Pituitary Disorders | Clinical Medicine

what's up Ninja nerds in this video today we're going to be talking about pituitary disorders this is part of our clinical medicine section if you guys enjoy these videos they make sense they help you please support us you can do that by hitting the like button commenting down the comment section and also subscribing additionally what I really recommend for you guys to really understand this topic I really think it's going to be helpful for you guys go down the description box below there's a link to our website on our website if you guys subscribe become

a member you'll have access to thousands of notes tons of illustrations thousands of quiz questions and if you guys even look into it more we're even developing courses for those exam prep courses such as your USM step one step two pants inlex Etc so be on the lookout for those all right let's talk a little bit my friends about the pituitary Disorder so there's two types one is hypop pituitarism so this is whenever you're not making enough of those pituitary hormones we know from physiology that the pituitary is the master indine gland right so it's

responsible for producing tons of hormones and they're more of like your stimulating hormones if you want to think about it what happens if the pituitary anti pituitary and postor pituitary stop being able to produce a lot of those hormones there's a lot of derangements that can result from this so let's talk a little bit about this so first thing is we have this kind of basic drawing here so we have to know that this is going to be the hypothalamus here this would be the mammary bodies and then there's the pituitary stalk or the pendulum

and then here we have the posterior pituitary and the anterior pituitary now whenever somebody has hypopituitarism there's really only comes down to it two particular problems one is something is compressing the pituitary right the anterior pituitary posterior pituitary there is significant compression of that and when you compress the tissue you reduce the ability of that tissue to get good good good blood flow as well as you reduce the ability of that tissue to produce hormones the other concept here is it could be due to direct destruction and there's multiple mechanisms of this destructive process that

we'll go into more detail of but if we're compressing the actual pituitary tissue or we're destroying the pituitary tissue in general you lose the ability of this pituitary tissue to produce hormones now what's really cool here is is that when you zoom in on the pituitary tissue there's multiple different cells or nuclei that are responsible for secreting these hormones if you look in the anterior pituitary you have all these different types of trophic cells and these trophic cells are the ones that are responsible for making specific hormones if unfortunately I have compression or destruction I

lose the capability of these somatotropes to produce a particular hormone somatotropes help to make what's called growth hormone and so as a result there will be a reduction and all of these let's actually just put down here all of these will have a reduction in the respective hormones now if the somatotropes don't release growth hor hormone what we will see out of this is a resulting growth failure which we'll talk about in the complications if the lactotropes are damaged from compression to destruction they will lose the capability of being able to produce another hormone which

is referred to as prolactin which will lead to lactation failure which we'll talk about if the gatot tropes are damaged you'll lose the capability of these cells to release two types of hormones one is called follicle stimulating hormone and the other one is called luttin hormone these are important for helping for spermatogenesis they help within the actual ovar ovulatory and menstrual cycles and they also play a role in your uh particularly testosterone production for luteinizing hormone and then progesterone production for the female but either way these patients will receive what's called hypogonadism the other one

is the thyrotropes if these are damaged they lose the ability to produce a very specific type of hormone which we refer to as TSH and this can result in secondary hypothyroidism if cortical trops are damaged they lose the capability of being able to produce a hormone referred to as act and this can lead to secondary Adrian lens efficiency lastly if there is damage enough compression or destruction that it extends to the posterior pituitary anterior posterior pituitary the posteri pituitary has multiple different nuclei often times we refer to it as the super optic nucleus but it's

responsible for secreting a hormone that's already been synthes si in the terminals known as vasopressin or also referred to as ADH and often times this will lead to a very interesting disorder that we'll talk about called diabetes inspius Central diabetes inspius so this is what we see as a result is that you have massive drops and hormones often times the most common ones that are usually affected here are going to be particularly things like growth hormone prolactin maybe the gatot tropins but usually these three are usually the ones that are lost last all right let's

go into this now talking about the actual things that cause compression of the pituitary or that cause destruction of the pituitary leading to a decreased production of these hormones first one is the pituitary compression this one's really common when you think about this in the vignette what it's really going to be due to is it's referred to what's called a pituitary macro adenoma now this is really important what I want you guys to remember about a pituitary macro adenoma is that these are causing compression of the anterior and to some degree maybe even the posterior

