Understanding Pituitary and Adrenal Disorders

this is chapter 54 care of patients with pituitary and adrenal gland problems our priority concepts are fluid and electrolyte balance cellular regulation and Immunity the pituary gland is H it has a significant role to produce and secrete hormones that help to regulate the body's endocrine functions it's divided into two lobes anterior and posterior the anterior portion is primarily responsible for uh synthesizing and and releasing essential hormones like growth hormone thyroid stimulating hormone lutenizing hor hormone follicular stimulating hormone and adrenocorticotropin hormone uh and prolactin the posterior lobe primarily stores and releases two essential hormones that include oxytocin and anti-diuretic hormone also known as vasopressin hypopituitarism can come from two primary sources first there could be pathology on the hypothalamus which is going to affect production of the Tropic hormones that affect the pituitary or there can be direct pathology that's uh influencing or affecting the pituitary gland itself the predominant cause in the majority of the cases is going to be an actual uh tumor in within the pituitary itself definition hypopituitarism is a medical condition that is insufficient hormone production of the pituitary gland the most life-threatening problems are when adrenocorticotropin or act or a thyroid stimulating hormone or TSH are deficient we mentioned that the most common cause is going to be a pituitary tumor this illustration shows that U that's the first one the adoma the second is an infar and it can come from a couple of different ways it could be actually through Hemorrhage and then the last empty Cella Could Happen by either the pituitary gland is flat it flattens or it's a small pituitary gland that could result from also from a hemorrhage where um the pituitary then goes under apoplexy or apoplexy which is basically it kind of shrinks and pushes off to the sides of the wall uh the other way that the the this pituitary CLI could become damaged is through like radiation uh radiation treatments or surgical Pro uh surgical procedure or trauma we will refer back to this illustration when we start talking about Addison and the clinical presentation hypopituitary arism carries more of an increased mortality risk from the cardiovascular and the respiratory diseases that are associated with it so early detection of this condition is really critical the symptoms that we find are actually related to the specific hormone that carries the deficiency table 54.1 we'll go over that in just a second um in your book describes some of those hormones and the the effects one of the first things that changes that you'll see first is vision changes especially the peripheral vision this table summarizes nicely the hormon secreted and the associated actions of specific interest want you to pay attention to the for the anterior pituitary act and growth hormone act its purpose is to stimulate synthesis and adrenal cortical St hormones and then growth hormone stimulates bone and muscle growth it promotes synthesis of of multiple things of fat metabolism uh protein synthesis and then decreases carb metabolism the posterior pituitary uh the one that want you to SP pay special note to is vasopressin um it's also called anti-diuretic hormone so what it does is it increases water reabsorption by the kidneys so you can see that if there's a deficiency in vasopressive then the body is not going to increase water reabsorption so there'll be quite a bit of excretion of very dilute urine the assessment for hypopituitarism can be kind of complex and a little bit puzzling uh because the pituitary stimulates other glands to secrete hormones and so when there's a deficiency the assessment can be all over the place so we're looking for signs associated with those hormone deficiency conditions if there's increase act that could lead to adrenal insufficiency the resulting symptoms could be fatigue postural hypotension if there's decrease and thyroid stimulating hormone then that's going to present as symptoms of hypothyroidism which we'll cover next week um the the presentation of the thyroid on palpation it's going to be softer a a smaller thyroid and then all the associated symptoms of hypothyroidism to include coarse dry skin thin hair or alopecia delayed tendon reflexes non-pitting edema cold skin and also a decreased ability to sweat if there's decreased growth hormone that's kind of self-explanatory in children they'll have short stature poor growth in adults that could present also with fatigue and weakness if there's a decrease in ADH U that could in turn cause diabetes and citus so they're going to have a dilute of large large amounts of urine and hypernatremia and then also some other other neuro and um vision changes that can occur and we kind of touched on this already they could result in Boral H Hemi anopsia which is a loss of that periperal peripheral vision and then extraocular paresis that basically is sluggish movement um of the eyes or the the triggering of the six muscles surrounding the eyes or uh could be result in um involuntary eye movement as far as the lab we could be testing for Baseline levels of pituitary hormones or the target gland hormones there's also a variety of dynamic function testing um you won't have to know the depths of this but just for your own information the dynamic testing could include an insulin tolerance test an act stem test um there's also a variety of different um x-ray radiological investigations that could be done to look at the pituitary also involves use the use of MRI they will use galum enhancement to visualize the pituitary the interventions and treatment are customized to address the underlying cause so typically if there's a mass then removal of a surgical removal of the mass is going to be a critical component and then the associated conditions have to be treated so that may mean replacement of the deficient hormones so that could include Androgen therapy hormone replacement therapy growth hormone replacement if there's anti-diuretic deficit then we're going to be replacing that um with baso pressin or desmopressin that could be either orally or intranasal hyper pituitarism is excessive production of the hormones that are secreted by the pituitary the most common cause again is a pituitary adenoma most of the tumors are going to cause hyper secretion of the hormones about 2/3 of the pituitary adoma are going to cause overproduction of hormones the path of can really vary quite a bit pomas that stimulate growth hormone could end up causing something called gigantism we'll talk about that here in just a second uh those that produce an increase in act will lead to over production of cortisol leading to something called Cushing disease we'll talk about that here in just a second as well there's a handful of different types of adenomas as well but we're going to focus primarily on the ones I already mentioned as well as acromegaly the symptoms are going to also vary depending on what the hormone is or hormones are that are NEX us we'll first want to assess for any local effects of a pituitary tumor will'll um try to assess for any changes in visual fields uh whether they have a presence of a headache you want to ask whether there's a family history of any kind of endocrine tumors and the um adomas may present on Imaging such as MRI then we'll assess for a variety of different symptoms that break off based on what the hormone is that's being produced in excess if there's an excess production of growth hormone uh then it could also Elevate insulin like growth factor that's going to result in symptoms of acromegaly there's a a graph or a a diagram we're going to show here next slide um unfortunately recognizing acromegaly that can take some time but for acromegaly some of the symptoms that we would look for or some of the signs would be uh skeletal overgrowth of flat bones like the mandible that'll be really super prominent um you'll ask the patient whether or not as they're an adult whether they've had an increase in shoe size like after growth should have already uh ceased uh they could have an overgrowth of skin and subcutaneous tissue they could have skin tags the issues could also present into organ systems like um they could develop cardiomyopathy which is an enlarged heart they could have uh symptoms such as carpal tunnel syndrome because of the compression of the medium median nerve they could have a variety of different osteoarthritis symptoms and they could have cardiovascular metabolic disturbances to include include hypertension dyslipidemia even obstructive sleep apnea they also could develop diabetes militis if the excessive production of growth hormone occurs in children before their growth plates are fused uh especially in the femur and the tibia then that could result in gigantism if there's an excess production of thyroid stimulating hormone then they're going to present with symptoms of hyperthyroidism which we're going to discuss next week uh but as TSH increases then um the hyperthyroidism symptoms are going to include weight loss heat intolerance um palpitations anxiety Etc if there's an excess production of Adeno corticotropic hormone then um we're going to look for features of Cushing syndrome which is hypercorticism so we'll look for things like muscle wasting um they can have that buffalo hump or that dorso cervical f pad um they could potentially have excessive bruising um blood pressure increases glucose intolerant they could have also that central obesity with um stria in the abdomen excessive production of prolactin could lead to decrease libido infertility osteoporosis in males um impotence could be a finding as far as diagnostic studies um we are going to potentially look at lab tests of the suspected excess hormones as far as Diagnostics um they could potentially use galum enhanced MRI galum it's um uh basically a contrast agent that has magnetic properties it helps for better visualization of non-bony tissues getting random growth hormone levels typically is not very helpful instead um well do suppression testing so a per the oral glucose solution um the suppression test involves the patient uh consuming a glucose formula and then growth hormones are then taken at set time frames usually like right away within an hour within a couple hours to assess for hypercortisolism confirmation um they can do something called a salivary cortisol test you might also be involved in a 24-hour urine collection for looking for free cortisol there could also be an overnight