Endocrinology Part 1 | The National EM Board (MyEMCert) Review

okay well work's not over unfortunately we got to keep going uh good morning everybody good to see you all glad to see everyone smiling faces here on day three of board of view i know you were you were really worried that you would have to wait this long for endocrine emergencies because it is just everyone's favorite topic in the entire world right i always say you know let's face it we went into emergency medicine to avoid this stuff right but here we are getting ready for the boards we got to relearn some of this some of the good news is that some of the stuff in endocrine emergencies is stuff we see all the time stuff like dka hypoglycemia you know hyperkalemia all right so we're going to cut through a bunch of hormones in the talk and then we're going to do a little bit of acid-base stuff and a little bit of electrolyte stuff and we'll actually be done with endocrine emergencies all right so we'll do part one now part two after the break and let's just forge on by the way if there are any endocrinologists in the room feel free to go out and gamble okay because this is definitely endocrinology for emergency physicians so let's start with simple things hypoglycemia remember that glucose is the only energy source of the brain it's the only thing that the brain can use and the symptoms of hypoglycemia depend on how low your sugar is and how rapidly it dropped okay and you know it can mimic all sorts of things that can make you altered it can mimic stroke seizures it can cause psychosis all sorts of things like that remember that insulin will of course drop your blood sugar but there are the counter regulatory hormones which will bring your blood sugar up these are things like glucagon and epinephrine okay glucagon and epinephrine will bring your blood sugar up remember that the way glucagon works is it breaks down and causes the relief of release of glycogen stores from the liver okay so i can imagine a board question where they say well who might not respond well to glucagon and it's going to be somebody with poor glycogen stores in their liver so somebody like with cirrhosis or some other you know chronic liver disease things like that may not respond as well to glucagon as somebody who's got normal glycogen stores okay and you know when you get hypoglycemic you get nervous and you get tremulous you get all that sympathetic sort of uh stuff going on and then you get the neurologic symptoms where you're altered and can have seizures and things like that remember that beta blockers can block all those sympathetic symptoms but not the neurologic ones and of course in the yellow box everyone is altered we got to check their sugar that's pretty basic emergency medicine right differential of hypoglycemia lots of things could do it you could have an insulinoma which is actually a tumor inside the body making insulin lots of different medications drugs and alcohol can do it you can have a tumor outside of the pancreas that can that can also make insulin so extra pancreas excuse me extra pancreatic cancers can do it as well liver disease because of depleted glycogen stores so again liver disease so the serratic patients who are altered it's not always hepatic encephalopathy it's not always alcohol intoxication they absolutely could be in liver failure with hypoglycemia make sure you're checking it if you just have a deficiency of your counter regulatory or hormones so for example you're a critically ill septic stressed out infant who's used up all of their epinephrine all their counter regulatory hormone you can get hypoglycemic from sepsis of course then there's this weird thing called dumping syndrome you know normally you're not going to get hypoglycemic after you eat right you just ate how are you going to get hypoglycemic but in dumping syndrome your gi motility is kind of altered where it kind of goes through really fast and because of that you get a little duodenal stretch and you over secrete insulin it's kind of like an overreaction to a meal so you eat a meal and you over secrete insulin and soon after the meal you get hypoglycemic okay that's pretty unusual that's dumping syndrome you can get an artifactual hypoglycemia if the blood's just sitting around in the tube for too long i'm sure you've seen this where the lab calls with some ungodly number makes no sense at all the blend the person is totally awake and doing fine the blood may have just been sitting there for too long there's continued glycolysis from the white cells and things like that also leukemia polycythemia whenever you've got too many cells think of it as chewing up your glucose so that's hypoglycemia here's a good question for the boards and just for practice too how do you tell whether somebody who keeps getting hypoglycemic actually has an insulinoma that is a tumor in their body making insulin versus they're just shooting themselves up with a bottle of insulin right they got like munchausen they're making themselves sick with a bottle of insulin just shooting themselves up how do you tell where that insulin is coming from the tumor in the body or outside of the body in the bottle and the answer to that is the c peptide it turns out that when um when insulin is made within the body it's made as a big pro peptide and that pro-peptide is cleaved into insulin and the c-peptide okay so if you have an insulinoma which is in the body it's making insulin it's also making a bunch of c-peptide but if you have insulin from the bottle they don't pack any c-peptide in there okay it's just the insulin itself so your c-peptide level is going to be elevated and an insulinoma and that's how you can tell that it's actually insulinoma not just shooting themselves up with insulin from a bottle okay treating hypoglycemia again you do this all the time this is pretty straightforward adults get d50 right you get an amp at d50 kids get d25 a little more dilute neonates get d10 even more dilute trying to help you know not irritate their veins and i just kind of remember the rule of 50 kind of helps me remember the dosing so an adult gets one amp of d50 right 1 times 50 is 50 kids get 2 ccs per kilo of d25 2 times 25 is 50. that's easy and neonates get 5 cc's per kilo of d10 5 times 10 is 50. pretty easy so d50 d25 or d10 depending how young they are glucagon of course we can give im or iv but you got to have glycogen stores for it to work recurrent hypoglycemia we stick them on a d10 drip i'm sure you've done that many times before if you think they are hypoglycemic because of adrenal insufficiency because they do not have the glucocorticoids from adrenal insufficiency you got to treat the adrenal insufficiency