pituitary but we have to Define what we what we mean by a macro adenoma so an adenoma is a t kind of tissue and what happens is this is kind of an abnormal tissue and usually what we refer to as a macro adenoma is it's usually greater than 10 millim if you have this tumor that's on the pituitary that's greater than 10 mm that is often times a pituitary macro ad what it'll do is is it'll compress that tissue and as a result you'll see a drop in the pituitary pituitary hormones so as we look

at this we have to ask ourselves a question pituitary macro adenoma big tumor greater than 10 mm compressing on the anterior poster pituitary leads to a drop in all these pituitary hormones that we talked about how am I supposed to think about this one what will give it away this is a big tumor and this tumor I mean the actual pituitary gland itself sorry sits in a bone called the cell Tura but right around that vicinity of where the actual pituitary is is this structure here called the optic Asma so here we have the eyeballs

here we have the optic nerve and then the optic nerve crosses right and usually right in this vicinity is where the pituitary gland is near if this mass is pretty big it can start leading to compression of the optic chasma and what happens is the optic kiasma is supposed to be picking up information from our medial retina which is from the lateral temporal fields and so this information would run here and then usually crosses over run here and then usually crosses over that Mass Effect from the tumor will compress this and will lose the actual

vision and our lateral fields right what is this called right this is referred to as bitemporal hemianopia let's write that down this is referred to as bitemporal Hemi enopia sometimes it's also referred to as anopsia but this is loss of your lateral visual Fields what what would that actually look like it looks like this so now we have an understanding here that if the tumor is big enough it can cause compression of not just the actual pituitary but it can cause compression of the optic kiasma which can lead to the loss of these particular visual

Fields the other thing is is that this mask can be somewhat big and so sometimes what can happen is if the mass is actually relatively bigger it's kind of taking up space now normally our you know there's What's called the Monro Kelly doctrine that says that the you know inside of the actual skull there's it's a space you don't have a lot of room for things to be able to you know get bigger or account you know move around and so what happens is is if you have something such as blood or CSF or tumor

or something abnormal there it's going to increase the OC cranial pressure and so this mass is taking up space and so often times what it may do is is it may increase a little bit of your intracranial pressure and that may lead to a headache and so often times these patients may experience what we call secondary headaches they're not primary headaches like migraines or tension headaches headaches or cluster headaches they're secondary headaches so it's important to remember is watch out for any evidence of secondary headaches so if a patient has evidence of growth failure lactation

failure hypogonadism hypothyroidism adrenal insufficiency and Central diabetes insipidus in combination with visual field loss and headaches you really want to go thinking about a big old tumor what could be another cause maybe it's not from compression maybe it's direct destruction of the pituitary gland this one's very interesting there's a condition that's referred to as shean syndrome this one's really interesting in the sense that whenever a patient is pregnant their pituitary really has a great degree of demand in other words the pregnant individual is depending upon the uh pituitary to produce an adequate amount of hormones

but if for some reason the patient experiences massive bleeding so let's say that they experien something that we refer to as post partum Hemorrhage how do you define postpartum Hemorrhage really well there's kind of two definitions I would say but often times the definition is whenever you lost greater than one liter of blood within a 24-hour period after giving birth or you've lost so much blood that the patient is becoming hemodynamically unstable that's how we would Define postpartum hemorhage when they lose a lot of blood often times we lean to the other factor which is

that they drop their blood volume if you drop blood volume what would you do to your blood pressure theoretically you'll drop your blood pressure so often times these patients experience hypotension on top of that postpartum Hemorrhage is also interesting it affects a lot of our like fibrinolytic factors and coagulation factors and it can lead to what's called DIC so patients can also experience something called DIC so if you have a combination of DIC which is we'll form clots all over the place but you're prone to bleeding and on top of that you also have low

blood pressure you know what this can really do this can clot up some of the vessels and then not peruse the tissue of the pituitary and so because of this you may lead to or represent this decrease perfusion of the pituitary and as a result the pituitary will become es schic and unfortunately necrotic and so now what can I see as a result here I'll have infarction or sometimes even necrosis of the pituitary as a result if I infar this tissue can I release hormones from it no and so as a result there's going to

be a drop in hormone production so there'll be a decrease in the pituitary hormones okay now that's one concept shean zendrum postpartum hamage losing a lot of blood dropping their blood pressure may even cause DIC which clot up some small vessels but prone to bleeding combination of those two poor profusion to the actual pituitary if the pituitary High has a high degree ofand demand in the scenario of pregnancy it may not meet it undergo esia infarction lose the hormone production that's how we get the hypopituitarism so you want to look for a patient who's just

