what's up Ninja nerds in this video today we're talking about hypothyroidism that's for a clinical medicine section and if you guys have been enjoying these videos they make sense to you they help you please support us and some of the simplest ways that you guys can do that is to hit the like button comment down in the comment section and please subscribe it goes a long way also for your benefit I really highly suggest this go down in the description box below there's a link to our website on our website we have extremely amazing high yield notes great illustrations to follow along with and then on top of that if you really want to test your knowledge and understand the topic we have nearly thousands of questions that can help you guys to understand these topics also we're developing exam prep courses so keep your eyes peeled open for things like step two the uh pants and so many more other exams all right let's talk about hypothyroidism so hypothyroidism is when a patient has very low thyroid hormone levels but there's two types one is called primary meaning the thyroid gland is the problem or secondary meaning that the pituitary or the hypothalamus are the problem let's talk about primary first we'll go over the basic pathophysiology and then we'll go over the causes so the first thing primary hypothyroidism we know that the problem is the thyroid gland itself the thyroid gland is responsible for making a hormone called T3 which is triot thyronine and T4 which is thyroxine together collectively they make what we refer to as the thyroid hormone but the problem is is that in hypothyroidism they're not producing an adequate amount of thyroid hormone so this production is reduced significantly now you have to ask yourself the question why is the thyroid hormone production reduced well then you have to take and zoom in to these actual thyroid follicular cells and take a better look at them so we'll look at them here we'll look at them here now these cells right if you're looking at one of these this is a thyroid follicle they're the actual structural and functional unit of the thyroid gland they make the thyroid hormone so the follicular cells what they do is is they make this black colloid here which is called thyroglobulin now thyroglobulin is like a clump of amino acids what happens is that thyroglobulin combines with iodine and then the iodine when it combines with thyroglobulin makes thyroid hormone and it gets pushed out to the bloodstream as T3 and T4 but what if I destroy these follicular cells can they make thyroglobulin no can they take and actually bind the thyroid globulin with iodine and make thyroid hormone no so the end result here is that these thyroid cells follicular cells won't be able to produce adequate amounts of T3 and T4 and there is a ton of causes for for this one that we'll go into great detail of the other one is interesting so let's see that these thyroid follicular cells are intact they're fine but the problem is is that you're supposed to take a molecule called iodine all right and iodine what happens is it gets taken and utilized and binds to thyroglobulin which is those Bunches of amino acids when you take the thyroglobulin combine it on to the actual iodine with it you'll make thyroid hormone and that thyroid hormone will then get released into the bloodstream but what if I have a decreased amount of iodine am I going to be able to take the iodine combine it with the thyroglobulin and then make thyroid hormone no and so the problem here is that I'm not going to be able to make functional thyroid hormone I'm not destroying the actual glands themselves the follicular cells but I am reducing the production so this is the concept here now big thing for iodine deficiency this is the most common cause of hypothyroidism worldwide so let's actually write that down this is the most common cause worldwide common cause worldwide so you want to think about this in areas where there's less iodine intake usually there's not enough sufficient intake third world countries Etc now let's come back a second we know that the thyroid gland is not producing thyroid hormone because the thyroid follicles are being destroyed or you're not having a sufficient amount of iodine to make functional thyroid hormone right that thyroid hormone it goes to many different tissues we'll talk about the downstream effects if we don't have enough of it but what happens is whenever the thyroid hormone levels are low or high our hypothalamus and pituitary is supposed to respond to it whenever it's low our hypothalamus in the pituitary will say hey we need more increase the actual production of very specific types of hormones and so what happens is your hypothalamus responds and says I'm going to make more TR and then I'm going to tell the pituitary to make more TSH and this is the actual downward Cascade that occurs here is that there'll be an increase in the production of TR an increase in the production of TSH so whenever you think about this this is actually super helpful diagnostically because primary is often times remembered as having two particular things a very low T3 and T4 and a very high TSH and that is the very very high yield component that I want you guys to remember you're probably like Zach what about the actual TR we don't necessarily monitor that these are the big things that we get from primary all right so primary hypothyroidism we have the two big terms we already covered one of them iine deficiency think about again iodine deficient areas third world countries poor iodine intake all right thyroid destruction what are some causes there is so many when we talk about these I want you to break them down into autoimmune causes of thyroiditis or inflammation of the thyroid that causes destruction infectious thyroiditis and iatrogenic thyroid destruction now when we talk about these autoimmune causes you know your plasma cells they make these things called antibodies antibodies can then actually be produced normally against pathogens right but sometimes we make Auto antibodies that attack our own tissues you know some of the things that they attack well you know that thing I told you called thyroglobulin that's inside of the thyroid follicles our body can sometimes generate antibodies against the thyroglobulin or we'll represent this in blue these little blue dots inside of these follicular