dexamethasone suppression test or ODST patient will take 1 milligram of dexamethasone uh usually very late at night close to midnight and then uh we'll draw a serum cortisol the very next day the very next morning between like 800 or 9:00 a.m. a normal finding will be that cortisol is going to be less than 1 .8 but also keep in mind that there are medications that could interfere with the test uh specifically photoin is one of the culprits and then finally they could order something called a lowd dose dexamethazone suppression test where the patient is taking a lower dose of dexamethasone in the morning and then uh they'll do it at set intervals usually every 6 hours for a couple of days the cortisol levels are measured at specific time frames again keeping in mind that there are not only medications there's also conditions that could interfere with these tests such as obesity alcoholism this illustration of acromegaly you'll notice that the prominence features the prominence of the forehead the jaw features that have continued to really roughen up and and continue to grow this is caused by growth Harmon hypers secretion and go ahead and put this video on pause and take a minute to just kind of read the different captions just kind of reiterates what we already discussed the goals and treatment of hyper pituitarism is going to be to return the hormone levels back to normal and reduce and remove symptoms if possible also to reverse body changes that's not always possible as far as pharmacological long-term management uh that typically tends to be only beneficial for prolactinomas um some of the strategies could be dopamine Agonist um and then possibly somatostatin analoges and competitive receptor antagonists two medications specifically that can be used for prolactinomas are going to be bromocryptine and cab GoLine radiation therapy targeting the adoma could also be potentially beneficial but ultimately for adenomas other than prolactinomas the definitive treatment is going to be a rem surgical removal of the pituitary and that's called a hypophysectomy they'll U use a transphenoidal approach that's typically the recommended route but then if the adenoma has become very very large uh removal may not be completely possible so the smaller the adenoma the higher the success rate of the surgical removal for posttop management of these patients remember they just went transphenoidal and it's kind of hard to see in this U illustration but they act the pathway is actually going right through the spinoid sinus and into the celera you can see the close proximity to the midbrain and the ponds because we're always concerned of um laceration or impeding into the subarachnoid space we're going to look for those potential signs and symptoms of leakage of cerebral spinal fluid um they just had surgery here so we want to teach the patient to report any signs of a post-nasal drip especially if it's a constant clear running uh kind of feeling um if they have any increased need for swallowing again that could indicate that they're leaking cerebral spinal fluid we want to make sure that we teach the patient to avoid coughing you don't want anything that has like these these surges of these this intense increase in interc cranial pressure um so other signs that we would look for that would indicate potential CSF leak would be if um we notice or they the patient notices that there's like a drop area or um fluid on the pillow that then turns into kind of a Halo pattern that could indicate that that's cerebral spinal fluid now let's move on to diabetes insipidus um that's kind of the the we're phasing that word out it's now called Arginine vasopressin deficiency or avpd and if it's Argan vasopressin resistance it's abpr if you remember from slide six earlier um we talked about the posterior pituitary is involved with secretion of ad DH or anti-diuretic hormone also known as vasopressin so when there's a problem here and there's a decrease in antidiuretic hormone the result is um that there's going to be an excretion of really hugely large amounts of very dilute urine there's the four different uh classifications we'll just touch on a couple um primary neurogenic also Central that can be caused by trauma um um decreased hypothalamus synthesis and Inter cranial masses this is resulting in a decreased um secretion of anti-diuretic hormone by the posterior pituitary then secondary neurogenic is really usually or renal in origin some potential drug related causes of diabetes and cidus could include um I'll just list three medications first lithium um it's an antimanic mood stabilizer as you know but I'm not really even sure if they even um prescribe that anymore another is foscarnet which is an antiviral that usually is used to treat Hepatitis B or CMV and then the last one is uh clopine not to be mistaken with clonazepam Kazaam is a benzodiazapine that's not what causes diabetes and citus but clopine is also an anti-choicers of Di our assessment is going to build on the categories that we just covered um we will ask whether or not the patients have had a recent cranial surgery do they have a history of head trauma what medications have they taken in the past and currently taking have they experienced the symptoms such as excessive thirst and then an increase and a tremendous increase in urination is what we're looking for and then do we have they reported any symptoms related to dehydration um we will probably um ask them to help or if they're impatient perform a 24-hour eyes and nose um when we run Diagnostics the urine is going to be very diluted with a specific gravity less than the lower end of normal of 1.005 and then Ur an osmolality um would be less than 300 we they would also exhibit hypernatremia and probably hypoy and what they need was anti-diuretic hormone so we're going to be giving them desmopressin um there's a couple of different ways you can give it if they're able to tolerate nasal spray is probably going to be the quickest way and the easiest way um you could also potentially give it IV or subq but it's going to be usually a nasal spray right away our goals are and interventions are going to be trying to prevent uh dehydration or manage the symptoms and the potential uh sequella of dehydration will encourage if they can uh fluid intake to equal urine output but in some cases it's just not easy to keep up so for these particular patients we're going to start IVs and um probably anticipate that we're going to give them pretty large volumes of fluid until the Vaso pressent takes effect and the urine output starts to decrease um if they're at risk for this being a recurring problem then they're going to need to wear Medic Alert bracelet um and then they should educated on the signs and symptoms of water toxicity water toxicity affects uh serum sodium that could very rapidly escalate and cause neuro neuros symptoms so they need to learn what those are and call 911 or go to the ER immediately um again so starting IVs um monitoring electrolytes and replacing those accordingly we can anticipate that we're going to be doing that around the clock I'm going to have you pause the video here in just a second so you can review the remainder of this illustration but first I wanted to point out again for diabetes and citus we're talking about posterior um the posterior portion of the pituitary and then if you focus on the bottom right you'll notice here the nursing care will also again emphasizing monitoring fluids replacing those fluids checking neurostatus will be uh critical uh following and trending Vital Signs and then assessing mucous membranes and other signs and symptoms of potential dehydration uh so we did review the other symptoms go ahead and pause the video and review the rest of the illustration let's talk about syndrome of inappropriate anti-diuretic hormone or sadh that's a condition that's caused by unsuppressed release of anti-diuretic hormone that can come from the pituitary gland or other sources that have continued action on the vasopressin receptors some potential other conditions that could lead to sedh could include things such as small cell lung cancer that's probably the most common tumor that's related to ectopic anti-diuretic hormone production Some central nervous system disorder uh disturbances like stroke Hemorrhage um mental illness and psychosis infection and Trauma there's some medications that could also cause sadh for example a couple of anti-convulsive one for example is carbamazapine oxcar bipen being another serotonin reuptake Inhibitors or ssris could also potentially lead to sadh some other malignancies that could cause it in addition to small cell lung cancer um head and tumor neck cancers um olfactory neuroblastomas those could all lead to ectopic anti-diuretic hormone release interestingly ecstasy um can also be associated with direct release of anti-diuretic hormone sometimes there are pulmonary diseases that have been Associated withh although the mechanism isn't exactly known what the connection is um it's a for example some of the you'll be surprised to know that some of those diseases could include um atelectasis acute respiratory failure or pneumothorax also pneumonia it doesn't matter if it's bacterial or viral there could be a connection and even tuberculosis there could also be a tie in between sidh and hormone Administration um let's say that somebody's getting um desmopressin to treat um hemophilia or platel dysfunction or they're getting they're getting oxytocin to induce labor um all of those can cause potentially an activation of the Vaso pressent 2 receptors that could then tie into siadh that's a little concerning the incidence of sadh tends to increase with age but uh that's not to say that children can get the get this as well so anti-diuretic hormone um we know we call that Arginine vasopressin is formed in the hypothalamus it's stored in the posterior pituitary and the most important function of anti-diuretic hor hormone is to maintain plasma tonicity in short sdh uh is water retention and fluid overload hyponatremia happens with the water retention there's dilutional hyponatremia and that increased blood volume uh leads to increased kidney filtration decreased renin and aldosterone there's an increased sodium loss via urine please review the medical history in your text in box 54.4 so when we assess these patients we're going to look for signs and symptoms of hyponatremia which would include um there's decreased extracell fluid osmolality that could cause water to move back into the cells causing cerebral cerebral edema so the early signs