lost a lot of blood recently postpartum that would tip this one away the other one is very interesting this one is what we refer to as pituitary apoplexy so we call this one pituitary Appo Plexi so Apple Plexi is basically where you have Hemorrhage you Hemorrhage into a particular structure often times pituitary epiplexis is you Hemorrhage a bunch of vessels around a pituitary adenoma so the patient usually has to have a tumor which is getting a lot of blood supply you know tumors they naturally create a lot of blood supply around them if what for

whatever reason this tumor you bleed into the tumor that's referred to as pituitary apoplexy what happens is from that blood you start causing a lot of compression of small vasculature around this area so imagine here I have some small blood vessels that are running here this Hemorrhage will start extending and pressing on these blood vessels so what you get is is you get vascular compression so vascular compression of the nearby pituitary vessels that are supposed to supply oxygen to the pituitary now because of that you're not going to get good vascular uh blood supply to

the pituitary tissue and so if you get increased vascular compression this will stimulate infrction of the tissue because it won't get the oxygen it needs the cells will die and they'll lose the ability to produce pituitary hormones so pituitary apoplexy often times will usually present with an adenoma how do adenomas present if they're big enough by temporal hopia and headaches so you may say how would I be able to identify the difference between a pituitary macroadenoma and pituitary apoplexy it would really come down to the Imaging you would have to get an MRI to say

oh there's Hemorrhage in the area of the pituitary and even a mass it's probably pituitary apoplexy where if I just see the mass I probably say it's a pituitary macroadenoma Shan syndrome is going to be the easy one though because it's going to come up with a classic clinical vignette one last thing is a quick little definition and some patients who have hypopituitarism they may only release some of they may only have deficiencies in some of these hormones if they have deficiencies in all of these hormones it's referred to as pan hypopituitarism so don't forget

that often times that's not too common you can see that in shean syndrome but often times it's usually only some of these but in shean syndrome it's often times pan hypopituitarism okay let's come down and talk about hyperpituitarism we've already built a pretty strong foundation so I think you guys would understand now that this one's pretty easy what if I have a pituitary that's just hyperfunction and there could be a couple different reasons why but often times the hyperfunction of the pituitary itself is usually due to a tumor now you're probably like wait a second

Zach you just said if I have a big tumor it's going to compress the pituitary and it won't it'll lose the ability to make these hormones yes I did often times this hyperfunctioning is from a tiny tumor we call it a m micro adenoma we'll talk about that all right but if this tumor is very tiny and it gains the capacity to secrete hormones that means that this tumor must have some of these cells that are hyperactive a little bit more hyperactive and if they're a little bit more hyperactive they'll increase the production of specific

hormones such as growth hormone prolactin TS and act so often times you may have increase in growth hormone which can lead to acrom megal increase in prolactin which can lead to galoria and gynecomastia increase in TSH which can lead to hyperthyroidism and increase in act which can lead to Cushings Disease so it's oftentimes really important to remember this now remember I told you that often times in hypopituitarism it's not common to have pan hypopituitarism it's usually uh in the scenario here where it's some of them like prolactin growth hormone FSH LH in hyperpituitarism it's also

similar it's not too common for you to have all of these the most common is going to be an increase in prolactin that's why often times 40 to 50% of cases of hyperpituitarism are due to what's called hyperprolactinemia due to a tumor which we refer to as a prolactinoma so we've built the foundation here of what hyper pituitary is is it's a hyper functioning of the pituitary likely due to a tumor that's causing increased production of these hormones but most likely prolactin well before I get into that it's likely a tumor you have to also

assume that sometimes tumors may not be the only reason why this thing is pumping out tons of pituitary hormones so I'm assuming that it's this right I'm assuming that oh we're just making a ton of pituitary hormones with the most common one likely being prolactin right that's likely the issue here so it's likely most commonly going to be what's called a pituitary micro adenoma how do we Define that well that one's greater than 10 mm therefore this one has to be less than 10 millimet so it's smaller has the actual capacity to become certain types

this tumor may contain certain types of lactotropes somatotropes thyrotropes corticotropes it just depends upon what the primary uh homogeneous or heterogeneity of that actual tumor is that's likely the most common cause but you have to assume that there's other reasons so sometimes in your boards there actually may be something because you know dopamine you have dopamine receptors that are present here on these lactotropes and you also have TR receptors I'm going to put here we'll put dop doine receptors and often times it's like dopamine 2 receptors so you have dopamine 2 receptors and TR receptors