too right so they're going to get some steroids some hydrocortisone something like that and then what about octreotide octreotide is an antidote for sulfonylureas and you remember sulfonylureas those are all those oral hypoglycemics that end in ide and they they obviously in overdose they cause hypoglycemia and the way a sulfoniaria works is it kind of tickles the pancreas and has it secrete insulin okay so it's like stimulates the pancreas so that it secretes out insulin octreotide does the exact opposite it blocks the release of insulin from the pancreas so it's a perfect antidote for sulfaniuria so a sulfonylurea will squeeze out the insulin whereas this octreotide will block the release of insulin from the pancreas so somebody's overdosed on a sulfonaria they're getting recurrent hypoglycemia octreotide would be the answer for that one okay so that's pretty straightforward the next thing i want to cover was one of these really painful llsa articles to be honest with you i think it was the most painful article i read of all the llsas it was the one that reviewed as many years ago but it reviewed all of the different oral agents you can treat diabetes and you know if you're not an internist this is like kind of painful stuff to be thinking about right uh painful for me to think about so what i'm going to try to do is just really summarize the points that i think are important and testable and not get into minutia from this article all right so big picture of these oral agents for treating diabetes think of it as two main classes you have your hypoglycemics which drop your blood sugar and your anti-hyperglycemics which really just keep your blood sugar from going up and the reason that's an important difference is when you overdose on a hypoglycemic you get hypoglycemic but if you overdose on one of these anti-hyperglycemics that just keeps your sugar from going up you're probably not going to get hypoglycemic okay and that certainly shows up in the ed and could show up on the board exam so let's kind of go over these the hypoglycemics the ones that will drop your blood sugar the big bad one of them of course are the sulfonylureas which we just talked about a little bit all the ones that end and eyed right glipizide glyburide all these eyed you know sort of medicines stimulate the pancreas to make insulin they have very long half-lives excuse me and because of that they can cause profound hypoglycemia and persistent hypoglycemia and overdose and that's why when people overdose on these sulfate ureas they're almost always going to be admitted right if they get if certainly if they get hypoglycemic at all you may as well just bring them in because it's going to be lasting a long long time so those patients who who overdose on it and do get hypoglycemic from it are going to be coming into the hospital so those are the sulfoneurias excuse me the other one is prandin which is replicanide or paglinite i don't know how you say it but basically all you got to know is it's also one of those that an overdose will cause hypoglycemia like the sulfonylureas okay so those are the hypoglycemic ones now the ones that keep your blood sugar from going up are less likely to cause hypoglycemia and overdose these are things like metformin which of course you know about and you see patients on all the time the other trivia point about metformin is that it can cause lactic acidosis especially in patients with renal insufficiency right renal impairment it's not like real common but it does happen so metformin can cause a lactic acidosis that's the trivia point to know about that one and an overdose it's not going to make you hypoglycemic you got these things called alpha glucose excuse me alpha glucosidase inhibitors these are basically sugar blockers they work in the gut they block the breakdown of these polysaccharides so that it doesn't get absorbed so again if you overdose on that you're not going to get hypoglycemic you're just not absorbing as much sugar okay that's what you need to know about that one and then there's this weird class of agents called the thiazilidine diones gotta love that name this is avandia and actos that you've heard about okay and the main thing to know about those again they're not gonna cause hypoglycemia probably an overdose trivia about those they cause fluid retention so they can cause worsening of chf so you've got a patient in chf whereas the history of chf they get put on avandia they get put on actos one of those agents now they come in the ed in pulmonary edema that's the medicine you need to know about associated with it and then avandia also has a black box warning for acute mri so just remember cardiac complications of those you know those of andy and actos medications and you're probably going to get those right on the exam too okay and then the more the more recent agent that was actually not in the article because that's more regent are these sglt2 inhibitors um basically these are like causing osmotic diuresis they basically increase the renal secretion of glucose so you just start pee out a whole bunch of glucose in your in your urine and because of that you know again you're not going to get hypoglycemic but you might get hypovolemic you may have orthostatic hypotension and things like that they have syncope but basically it's just an osmotic diuresis it's like given a mannitol or something like that in some ways right think of it that way you secrete glucose out it's an osmotic diuresis all right so those are the oral agents the hypoglycemics which will drop your sugar the anti-hyperglycemics which just keep it from going up and i think that's all you got to know about the factoids and the mechanisms of those agents and if you know that you should get all those exam questions right so some final pearls for hypoglycemia again we already mentioned always admit the sulfonylurea overdoses most will be symptomatic within four hours but it can be delayed octreotide is the an adult for the sulfonylureas malnourished patients who are hypoglycemic or you're giving them glucose you also want to give them thymine what are we trying to prevent here wernicke's encephalopathy right wernicke's encephalopathy so if they're thiamin depleted and you give them their sugar you want to make sure you're also giving them some thyme and as well so they do not develop wernicke's encephalopathy now we were all taught in medical school at least of my generation in medical school i don't know about the newer generation we're all taught you got to give the finemen before the glucose right that's what we were supposed to do the reality is those were like studies of people who were on days i mean glucose and fusion drips and