're going to treat by
14:03 giving an aldosterone receptor
14:05 antagonist and
14:06 spironolactone so you're just inhibiting
14:08 the effects of aldosterone on the body
14:10 and then there's two other more rare
14:12 types of disease include a deficiency in
14:15 21 beta hydroxylase which is one of
14:17 those
14:17 enzymes that's involved in synthesizing
14:20 both mineral corticoids and
14:21 glucocorticoids so you end up with
14:23 addison's disease
14:25 or the deficiency in 17 alpha
14:27 hydroxylase
14:29 which is only involved in really the
14:30 production of glucocorticoids
14:32 or androgens so you still have normal
14:35 mineral corticoids so you end up with
14:37 something called
14:37 atypical addison's because you have
14:40 normal mineral corticoids but you have a
14:42 lack of cortisol
14:43 and that will end the chapter for today
14:45 join us
14:46 in the next video where we're going to
14:47 go over the endocrine pancreas
14:49 otherwise feel free to drop a comment
14:51 and we'll see on the next one
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