if a patient is taking anti- dopam menics or or if they have hypo thyroidism Watch What Happens anti-dopaminergic will then lead to what will they do to this D2 receptor well dopamine actually wants want to inhibit prolactin production so if I block dopamine I will stimulate prolactin production so anti-dopaminergic will actually work here at this receptor site and actually believe it or not lead to stimulation of these lactotropes which will lead to a increased production of prolactin okay so I have to then look is the patient on antipsychotics antiemetics tcas some type of antidopaminergic the

the other thing is that hypothyroidism hypothyroidism is when you have low T3 low T4 that comes back to the hypothalamus and what does the hypothalamus release lots of TR if there's lots of TR what is that going to do it's going to bind onto the TR receptor and if you bind onto the TR receptor TR loves to stimulate the lactotropes to increase prola production we talked about this in our hypothyroidism video how you can have hyperprolactinemia as a result here this is usually severe hypothyroidism so it's important and it's a very great value for you

to look through the clinical vignette and history to see are they taking any antidopaminergic or do they have severe hypothyroidism before assuming that it's a pituitary microadenoma you want to know why pituitary microadenomas you just know okay these patients will have a high pituitary hormones most most commonly it's going to be prolactin same thing a lot of these are going to be prolactin this you'll have maybe a history of the drugs this one you won't really have history and then you'll be like oh well Zach I'll know cuz it's a tumor right so it's going

to compress the optic Asma no that's the thing with pituitary microadenomas there's usually little Mass Effect little or no Mass Effect because it's a tiny tumor so since it's a tiny tumor are you going to have bitemporal hemianopia are you going to have these secondary headaches due to maybe due to a little increase in intracranial pressure no because the tumor isn't big enough to cause compression or increase the intracranial pressure so that's why it's really important to look at the history to see if you can find this ainet before saying hey let me get an

MRI all right all right my friends we've talked about the pathophysiology the causes now we go into the grunt work which is talking about what is the problem with all these low levels of hormones and high levels of hormones all right my friends so we talked a lot about the pathophysiology behind hypopituitarism and hyperpituitarism we understand that you're either not making enough of particular hormones we talked about all those or you're making too many of them we went over a lot of the causes particularly to with hypop pituitaries like Shihan Singin pituitary apoplexy pituitary macro

adenomas and there's other things like TBI and radiation therapy with Hyper pituitarism we talked about it's primarily a pituitary microadenoma with that being said I want you guys to start thinking kind of changing gears here okay I know the causes I know the path ofas a little bit but what are the complications of having few levels of these hormones or deficient levels of these hormones well let's say that a patient has a deficient production of one of these and that is ADH whenever there's low amounts of ADH I kind of mentioned this in kind of

passing that it can lead to something called Central di di is for diabetes in citus what happens in this process is ADH is supposed to bind onto these little receptors they're called the vasopressin receptors or the V2 receptors and when ADH binds here what it's supposed to do is it's supposed to stimulate the movement of water so water is supposed to move through the collecting duct and as it moves through the collecting duct there is ADH present which will help to stimulate the presence of aquapore and channels and so generally some of the water may

go out into the urine but some of this water should be absorbed but it's dependent upon the presence of ADH if there's very little ADH present what's the problem here well less ADH means I will not stimulate this process this will be inhibited I won't reabsorb water so there'll be less water that is reabsorbed if there is less water reabsorbed that means I'm going to have a massive water loss in the urine so with that being said you're losing tons of water in the air and what's the end result of all of this well I'm

not reabsorbing a lot of water and because of that my osmolarity of the plasma starts kind of going up and I start getting really thirsty and often times this will present with what we call poly dipsia this is a super common presentation on top of that you're losing tons of water in the urine and it's very large volumes and you're pring quite frequently and so this is called poly Uria it kind of sounds like diabetes these malius right except they have polyphasia the big difference here is that the polyer and polydipsia are often times accompanied

with hypernia and so another thing that you want to watch out for is do these patients have high levels of sodium so hypernia and sometimes from the massive massive polyurea they may also have dehydration so watch out for hypernut treia polydipsia and polyuria and patients who have hypopituitarism presenting with Central di all right cool what if this one's not too hard what if in this process I don't produce an adequate amount of growth hormone well growth hormone is obviously important for growth that's the within the name right growth hormone you have receptors that are present