they they got wernicke's without getting thiamin so i don't think you have to get the thiamin right before the glucose but you should give the thiamin soon right so give the glucose if their sugar is 20 give them the glucose but if they're really malnourished chronic alcoholics folks like that make sure they're getting some thymine and the ed as well so they don't develop ortiki encephalopathy and we already talked about where glucagon may not work in anybody who has bad glycogen stores so basically liver disease okay so that's low sugar pretty simple let's move on to dka which is something that you see all the time quick review of the pathophysiology if you remember basically the problem here is a lack of insulin if you don't have insulin your blood sugar goes up your blood sugar goes up you start peeing it out osmotic diuresis so you get dehydrated you lose fluids you use electrolytes you know potassium phosphate all that good stuff you also have this lack of insulin with your blood sugar going up but your body can't use that sugar because it can't get into the cells so you start to break down the fats into the fatty acids and that's why you have the ketoacidosis all right so it's all lack of insulin problem osmotic diuresis lose electrolytes and the ketoacidosis and remember that acidosis is why you'll see patients with coo small respirations those big real big fast and real deep respirations you see that thin patient coming in you're like i think that patient's in dka all right they're trying to compensate for that metabolic acidosis precipitants of dka uh before i get into the eyes i want to give you a general thing about all of the endocrine emergencies we're going to talk about today almost every endocrine emergency can be precipitated by almost any acute stressor you really don't have to memorize a list of all the bad things that can precipitate adrenal insufficiency or a thyroid storm or dk all these sort of things because the reality is any acute stressor will precipitate any of them the glands just do not like acute stressors so you don't have to really memorize a hopeful list these are a bunch of eyes that can precipitate dka but again any acute stressor can do it i usually remember the first four eyes because it just gives me a place to start when i'm looking at somebody in dki just to think about and that's you know do they have an infection they had an infarction acute mi they have insulin lack of insulin so insulin non-compliance or iup in tutor and pregnancy or are they pregnant all right so i'm thinking hmm are they infected they've been taking their insulin are they having an mi are they pregnant that's a good place to start but the reality is any acute stressor can precipitate these things glands do not like stress fluid and bicarbonate dka you know these patients are all dry they're going to get lots of fluid you want to give them initial fluid resuscitation to get rid of their hypovolemia you want to replace their electrolytes you want to start them on an insulin drip right to start reversing that ketoacidosis but remember you do not start them on an insulin drip until you know what their serum potassium is because insulin is going to do what to your potassium drop it right and when you fix someone's acidosis with all the fluids you're giving them what's that going to do to your potassium drop it so everything you do to treat dka is going to drop their potassium so you need to know where you're starting and if you're starting high or normal that's one thing but if you're starting low and you start giving them insulin you can give them severe hypokalemia and they can arrest in front of you not a good shift okay so always know the potassium level before you start the insulin drip really important and let's talk for a moment about sodium bicarb those of you have been practicing for a while understand that this has always been controversial in dki right should we use bicarb should we not use bicarb how much should we use the reality is the boards are not going to test you on controversial things we don't use it very much now as you know if maybe at all but there are some testable factoids about bicarb that i think are fair game for the exam okay so let me give you what i think are testable factoids that are fair game the first is when you give someone bicarb you're making their blood right look better you're getting rid of their acidosis from their blood but you give them the bicarb it kind of gets up across the blood-brain barrier you know turns into co2 goes across the blood-brain barrier and then gets trapped in the brain and because of that you get a csf acidosis so even though you're making their blood look better you're fixing the acidosis in their blood you can have a paradoxical worsening acidosis in the brain you know when acidosis in your brain makes you altered leaky brain cerebral edema those sort of things right so that's one of the hazards of bicarb is this paradoxical csf acidosis the other thing bicarb does if you remember i know it's kind of painful but that oxygen hemoglobin dissociation curve remember that thing it shifts it to the left what that means is that hemoglobin is stingy it doesn't want to drop off oxygen at the tissues as much as it used to all right and if you're acidemic you kind of want some at you want some oxygen at your tissues right you don't want to be hypoxic at your tissues so this makes it worse as well so it messes up with the brain it's getting less tissue delivery of oxygen that's another bad thing and of course bicarb is sodium bicarb so you can get sodium overload volume overload bicarb will drop your potassium so that can also make you hypokalemic okay and it turns out in kids it has been independently predicted of kids in dka who will develop cerebral edema this was a study many years ago in new england journal they took a bunch of kids in dka and they said which kids go on to develop cerebral edema which will predict this bad outcome in kids you know who have dka and they looked at all sorts of predictors and did their fancy statistics in new england journal right and they found that there were three things that predicted which kids were going to develop the cerebral edema two of them were just lab markers we can't fix a lab marker it's just a lab value but only one thing was something we actually did as doctors and that's given bicarb so giving bicarb to kids in dka is independently associated with them developing cerebral edema so i would really avoid it in kids all right so those are the testable factoids of bicarb all right for dka okay sodium phosphate if you remember as your blood sugar goes up your serum sodium goes down okay and what hap the reason