that you might see would be that they complain of headache um they're having problems concentrating or they could become lethargic and even obtunded so changes in level of Consciousness would be something to assess for in severe cases they could actually even seize or even go into respiratory arrest treated it could proceed into a coma State interestingly if patients have a chronic state of hyponatremia they could somehow adapt where they could potentially be asymptomatic despite having a low serum sodium other signs and symptoms could include fatigue dizziness muscle cramps nausea and vomiting again all these symptoms potentially associated with hyponatremia there risk at Falls uh fall risk RK you want to ask them whether they have a history of a head injury um what's their weight done has it fluctuated have they lost a lot of weight do they have any pulmonary symptoms are they abusing any substances heroin ecstasy and myth other assessment points um are tied into volume status we will place them on daily weights have they noticed that they've gained weight as they're holding on to water uh pulses will probably be re bounding unless there are also exhibiting signs of heart failure they might be hypothermic as well keep in mind that they may be starting to hang on to fluid but not yet exhibiting signs of overload such as jvd um Etc so that's something to keep into consideration dep paying on hard early in the game we're catching them um their urine output we'll probably be measuring eyes and nose because we would expect that that's going to decrease and the urine osal ity is probably going to increase as well the lab panels that we'll do for sidh patients are listed here we'll check serum osmolality serum of sodium urine sodium and osmolality bu and creatinin blood glucose thyroid profile serum cortisol and then uh we're looking for electrolyte shifts so potassium and chloride and also looking for bicarb additional tests might include a fasting lipid profile and liver function tests for these patients we're going to absolutely place them on eyes and no and daily weights we need to restrict their fluids um we're going to monitor them for signs of fluid overload their fluid restriction for 24 hours is usually going to be 800 Ms or less and the goals of therapy are going to be to correct hyponatremia and hopefully increase water excretion couple of different medications that could be used are a couple of VAP Tans uh vasopressin re antagonist conivaptan and Tall vaptan to correct sodium assuming that the patients are not in Dire Straits uh they might get uh sodium po or sodium tablets in addition they might actually add a loop diuretic such as feros amide that combination will help decrease urine concentration and hopefully increase water excretion if the patients are more critical we might give a hypertonic saline but generally that's held more for the ICU environment we'll talk more about that in complex 2 um if we correct sodium too quickly we could potentially cause a complication called omotic demyelination syndrome or locked in syndrome that's rever not non-reversible and could be actually lethal these folks will absolutely have no free water whatsoever we want to use saline to dilute any inal feeds at all um we need to obviously perform frequent neuro checks and continue to monitor Vital Signs and any signs and symptoms of ongoing fluid overload moving on to Cushings And Addison's disease um at your leisure take a look at this video it's about 19 minutes long and she does a very nice job of summarizing the differences between Cushings and Addison um the link is on the bottom left there just in case this active link um if we lose that in the video conversion and we'll come back to this illust ation a little bit later uh but side by side looking at Addison versus Cushings on the left Addison is a result of under reactive adrenals uh causing an adrenal crisis and then on the right Cushing syndrome is on the other side of the spectrum now you've got overreactive adrenals or too much circulating cortisol and again we'll come back to that after we describe each in detail first will cover adrenal gland hypo function that can be categorized into three causes the first uh primary secondary and tertiary causes so the adrenal cortex as you know is responsible for producing glucocorticoids mineral corticoids and androgens primary adrenal insufficiency occurs when there there's something that's affecting the adrenal gland itself secondary um insufficiency results from there's a decreased level of act that's being relased from the pituitary and then then tertiary adrenal insufficiency is caused by a decreased level of corticotropin releasing hormone that's being released from the hypothalamus Addison's disease is categorized as primary the other thing to consider is whether this is a chronic onset or an acute onset chronic presentation can be actually kind of tough to to pick up on whereas an acute onset of adrenal insufficiency can be life-threatening and can occur when the patient's already in a critical state for our assessment for these patients make sure that you review box 54.5 in your text as that will present the causes that can help tailor your um history approach and also your assessment of these patients we want to ask these patients history wise um whether they have a history of autoimmune disease and what medications have been taken of particular interest is going to be whether they've been taking exogenous steroids um you learned in your Pharmacy class the importance of tapering off steroid use and the reason for that is we're trying to prevent these um the patients from kicking into acute onset uh adrenal insufficiency the symptoms could be actually quite varied they might present with hypotension altered mental status uh they could have GI symptoms as well anorexia vomiting uh weight loss fatigue um and they could also have recurrent abdominal pain there are reproductive complaints that could occur as well in women Amara loss of libido and a decreased axillary and pubic care they could be craving salt and have orthostatic hypotension especially with primary adrenal insufficiency because of the volume depletion um so everything is kind of going low and slow patients could have poor skin turer and increased skin pigmentation some patients will develop shock um and hypotension can be present in any form of adrenal insufficiency additional things to ask and assess for is um hypoglycemia and fluid depletion there's a variety of multiple lab tests that could be done and including also di um CT and MRI imaging that could be helpful potentially common lab findings uh with somebody that has primary adrenal insufficiency are anemia hyponatremia and Hyper calmia this information is also in your text it's a nice summary of the systems and the symptoms and the Diagnostics we already me mentioned the only thing that we haven't touched on is we could do something called an act stimulation provocative test uh so go ahead and pause the video and review the systems that are listed here and the associated symptoms the treatment strategies are hoping to promote fluid balance um regardless of whether the onset is chronic or acute it's probably going to involve replacement of glucocorticoids probably mineral corticoids as well um we'll do a variety of different things we'll monitor them for fluid volume status and preventing hypoglycemia we want to assess not only cardiac function but um all the body systems that were listed previously will weigh them daily and we're going to monitor electrolytes and a variety of different other diagnostic exams the steroid replacement could be hydrocortisone prazone or dexamethazone and there's a variety of different regimens that could be used if this is an acute onset and there's an adrenal crisis um we're going to start two large boore IVs we're going to send off Electro ites will check their glucose and then we're also going to measure plasma C cortisol and act we should be prepared to administer uh at least a couple of liters of isotonic saline these patients could become very unstable and hypotensive so U they'll probably have some sort of hemodynamic monitoring you can prepare for and anticipate that we're going to probably be given a hydrocortisone about 100 milligrams IV and then every 6 hours we'll give a dose usually about half of that for the first 24 hours and it'll they'll be tailored depending on the patient's condition in addition we'll be replacing any potential deficient electrolytes after hyponatremic that's usually self-correcting once we get the cortisol and the volume repleted once they start stabilizing we'll slow down the IV fluid replacement and then again of course we know that we're going to have to taper the steroids off slowly over one to three days we talked about hypofunction of the adrenal glands now let's talk about hyperactive uh let's talk about the difference between Cushing syndrome and Cushing disease syndrome is a group of symptoms that occur together for Cushing syndrome that typically occurs when C levels go up and it could be through a variety of different causes but medications tends to be the most common Cushings Disease or disease in general is a disorder with a known cause a distinctive group of signs and symptoms Andor anatomical changes and cushion Cushing's Disease uh then tends to be caused by usually a pituitary aboma which then leads to increased act which then increases uh cortisol production by the adrenals and that's what leads to the distinctive disease signs and symptoms and presentation ping syndrome as we mentioned the ideology is going to be prolonged exposure to high cortisol so it's going to be caused typically caused by drug therapy for another health problem for example um somebody has an inflammatory process going on that needs significant corticosteroid treatment if it's a non-drug cause that tends to be a pituitary abnoba but again keep in mind that for syndrome typically it's it tends to be exogenous corticosteroids women tend to be affected more than men and so ideally for disease prevention providers will um if they're going to start with high doses of steroids they'll try to taper down to the lowest effective dose and as we've mentioned previously when it comes time to discontinu therapy there'll be a taper down versus cutting off the cortico steroids abruptly so for purposes of our remaining discussion just go ahead and view Cushing syndrome and Cushing disease together uh the clinical presentation and the treatment strategies are going to be relatively the same and you won't run into a scenario