on the liver and what happens is growth hormone is supposed to bind onto these receptors and what they're supposed to do is stimulate the production of a molecule called insulin like growth factor type one igf1 some people put I gf1 same concept but if GH is not present or deficient amounts you're not going to produce an adequate amount of igf-1 if I don't produce an adequate amount of insulin like growth factor one what happens is I don't allow for proper growth I'm not stimulating the skeletal muscles to grow I'm not stimulating the bones and the

cartilage to grow so because of that children usually exhibit growth failure and the way that that looks is it's usually exhibit in the form of short stature kind of like dwarfism if you want to think about that and then on top of that they may even have decreased muscle mass and so that's one thing I want you guys to be able to think about okay this could be a very common presentation this is another common presentation whenever the actual pituitary is not producing an adequate amount of another hormone referred to as prolactin prolactin is really

important because what it does is it works on some of the actual alveolar cells present within the breast tissue and it helps with increased produ of milk it also plays a role within some of the actual structure of the the actual breast tissue especially in males and so growth of the breast tissue and production of milk so if there is a deficiency in prolactin there'll be an inadequate stimulation of the breast tissue to produce milk and to grow as a result when a baby is born they depend upon the suckling for the breast milk however

since prolactin is deficient there'll be an ability to lactate postpartum and so that's again a problem with a decrease or deficient prolactin production so there'll be a an ability to lactate postpartum this is a very common presentation that I want you guys to remember so inability to lactate postpartum if the pituitary is failing it may lose the ability to produce another hormone here and one of those hormones is called FSH and LH so so this is referred to as follicle stimulating hormone and luteinizing hormone these may be produced in deficient amounts now both of these

hormones work on the male testes and they also work on the female ovaries all right so you're going to get a combination of effects with these we're going to talk more about this when we get into the reproductive system particularly but for the most part here the basic thing that I want you guys to remember is that FSH helps with sperm production and LH helps with testosterone production same thing FSH help plays a role with an estrogen production and LH plays a role with an testosterone production so the basic concept here is that these are

really helping to stimulate the production of hormones and again just as a reminder one would be testosterone and the other one for females would be estrogen and progesterone now these hormones play a lot of different roles and I don't want to get bogged down too much but if we lose this ability to have an adequate amount adequate amount you're not going to produce enough testosterone not enough estrogen not enough progesterone that's the downfall of this but what would this look like you're not just be ah man my tea levels be low no you're going to

have some common presentations often times for males this could lead to like atrophy of the goads of some sort but another common one is usually libido so libido may be reduced in this patient population this could also happen again with females when there's a reduction in their estrogen progesterone production another thing is really important for females they may have menstrual irregularities and they also may have issues with fertility so you want to watch out for infertility and watch out for menstrual irregularities or dysfunction if you will what do I mean by menstrual dysfunction what I

mean is is that these patients can can have very abnormal menstrual cycles they may not have a menstrual cycle referred to as amenorrhea or they may have very few periods of menal cycle referred to as aligo Menara so infertility menual dysfunction and reduced libido is relatively common in this scenario okay what else so the next one here and I think this is really really important to remember for these last two is these are often lost last in the hypopituitarism picture so if a patient has panhypopituitarism they'll lose all of these hormones if they're only kind

of losing some function they often times lose these and it's uncommon for them to lose these however if they did they'll lose the ash uh the production of TSH and they'll lose the production of act now there is a profound effect of these hormones I can't go through all of the dysfunctions that we would see in hypothyroidism and adrenal insufficiency we will talk about these more in these individual lectures I'll give you a quick run through though so whenever there's an inadequate TSH we know TSH is supposed to hit the TSH receptors and help play

a role in T3 and T4 production if there's inadequate TSH there'll be an inadequate production of T3 and T4 by the pituitary I'm Sorry by the thyroid from here how will hypothyroidism present so many different dysfunctions you can have a metal AB abolic dysfunctions with weight gain with cold intolerance hyponatremia bradicardia diastolic hypertension lethargy faue generally you can have very dry skin brittle nails hair loss many different types of dysfunction can present in this disease we're not going to write all of these down and go through all of them adrenal insufficiency is another one so

act is really important because what it does is is it works to stimulate the adrenal cortex there's different layers of the adrenal cortex like the zon glosa and the facula and the reticularis it primarily stimulates the facula to produce something called cortisol and to a small degree it may even stimulate DHEA which is like these androgens that are really important in females now if this happens and you have a reduced act you'll have a reduced production of cortisol and to some degree you may even have a reduced production of DHEA how would this present well