cells is called TPO thyroid peroxidase we sometimes can generate antibodies against those when you generate anti bodies against this tissue unfortunately creates an immune reaction and causes destruction of the thyroid follicle what happens you lose the ability to produce T3 and T4 because you lose the follicular cell function right so we have to ask ourselves the question what are these antibodies well there's three diseases that produce Auto antibodies against the thyroid gland leading to a reduction in T3 and T4 what are they Hashimoto is one postpartum and rles or uh rles thyroiditis now with these Hashim Modas is by far going to be the most common cause of hypothyroidism in the United States this one worldwide this one United States remember that Hashim Modas what are the antibodies it actually is the really important one that you remember it makes it against both of these things that I pointed out so you're going to have two different types one is going to be What's called the anti we represent this as TG thyroglobulin antibodies and anti- TPO thyroid peroxidase antibodies these are positive in people who have Hashimoto now the question is is why do we produce these antibodies in this particular situation they believe that it's related to Young individuals who have abnormalities in their HLA genes like what well there's very specific HLA mutations one is this may be related to What's called the HLA dr3 mutation or the HLA dr4 mutation now this is not something that you test for what happens is that these mutations lead to alterations in immune function and the alterations in the immune function is what leads to the undesirable production of these antibodies against our own tissues usually these patients will also have diabetes and maybe other types of disorders as well so that's one big thing postpartum it's literally within the name it's a patient who is pregnant so that one's not hard what about the antibodies this one it really only has the anti-tpo now the key thing that's really different here is because you're like okay well how do I know it's not Hashimoto well Hashimoto one of the big things for this one is the hypothyroidism is permanent you don't gain that function back with postpartum they do make these antibodies and the trigger guess what it's pregnancy or it's postpartum so usually within one year of birth of of a child this may stimulate the anti- TPO production but the key thing is it will cause destruction but then the actual thyroid follicle cells will regenerate and you'll gain normal thyroid function or you thyroid function back so one of the big things to remember about postpartum is that this is what we call a transient hypothyroidism it is a transient hypothyroidism it is not chronic and that is super super important often times this type of like hypothyroidism exhibits a triphasic response we'll talk about it more in hyper thyroidism but usually you destroy the follicles release the thyroid hormone hyper thyroid you destroy them so they end up going into a hypothyroid phase and then eventually they regenerate and they go into a u thyroid state so this is Po postpartum uh thyroiditis and again usually less than one year postpartum so we'll put less than one year postpartum is the trigger here it's some type of hormonal relationship which hormone we don't know last one is rles now rle thyroiditis is very interesting it's a part of a group of diseases and they're called the IG G4 systemic diseases this igg4 antibodies are produced and they cause destruction of the thyro gland but more particularly they do something really interesting what they do is they cause destruction but it's a very interesting way what they do is they activate fibroblast and fibroblasts release lots of fibrous tissue and this leads to increased fibrosis of the thyroid gland look at this thing this thing gets like super super fibrotic so clumps of fibrous tissue all over the thyroid gland now if I replace a lot of the normal thyroid follicle tissue with fibrous tissue I will lose thyroid function but believe it or not and here's what's really interesting here these patients maybe 30% of them will develop hypothyroidism so it can cause fibrosis and I think the big thing to remember here is approximately 30% approximately 30% will develop hypothyroidism so that's not like a super super large population now one thing that's really important to remember here is yes you can see this in hypothyroidism but the igg4 is the giveaway so this one is usually associated with these mutations and other autoimmune diseases this one pregnancy this one not a lot except for a couple things one is the igg4 is a present in other Advanced systemic diseases I would only want you to remember three of them though so these IG G4S can also be present in what's called autoimmune pancreatitis so autoimmune pancreatitis so if they have autoimmune pancreatitis and a fibrotic thyroid gland I want you to think about potentially what Ral thyroiditis the other one is it can cause aortitis which is inflammation of the aorta and the last one is it can cause fibrosis of the retrop perenium and so I'm going to abbreviate that RP retr paranal fibrosis all right what is the big thing that I really want you to remember though because that's hard to remember right I can remember the igg4 antibodies I can remember the fibrosis I can remember some of them get hypothyroidism here's the easy thing to remember the fibrosis causes compression of nearby structures which makes it different from other types of hypothyroidism diseases so whenever there's this fibrosis it compresses on three things nearby so here's the compressive effect let's actually write that down let's write down here's our compressive effects and the compressive effects in order is I will compress the recurrent lenial nerve so I'm going to abbreviate that R Ln recurrent lenial nerve if I compress that Poppy what will be the symptom horseness right so I have horseness the other thing is I can compress the trachea if I compress the trachea I'll have difficulty being able to entrain air so this can lead to disia or it can lead to Strider and then lastly I can compress the esophagus which makes it difficult for food and fluids to move down which can lead to dysphasia more particularly esophageal dysphasia so if I compress these particular structures I can see the you know devastating