that happens as your sugar is going up your body pulls fluid in to dilute it out right and as it dilutes out the sugar it's also diluting out your serum sodium they call that pseudohyponatremia but it is real it's not pseudo like it's fake it's just pseudo because it's not that you've lost the sodium particles you've just diluted it out but it is a real hyponatremia for whatever cause as your blood sugar goes up your serum sodium is going to drop because you're starting to pull in more fluid into your body okay excuse me into your into your bloodstream okay and there is a formula there's actually a couple different formulas but there's a formula that you can use to try to predict depending on how high your glucose is how low is your sodium going to go okay i'll start with like one formula and i'll tell you a little twist on it okay one formula is that for every hundred that your blood sugar goes up over a hundred your serum sodium is going to drop by about 1.6 okay so that would mean for example if you had a serum glucose of 600 600 is 500 above 100 5 times 1.6 is 8. so that would mean instead of your serum sodium being 140 normal it'll drop down to 132. so what i mean by that is if you've got someone's chemistries and it says glucose 600 sodium 132 you could say if you're using that formula that that makes perfect sense that's a perfect balance the sugar went up the sodium went down okay some people like a bigger number they like to use 2.4 this comes from a study of like it was like four or six like healthy volunteers that they made hypoglycemic and they said actually we think 2.4 is a better number than one point six if that were the case the example i i gave you instead of dropping by eight it would drop by twelve okay so it's about fifty percent more all right and i don't think it's so important that you know the exact number but i think it's important that you understand the concept and you have some idea of the range of what's going to happen with this and why would this ever be important other than the board exam why would it ever be important in your life well you can imagine a patient in front of you where their sugar is elevated it's 600 it's 700 something like that and their serum sodium is normal it's 140. it would be really easy to blow by that and just say oh sodium is normal that's not a problem but if you correct that if you add that 8 or 12 back on to that number right it's not 140. it's 148 or 152. it's something like that that patient is really really dehydrated okay so if you see somebody who's sugar six or 700 and their sodium is normal they're actually really really dry because their sodium should be low all right that's the reason i want you to understand that point okay phosphate you know you in dka you pee out everything you pay out your sugar p out potassium you pee out phosphate so they got hypophos as well you need phosphate to make atp atp for energy so when they get hypophos they get weak so you want to replete their phosphate okay potassium really important total body potassium is probably down because you're peeing out your potassium but your serum potassium could be low normal or high depending on their acid-base status and depending on their renal function if their kidneys are still working so you really do not know what their serum sodium is even though their their total body is probably down that's why you have to check it before you start that insulin drip and the way it kind of works is you know if their serum sodium is you know let's just say um low you got to start repleting their potassium not sodium i'm sorry if their serum potassium is low you start to replete their potassium and then once you get it up to normal you can start your insulin drip if their first serum potassium is normal you start your insulin drip and you give them a little bit of potassium along with it too right because you don't want them to drop too much and if their initial potassium is high you start your insulin drip you wait till their potassium comes down into normal and they're peeing so that you know their kidneys work then you start adding your potassium in as well so they don't get too low all right so just watch the potassium and dka that's really really important complications of treating dka they can get hypoglycemic from all the insulin we're giving them you can get hypokalemia we already talked about that the insulin the fixing the acidosis if you give them bicarb bicarb can cause that csf acidosis and we talked about cerebral edema as well these are patients that are getting altered mental status bad complication of dka so that's dka we went over it and hopefully now you know all the other testable points that could show up because i know you know how to take care of these patients now let's do aka alcoholic ketoacidosis you are at a board review course in las vegas it is day three you had to sit through endocrine emergencies okay and you said i'm out you said i'm going to go drinking forget the review session i'm going drinking so you go out and you start drinking alcohol and drinking and drinking and drinking and of course you're not eating so much food because hey you got your liquid diet that you're on there right and you drink for a couple of days and then you stop and of course the next morning you feel bad but but you know a day to two after that you start to feel really bad not just hung over but like really really bad nausea vomiting abdominal pain you just feel horrible okay you have a really bad acidosis is what's going on now you kind of feel like somebody was in dka you feel like really really miserable you present to the ed nausea vomiting abdominal pain so what is going on there is what's called alcoholic ketoacidosis binge drinking heavy alcohol not taking a lot of food so you get this kind of relative hypoglycemia the alcohol itself ethanol will inhibit gluconeogenesis it's another reason you get this relative hypoglycemia and because you have this hypoglycemia you develop a ketoacidosis just like in dka all right so you're dry you've got belly pain you've got a ketoacidosis that's going on you feel really really sick alcohol levels in aka should be normal zero right this is not when you're drunk this is when you're undrunk this is when you've stopped drinking you're now in alcoholic ketoacidosis all right um you know you've got again you've got a metabolic acidosis so you're gonna have an elevated anion gap with alcohol ketoacidosis it's a metabolic acidosis that makes sense what about the ketones though if you measure their serum of course you're going to have positive ketones because i just told you it's alcoholic ketoacidosis you have lots of ketones but in your urine the urine