primarily when a patient has secondary adrenal insufficiency low cortisol they can have low glucose they can have fatigue they can have lethargy they can have orthostatic hypotension they can have eosinophilia they can have so many different types of problems again we're not going to go through all of these effects we'll talk about them more in the adrenal insufficiency lecture again it's also important these are lost last so they're not going to be super common with that being said we've really dedicated a good amount of time to the hypopituitarism effect what if I now say we're

going to go the other direction now a patient has hypopituitarism we know based upon that definition they probably most likely have a pituitary microadenoma less than 10 millim that is just pumping out this particular hormones and now we're just going in the opposite direction of what we were doing so in this scenario acromegaly is the opposite of growth failure they're going to be pumping out way too much growth hormone and if you're pumping out way too much growth hormone you're stimulating an increase in insulin like growth factor type one so increased here means increased here

which means you're going to have an increase in skeletal muscle production an increase in bone growth cartilage growth so many different things so what are some of the effects well some of the big ones that I really want you to know here is a three-part thing one is it affects your sweat glands right so it helps to be able to promote sweat if you have increased in insulin like growth factor one and growth hormone you're going to have an increase in sweating we refer to this as dieresis sometimes in the exams I don't know why

but they say that these are big people with like doughy wet hands because they're big tissue and they have very wet moist hands because of the sweating the other thing is that it also affects insulin so what it does is it actually increases insulin resistance because you know the growth hormone helps to increase your glucose if you increase your glucose your body produces more insulin if you produce more insulin and over time those receptors become a little bit more agitated and less sensitive to The receptors less sensitive insulin so they can experience insulin resistance now

when patients develop insulin resistance what does that sound like sounds like diabetes right so these patients can develop diabetes metis often times times type two so there're an increased risk for diabetes metis type two so think about a doughy sweaty hand with with diabetes and then on top of that let's add more to this it increases a lot of the actual so patients don't usually get tall unless they kind of have this produced during their actual growth period if it's more in adults which we're kind of seeing with these patients what happens is some of

their bones and cartilage in the face gets really thick so they get enlarged face and facial features when you have enlarged facial features what happens is so you're going to get facial features are going to kind of become more prominent and the hands and the fingers will become elongated hands and fingers get bigger so all of this things get enlarged so you have enlargement of the facial features and the hands and the fingers the problem with that is that with the facial features especially up here air is supposed to run in through your nose and

through your mouth when you're sleeping and you're not supposed to have all that stuff there if it is there it's obstructing the air flow these patients are at super high risk of obstructive sleep apnea and on top of that all this thickening the doughy hands especially near the wrist area you're compressing the median nerve and so these patients are also at high risk of carpal tunnel syndrome I'm going to abbreviate that C TS so now with that being said I can already tell that a patient who has acromegaly which is actually kind of common if

we're talking about these it's usually this one is the most common 40% and then this one would come up as a as a as a second like a runner up all right think about en llarge facial features big fat hands and fingers think about diabetes and sweaty individual the next one is hyperprolactinemia and I have to again kind of put this next to it it is the most common so it's in therefore the most important one to remember if you forget most of these which is okay cuz it's a lot when you produce prolactin levels

and they're up above like 200 generally what happens here is that prolactin we already know based upon what we talked about above is that it helps with uh the production of milk the thickening of the breast tissue now when it does this one of the things that you'll see here sadly is that these patients May unfortunately uh lactate can produce milk uh even when they're not supposed to so it's inappropriate and you know what we call that we call that galacta so one very common presentation is usually going to be inappropriate milk production which we

refer to as galacto Ria the other thing is that not only does this stimulate and increase in milk production it also stimulates breast tissue production especially in the male population and so sometimes this can stimulate what we refer to as gyo mastia especially in the male population so you may see galacta and gynecomastia especially in the male population the other thing is Prolactin actually inhibits FSH and LH production so you'll see all the things that you would see in hypogonadism menstrual regularities decreased libido infertility as well so this is really big things to remember by

far the most common the next concept here is with this this microadenoma it also may be pumping out too much of this hormone here which we refer to as TSH and too much act now if I'm pumping out too much TSH and I'm pumping out too much AC we already know how this works TSH increase the production of T3 and T4 act increases the production of cortisol and to a degree the androgens for females so if there is too much of this you'll get too much of this too much of this you'll get too much