from the assessment perspective where you'll have to distinguish Syndrome from disease interestingly so in Cushing's disease um Act production can stay the same but then there's loss of that circadium Rhythm um the normal circadium Rhythm response so when it when things are supposed to power down they aren't so there's a consistent higher level of act production that leads to adrenal hyperplasia and then there's um overproduction of cortisol more than is needed then the consequences of that persistently High cortisol is what's going to lead to some complications at that there's going to feed our um assessment points it could lead to hypertension hypokalemia um through the e and this summarizes what we just discussed go ahead and pause the video and take a second to kind of go around and review these signs and symptoms of Cushing syndrome our assessment continues with Diagnostic lab and imaging some of these tests are going to sound very familiar uh we could potentially participate in helping the patients with blood salivary and urine cortisol levels um we'll look for increase increases in serum glucose and sod will'll expect to send off cbcs and electrolytes look for decreased lymphocytes look at calcium levels um these folks may also have a dexamethasone suppression test the late night salivary cortisol test tends to be most popular probably because it's easier but if done correctly they have a sensitivity of specificity pretty high nearing 98% as far as a urine cortis all testing keep in mind that um these are snapshots so typically that those tests are going to be repeated three times just to make sure that we didn't catch kind of a snapshot during a high stress U period there are other some other interfering factors such as alcoholism um sleep apnea and a couple of other things so that's why we would repeat the test three times the dexasone suppression testing so it will there's a couple of different approaches and we mentioned these already um they could be um administered either kind of like a a a dose and then excuse me the dose can be given very late at night close to midnight and then we'll measure the serum cor cortisol first thing in the morning so we would expect uh the normal response would be that the cortisol level is going to remain less than 1.8 another approach would be um to give half a milligram uh po at 6 hour intervals for a couple of days and then we're still going to measure the cortisol levels uh typically at 6 hour marks or we may actually wait until the last dose is administered and give that um send that that off to lab unfortunately there are some interfering drugs uh that could generate a false positive such as oral contraceptives and estrogens the Diagnostics are also going to sound familiar unfortunately if the culprit is a small adenoma or a micro adenoma it might not be picked up in CT or MRI ultimately the things that we want to prioritize as a team is um want to manage any potential fluid overload um we're going to watch inbalance electrolytes specifically calcium and sodium uh there's that potential for injury due to that skin thinning that becomes very very fragile so for us the implications are going to be that we don't want to put any tape on these folks we're going to really rip their skin to Pieces um also their decreased density loss we need to be mindful of that and educate the patient as well there's a potential for infection because of the reduced immunity so we need to not necessarily need to put them on precautions or isolation but uh we need to make sure that we use good clean and aseptic technique when appropriate and teach the patients good handwashing as well as visitors so our plan is to restore that fluid balance prevent injury and prevent infection first line treatment if it's an act secreting tumor U then it's going to be surgical reection of that tumor again this is going to sound very familiar they'll use a transphenoidal approach uh but they can also go endonasal or sublabial either way the precautions and the posttop care is going to be the same we don't want anything that's going to raise intracranial pressure we're going to watch them for leaks for CSF um make sure that we you go back back and review the recovery for these patients and even after after attempted resection if the syndrome and disease persists there might be additional therapies that we'll try we could do um external beam pituitary radio therapy or radiation therapy they might actually try the resection again although the second time around tends to be even less successful and something to keep in mind is with all that manipulation there could be complications to include the development of fluid and electrolyte abnormalities neuro deficits you know think of the anatomy again and the development of diabetes and citus and lastly if all Elis is failing they could potentially have a bilateral adrenalectomy um if that's going to ultimately immediately reduce uh cortisol levels but then of course these patients are going to have lifelong therapy they're going to have to take glucocorticoids and mineral corticoid replacement therapy our evaluation is going to focus on what our priorities were we're going to hopefully have prevented um shifts and fluid and electrolytes so they'll be back to homeostasis they they will have remained free from injury and again remember that includes things that we do to the patient as well uh that the patient remained free from infection and also it's knowledgeable so they're able to participate in those prevention strategies and that that we didn't kick them over to the other side where they're exp experiencing acute adrenal insufficiency to prepare them for transitioning and Home Care um the self-management remember that they they're going to have that muscle weakness so maybe they're going to have to live on one floor for a while if they've got a two-story or three-story home uh if they need assistance we'll have to make sure that case management is is working with them to get them assistant devices or maybe even some Home Care they're going to Le require lifelong therapy of exogenous glucocorticoids then we'll get them educated with with that there's an ongoing concern with fluid and electrolyte balances we'll need to address those as well if they had a bilateral adrenalectomy then additionally they're going to have to have hormone replacement therapy and then any uh precautions that they'll need to take if they have reduced immunity coming back to this this illustration that we showed earlier I want you to pause the video and take a look comparison comparing Addison's disease to Cushing syndrome Cushing's disease um Addison on the left there's this is a result of under reactive adrenals there's not enough production of cortisol and AD aldosterone so when you look at the patient um the signs and symptoms everything's kind of getting low and slow and then on the right hand side you've got over adrenal over production of cortisol overactive adrenals and as you go around the symptomology that uh some of those S tend to be increasing symptoms related to the cortisol such as uh potentially hyperglycemia the CNS irritability um GI distressed and increased acid fat deposits on the face the back of the shoulder so they'll get that buffalo hump the face is starting to look really really round it's called a moon face then there's this the um atypical but very unpleasant symptoms you know that thin skin the purple stri this is pointing to the leg but keep in mind that you'll see them especially around the belly area so the abdomenal they'll look like stretch marks except with a lot of uh it's not pigment they'll just look kind of a deep purple and again pause the video and review these symptoms aldosteronism happens because there's excess production of aldosterone from the adrenal glands aldosterone is a mineral corticoid hormone that increases sodium and water retention so ultimately it's going to raise blood pressure initially can be very tricky to diagnose because clinically it's going to present as either mild or a severe refractory hypertension so that blood pressure could be elevated um mildly or it could be significant and persistent as kidneys retain sodium and excrete potassium there's the development also of metabolic alkalosis primary hyper ostrin ism is due to an excess and production of um aldosterone by the adrenal gland and secondary hyper aldosteronism is potentially inappropriate activation of the RASS and then that results in increased ostrin production some key points for assessing these folks is their clinical presentation may be that they have again as I mentioned refractory hypertension so somebody that presents and they're already on three anti-hypertensive meds but they're not having good results and a complication of long-term hypertension might be for example um enlargement of the left ventricle so you might hear an S4 as a result some increased risk factors for developing hyperaldosteronism include um hypokalemia whether um they developed spontaneously or due to thide use of diagnosis of an adrenal adoma and then have a familial history of cardiovascular events at a younger age most common treatment is going to be removal of either one or both adrenal glands there's a handful of different tests that could be done by suppressive testing an example of why maybe perhaps both adrenals are not removed is that for example if they do find an adoma in Diagnostic Imaging on only one of the adrenals then it would make sense to just remove that one adrenal gland Imaging studies again include CT or MRI a big concern is going to be the development of cardiovascular complications as a result of longstanding hyperaldosteronism and these could include things like like myocardial fibrosis LT ventricular hypertrophy uh even an MI myocardial infection cium sparing diuretics spol lactone is typically administered this concludes the voiceover presentation the remainder of the slides are for you to review at your leisure um go ahead and pause the video and make sure that you do go over the questions e e