dip may be only weakly positive so you're thinking shouldn't it be really positive it may be only weakly positive if you remember there's two main types of ketones acetoacetate and beta-hydroxybutyrate it turns out that in alcohol ketoacidosis the main ketone is beta-hydroxybutyrate so they're making lots of beta-hydroxybutyrate and a little bit relatively of acetoacetate and it turns out the urine dipstick only picks up acetoacetate not beta-hydroxybutyrate and the way i remember it is very simplistically i just think to myself like when they invented the urine dipstick test they invented it and they got the a and they didn't get the b all right so the dipstick will pick up the acetoacetate but it won't pick up beta-hydroxybutyrate and that's what you get in alcoholic ketoacidosis so even though they've got plenty of ketones in their blood their urine is only weakly positive for ketones really testable point that could show up on the exam okay so the patient has come in your emergency department belly pain nausea vomiting alcohol ketoacidosis and you're thinking yeah i know how to deal with this i give them some fluids i give them some zofran i do that all the time right the special thing here is you want to give them d5 normal saline so they need some substrate there right because they have this ketoacidosis with this relative hypoglycemia so it's not just normal saline and zofran it's d5 normal saline and some zofran all right so that's what they need and then they're going to get better that's alcoholic ketoacidosis okay so it's another ketoacidosis like decay but not the same the next thing we need to cover hyperoz molar hyperglycemic non-ketotic state so this is another state where you have really high blood sugars so kind of like dka but there are some differences and very testable differences i could write a number of questions for the boards just about differences between dka and this state this h and and you know and s this hyper osmolar hyperglycemic non-ketotic state okay so it's similar to dka they both have elevated blood sugars but there are some differences so for example there is no ketoacidosis in this dka has ketoacidosis this is non-ketotic okay or or at least low ketones all right so it's not a it's not a big keto keto acidosis state like dka is the glucose here is oftentimes really high 800 900 1000 1200 you've seen these patients right elderly patient from nursing home pneumonia comes in really dry sugar's 1400 that's this state that's not dka that's this state okay really high blood sugar whereas dka it's usually not more than 600 or so right it's not like 1200. osms are very very high this usually occurs in non-insulin dependent diabetics whereas decay of course it's type 1 insulin dependent diabetics in fact for this state about half of the patients did not know they even had diabetes until they showed up with this okay so this is their first presentation for about half of these patients so non-insulin dependent diabetics with this and the mortality is higher than in dka uh these patients tend to be older they have more comorbid conditions um uh you know lots of lots of and it's been going on for a longer period of time so this has a higher mortality than decay on average not not not everybody of course but on average higher mortality than dka and dka is a shorter onset right you stopped your insulin yesterday and now you're in the emergency department in dka whereas this thing has been going on over a couple of weeks they got sick they got a little pneumonia a little cough they didn't drink so much they got dehydrated worse and worse and over the couple of weeks they got really bad okay so those are the differences very testable know the differences precipitating factors anything bad any acute stressor don't even bother memorizing the list any acute stressor will do it okay comorbid conditions they tend to have renal and cardiac disease and they tend to be on renal and cardiac meds that's the way i remember it you're not going to remember everything just remember renal and cardiac disease renal and cardiac meds so these are elderly patients with renal disease and vascular disease and you know they don't have great access to water so they get dry whether on renal or cardiac meds like diuretics beta blockers calcium channel blockers those are the things to remember okay when they come into the ed they are profoundly dehydrated and they're altered so they are altered and they look really really dry with their blood sugars of 1200 and things like that they can they can have focal neurologic science but that's pretty rare they're usually just altered and very very dry the treatment for this is to rehydrate them is the most important thing so they're very very dry you give them some normal saline remember they're really dry big deficits of like 8 to 12 liters and remember we want to fix things slowly in general with endocrine emergencies in general not hypoglycemia but most things fix it slowly so half their deficit in the first 12 hours and the other half over the next you know 24 hours something like that fix it slowly get them volume repleted but slowly and then of course and then insulin as well you can start them on instance at the bottom there insulin infusion as well low dose insulin infusion they don't need a bolus you don't need to bring their sugar down real fast but some fluids a little insulin fusion and then try to figure out what the underlying condition was oftentimes they have some acute precipitate as well all right if you treat this too fast they can develop cerebral edema remember these patients are probably hypernatremic because they're dry fixing that too fast correcting it too fast can cause cerebral edema so don't do it too quickly all right so we did a bunch of sugar low sugar high sugar all sorts of stuff like that now let's move on to our friend the thyroid let's do a couple of glands here the thyroid okay if you remember the way this works you got your hypothalamus which secretes some thyroid uh releasing hormone which goes your pituitary your anterior pituitary anterior pituitary secretes out tsh that's thyroid stimulating hormone right so the anterior pituitary makes tsh that goes to your thyroid and it binds to the tsh receptors and it stimulates the thyroid like it says it stimulates the thyroid to make thyroid hormone the thyroid makes a bunch of t4 remember that t4 then peripherally gets deiodinated into t3 and that both t4 and t3 are active but t3 is like the big guns right it's like the more biologically active of the two things you got your t4 and your t3 which is really active and then of course the thyroid hormone the t4 and t3 feed back at the pituitary to you