of these how would this look we're not going to write all these down the reason why is we're going to discuss this in way more detail in the respective lectures of hyperthyroidism and Cushing's Disease but a quick little undergoing of this kind of like a recap of it is that it would generally be presenting with uh usually weight loss heat intolerance usually these patients will also be pretty sweaty the other concept is that they'll have tacac cardia they may have systolic hypertension they may have hyperactive deep endon reflexes they may be anxious they may have

diarrhea they may even have pretibial miedema um and engraves disease patients you'll see like some of the exop thalos you won't really see that in these patient populations so with this being said you're going to see a lot of presentations on hyperthyroidism right you just have to think could it be due to a secondary cause like a pituitary problem so you think about this more in the thyroid lectures same thing with this one in Cushing syndrome you're going to get an increase in cortisol you're going to get all that like pocis and fat redistribution presentations

like the moon face the buffalo hump the trunkal Obesity the abdominal strier hyperglycemia hypertension increased uh risk of infections so so many different things can present in that as well with that being said we have really covered a lot of the down ex consequences of having decreased production of these hormones pituitary hormones and increased production of these pituitary hormones how do we go about diagnosing this let's talk about that now well the first thing to think about is again check the pituitary hormone testing if a patient comes in with any symptoms for example if I

think that they're having growth failure lactation failure hypothyroidism uh maybe some type of adrenal insufficiency or Central di in any of these scenarios or secondary hypogonadism I'm going to send off all of the pituitary hormone tests so for example I'll send off the cortisol and act levels if I have any inclination that they have some type of adrenaline sufficiency if their cortisol is low and act is low it's secondary AI it's not primary I got to go looking for the problem with the pituitary is it an infarction from Shihan from a pituitary apoplexia a macro

adenoma TBI or radiation therapy that's where I would get my pituitary MRI look at this big goach hanging in their head that's a pituitary macat which is pretty common cause that would identify if it's a pituitary lesion as the source now continue to go on I think the patient has hypothyroidism but I'm not sure which type I check a TSH and I check a T3 T4 if both of them are low it suggests secondary I'm going to go look at the pituitary and see if there's a leion there I'm going to check my FSH and

LH and estrogen test testosterone progesterone if I think of patients having menual irregularities if I think having poor libido sexual dysfunction uh and maybe even difficulty getting pregnant if the FSH LH is low if their estrogen and testosterone and progesterone's low well then I think it's secondary hypogonadism it's not a primary problem check the pituitary see if they have a mass or any type of lesion next thing is if I have a patient who's difficulty with growth they're short statured they don't have a lot of muscle mass it's a child I'm going to check the

igf-1 if that's really low it definitely suggests that they could have some type of growth hormone failure so what I do is I do what's called a growth hormone stimulation test you basically give them Arginine and glucagon and what this is supposed to do is tell the somatotropes to be able to produce growth hormone but in this scenario if I give them Arginine gugan and they don't make the igf-1 that tells me that something's wrong with the seatat tropes another thing you could do is you could give them insulin which produce like a mild hypoglycemia

and if that hypoglycemia is strong enough it can tell the somatotropes hey release growth hormone so that you can increase the actual uh glucose but if I give them insulin or I give them Arginine and glucagon and it does not result in an increase in growth hormone I know something's wrong with the somatotropes so therefore I have to go ahead and check at the pituitary and make sure that it's not having a lesion there that's causing a reduction in growth hormone production the last thing is if I have a patient come in with polyurea polydipsia

maybe they have a high serum sodium and I'm concerned that they have Central di I can obtain an osmolal what would this be well if I do this I'm going to check serum and urine I have to think about this a no ADH being present it won't reabsorb water into the bloodstain that means the serum osmolality will go up all the water will go into the urine so the urine osmolality should go down all right if that's the case then this person has di likely the only way that I can truly determine if it's Central

or if it's nephrogenic di is I have to do something called a ddavp test give them DD AVP which is ADH if I give them that and their urine osmolality flips and their serum osmolality flips then it's likely Central Di and I've determined that it's PR Central di let me look at the pituitary see if there's a mass infarction radiation necrosis or some type of trauma that's likely to cause here all right in the same way I got to do this for hyperpituitarism if I have a patient who's coming in and I think okay I