this is chapter 54 care of patients with pituitary and adrenal gland problems our priority concepts are fluid and electrolyte balance cellular regulation and Immunity the pituary gland is H it has a significant role to produce and secrete hormones that help to regulate the body&#39;s endocrine functions it&#39;s divided into two lobes anterior and posterior the anterior portion is primarily responsible for uh synthesizing and and releasing essential hormones like growth hormone thyroid stimulating hormone lutenizing hor hormone follicular stimulating hormone and adrenocorticotropin hormone uh and prolactin the posterior lobe primarily stores and releases two essential hormones that include oxytocin and anti-diuretic hormone also known as vasopressin hypopituitarism can come from two primary sources first there could be pathology on the hypothalamus which is going to affect production of the Tropic hormones that affect the pituitary or there can be direct pathology that&#39;s uh influencing or affecting the pituitary gland itself the predominant cause in the majority of the cases is going to be an actual uh tumor in within the pituitary itself definition hypopituitarism is a medical condition that is insufficient hormone production of the pituitary gland the most life-threatening problems are when adrenocorticotropin or act or a thyroid stimulating hormone or TSH are deficient we mentioned that the most common cause is going to be a pituitary tumor this illustration shows that U that&#39;s the first one the adoma the second is an infar and it can come from a couple of different ways it could be actually through Hemorrhage and then the last empty Cella Could Happen by either the pituitary gland is flat it flattens or it&#39;s a small pituitary gland that could result from also from a hemorrhage where um the pituitary then goes under apoplexy or apoplexy which is basically it kind of shrinks and pushes off to the sides of the wall uh the other way that the the this pituitary CLI could become damaged is through like radiation uh radiation treatments or surgical Pro uh surgical procedure or trauma we will refer back to this illustration when we start talking about Addison and the clinical presentation hypopituitary arism carries more of an increased mortality risk from the cardiovascular and the respiratory diseases that are associated with it so early detection of this condition is really critical the symptoms that we find are actually related to the specific hormone that carries the deficiency table 54.1 we&#39;ll go over that in just a second um in your book describes some of those hormones and the the effects one of the first things that changes that you&#39;ll see first is vision changes especially the peripheral vision this table summarizes nicely the hormon secreted and the associated actions of specific interest want you to pay attention to the for the anterior pituitary act and growth hormone act its purpose is to stimulate synthesis and adrenal cortical St hormones and then growth hormone stimulates bone and muscle growth it promotes synthesis of of multiple things of fat metabolism uh protein synthesis and then decreases carb metabolism the posterior pituitary uh the one that want you to SP pay special note to is vasopressin um it&#39;s also called anti-diuretic hormone so what it does is it increases water reabsorption by the kidneys so you can see that if there&#39;s a deficiency in vasopressive then the body is not going to increase water reabsorption so there&#39;ll be quite a bit of excretion of very dilute urine the assessment for hypopituitarism can be kind of complex and a little bit puzzling uh because the pituitary stimulates other glands to secrete hormones and so when there&#39;s a deficiency the assessment can be all over the place so we&#39;re looking for signs associated with those hormone deficiency conditions if there&#39;s increase act that could lead to adrenal insufficiency the resulting symptoms could be fatigue postural hypotension if there&#39;s decrease and thyroid stimulating hormone then that&#39;s going to present as symptoms of hypothyroidism which we&#39;ll cover next week um the the presentation of the thyroid on palpation it&#39;s going to be softer a a smaller thyroid and then all the associated symptoms of hypothyroidism to include coarse dry skin thin hair or alopecia delayed tendon reflexes non-pitting edema cold skin and also a decreased ability to sweat if there&#39;s decreased growth hormone that&#39;s kind of self-explanatory in children they&#39;ll have short stature poor growth in adults that could present also with fatigue and weakness if there&#39;s a decrease in ADH U that could in turn cause diabetes and citus so they&#39;re going to have a dilute of large large amounts of urine and hypernatremia and then also some other other neuro and um vision changes that can occur and we kind of touched on this already they could result in Boral H Hemi anopsia which is a loss of that periperal peripheral vision and then extraocular paresis that basically is sluggish movement um of the eyes or the the triggering of the six muscles surrounding the eyes or uh could be result in um involuntary eye movement as far as the lab we could be testing for Baseline levels of pituitary hormones or the target gland hormones there&#39;s also a variety of dynamic function testing um you won&#39;t have to know the depths of this but just for your own information the dynamic testing could include an insulin tolerance test an act stem test um there&#39;s also a variety of different um x-ray radiological investigations that could be done to look at the pituitary also involves use the use of MRI they will use galum enhancement to visualize the pituitary the interventions and treatment are customized to address the underlying cause so typically if there&#39;s a mass then removal of a surgical removal of the mass is going to be a critical component and then the associated conditions have to be treated so that may mean replacement of the deficient hormones so that could include Androgen therapy hormone replacement therapy growth hormone replacement if there&#39;s anti-diuretic deficit then we&#39;re going to be replacing that um with baso pressin or desmopressin that could be either orally or intranasal hyper pituitarism is excessive production of the hormones that are secreted by the pituitary the most common cause again is a pituitary adenoma most of the tumors are going to cause hyper secretion of the hormones about 2/3 of the pituitary adoma are going to cause overproduction of hormones the path of can really vary quite a bit pomas that stimulate growth hormone could end up causing something called gigantism we&#39;ll talk about that here in just a second uh those that produce an increase in act will lead to over production of cortisol leading to something called Cushing disease we&#39;ll talk about that here in just a second as well there&#39;s a handful of different types of adenomas as well but we&#39;re going to focus primarily on the ones I already mentioned as well as acromegaly the symptoms are going to also vary depending on what the hormone is or hormones are that are NEX us we&#39;ll first want to assess for any local effects of a pituitary tumor will&#39;ll um try to assess for any changes in visual fields uh whether they have a presence of a headache you want to ask whether there&#39;s a family history of any kind of endocrine tumors and the um adomas may present on Imaging such as MRI then we&#39;ll assess for a variety of different symptoms that break off based on what the hormone is that&#39;s being produced in excess if there&#39;s an excess production of growth hormone uh then it could also Elevate insulin like growth factor that&#39;s going to result in symptoms of acromegaly there&#39;s a a graph or a a diagram we&#39;re going to show here next slide um unfortunately recognizing acromegaly that can take some time but for acromegaly some of the symptoms that we would look for or some of the signs would be uh skeletal overgrowth of flat bones like the mandible that&#39;ll be really super prominent um you&#39;ll ask the patient whether or not as they&#39;re an adult whether they&#39;ve had an increase in shoe size like after growth should have already uh ceased uh they could have an overgrowth of skin and subcutaneous tissue they could have skin tags the issues could also present into organ systems like um they could develop cardiomyopathy which is an enlarged heart they could have uh symptoms such as carpal tunnel syndrome because of the compression of the medium median nerve they could have a variety of different osteoarthritis symptoms and they could have cardiovascular metabolic disturbances to include include hypertension dyslipidemia even obstructive sleep apnea they also could develop diabetes militis if the excessive production of growth hormone occurs in children before their growth plates are fused uh especially in the femur and the tibia then that could result in gigantism if there&#39;s an excess production of thyroid stimulating hormone then they&#39;re going to present with symptoms of hyperthyroidism which we&#39;re going to discuss next week uh but as TSH increases then um the hyperthyroidism symptoms are going to include weight loss heat intolerance um palpitations anxiety Etc if there&#39;s an excess production of Adeno corticotropic hormone then um we&#39;re going to look for features of Cushing syndrome which is hypercorticism so we&#39;ll look for things like muscle wasting um they can have that buffalo hump or that dorso cervical f pad um they could potentially have excessive bruising um blood pressure increases glucose intolerant they could have also that central obesity with um stria in the abdomen excessive production of prolactin could lead to decrease libido infertility osteoporosis in males um impotence could be a finding as far as diagnostic studies um we are going to potentially look at lab tests of the suspected excess hormones as far as Diagnostics um they could potentially use galum enhanced MRI galum it&#39;s um uh basically a contrast agent that has magnetic properties it helps for better visualization of non-bony tissues getting random growth hormone levels typically is not very helpful instead um well do suppression testing so a per the oral glucose solution um the suppression test involves the patient uh consuming a glucose formula and then growth hormones are then taken at set time frames usually like right away within an hour within a couple hours to assess for hypercortisolism confirmation um they can do something called a salivary cortisol test you might also be involved in a 24-hour urine collection for looking for free cortisol there could also be an overnight dexamethasone suppression test or ODST patient will take 1 milligram of dexamethasone uh usually very late at night close to midnight and then uh we&#39;ll draw a serum cortisol the very next day the very next morning between like 800 or 9:00 a.m. a normal finding will be that cortisol is going to be less than 1 .8 but also keep in mind that there are medications that could