effects that a patient could experience and so I want you to think about this in a patient with hypothyroidism and compressive effects from the actual nasty fibrosis if you happen to remember these try your best to remember autoimmune pancreatitis okay now 30% chance of hypothyroidism transient hypothyroidism permanent hypothyroidism we come to the next one infectious thyroiditis this one is not super common but it is something to be able to remember it's usually triggered by a viral upper respiratory tract infection so a patient experiences a viral upper upper respiratory tract infection so I think one of the big things to look for here is in these patients they make come in with low-g grade fevers muscle aches they may come in with stiff or painful joints they may also come in with a runny nose congestion sore throat and if they also have a painful thyroid goer that also makes me think of dequan's thyroiditis so this will be a viral upper respiratory tract infection and it'll cause direct injury and destruction of the thyroid follicle tissue which will drop your T3 and T4 levels now with this one the thing I want you to remember is remember that it's going to be causing a painful thyroid so it's a painful thyroid and usually there's even a goiter and we'll talk about what a goiter is in a second but it's going to cause a painful thyroid the other thing here is again look for upper respiratory tract infection symptoms so look for viral upper respiratory tract infection sympt Syms again headache congestion sore throat fevers myalgias Etc and here's the kicker this patient will also have a elevated ESR from inflammation it's nonspecific but it's great on your exams so whenever you see a significantly increased arthrite sedimentation rate in the context of a painful thyroid and positive viral upper respiratory tract infections and hypothyroidism think about dequin thyroiditis one big thing to remember remember how I told you postpartum is transient dequin is transient this is a transient hypothyroidism it's not permanent that is another high yield fact this is a part of that triphasic response I mentioned before and again we'll repeat that when whenever we get into hyperthyroidism all right autoimmune infectious iatrogenic these are the easiest ones so a thyroidectomy would probably be the most obvious thing possible right I don't even do I even really need to explain this no if a patient had a recent surgery and you cut out their thyroid because they had thyroid cancer or they had Hyer thyroidism now they don't make thyroid hormone that is super obvious okay look for a patient who has a recent history of thyroid surgery that's all I want you guys to remember recent thyroid surgery maybe even take a look examine their neck look to see if you can actually see um any evidence of a surgical scar there the last one is a wolf chai cough effect this one's really interesting it's kind of weird but it's interesting your thyroid follicles what they do is they take thyroglobulin that's made by the follicular cells when they do that they interact with that enzyme that I told you is found inside of these follicular cells it's a weird enzyme where it's found inside like around the edges and it's found inside the cells it's called TPO right so this enzyme is called T po thyroid peroxidase that's the same one that you have antibodies against in Hashimoto and postpartum this enzyme is supposed to stimulate the conversion of thyroglobulin into thyroid hormone by adding what into it it adds iodine into the mixture so if iodine is added into the mixture and the presence of thyroid peroxidase it will stimulate the formation of thyroid hormone what if and this is weird what if I gave way way way too much iodine to a patient I give them insanely large doses of iodine that large doses of iodine can work via kind of a negative feedback mechanism because what it'll do is it'll say hey I have lots of iodine for me to make thyroid hormone but then your thyroid peroxidase enzyme says oh crap this is this this reaction is going way too fast I need to regulate this and so these high high levels of iodine can actually inhibit this enzyme if you inhibit this enzyme can you take and convert thyroglobulin into thyroid hormone now no can I make thyroid hormone no this is called the wolf chai cough effect it's very paradoxical where super high levels of iodine and what scenarios well one one reason is patients who take am odone long term this is used in apib right so chronic atrial fibrillation that' be one cause another one is Radio iodine therapy all right so radio iodine therapy is another very very common one so if a patient received heavy amounts of radioiodine therapy or chronic emodin use this can lead to the wolf chof effect so this is what I want you guys to think about here that's a ton of causes we'll actually review a lot of this stuff when we go through the diagnostic algorithm but this is the big thing I want you guys to know for primary hypothyroidism now let's talk about secondary hypothyroidism this one's actually super straightforward not too crazy in this problem it's the hypothalamus of the pituitary that's dysfunctional so what's happening here is you're supposed to again make that hormone called TR from the hypothalamus that's supposed to tell the anterior pituitary to make TSH right so hypothalamus makes TR travels through What's called the hypohyal portal system which is a little vascular system between the hypothalamus and the anter pituitary tells the anter pituitary to make TSH and then TSH will go and bind onto the what are these little suckers here called These are called your TSH receptors which is on your thyroid gland and it tells it to make T3 and T4 right same thing these little if you kind of zoomed in here and looked this is a TSH receptor TSH will bind right here stimulate the thyroglobulin synthesis help with iodine if it's there to bind with the thyroglobulin and then make thyroid hormone and put it into the bloodstream but let's say I have some type of problem where there's injury to the hypothalamus I have injury to the anterior pituitary now now I can't make TR if I can't make TR can I make TSH no and if I can't make TSH can I stimulate the TSH receptor no can I make T3 and T4 no and so because of all this I'll have low levels of thyroid hormone inside of the bloodstream and so the key thing