[Music] all right you guys welcome back to the second lesson in our series of lessons covering the endocrine system and in this lesson we're going to be covering the differences between Addison's and Cushing's this is going to be the first dive into some of the disorders that we find within the endocrine system but before we begin if this is your first time to our channel and watching our videos I do invite you guys to subscribe to our channel below make sure though you hit that Bell notification icon that way you will be notified as soon as our new lessons become available as always I truly value the subscriptions the likes and the comments that you guys leave for us and so for that I do want to thank you guys my name is Eddie Watson and this is ICU advantage all right so let's go ahead and begin with this lesson here like I said we're going to be talking about the differences between Addison's disease and Cushing's syndrome so both of these disease processes are very different from one another but they're also very similar in the fact that they both are dealing with a problem with our corticosteroid production and so to understand that let's do a quick review of some of the anatomy that we talked about from the last lesson so as we know right here we have our hypothalamus here we have our pituitary gland and down here we have our adrenal glands and so what normally happens is we have the hypothalamus here that will release what we call corticotropin-releasing hormone or CRH and CRH is going to go to our pituitary gland and this is going to cause the pituitary gland to release what we call the adrenocorticotropic releasing hormone or ACTH and so for a quick check of understanding from the last lesson in the comments below let us know if you remember which part of the pituitary gland it is that's responsible for releasing ACTH but so this release of ACTH by the pituitary gland is going to go down to our adrenal gland and in particular the adrenal cortex and that's going to stimulate the cortex to release several hormones we have our cortisol or aldosterone as well as the androgens for the sex hormones and this is how this particular hormone pathway within the endocrine system is supposed to work and so with that out of the way let's go ahead and start to talk about the first of the disorders that we're going to talk about and that is going to be Addison's disease and so we know that we're gonna have a problem with our corticosteroid production and so in the case of Addison's disease what we're dealing with is an acute adrenal insufficiency and this can progress into what we call Addison's crisis and so really what this means for us is that this is an acute form of a chronic adrenal dysfunction and so what this means is we're gonna have inadequate secretion of our glucocorticoids which are going to be our cortisol as well as an inadequate secretion of our mineral corticoids which is going to be our aldosterone and these hormones are going to play an important part in what we see in Addison's disease and so just think about this as inadequate or insufficient amount of these hormones and so let's talk about some of the causes that are going to lead our patient into Addison's disease and for these causes we can really divide this up into three sub categories the first one is our primary causes and our primary causes are going to be the result of damage to our adrenal cortex and so these are going to be things like our idiopathic autoimmune diseases metastatic cancer trauma sepsis AIDS even drugs like fina toen barbituates so anything that destroys the adrenal cortex that this is going to lead to an inability to produce these corticosteroids so the next category we have is what we call secondary and these are going to be anything that interferes with our hormone secretion and really we're talking about interference with our ACTH secretion so here things like pituitary tumors radiation hemorrhage again trauma or surgery or even any hypothalamic disorders things that are going to lead to an inability of the pituitary gland to secrete ACTH and thus stimulating the adrenal cortex to release its corticosteroids and finally the last category that we have here is what we call the tertiary and this is really gonna be the result of long term steroid use and so what happens here is we have a failure of the adrenal gland to resume production of cortisol as a result all right so knowing that we have these different types of causes that are ultimately going to lead to a problem producing the corticosteroids from the adrenal cortex let's talk a little bit about the the pathology of what's happening in our patients who have Addison's disease there's two major pathways that are really going to contribute to these problems that we see the first is going to be as a result of our decrease in our cortisol level and because cortisol is one of our stress response hormones we're gonna see things like decrease in our glucose production we're also gonna see a decrease in the metabolism of our fats and proteins a decreased appetite a decreased intestinal motility a decreased vascular tone as well as a decrease in our catecholamine effectiveness and these are our EPI and Nour epi and so really you can think about this as our body having less of an ability to handle stress because we have less of this stress hormone that's available and so when our patients become stressed due to many different sources that this can often lead to profound cardiovascular collapse and so this is our big concern with these patients and oftentimes why you may be monitoring them within the ICU because they've perhaps experienced one of these stressing events and has ultimately landed them in the unit in your care now in addition to the decreased cortisol levels like we talked about we're also going to have a decrease in our levels of our aldosterone and we know aldosterone plays a very important role in our body's fluid regulation and so this is going to lead to a loss of sodium a loss of fluid and as a by-product a retention of potassium and so what this means for our patients is they're gonna end up with a decreased blood volume which if we add that on top of a stressing event that once again they become high risk for this cardiovascular collapse and so now let's talk some of the signs and symptoms that we're gonna see with these patients with Addison's though it's important to note that our signs and symptoms are often going to be nonspecific so here we're talking about things like headache fatigue