know say hey don't make so much more tsh we got plenty of thyroid hormone right so that's the usual loop you kind of remember that and remember that the thyroid hormone just increases your metabolic state it revs everything up that's what it does okay let's start with hyperthyroidism rule of thumb i want you to remember when there's a problem with the thyroid whether it's high thyroid or low thyroid it is usually the thyroid itself it is not usually the hypothalamic pituitary axis that's messed up when it's the thyroid it's usually the thyroid itself primary hyper or hypothyroidism okay something is wrong with the thyroid the most common cause of hyperthyroid which is at the thyroid is graves disease if you remember what graves disease it's an autoimmune disorder where your body is making antibodies and the antibodies look just like tsh they look like tsh so they go to the thyroid and they stimulate the thyroid and they make you hyperthyroid that's exactly what graves disease does okay it makes you very hypothyroid that's what it does you can have other causes within the thyroid itself uh toxic adenoma multi-nodular goiters thyroiditis you know meaning which can be viral or it can be autoimmune there's this thing called hashimoto thyroiditis which is when you get lymphocytes that infiltrate your thyroid they kind of get in there and infiltrate and when they first infiltrate it'll make you hyperthyroid now eventually it burns out the thyroid and then they get hypothyroid okay but thyroiditis either viral or autoimmune can cause it as well usually the thyroid itself yes you can have a pituitary adenoma secreting out tsh but it's just less common than the thyroid itself and too much iodine can do it too okay so it's usually the thyroid itself graves is the most common signs and symptoms of hyperthyroidism remember everything's revved up so you know you're nervous you're tremulous you can't sleep because you're revved up you don't tolerate heat because you're already making plenty of heat on your own right uh you get weak you uh you know you got weight loss you get tachycardic and palpitations maybe afib things like that hyper-defecation everything's moving quickly bowels moving real quickly all those sort of things maybe a big goiter with a brewee over it that's always a nice hint on exam if you see that [Music] look at the picture here this is some exophthalmos here right that kind of looks like kind of proptosis sort of thing the eyeball's very prominent there this is seen only in graves disease so not the other causes of hyperthyroidism this is only in graves disease and the reason you see this in graves disease is it turns out that back behind the eye there there are these fibroblasts and fat cells those adipocytes and they have tsh receptors on them so that antibody that's going to your you know to your thyroid looking like tsh and making you hyperthyroidism that same antibody is going to those fat cells and fibroblasts behind your eyes and causing them to like proliferate and secrete stuff and things like that so stuff starts to accumulate behind the eyeball and it starts to get proptotic so that's only in graves disease because it's the antibody thing that's doing it okay you don't get it from the other causes so they get proptosis they get this other thing called lid lag lid lag so normally in a patient if i'm having them look forward and i just say look down at your feet not your whole face just your eyeballs look down at your feet as their eyes look down eyeballs move down and the lid moves right with your eye that's a normal thing to happen right if you just look at each other and you look down you'll see your eyelid kind of moves with your eye that's a normal thing to happen but in lid lag it's just like it says the lid lags so the eyeballs move down the lid is kind of more slow and you may see the sclera on the top of the eyeball and things like that okay so that's lid lag so um the the exophthalmos and the lid lag are with graves disease also in graves disease you can get pre-tibial myxedema i'm not talking general mixed edema i'm talking just pre-tibial kind of this infiltrative stuff there's this nodular plaques that develop there again it's the fibroblast there it's all the same thing that's happening making these like polysaccharides all right so basically it's the same thing they get all stimulated they they make this stuff so they make it behind the eye they make it in front of the legs that's graves disease okay yellow waxy nodules pre-tibial mixed edema okay any sort of thyroid disorder family history is is a risk factor and being a female so women are more common to have either hyper or hypothyroidism thyroid disease is more common in women okay let's do about the labs in hyperthyroidism because it's usually the thyroid itself making too much thyroid hormone your t3 your t4 those are going to be elevated and your tsh is going to be low right because of feedback at the hypoth at the hypothalamus okay that makes that makes pretty much sense okay um treating hyperthyroidism if it's mild hyperthyroidism somebody you're sending home uh they may just they may get a beta blocker or they may just get something like uh ptu or methymizole more likely methymizole okay turns out that um ptu has more liver toxicity so more likely they're going to put somebody home on methymizole right so they may get a little beta blocker they may get some ethymizal when they go when they go out more likely and then of course there are things that you do to treat the disorder so they may get radioactive iodine for their thyroid or surgery for their thyroid for example if they have graves they may try to blast out the thyroid depending on what's going on just depends okay so that's mild hyperthyroidism now thyroid storm really important stuff sick patients in the ed this is when you have life-threatening manifestations of hyperthyroidism it's the extreme end of it now okay precipitating events again anything bad you do not have to memorize the whole list the only thing i would remember is iv contrast so it's any acute stressor anything you can think of stroke bleeds drugs whatever trauma but infection but iv contrast so i can imagine you know so they have iodinated contrast so somebody you know they say walked into your emergency department oh recently had an iv contrast study and now they're triuming tachycardic and blah blah blah right think about iv contrast is something that precipitates thyroid storm but any acute stressor can do it what makes it thyroid storm it's not a lab test it's not a tsh level it's not a t3 level it's all about a clinical diagnosis it's basically when you're starting to get cns disorder so altered mental