here for being able to remember this is primary was this one secondary would be low and low right so for this one I would have both low T3 and T4 and low TSH as compared to primary so that's a very helpful diagnostic tool now the question comes what's leading to this pituitary it's primarily the pituitary but hypothalamus or pituitary dysfunction so I'm going to come over here and talk about the causes of pituitary pituitary dysfunction all right and there's two big ones that I want you guys to be able to remember one is called a pituitary adenoma but I want to actually be a little bit more specific it's like a pituitary macro adenoma this sucker is huge whenever you have this huge tumor remember what I told you TR is produced by the hypothalamus right and whenever TR is produced by the hypothalamus it's supposed to run through the hypohyal portal system well what if here's this little blood vessel let's say here's a blood vessel it's being compressed by the tumor if it's being compressed by the tumor is the signal of the TR going to reach the anter pituitary and Trigger the anti pituitary to make TSH no and so that's a really really important point is TR may be being produced in high amounts or in normal amounts but the signal of receiving it via the portal system is being impeded so this process here is being impeded and because of that TSH production is low how do I usually think about this one this one's really interesting because I have a big old socker uh a big Mass right there at the pituitary that thing pushes on a couple things and so what happens with this is you get Mass Effect and this is one of the key things that I really want you guys to think about with secondary hypothyroidism when it compresses on things it can lead to a headache that's one super common effect it can lead to compression of nearby structures and lead to a intracranial kind of presenting headache but here's the other one and this is the giveaway it compresses the optic Asma when you compress the optic Asma it leads to what called bi temporal Hemi anopia this is where you lose your vision in the bilateral temporal Fields so what do B hopia look like it looks like this whenever we have a patient who comes in with headache B and proh hemianopia and again it's important to remember why does this happen we'll talk about it more in pituitary disorders but a quick recap is here's an eyeball here's an eyeball and you guys have to remember that you have that structure here called the optic Asma the pituitary gland sits right here in this area so if I have a mass that's compressing right here I'm hitting all the fibers that are actually going to be coming from these areas here and so that's why is that generally this is a visual field here this is a visual field here and it picks up your lateral and your lateral it's running right through this area here and that's why you're getting this in injury here it's because it's supposed to cross here supposed to cross here and I'm losing the visual field and my temporal Fields all right pituitary adoma big one to remember last one here is really helpful for your boards and I think it's because of the his shean syndrome so if a patient gives birth and from that birth they lose a large volume of blood so we call this this postpartum Hemorrhage to the point where they've lost so much blood that they're becoming hypovolemic they've lost more than like a liter within 24 hours massive blood loss in this particular scenario where they have blood loss this can lead to very severe hypovolemia so their blood volume will drop if blood volume drops what can that do to your blood pressure it can drop your blood pressure if you drop your blood pressure you drop the profusion to various tissues and one of these areas that seems to be somewhat susceptible is the pituitary and so the pituitary doesn't get good perfusion if it doesn't get good perfusion you're going to lead to necrosis of this tissue if you cause death of this tissue can it release particular hormones no and so we actually lose a ton of hormones but in this particular example here you'll have a reduction of TSH as being one of those big ones here but again you'll lose all the other hormones in in response to that so these are the two big things I want you to remember for secondary another one could be traumatic brain injuries but less likely to be presented in your exams all right we've gone over the pathophysiology the causes of hypothyroidism now I need to talk about how do these patients classically present and what's the worst case scenario for hypothyroidism all right my friends now we're going to move on to the next component here so a patient with hypothyroidism generally would come in with multifactorial involvement there's multi-stem involvement it's so crazy so it's not something as simple as that you can just point to oh there's just one common or two common findings in hypothyroidism there's many because the thyroid hormone affects so many systems of the body so whenever a patient comes in and you think that they have hypothyroidism these are the classic findings that I want you guys to think about classify them in this particular manner one is do they have the presence of a goer so a goer is kind of like an enlargement of the thyroid gland now let's talk about the goer first the path of physiology of how it forms because it'll help you to understand which types of hypothyroidism present with a G now generally when a patient has hypothyroidism let's say that it's because their thyroid gland is producing an inadequate amount of T3 and T4 if that's the case if it's producing an inadequate amount it'll then tell what it'll tell the hypothalamus and the pituitary gland to start producing large amounts of TSH and so whenever you produce large amounts of TSH what it does is it goes to the actual thyroid follicles starts triggering them to undergo replication increase more thyroid globulin production and because of that the follicles get bigger and bigger and bigger multiple follicles make up a thyroid gland that thing is huge so because of that now I'm going to start seeing this thyroid gland get all kinds of Lage now look at this it's going to be a big old beefy thyroid gland as a result now now enlargement of the thyroid gland right you may be able to palpate this you may be able to visibly see this one of the big things