anorexia depression nausea vomiting fever hair loss you could also experience hyperpigmentation hypotension even shock in these patients you're gonna see decreased sodium increased potassium and a hypoglycemia that's really unresponsive to therapy so none of these signs and symptoms are really going to jump out at us and tell us that this patient has Addison's disease we're going to really need to look into these symptoms as well as some specific tests that we can perform to really figure out how to diagnose these patients so first and foremost we're going to need to take a look at our labs so we want to check CBC CMP ABG cortisol and aldosterone levels and really we're looking for that hypoglycemia hyponatremia hyperkalemia and that decreased cortisol and so based on these signs and symptoms in these lab values we really may be suspecting that our patient has Addison's disease and so if we do suspect this then we're going to want to perform what we call the Kosan tropen stimulation test and so what we do here is we give them a dose of this Kosan tropen and 30 to 60 minutes later we should see a rise in our cortisol level and so if we don't see this rise that this is going to be diagnostic for this adrenal insufficiency that the patient has and so lastly let's talk about the treatment and our treatment for these patients are going to consist of primarily three things steroids fluids and glucose and so as you know here our patients don't have enough steroids so here we want to make sure that we're adding steroids in and our glucocorticoid replacement is going to be our first line treatment so these are things like our hydrocortisone we need to get these levels up which is really important and for our patients to help prevent that cardiovascular collapse now when we talk about our fluid volume replacement we might be replacing as much as five liters in these patients in the first 12 to 24 hours and so we're gonna need to replace this volume and we want to use either normal saline or normal saline with 5% dextrose but early on in these patients because of this volume loss as well as that possible cardiovascular collapse you may need to use vasopressors as well until you can get this volume replaced and finally like I said you want to replace the patient's glucose and this is why you may choose to add that dextrose in with the normal saline fluid replacement but it's gonna be very important that we're providing glucose to our patients because right now they're just not going to be producing their own alright so that pretty much concludes our talk on Addison's disease hopefully this makes us a little bit clearer for you guys and just remember that Addison's is a problem with not having enough of the corticosteroids and so this is why in our treatment we want to add those steroids back in so if you're trying to really understand this think about the problems that are gonna come from having too low levels of cortisol and aldosterone alright and so moving on now we're gonna talk about our Cushing's syndrome and so once again we're gonna have a problem with our corticosteroid production but as you can probably figure out where as in Addison's we didn't have enough and Cushing's syndrome we're actually going to end up with too much and so you may also hear Cushing's syndrome referred to as hyper courtesan and so like I said this is where we're gonna have an increased production of our glucocorticoids mineral corticoids as well as the androgen steroids and so in this case think we've got too much of the cortisol and too much of our aldosterone and so once again the increase in the amount of these hormones are where they're going to lead to the problems that we see in Cushing's syndrome so once again let's talk about some of the causes in this case for Cushing's syndrome and there's really just a few causes for this the first is going to be some sort of adrenal cortex tumor so these are usually like our adenoma 's and so in this case a tumor in the adrenal cortex is going to be causing an increase in these corticosteroids you also can see this in patients with pituitary tumors and so what's happening here is the pituitary tumor is causing the pituitary gland to release too much of the ACTH therefore over stimulating the adrenal cortex to over produce these corticosteroids you can sometimes see this in the case of long term steroid use and while this last case is pretty where it can be a result of some sort of ovarian or pulmonary neoplasms that are basically causing some sort of ectopic ACTH production basically you end up with these tumors that themselves produce ACTH thus over stimulating the adrenal cortex so let's go ahead and move on and talk about the patho involved here because it is going to be a bit different than what we see in Addison's disease so once again our normal process hypothalamus releases CRH tells the pituitary gland to release ACTH which goes to the adrenal cortex and thus produces its corticosteroids now as we had talked about in the first lesson we talked about that negative feedback mechanism and in this case the production of cortisol is actually going to cause the hypothalamus to decrease the production of CRH and so this should lead thus to a decrease in production of ACTH and thus ultimately a decrease in our cortisol production but we know in the case of Cushing's syndrome we have too much of this cortisol and like we talked about in the case of these adenoma 's that this is going to itself cause the higher release of cortisol independent of the normal process or pathway within the endocrine system a tumor in the pituitary gland is not going to be impacted by the release of CRH or the lack thereof and so we're going to continue to see that increase in the ACTH secretion and thus ultimately the increase in cortisol levels and as it's pretty obvious in the ectopic causes we're going to see high levels of ACTH and thus high levels of cortisol as a result and so one of the things that we're going to see as a result of this increased cortisol is where this is going to stimulate our glucose in Isis and our glycogenolysis and so this means that we're going to have an increase in our serial glucose level as well as an increase in our glycogen stores in the liver and you can think about these because these are normal processes that our body is going to go through in a normal stress response and here we have too much of these stress hormones floating around you're also going to see a decrease in protein synthesis as well as the catabolism of