status so somebody starts to get altered now they're in thyroid storm okay so they're altered they may have a little elevated temperature they'll be very tachycardic even out of proportion of that temperature okay and again all the other symptoms of hypothyroidism we talked about there but it's a clinical diagnosis they're really sick labs again because it's usually the thyroid itself elevated t4 elevated t3 but a low tsh and then i want to talk to you about these other labs okay the ones below those all this stuff down here okay the sugar the calcium the lfts everything goes up all these other labs go up the sugar goes up the calcium goes up because of blood turnover the lfts goes up the only thing that goes down are the cholesterol okay the lipids the cholesterol goes down and the way i think of it is you're hyperthyroid everything's revved up you're tachycardic things are going everything's going up right all of your blood tests all these you know these these glucose calcium melodies they all go up except for your cholesterol which goes down because you know you're so active with your hypothyroidism that you drop your cholesterol all right not the actual mechanism but it'll help you remember it all right so all these other labs go up just like the thyroids up the cholesterol goes down treating thyroid storm this is actually really important okay it's important for your practice and for the exam you need to know the steps of treating this it does matter to the order of these at least to some degree so the first thing you do is in general you give supportive care right so you give some iv fluids you fix your electrolytes things like that but you give them a dose of steroids so you're giving this person in thyroid storm a dose of corticosteroids like a hydro hydrocortisone why are we doing it somebody tell me why are we getting steroids yeah i heard the word adrenal that's right it's they have a relative adrenal insufficiency okay so a normal person wouldn't need some steroids but because their metabolic rate is you know doubled and tripled and quadrupled or whatever it is with a thyroid storm their their their adrenals even though they're working normally they need help they need stress dose steroids right so anybody in thyroid storm they need some additional help they get some corticosteroids they give a hydro hydrocortisone okay now let's start fixing things um they're real tachycardic so we start giving them some propranolol they get their heart rate under control the truth is you could use any beta blocker the reason we like propranolol at least one of the reasons that we like propranolol is it also blocks the peripheral conversion of t4 to t3 so you don't make as much of that really active stuff so an extra bonus with that beta blocker is it blocks the peripheral conversion of t4 to t3 by the way so do the steroids that we gave for the adrenaline deficiency that'll also reduce the peripheral conversion of t4 to t3 okay so it's extra bonus so that's why we like for parental so you give them a little propranolol you know milligram at a time get their heart rate under control things like that okay now we got the heart rate under control we want to stop them from making all this thyroid hormone so you can either put them on ptu or methymizole but here i want you to use the ptu the propafia uracil it blocks the enzyme so you stop making thyroid hormone why ptu over methamphol well ptu also will block that peripheral conversion of t4 to t3 okay so you get less so it means it's going to work faster and better than the methymizole is and even though methimazole has a less risk of liver toxicity if someone's in thyroid storm you want the ptu if someone's in mild hyperthyroidism and going home you can put them on a themselves when they're in storm you want the ptu you want the big guns right and then later when you get under control they can transition them to methamphetal but you start with the pto so you gave me some steroids to help their adrenals and block peripheral conversion you gave them some beta blocker to control their heart rate and block peripheral conversion and you gave them some ptu to stop making hormone and a block peripheral conversion and then the last thing or not the last thing but the next thing you want to do is to give them iodine you want to basically block the release of whatever hormone was already made in the gland okay so they're not making any more we've shut it down but there's still some in there and we want to stop its release and for that you give iodine you can use iodinated you know oral contrast you can use sski that saturated solution of potassium iodide basically you're going to look it up okay but you know that you're going to give them some iodine is what you're going to end up giving them for that and this is a really important point you have to wait you have to wait at least an hour after you've given the ptu so that the ptu will shut down the machinery before you give the iodine otherwise the iodine is sucked up into the thyroid and you make more thyroid hormone okay so you've got to wait at least an hour so some steroids some beta blocker get it under control some ptu shut down the machinery wait an hour then give them some iodine to block the release and then the final thing is you know figure out what was the precipitating event right what was their stroke their bleed their pneumonia what was it what was going on all right so that is thyroid storm really important some testable stuff in there okay you know how in elderly patients they present differently with everything right you know like their appendicitis is different they're not as tender they don't get as much of a white count their everything like always presents a little more subtly in elderly patients hyperthyroidism can also present a little differently in in elderly patients and it's this thing called apathetic thyrotoxicosis they look apathetic but they've got thyrotoxicosis okay so instead of looking all revved up they look more like you know you know stare droopy eyelids you know slowed mentation lethargy they look more like the press or something like that but they're hyperthyroid and their heart knows they're hypothyroid because it's tachycardic and they're an afib and maybe they've got you know high output chf and things like that so they are hyperthyroid it's just in these elderly patients kind of like many things the external signs look a little different okay they look more mass face so that's what apathetic thyrotoxicosis is i just don't want you to miss that when you see somebody who's you know elderly and altered or looking depressed or whatever in the ed it could be this you know apathetic thyrotoxicosis okay