that add on to this component here is is this enlargement of the thyroid gland painful or painless this helps with the actual differential of the cause so painful you want to think about infectious this is is the one that we refer to as day querin thyroiditis now if I said pain less this is all the autoimmune causes so this is the one that you want to think about in patients who have what particularly Hashimoto this is a big one that I would want you guys to think about postpartum and then one more that's not a thyroiditis I deficiency iodine deficiency causes massive massive goers so another one would be iodine deficiency and we'll represent that with a down arrow all right iodine deficiency most common worldwide deficient areas across an endemic populations Hashimoto is most common United States now painless painful goers really help you with being able to differentiate a little bit of the cause let's move to the next component here next one is metabolic dysfunction metabolic dysfunction consists of multiple parameters but let's say here a patient is producing an inadequate amount of T3 and T4 thyroid hormone if there's an inadequate production this affects a couple different things you know multiple tissues in our body they have a pump on them called the sodium potassium atps the sodium potassium pump is supposed to be able to move particular ions across it so it'll move potassium into the cell move sodium out of the cell right so it helps to be able to move sodium and potassium across these cells problem is it requires large amounts of ATP if I have less thyroid hormone I inhibit the sodium potassium pumps if I inhibit the sodium potassium pumps I will then as a result lead to less consumption of metabolic activity now if there is a reduction in metabolic activity that leads to two problematic issues here one is it leads to a reduction in catabolism of multiple things like what fats it leads to a reduction in metabolism of glycogen and multiple other substances because of that will I be able to break down fat will I be able to break down macronutrients easily no because of that these patients often times gain a ton of weight all right so weight gain tends to be a very common feature here all right the other compon component is that these sodium pottassium ATP Aces whenever you're actually helping to generate energy through these metabolic processes you generate heat but if you're having holy crap decreased metabolism of these sodium pottassium pumps you're going to be leading to decreased heat production so heat production will decrease if I have decreased heat production what will happen to my body temperature it starts to become a little bit lower so we refer to these patients as being what's called cold intolerant they feel cold all the time so if I think about weight gain and I think about cold intolerant in a patient with a goiter I really want to be thinking about a patient who has hypothyroidism I'm not kidding these are super super important ones that I need you to remember all right goiter cold intolerance weight gain the other component here that I wouldn't say is as crucial but think about it especially in um some kind of like minor suggestive causes or minor suggestive findings hypothyroidism May stimulate your poster pituitary to make a hormone called ADH now when ADH is produced in large amounts what it does is is it goes to your kidney tubules here you have your Bowman's capsule PCT Loop of Henley DCT collecting duct right the collecting duct is the site of ADH and what it'll do is it will reabsorb tons of water now when I reabsorb a lot of water what will that do to my sodium well I'll dilute down my sodium and when I dilute down my sodium this will lead to hypo nemia so one of the other classic findings that you may see is a patient who has what's called hyponatremia and it's kind of like a subcategory of what we refer to as ADH so hyponatremia weight gain cold intolerance goiter classic findings what else whenever your thyroid is not acting correctly it's not pumping out that T3 and T4 in an adequate amount that we should again basil metabolic rate for tissues this is tissues everywhere this includes the neurons of your brain when you don't have thyroid hormone the neurons aren't firing at an appropriate rate imagine all the neurons are slowed down dude it's like all my tissues are just like chilling bro my neurons are just chilling bro same thing with the brain so because of that the decreased neuron activity within the central nervous system will lead to severe lethargy and fatigue so lethargy which is just ex you know just generalized tiredness and fatigue are very common findings sometimes depression is also another really big one but that also makes sense it's slowing everything down dude the other thing is that it also will affect on transmission that's important with our reflexes so you tap the tendon and you're like man that that reflex took in crazy long amount of time because everything's jail the delayed dtrs or deep tendon reflexes is super super suggestive of hypothyroidism so if I say delayed deep tender reflexes lethargy weight gain cold intolerance and goiter you're thinking hypothyroidism all right let's come over here and move on to the next next dysfunction here is the cardiovascular system the thyroid hormone has a very profound effect on on your cardiovascular system so whenever there's inadequate amounts of T3 and T4 one of the big things is your thyroid hormone affects your cardiovascular system specifically it works on the beta 1 receptors you know there's uh beta 1 receptors that are present on The myocardium of your heart what happens is when there's low thyroid hormone there's less beta 1 sensitivity beta 1 receptor sensitivity that means whenever norepinephrine and epinephrine bind onto these receptors they're less active less functional that leads to decreased conduction which leads to a reduction in their heart rate and also a little bit of reduction in contractility but primarily a reduction in heart rate so I have decreased sensitivity of The myocardium decreased action whenever epinephrine and norepinephrine bind onto it and a reduction in heart rate what's that called braic cardia now this could be present but it's usually found in severe cases of hypothy which we'll talk about here the other thing which is super weird is low levels of