proteins and then finally there's a series of responses that we can really remember through the acronym big which is BB III G so the first B is for elevated blood pressure and so cortisol is going to activate the alpha-1 receptors thus leading to a higher blood pressure the next B is for inhibition of bone formation then the first eye is going to be for our anti-inflammatory the next eye is going to be a reduction in our immune system response and so finally the gia is for gluconeogenesis our lipolysis and our protein lysis and these again are all a response of that elevated cortisol level and thus that exaggerated stress response and these are all going to come in and play an important role when we talk about the signs and symptoms that we're going to expect to see in fact a lot of them go along with some of these issues we see summed up within this big acronym and so these are going to be things like hypertension osteoporosis our immune suppression and so that's gonna mean things like slow wound healing you're gonna see muscle weakness and this is because of that protein lysis and you're really gonna often see this with thin extremities and due to the increase in the storage of fat you're gonna see things like moonface which is that big round face the Buffalo Hump just fat storages on the back as well as just a general truncal obesity as a result of all this you're typically gonna see weight gain in these patients you'll have that hyperglycemia as well as the abdominal striae for those red stretch marks on the abdomen partially due to the increase in size but also as a result of the impaired collagen production because of that protein lysis now in these patients because of the increased aldosterone production you're now going to see hypernatremia and hypocalcemia so the opposite of what you'd see in Addison's you can also see excessive body hair particularly in women as well as these patients may be more prone to bruising so there definitely are some very telltale signs and symptoms that you're potentially going to see in your patient here especially with the the round face and the Buffalo Hump these can be dead giveaways that your patient has syndrome all right so with all that said let's talk about how we diagnose these patients so really our gold standard for this is going to be the 24-hour urine free cortisol but we can also do what we call the dexamethasone suppression test and so if we give a dose of dexamethasone we should see the body respond by suppressing the endogenous cortisol production you could also look at imaging studies like an MRI particularly of the head chest or abdomen but once you've done these and you've diagnosed your patient with Cushing's syndrome there are other tests that we can do to help differentiate between is this an adenoma or as a Cepheid - eteri tumor or some sort of ectopic ACTH production and so if we check our serum cortisol as well as our serum ACTH levels that this can help differentiate between is this an adrenal or a pituitary or ectopic source so if we have a low ACTH level we know the hypothalamus and thus the pituitary glands are responding appropriately to the negative feedback and thus suppressing our acth production therefore we know that those are fine and so this must be an adrenal source but in the cases where our ACTH is high we know that this should be low because we have high cortisol therefore we know that this is either a problem with the pituitary or some sort of ectopic ACTH production and so if we do find the case where the patient has this high ACTH level then we can actually do a high dose dexamethasone test and so by giving a very high dose of the dexamethasone that if this is a problem originating with the pituitary gland that with this high dose that we should be able to suppress the cortisol production and so if we see the cortisol level is suppressed after this dose we know that this is a pituitary problem whereas these ectopic sources of ACTH are not going to be affected or have any sort of negative feedback from this dexamethasone test and therefore we're not going to see any suppression of the cortisol and so finally if we talk about the treatment for these patients so it's really all going to revolve around controlling the cause so if our cause is from long-term steroid use then we're gonna do things like slowly decreasing our steroid dose if it's one of our other causes we can look at things like surgery and this could just be a surgery to remove the ectopic source of acth production this could mean adrenalectomy or you can also do a transfer noodle surgery to take care of a pituitary tumor but it's important to know that this may require lifelong hormone replacement therapy for these patients and then finally in the case of some of these pituitary tumors where surgery may not be an option then we can look at things like radiation therapy with the hope of shrinking and treating that pituitary tumor alright so that is gonna finish things up in talking about Cushing's syndrome so as you can see it's quite a bit different than Addison's disease well they ultimately are both dealing with some sort of problem with the corticosteroid production in the case of Addison's disease we don't have enough of it and so we're gonna see different effects as a result of this decrease in cortisol and decrease in aldosterone and typically you're going to see these thin week patients whereas in the case of Cushing's syndrome we actually have too much of the cortisol and aldosterone and so we're gonna see a different set of effects as a result of that and this is oftentimes very gonna see these large potentially hairy patients which really has this stand out when you compare these patients to the patients that you're gonna see with Addison's disease to opposite ends of the spectrum when dealing with a disorder within the same part of the endocrine system and so with that said as always I want to thank you so much for watching if you enjoyed this video and you found it useful please leave us a like down below as well as if you'd be interested in more of this critical care education then subscribe to our channel as well in the next lesson in this series we're gonna go on to talk about hypoglycemia as well as hyperglycemia and diabetes so make sure and subscribe to be notified when that lesson becomes available and in the meantime feel free to check out the last series that we did in which we did a good breakdown of heart failure as always thank you guys so much for watching and you have a wonderful day