think they have cushions they have that type of presentation I'm going to send off the cortisol and the AC levels if it's high cortisol High act it's probably a good confidence that it could be coming from the pituitary they probably have cushions disease I would get a pituitary MRI and here I see a tiny little micro adenoma that's sorry right here a tiny little pituitary microadenoma that's present that would tell me that there's definitely a pituitary microadenoma is the lesion and the source of this increased act and then subsequently The increased cortisol levels if I

check a prolactin because a patient's having galoria gynecomastia menro like irregularities uh low libido erectile dysfunction difficulty getting pregnant I check the prolactin it's greater than 200 all right it's probably hyperprolactinemia make sure I rule out dopamine antagonist make sure I rule out hypothyroidism and if I do get a pituitary MRI look to see if they have a microadenoma that's causing this same thing I think that the patient has hyper thyroidism they're presenting with features that are concerning for that check the TSH if it's elevated and then the subsequent T4 is elevated it's secondary get

a pituitary MRI find the lesion if I get an igf-1 and I'm suspecting that they have acromegaly it'll be elevated what I do is I want to try to see something really interesting I'm going to do something called an oral glucose tolerance test you give them glucose that should trigger hypoglycemia so hypoglycemia was supposed to stimulate GH release hyperglycemia would then suppress GH release if this is a tumor it doesn't care about glucose or anything it's going to continue to produce GH so if the GH is still being in high levels it's a tumor that's

pumping out GH and nothing is shutting it down so in this particular situation I think that they have acromegaly get a pituitary MRI see if I can find a m groma all right that's a lot I think the question arises I find the lesion I find that the patient has hypopituitarism based upon one of those millions of presentations I get the pituitary marai and I see they have a pituitary macoma I find that it's maybe Shihan or um you know potentially apoplexy that caused infarction or some other potential ethology how do I treat these patients

well with any of these situations it's always about replacing the hormones that they're missing so if they have adrenal insufficiency you give them hydrocortisone you give them steroids because that's what they're missing if they have hypothyroidism you give them thyroid hormone if they have hypogonadism you give them the respective hormones that they need testosterone for males estrogen for females if they have a growth hormone deficiency you give them growth hormone if they have Central diabetes and CPUs you give them ADH in the form of deso pressin and if you have the capability to remove the

tumor remove the tumor so in patients who have like Shan syndrome pituitary apoplexy maybe radiation TBI it may be hard to treat the underlying cause but if they have a big adenoma that's causing these problems and you're trying to replace it in the meantime if you can remove this they do something where they actually go in transphenoidal and then they resect the tumor if possible all right and hyperpituitarism you have a pituitary micro adenoma that's just pumping these things out the treatment can actually vary depending upon the presentation for example if they present with Cushings

it's best to just cut that thing out if possible if they present with hyperthyroidism it's best to cut that thing out if possible in the other particular scenario if they present with aquoral so in other words they present with long hands fingers lots of sweating they also present with you know large uh coarse facial features and hyperglycemia you want to determine if the patient feels like they're a good candidate to operate and remove the tumor if they are a good candidate go ahead remove the tumor but if the patient doesn't want to get surgery or

if it's not really an operable tumor there is Alternatives things that you can use in these patients to try to in other words suppress growth hormone release this would be things like octreotide or pegvisomant pegvisomant octreotide is usually first line and pegvisomant is usually second the concept behind this is that octra Tides will directly inhibit the somatotropes from producing growth hormone whereas the pisat actually works a little bit more Downstream it prevents the G from hitting on these potential Target organs and causing the release of igf1 so again octreotide will suppress the somatotropes and shut

down the actual GH production and then pegvisomant will shut down the liver from producing igf1 the other thing is if a patient has a hyper prolactinoma all right so a prolactinoma causing hyper prolactinemia in this situ particular situation it actually is best that these patients can respond relatively well to Medical therapy all I want to do is shut down the lactotropes from producing prolactin and so first line in all these patients at least try and one of the benefits of this is twofold one is I can avoid a surgery potentially second is usually cabergoline and

bromocryptine can actually have some degree of shrinking the tumor a little bit which makes it easier for them to actually reect so if I give cabergoline or bromocryptine what are these going to do they're literally going to act as dopamine Agonist and they're going to shut down the prolactin production and so this is something that we would go to First usually kglin first line bromocryptine is an alternative if they do not respond to the cabergoline or the bromocryptine they still have symptoms then you can go ahead and you can try to cut that tumor out

all right my friends that is the pituitary disorders I really hope it made sense I hope that you guys enjoyed it and as always until next time [Music]