thyroid also control the tone of your blood vessels naturally thyroid helps to maintain a balance between constriction and dilation but whenever there's very little constriction overpowers and so because of that what we'll see here is we'll see what's called an increase in vasil constriction you're like oh my gosh I'm going to Vaso constrict my vessels what that going to do well it's going to cause your vessels to have more resistance to blood flow so your systemic vascular resistance will go up and if systemic vascular resistance goes up your diastolic blood pressure will go up and so sometimes in these patients what we say is is that because their Vaso constricting a little bit too much their resistance is going up they may have diastolic hypertension now with these I would prefer that you remember braic cardia all right as the profound effect on the cardiovascular system it can cause diastolic hypertension by vas or constricting one other effect it also acts on the liver now what it does is is it controls the uptake of LDL receptors you see these little receptors here these are your LDL receptors right here what happens is less thyroid hormone means I have less LDL receptors that are going to be expressed if I have decreased numbers of LDL receptors will I bind the LDL in my bloodstream and bring it into the liver no so then what happens is this uptake becomes inhibited and LDL builds up in the blood and so because of that if l LDL builds up in the blood what is that disease called whenever it's super high hyperlipidemia so these patients can also develop hyper lipidemia all right increased LDL can trigger hyperlipidemia now this is the cardiac dysfunction so if I say a patient has braic cardia they have lethargy and fatigue they have delayed dtrs they have weight gain cold intolerance and a goer you think hypothyroidism let's add another one this one's interesting usually this is helpful whenever we get into the OBGYN system because in patients who come in and they're like man I can't get pregnant or I'm having a lot of problems with my menstrual cycles or I'm having infertility issues libido issues this can be something that you'll say let me check your thyroid and make sure that's it's appropriate so what happens behind this is that your thyroid gland whenever it's not producing enough T3 and T4 this is a really interesting concept here T3 and T4 whenever not producing an adequate amount affect your levels of prolactin so now my pituitary gland will start producing larger than normal levels of prolactin now prolactin is really a dangerous kind of guy whenever it's producing large large amounts because what it does is is it Alters your estrogen levels and it Alters your progesterone levels and so now because of me altering those levels of my estrogen progesterone I will then experience menstrual dysfunction and this can look a lot of different ways when I talk about like menstrual irregularity or dysfunction this could be not having a cycle a in ARA or they could have heavy bleeding so minasia so there's a lot of dysfunction there the other component here is they could have problems with fertility so infertility would be another really big one and then even libido can also be altered as well so libido may also be reduced in women and men all right so reduced libido menstrual regularities and infertility tend to be the kind of reproductive dysfunction I don't want you to spend too much time worrying about those they'll become more apparent when we talk about that in the OBG L system gastrointestinal dysfunction what about this one whenever there's hypothyroidism inadequate T3 and T4 this also plays a role in metabolic activity of the smooth muscle in your git so now if I have some degree of kind of function here all right so T3 T4 it's supposed to affect motility so I'm going to have decreas decreased smooth muscle contraction if I have decreased smooth muscle contraction we refer to that as decreased GI motility or just motility so decreased motility of the git if I have decreased motility that means that I'm not moving substances through the GI tract effectively it's taking a longer time for them to Transit they build up they get bulky and now a patient can start experiencing prolonged time frames between bowel movements referred to as constipation and so constipation is actually a high yield one that you want to remember so if I said that a patient has constipation they also have braic cardia wak Ging cold intolerance goiter as well as lethargy And Delay de deep tend reflexes you really want to think about hypothyroidism but let's add the big one in integumentary system whenever a patient is producing an inadequate amount of T3 and T4 this has a really interesting effect so what happens here and this would only be seen in primary this one here only in primary really most of these would be seen in you can see this in secondary but this one's really really big in primary hypothyroidism M low T3 T4 what does that do to your hypothalamus in pituitary increase TR and increase TSH so now pump out more TSH if I pump out more TSH there is fibroblast and these fibroblasts heavily respond to TSH now what fibroblasts do is that they can produce a bunch of different types of molecules but one of the big ones that they start to release a lot of is called gags all right they release tons and tons of these molecules called glycose Amino glycans we're going to refer to them as gags though because that's a long word I don't know how to spell it so gags tons of glycosamino glycoproteins now these glycosaminoglycans what happens is Imagine them as like um like water retenes like they love to retain tons of water so what they'll do is they're going to retain tons and tons of water retention of water but it loves to retain this water in lots of soft tissues very specific soft tissues I may add so there's going to be an increased retention of water and particular tissues this retention of water causes somewhat of an ademi dis appearance but it occurs in very very interesting areas one is right in like the tibial region like the pre-tibial region honestly it looks like a roughened orange type of appearance and this is kind of like a non-pitting edema all right non-pitting that means if you push into it it doesn't cause the divot to say there so we call this one pretibial mix edema this is like high yield my friends