interfere with the test uh specifically photoin is one of the culprits and then finally they could order something called a lowd dose dexamethazone suppression test where the patient is taking a lower dose of dexamethasone in the morning and then uh they&#39;ll do it at set intervals usually every 6 hours for a couple of days the cortisol levels are measured at specific time frames again keeping in mind that there are not only medications there&#39;s also conditions that could interfere with these tests such as obesity alcoholism this illustration of acromegaly you&#39;ll notice that the prominence features the prominence of the forehead the jaw features that have continued to really roughen up and and continue to grow this is caused by growth Harmon hypers secretion and go ahead and put this video on pause and take a minute to just kind of read the different captions just kind of reiterates what we already discussed the goals and treatment of hyper pituitarism is going to be to return the hormone levels back to normal and reduce and remove symptoms if possible also to reverse body changes that&#39;s not always possible as far as pharmacological long-term management uh that typically tends to be only beneficial for prolactinomas um some of the strategies could be dopamine Agonist um and then possibly somatostatin analoges and competitive receptor antagonists two medications specifically that can be used for prolactinomas are going to be bromocryptine and cab GoLine radiation therapy targeting the adoma could also be potentially beneficial but ultimately for adenomas other than prolactinomas the definitive treatment is going to be a rem surgical removal of the pituitary and that&#39;s called a hypophysectomy they&#39;ll U use a transphenoidal approach that&#39;s typically the recommended route but then if the adenoma has become very very large uh removal may not be completely possible so the smaller the adenoma the higher the success rate of the surgical removal for posttop management of these patients remember they just went transphenoidal and it&#39;s kind of hard to see in this U illustration but they act the pathway is actually going right through the spinoid sinus and into the celera you can see the close proximity to the midbrain and the ponds because we&#39;re always concerned of um laceration or impeding into the subarachnoid space we&#39;re going to look for those potential signs and symptoms of leakage of cerebral spinal fluid um they just had surgery here so we want to teach the patient to report any signs of a post-nasal drip especially if it&#39;s a constant clear running uh kind of feeling um if they have any increased need for swallowing again that could indicate that they&#39;re leaking cerebral spinal fluid we want to make sure that we teach the patient to avoid coughing you don&#39;t want anything that has like these these surges of these this intense increase in interc cranial pressure um so other signs that we would look for that would indicate potential CSF leak would be if um we notice or they the patient notices that there&#39;s like a drop area or um fluid on the pillow that then turns into kind of a Halo pattern that could indicate that that&#39;s cerebral spinal fluid now let&#39;s move on to diabetes insipidus um that&#39;s kind of the the we&#39;re phasing that word out it&#39;s now called Arginine vasopressin deficiency or avpd and if it&#39;s Argan vasopressin resistance it&#39;s abpr if you remember from slide six earlier um we talked about the posterior pituitary is involved with secretion of ad DH or anti-diuretic hormone also known as vasopressin so when there&#39;s a problem here and there&#39;s a decrease in antidiuretic hormone the result is um that there&#39;s going to be an excretion of really hugely large amounts of very dilute urine there&#39;s the four different uh classifications we&#39;ll just touch on a couple um primary neurogenic also Central that can be caused by trauma um um decreased hypothalamus synthesis and Inter cranial masses this is resulting in a decreased um secretion of anti-diuretic hormone by the posterior pituitary then secondary neurogenic is really usually or renal in origin some potential drug related causes of diabetes and cidus could include um I&#39;ll just list three medications first lithium um it&#39;s an antimanic mood stabilizer as you know but I&#39;m not really even sure if they even um prescribe that anymore another is foscarnet which is an antiviral that usually is used to treat Hepatitis B or CMV and then the last one is uh clopine not to be mistaken with clonazepam Kazaam is a benzodiazapine that&#39;s not what causes diabetes and citus but clopine is also an anti-choicers of Di our assessment is going to build on the categories that we just covered um we will ask whether or not the patients have had a recent cranial surgery do they have a history of head trauma what medications have they taken in the past and currently taking have they experienced the symptoms such as excessive thirst and then an increase and a tremendous increase in urination is what we&#39;re looking for and then do we have they reported any symptoms related to dehydration um we will probably um ask them to help or if they&#39;re impatient perform a 24-hour eyes and nose um when we run Diagnostics the urine is going to be very diluted with a specific gravity less than the lower end of normal of 1.005 and then Ur an osmolality um would be less than 300 we they would also exhibit hypernatremia and probably hypoy and what they need was anti-diuretic hormone so we&#39;re going to be giving them desmopressin um there&#39;s a couple of different ways you can give it if they&#39;re able to tolerate nasal spray is probably going to be the quickest way and the easiest way um you could also potentially give it IV or subq but it&#39;s going to be usually a nasal spray right away our goals are and interventions are going to be trying to prevent uh dehydration or manage the symptoms and the potential uh sequella of dehydration will encourage if they can uh fluid intake to equal urine output but in some cases it&#39;s just not easy to keep up so for these particular patients we&#39;re going to start IVs and um probably anticipate that we&#39;re going to give them pretty large volumes of fluid until the Vaso pressent takes effect and the urine output starts to decrease um if they&#39;re at risk for this being a recurring problem then they&#39;re going to need to wear Medic Alert bracelet um and then they should educated on the signs and symptoms of water toxicity water toxicity affects uh serum sodium that could very rapidly escalate and cause neuro neuros symptoms so they need to learn what those are and call 911 or go to the ER immediately um again so starting IVs um monitoring electrolytes and replacing those accordingly we can anticipate that we&#39;re going to be doing that around the clock I&#39;m going to have you pause the video here in just a second so you can review the remainder of this illustration but first I wanted to point out again for diabetes and citus we&#39;re talking about posterior um the posterior portion of the pituitary and then if you focus on the bottom right you&#39;ll notice here the nursing care will also again emphasizing monitoring fluids replacing those fluids checking neurostatus will be uh critical uh following and trending Vital Signs and then assessing mucous membranes and other signs and symptoms of potential dehydration uh so we did review the other symptoms go ahead and pause the video and review the rest of the illustration let&#39;s talk about syndrome of inappropriate anti-diuretic hormone or sadh that&#39;s a condition that&#39;s caused by unsuppressed release of anti-diuretic hormone that can come from the pituitary gland or other sources that have continued action on the vasopressin receptors some potential other conditions that could lead to sedh could include things such as small cell lung cancer that&#39;s probably the most common tumor that&#39;s related to ectopic anti-diuretic hormone production Some central nervous system disorder uh disturbances like stroke Hemorrhage um mental illness and psychosis infection and Trauma there&#39;s some medications that could also cause sadh for example a couple of anti-convulsive one for example is carbamazapine oxcar bipen being another serotonin reuptake Inhibitors or ssris could also potentially lead to sadh some other malignancies that could cause it in addition to small cell lung cancer um head and tumor neck cancers um olfactory neuroblastomas those could all lead to ectopic anti-diuretic hormone release interestingly ecstasy um can also be associated with direct release of anti-diuretic hormone sometimes there are pulmonary diseases that have been Associated withh although the mechanism isn&#39;t exactly known what the connection is um it&#39;s a for example some of the you&#39;ll be surprised to know that some of those diseases could include um atelectasis acute respiratory failure or pneumothorax also pneumonia it doesn&#39;t matter if it&#39;s bacterial or viral there could be a connection and even tuberculosis there could also be a tie in between sidh and hormone Administration um let&#39;s say that somebody&#39;s getting um desmopressin to treat um hemophilia or platel dysfunction or they&#39;re getting they&#39;re getting oxytocin to induce labor um all of those can cause potentially an activation of the Vaso pressent 2 receptors that could then tie into siadh that&#39;s a little concerning the incidence of sadh tends to increase with age but uh that&#39;s not to say that children can get the get this as well so anti-diuretic hormone um we know we call that Arginine vasopressin is formed in the hypothalamus it&#39;s stored in the posterior pituitary and the most important function of anti-diuretic hor hormone is to maintain plasma tonicity in short sdh uh is water retention and fluid overload hyponatremia happens with the water retention there&#39;s dilutional hyponatremia and that increased blood volume uh leads to increased kidney filtration decreased renin and aldosterone there&#39;s an increased sodium loss via urine please review the medical history in your text in box 54.4 so when we assess these patients we&#39;re going to look for signs and symptoms of hyponatremia which would include um there&#39;s decreased extracell fluid osmolality that could cause water to move back into the cells causing cerebral cerebral edema so the early signs that you might see would be that they complain of headache um they&#39;re having problems concentrating or