for particularly patients who have hypothyroidism it can cause kind of an aditus appearance in other areas as well it may occur around the the orbits so periorbital edema but that's not always as specific for thyroid disorders so you may see this in periorbital edema and there's one other thing that it can do I'd say It's relatively uncommon but it's something to kind of at least think about if I mention it here is um you can get edema that occurs around the soft tissue in the carpal tunnel region and what happens is it kind of causes so much edema that it compresses on the nerve that runs right through there called the median nerve and so patients can develop carpal tunnel syndrome as a result as well so watch out for periorbital edema and carpal tunnel syndrome as potential effects of the glycos aminoglycan amounts and retention of water in the soft tissues other things that can happen with hypothyroidism it also affects just the generalized texture of the skin so they'll be having more dry skin they'll have brittle hair and nails as well and they even have lots of hair loss all right with that being being said we have covered the classic findings you're like man this is a this is a lot well we got one more this is mixed deacom mixed deacom is chronic hypothyroidism on steroids and it's very specific types of classic findings that are Amplified what is mixoma mixed deacom is when a patient who has so it's kind of like a combination if you will it's a patient who has chronic hypothyroidism so you'll have chronic low levels of T3 and T4 right so chronic hypothyroidism and an increased stress on the body like a massive massive metabolic stress on the body now what happens is this stressor that is occurring in these patients who have chronic hypothyroidism is very specific specific what are some of these stressors some of these stressors could be infection so if a patient has what's called sepsis that can really produce a very large metabolic Demand on the body another one is just if they had surgery so if you had surgery your body is kind of going into this catac colomine Surge and that could also produce a lot of stress on the body another one and this one's really interesting is if a patient has hypothermia so they're in really cold environments and often times that's classic in the clinical vignette is this old kind of rickety woman who was kind of caught outside in the cold weather so hypothermia is another really really big trigger that puts this the insane amount of stress on the body and then lastly is non-compliance with thyroid meds we're going to put the most common thyroid Med here is Leo thyroxine so if a patient is either non-compliant with their levo thyroxine that they're supposed to be taking for their hypothyroidism and they say I'm not going to take it or if they have hypothermia recent surgical procedure or severe infection this puts an insane amount of stress on the body that stress will increase metabolic demand so now what this is going to do is the stress will increase metabolic demand but if you have hypothyroidism can your body meet that metabolic demand no and so that's the problem is there's so much stress but your thyroid hormone isn't able to be produced in adequate amounts to help you to adapt to that stress that's when this starts to happen so what you see here as a result of this is you see a profound effect on a couple different tissues one is you'll see the metabolic Factor insane metabolic Factor here you'll have a basic shutdown of the sodium potassium pumps these things done these things are shut down and because of that you basically generate almost no heat and so your heat production is significantly significantly reduced if it's reduced your body has significant difficult time being able to generate heat and body temperature these patients often present with hypothermia this is when the body temperature gets to at least below 35° that is a super common manifestation it's basically the uh decrease heat production on steroids the other effect here is it affects the cardiovascular system it basically shuts down the AV node it says all right no beta 1 kind of sensitivity okay I'm going to shut down the AV node and because of that I'm going to cause a massive reduction in heart rate so these patients can have severe severe bra cardia that's one feature the other thing is is it's going to reduce the sensitivity of the beta 1 receptors for contractility and then on top of that it's also going to squeeze the arteries and so Vaso constriction is intense so now because of that imagine this my svr is significantly increased if my heart rate's dropping what does that do to my cardiac output drops it if my SV R goes up that increases my afterload what does that do to my cardiac output drops it the combined effect here will drop my cardiac output and put me into acute heart failure so often times these patients can develop acute heart failure and this is actually kind of terrifying so look for a patient who is severely braic cardic with acute presenting heart failure they may be hypotensive they may have pulmonary edema hypothermia and here's the big one ready for the next one severe severe hypoactive encylopedic incopy and it's referred to sometimes as hypoactive incopy what could that look like they could go from being confused they could go to being obtunded where it's hard to arouse them they could even go completely into a comos state where you can't even arouse them with painful stimuli this is the range for the encylopedic cardia and severe encylopedic coma and then if I add on mix edema then I have a recipe for a patient who has likely miedema coma and what do I mean by miedema usually it's pre-tibial but it could be periorbital or it could be carpotonal syndrome but pre-tibial is often times the most common manifestation so if a patient has chronic hypothyroidism they have a recent stressor and now they have a come State worsening mix edema and hypothermia and bra a cardia with acute heart failure you're really want to be thinking about mix ademac coma all right we've covered a lot about hypothyroidism the next part here is going into how do we diagnose it all right my friends let's now move into the diagnostic approach to hypothyroidism so when a patient comes in that you think has hypothyroidism the first thing to do is order your tfts your thyroid function test this consists of your TSH and your T4 now when you do this if the TSH comes back low and the T4 comes back low it definitely suggests a pituitary source so with that being said it's probably secondary hypothyroidism I'm going to throw a little caveat in there there is this weird disease it's called U thyroid 6 syndrome and you usually see this in critically ill patients due to like massive cyto release and they're very sick the concept behind this is really looking at two things one is if the TSH and the T4 is low and both of these diseases T3 will also be low the pathophysiology of how that happens is not important but it we'll talk about it briefly what really is the differentiating factor between these two is the reverse T3 so it's always important to obtain a T3 and to obtain a reverse T3 if the T3 is low and the reverse T3 is high this definitely suggest U thyroid 6 syndrome the concept behind this is a little bit different in the sense that these patients are critically ill so they degrade their TSH they degrade their T4 and then again they convert most of their remaining T4 to reverse T3 and they don't convert as much of their T4 to like your normal T3 so that's their mechanism in comparison to a patient to a secondary hypo thyroidism their problem is that they again don't release TSH their thyroid gland as a response doesn't make T3 and T4 but again the important thing to remember is the reverse T3 will not be high in a patient with secondary hypothyroidism now with that being said when you have a patient that kind of their Labs suggests more of a secondary hypothyroidism picture get a pituitary MRI and the reason why is look for that pituitary macro adenoma that potentially could be causing this process or pituitary infarction in the place of shean pituitary apoplexy or maybe even the scenario of trauma and radiation once we've done this and we've gone down this arm let's move down the next arm here which is okay the TSH is high that means it's a compensatory response if the T4 is low it is this is primary all day in primary hypothyroidism the concept is pretty straightforward again this patient has a problem with their thyroid they're not making T3 T4 as a response this feedback cycle will then generate an increase in TSH to try to make more T3 T4 but it will not respond so if that happens I then need to say okay TPO anti the anti-tpo and thyroglobulin antibodies if these are elevated it could be postpartum it could be Hashimoto but the big thing to remember here is if I do that if they come back positive consistently I really want to think about a patient with Hashimoto's thyroiditis the other thing to remember is that often times when they're negative it could be a bunch of other causes how do I really determine it you base it off their history did they recently give birth do they have any recent features of a viral upper respiratory tract infection do they have a painful Gorder with an elevated ESR do they have any features of igg4 related diseases autoimmune pancreatitis retrop pertino fibrosis aortitis do they have a hard goer with compressive effects it could be rles do they have any recent um amiodarone or lithium use any recent thyroid ectomy or radioiodine ablation have they also potentially have a deficiency in iodine these are all things that can be obtained from the history and elucidate the cause it's often important just to know is it Hashimoto or not now that covers the diagnostic approach to True primary and true secondary there is a weird purgatory and this Purgatory is when a patient has a very elevated TSH but a normal T4 this is called sub clinical hypothyroidism the P the point of this is that patients can have subclinical hypothyroidism meaning that they don't truly have a low T4 so they're not going to have a lot of the pathological effects of this we don't really treat this until the TSH is super super high generally like greater than 20 so that's an important thing to be able to Define here all right let's now move into the treatment of hypothyroidism it's actually pretty straightforward it's all about just giving them back the thyroid hormone that they're missing so often times for these patients you're going to give them something called Leo thyroxine also known as Synthroid and what happens is when you give them this drug it's hopefully going to improve their T3 and T4 levels which will then hopefully lead to the suppression of the anter pituitary leading to a drop in the TSH levels and so what you'll do is you'll check their tfts every couple months and look to see where's their TSH has it dropped down is it no longer high is it kind of improved and it's normal okay great we're in a sweet spot and that's important what about the patient that comes in terribly sick with bra cardia with hypotension with hypothermia with maybe hypoactive encylopedia and I'm terrified that they have a mix ofoma I have to pump their thyroid hormone up quickly and oral is not going to cut it often times they need IV T4 in the form of Levothyroxine and IV T3 because this is the physiological type of thyroid hormone the other thing is that these patients will be very cold it's important that as you give them thyroid hormone during that process of where you're trying to get this hormone into them you may need to warm them up with things like a bear hugger or warm blankets potentially even warm fluids I think the big thing to remember especially for your exams is when a patient comes in and you think that they could potentially have hypothyroidism uh that's caused mix ademac coma you should treat them as a patient that may also look like adrenal insufficiency and so oft times these patients you're going to give them steroids like IV Hydrocortisone and this is just going to be a long enough until you actually send off their labs for adrenal insufficiency send off their cortisol send off their act and if that comes back with no evidence of adrenal insufficiency you can cut the IV hydrocortisone so that's an important thing to remember and the only reason why is mixed deacom and adrenal sufficiency can sometimes Sprint that somewhat similarly so it's important to be able to make sure that you rule that out and treat them until it's completely ruled out all right my friends that's hypothyroidism I hope it made sense I hope that you guys enjoyed it and as always until next time [Music]