they could become lethargic and even obtunded so changes in level of Consciousness would be something to assess for in severe cases they could actually even seize or even go into respiratory arrest treated it could proceed into a coma State interestingly if patients have a chronic state of hyponatremia they could somehow adapt where they could potentially be asymptomatic despite having a low serum sodium other signs and symptoms could include fatigue dizziness muscle cramps nausea and vomiting again all these symptoms potentially associated with hyponatremia there risk at Falls uh fall risk RK you want to ask them whether they have a history of a head injury um what&#39;s their weight done has it fluctuated have they lost a lot of weight do they have any pulmonary symptoms are they abusing any substances heroin ecstasy and myth other assessment points um are tied into volume status we will place them on daily weights have they noticed that they&#39;ve gained weight as they&#39;re holding on to water uh pulses will probably be re bounding unless there are also exhibiting signs of heart failure they might be hypothermic as well keep in mind that they may be starting to hang on to fluid but not yet exhibiting signs of overload such as jvd um Etc so that&#39;s something to keep into consideration dep paying on hard early in the game we&#39;re catching them um their urine output we&#39;ll probably be measuring eyes and nose because we would expect that that&#39;s going to decrease and the urine osal ity is probably going to increase as well the lab panels that we&#39;ll do for sidh patients are listed here we&#39;ll check serum osmolality serum of sodium urine sodium and osmolality bu and creatinin blood glucose thyroid profile serum cortisol and then uh we&#39;re looking for electrolyte shifts so potassium and chloride and also looking for bicarb additional tests might include a fasting lipid profile and liver function tests for these patients we&#39;re going to absolutely place them on eyes and no and daily weights we need to restrict their fluids um we&#39;re going to monitor them for signs of fluid overload their fluid restriction for 24 hours is usually going to be 800 Ms or less and the goals of therapy are going to be to correct hyponatremia and hopefully increase water excretion couple of different medications that could be used are a couple of VAP Tans uh vasopressin re antagonist conivaptan and Tall vaptan to correct sodium assuming that the patients are not in Dire Straits uh they might get uh sodium po or sodium tablets in addition they might actually add a loop diuretic such as feros amide that combination will help decrease urine concentration and hopefully increase water excretion if the patients are more critical we might give a hypertonic saline but generally that&#39;s held more for the ICU environment we&#39;ll talk more about that in complex 2 um if we correct sodium too quickly we could potentially cause a complication called omotic demyelination syndrome or locked in syndrome that&#39;s rever not non-reversible and could be actually lethal these folks will absolutely have no free water whatsoever we want to use saline to dilute any inal feeds at all um we need to obviously perform frequent neuro checks and continue to monitor Vital Signs and any signs and symptoms of ongoing fluid overload moving on to Cushings And Addison&#39;s disease um at your leisure take a look at this video it&#39;s about 19 minutes long and she does a very nice job of summarizing the differences between Cushings and Addison um the link is on the bottom left there just in case this active link um if we lose that in the video conversion and we&#39;ll come back to this illust ation a little bit later uh but side by side looking at Addison versus Cushings on the left Addison is a result of under reactive adrenals uh causing an adrenal crisis and then on the right Cushing syndrome is on the other side of the spectrum now you&#39;ve got overreactive adrenals or too much circulating cortisol and again we&#39;ll come back to that after we describe each in detail first will cover adrenal gland hypo function that can be categorized into three causes the first uh primary secondary and tertiary causes so the adrenal cortex as you know is responsible for producing glucocorticoids mineral corticoids and androgens primary adrenal insufficiency occurs when there there&#39;s something that&#39;s affecting the adrenal gland itself secondary um insufficiency results from there&#39;s a decreased level of act that&#39;s being relased from the pituitary and then then tertiary adrenal insufficiency is caused by a decreased level of corticotropin releasing hormone that&#39;s being released from the hypothalamus Addison&#39;s disease is categorized as primary the other thing to consider is whether this is a chronic onset or an acute onset chronic presentation can be actually kind of tough to to pick up on whereas an acute onset of adrenal insufficiency can be life-threatening and can occur when the patient&#39;s already in a critical state for our assessment for these patients make sure that you review box 54.5 in your text as that will present the causes that can help tailor your um history approach and also your assessment of these patients we want to ask these patients history wise um whether they have a history of autoimmune disease and what medications have been taken of particular interest is going to be whether they&#39;ve been taking exogenous steroids um you learned in your Pharmacy class the importance of tapering off steroid use and the reason for that is we&#39;re trying to prevent these um the patients from kicking into acute onset uh adrenal insufficiency the symptoms could be actually quite varied they might present with hypotension altered mental status uh they could have GI symptoms as well anorexia vomiting uh weight loss fatigue um and they could also have recurrent abdominal pain there are reproductive complaints that could occur as well in women Amara loss of libido and a decreased axillary and pubic care they could be craving salt and have orthostatic hypotension especially with primary adrenal insufficiency because of the volume depletion um so everything is kind of going low and slow patients could have poor skin turer and increased skin pigmentation some patients will develop shock um and hypotension can be present in any form of adrenal insufficiency additional things to ask and assess for is um hypoglycemia and fluid depletion there&#39;s a variety of multiple lab tests that could be done and including also di um CT and MRI imaging that could be helpful potentially common lab findings uh with somebody that has primary adrenal insufficiency are anemia hyponatremia and Hyper calmia this information is also in your text it&#39;s a nice summary of the systems and the symptoms and the Diagnostics we already me mentioned the only thing that we haven&#39;t touched on is we could do something called an act stimulation provocative test uh so go ahead and pause the video and review the systems that are listed here and the associated symptoms the treatment strategies are hoping to promote fluid balance um regardless of whether the onset is chronic or acute it&#39;s probably going to involve replacement of glucocorticoids probably mineral corticoids as well um we&#39;ll do a variety of different things we&#39;ll monitor them for fluid volume status and preventing hypoglycemia we want to assess not only cardiac function but um all the body systems that were listed previously will weigh them daily and we&#39;re going to monitor electrolytes and a variety of different other diagnostic exams the steroid replacement could be hydrocortisone prazone or dexamethazone and there&#39;s a variety of different regimens that could be used if this is an acute onset and there&#39;s an adrenal crisis um we&#39;re going to start two large boore IVs we&#39;re going to send off Electro ites will check their glucose and then we&#39;re also going to measure plasma C cortisol and act we should be prepared to administer uh at least a couple of liters of isotonic saline these patients could become very unstable and hypotensive so U they&#39;ll probably have some sort of hemodynamic monitoring you can prepare for and anticipate that we&#39;re going to probably be given a hydrocortisone about 100 milligrams IV and then every 6 hours we&#39;ll give a dose usually about half of that for the first 24 hours and it&#39;ll they&#39;ll be tailored depending on the patient&#39;s condition in addition we&#39;ll be replacing any potential deficient electrolytes after hyponatremic that&#39;s usually self-correcting once we get the cortisol and the volume repleted once they start stabilizing we&#39;ll slow down the IV fluid replacement and then again of course we know that we&#39;re going to have to taper the steroids off slowly over one to three days we talked about hypofunction of the adrenal glands now let&#39;s talk about hyperactive uh let&#39;s talk about the difference between Cushing syndrome and Cushing disease syndrome is a group of symptoms that occur together for Cushing syndrome that typically occurs when C levels go up and it could be through a variety of different causes but medications tends to be the most common Cushings Disease or disease in general is a disorder with a known cause a distinctive group of signs and symptoms Andor anatomical changes and cushion Cushing&#39;s Disease uh then tends to be caused by usually a pituitary aboma which then leads to increased act which then increases uh cortisol production by the adrenals and that&#39;s what leads to the distinctive disease signs and symptoms and presentation ping syndrome as we mentioned the ideology is going to be prolonged exposure to high cortisol so it&#39;s going to be caused typically caused by drug therapy for another health problem for example um somebody has an inflammatory process going on that needs significant corticosteroid treatment if it&#39;s a non-drug cause that tends to be a pituitary abnoba but again keep in mind that for syndrome typically it&#39;s it tends to be exogenous corticosteroids women tend to be affected more than men and so ideally for disease prevention providers will um if they&#39;re going to start with high doses of steroids they&#39;ll try to taper down to the lowest effective dose and as we&#39;ve mentioned previously when it comes time to discontinu therapy there&#39;ll be a taper down versus cutting off the cortico steroids abruptly so for purposes of our remaining discussion just go ahead and view Cushing syndrome and Cushing disease together uh the clinical presentation and the treatment strategies are going to be relatively the same and you won&#39;t run into a scenario from the assessment perspective where you&#39;ll have to distinguish Syndrome from disease interestingly so in Cushing&#39;s disease um Act production can stay the same but then there&#39;s loss of that circadium Rhythm um the normal circadium Rhythm response so when it when things are supposed to power down they aren&#39;t so there&#39;s a consistent higher level of act production that leads to adrenal hyperplasia and then there&#39;s um overproduction of cortisol more than is needed then the consequences of that persistently High cortisol is what&#39;s going to lead to some complications at that there&#39;s going to feed our um assessment points it could lead to hypertension hypokalemia um through the e and this summarizes what we just discussed go ahead and pause the video and take a second to kind of go around and review these signs and symptoms of Cushing syndrome our assessment continues with Diagnostic lab and imaging some of these tests are going to sound very familiar uh we could potentially participate in helping the patients with blood salivary and urine cortisol levels um we&#39;ll look for increase increases in serum glucose and sod will&#39;ll expect to send off cbcs and electrolytes look for decreased lymphocytes look at calcium levels um these folks may also have a dexamethasone suppression test the late night salivary cortisol test tends to be most popular probably because it&#39;s easier but if done correctly they have a sensitivity of specificity pretty high nearing 98% as far as a urine cortis all testing keep in mind that um these are snapshots so typically that those tests are going to be repeated three times just to make sure that we didn&#39;t catch kind of a snapshot during a high stress U period there are other some other interfering factors such as alcoholism um sleep apnea and a couple of other things so that&#39;s why we would repeat the test three times the dexasone suppression testing so it will there&#39;s a couple of different approaches and we mentioned these already um they could be um administered either kind of like a a a dose and then excuse me the dose can be given very late at night close to midnight and then we&#39;ll measure the serum cor cortisol first thing in the morning so we would expect uh the normal response would be that the cortisol level is going to remain less than 1.8 another approach would be um to give half a milligram uh po at 6 hour intervals for a couple of days and then we&#39;re still going to measure the cortisol levels uh typically at 6 hour marks or we may actually wait until the last dose is administered and give that um send that that off to lab unfortunately there are some interfering drugs uh that could generate a false positive such as oral contraceptives and estrogens the Diagnostics are also going to sound familiar unfortunately if the culprit is a small adenoma or a micro adenoma it might not be picked up in CT or MRI ultimately the things that we want to prioritize as a team is um want to manage any potential fluid overload um we&#39;re going to watch inbalance electrolytes specifically calcium and sodium uh there&#39;s that potential for injury due to that skin thinning that becomes very very fragile so for us the implications are going to be that we don&#39;t want to put any tape on these folks we&#39;re going to really rip their skin to Pieces um also their decreased density loss we need to be mindful of that and educate the patient as well there&#39;s a potential for infection because of the reduced immunity so we need to not necessarily need to put them on precautions or isolation but uh we need to make sure that we use good clean and aseptic technique when appropriate and teach the patients good handwashing as well as visitors so our plan is to restore that fluid balance prevent injury and prevent infection first line treatment if it&#39;s an act secreting tumor U then it&#39;s going to be surgical reection of that tumor again this is going to sound very familiar they&#39;ll use a transphenoidal approach uh but they can also go endonasal or sublabial either way the precautions and the posttop care is going to be the same we don&#39;t want anything that&#39;s going to raise intracranial pressure we&#39;re going to watch them for leaks for CSF um make sure that we you go back back and review the recovery for these patients and even after after attempted resection if the syndrome and disease persists there might be additional therapies that we&#39;ll try we could do um external beam pituitary radio therapy or radiation therapy they might actually try the resection again although the second time around tends to be even less successful and something to keep in mind is with all that manipulation there could be complications to include the development of fluid and electrolyte abnormalities neuro deficits you know think of the anatomy again and the development of diabetes and citus and lastly if all Elis is failing they could potentially have a bilateral adrenalectomy um if that&#39;s going to ultimately immediately reduce uh cortisol levels but then of course these patients are going to have lifelong therapy they&#39;re going to have to take glucocorticoids and mineral corticoid replacement therapy our evaluation is going to focus on what our priorities were we&#39;re going to hopefully have prevented um shifts and fluid and electrolytes so they&#39;ll be back to homeostasis they they will have remained free from injury and again remember that includes things that we do to the patient as well uh that the patient remained free from infection and also it&#39;s knowledgeable so they&#39;re able to participate in those prevention strategies and that that we didn&#39;t kick them over to the other side where they&#39;re exp experiencing acute adrenal insufficiency to prepare them for transitioning and Home Care um the self-management remember that they they&#39;re going to have that muscle weakness so maybe they&#39;re going to have to live on one floor for a while if they&#39;ve got a two-story or three-story home uh if they need assistance we&#39;ll have to make sure that case management is is working with them to get them assistant devices or maybe even some Home Care they&#39;re going to Le require lifelong therapy of exogenous glucocorticoids then we&#39;ll get them educated with with that there&#39;s an ongoing concern with fluid and electrolyte balances we&#39;ll need to address those as well if they had a bilateral adrenalectomy then additionally they&#39;re going to have to have hormone replacement therapy and then any uh precautions that they&#39;ll need to take if they have reduced immunity coming back to this this illustration that we showed earlier I want you to pause the video and take a look comparison comparing Addison&#39;s disease to Cushing syndrome Cushing&#39;s disease um Addison on the left there&#39;s this is a result of under reactive adrenals there&#39;s not enough production of cortisol and AD aldosterone so when you look at the patient um the signs and symptoms everything&#39;s kind of getting low and slow and then on the right hand side you&#39;ve got over adrenal over production of cortisol overactive adrenals and as you go around the symptomology that uh some of those S tend to be increasing symptoms related to the cortisol such as uh potentially hyperglycemia the CNS irritability um GI distressed and increased acid fat deposits on the face the back of the shoulder so they&#39;ll get that buffalo hump the face is starting to look really really round it&#39;s called a moon face then there&#39;s this the um atypical but very unpleasant symptoms you know that thin skin the purple stri this is pointing to the leg but keep in mind that you&#39;ll see them especially around the belly area so the abdomenal they&#39;ll look like stretch marks except with a lot of uh it&#39;s not pigment they&#39;ll just look kind of a deep purple and again pause the video and review these symptoms aldosteronism happens because there&#39;s excess production of aldosterone from the adrenal glands aldosterone is a mineral corticoid hormone that increases sodium and water retention so ultimately it&#39;s going to raise blood pressure initially can be very tricky to diagnose because clinically it&#39;s going to present as either mild or a severe refractory hypertension so that blood pressure could be elevated um mildly or it could be significant and persistent as kidneys retain sodium and excrete potassium there&#39;s the development also of metabolic alkalosis primary hyper ostrin ism is due to an excess and production of um aldosterone by the adrenal gland and secondary hyper aldosteronism is potentially inappropriate activation of the RASS and then that results in increased ostrin production some key points for assessing these folks is their clinical presentation may be that they have again as I mentioned refractory hypertension so somebody that presents and they&#39;re already on three anti-hypertensive meds but they&#39;re not having good results and a complication of long-term hypertension might be for example um enlargement of the left ventricle so you might hear an S4 as a result some increased risk factors for developing hyperaldosteronism include um hypokalemia whether um they developed spontaneously or due to thide use of diagnosis of an adrenal adoma and then have a familial history of cardiovascular events at a younger age most common treatment is going to be removal of either one or both adrenal glands there&#39;s a handful of different tests that could be done by suppressive testing an example of why maybe perhaps both adrenals are not removed is that for example if they do find an adoma in Diagnostic Imaging on only one of the adrenals then it would make sense to just remove that one adrenal gland Imaging studies again include CT or MRI a big concern is going to be the development of cardiovascular complications as a result of longstanding hyperaldosteronism and these could include things like like myocardial fibrosis LT ventricular hypertrophy uh even an MI myocardial infection cium sparing diuretics spol lactone is typically administered this concludes the voiceover presentation the remainder of the slides are for you to review at your leisure um go ahead and pause the video and make sure that you do go over the questions e e

Transcript for:Understanding Pituitary and Adrenal Disorders

Transcript for:
Understanding Pituitary and Adrenal Disorders