so that was the high thyroid now we're going to do the low thyroid and since we covered a lot i think it'll be easier with the low thyroid again what causes it usually the thyroid itself most commonly treatment of graves disease someone had graves which is very common and now we treated it with iodine and where we took the thyroid out or something like that and they're hypothyroid iodine deficiency in the diet can do it remember the autoimmune the hashimoto's thyroiditis where the lymphocytes come in and make your make you elevated initially and then burn it out and make you hypothyroid and then there's some medicines that i think you should know are associated with hypothyroidism lithium and amiodarone are two to remember you know there's obviously other things but those are ones that i think are pretty testable lithium and amiodarone associated with hypothyroidism and of course it could be the pituitary or hypothalamic stuff you got a you got a stroke in your pituitary or a tumor or something and it's not making tsh but those are less common than the thyroid itself signs and symptoms of hypothyroid everything is slow everything is sluggish so you're weak lethargic you don't tolerate the cold because you're not making heat to begin with hypothermia you're gaining weight you're constipated things are moving slowly dry skin right these sorts of things you can see the picture there the before and after of what it looks like you know you know before when they had hypothyroidism and then after some treatment back to normal okay but that's the slow sluggish and big and puffy stuff going on too you can look at hair loss particularly the lateral thirds of the eyebrows that's a kind of a good good kind of just clinical pearl lateral thirds of the eye eyebrows lose some hair loss it's good place to look they get slowed mentation psychosis things like that cardiac of course they can get bradycardia they can get chf and they tend to kind of accumulate fluid so they can get pleural effusions and pericardial effusions and generalize mixed edema things like this okay so so basically hypothyroidism they accumulate fluid labs because it's the thyroid itself your t4 your t3 are going to be low your tsh is going to be high trying to get that thyroid to work okay and then what about the other labs not the not the hormone level labs but the other labs with hypothyroidism you get all the hypos now you get hypoxia okay hypoxemia low oxygen hypothermia and mix of the vacuum hyponatremia everything's low anemia low blood count okay so everything's low except for the lipids the lipids are going up and again i just think about hypothyroidism all those other like chemistries and stuff are low but your cholesterol has gone up because you're so slow and sluggish that your lipids gone up all right that's the way to remember for the test that's hypothyroidism mixodemocoma kind of like thyroid storm it's just the end of the spectrum thyroid storm at this end mixing emo coma at the other end right life-threatening hypothyroidism lots of different precipitating factors any acute bad thing can do it don't have to memorize the list the things i would remember are cold exposure so it's more common in winter and in cold exposures so for those of you who live in areas of the country where it gets really cold particularly during winter somebody gets outside you know you get a 55 year old woman comes in your emergency department a little bradycardic hypothermic altered maybe was out in the cold a little too much think about mixing mixodemocoma she probably had hypothyroidism and got that acute stressor and now is there with myxoneemacoma all right so cold is the other thing i would remember for precipitating mixidimencoma okay again signs of mixademocomas i already talked about their hypothermic they're altered they get these um what they call hung up reflexes so it's delayed relaxation phase so here let's just do my arm here normal patient reflexes right that's normal up and down we've seen that before normal biceps these are the hung up ones okay hung up so slowed relaxation phase the patient that i just described to you comes into your emergency department i know we're not big into checking reflexes but just check a reflex and see what happens and if they do this thing you can look like a superstar and say you know what i think that might be mixodemocoma all right start sending off the labs check up for those hung up reflexes and again they get generalized pitting edema they look like that when they come into your emergency department treating mixodemocoma again supportive care so warm fluids you know external rewarming things like that iv fluids rewarming and then they need the thyroid hormone okay so they need some thyroid hormone back uh and you can even give t4 or t3 or both uh the only thing i'll tell you is that t3 remember i said it's more active so it can cause some ventricular arrhythmias not so fun right so you know you can do t4 you can do t3 you can do both depends on what your endocrinologist wants me personally i just start with some t4 because i know they're getting something and it feels less dangerous than starting with the t3 all right and then i call upstairs and say hey what do you really want you want more of this more that and i give them whatever they say okay but some iv thyroxine they need the hormone back patients in mixodema coma also get a dose of steroids okay they also get like 100 hydrocortisone for example why do we do that in mixodema coma here we're worried again about adrenal insufficiency but we're worried maybe it's not the thyroid itself maybe it was a pituitary cause of hypothyroid and maybe with that pituitary being messed up they're also adrenal insufficient so we're going to just go ahead and empirically give them a hundred hydrogen cortisone as well so easy to remember for us whether it's thyroid storm at this end or mixidemo coma at this end either bad end of thyroid disease you go ahead and give them stress dose of steroids pretty simple for different reasons but it works all right so supportive care warm them up give them their stress dose of steroids give them some thyroid hormone and emit them okay so that's our friend the thyroid we made it through that one we get to move on to our next exciting gland the adrenal all right so let's do the adrenal now remember the adrenal the cortex makes all these things like the glucocorticoids like cortisol the mineralocorticoids like aldosterone and remember that the middle the medulla there makes all those like other things like epi and norepinephrine okay more of those like presser sort of things right but the but the the periphery the cortex makes the mineralocorticoids and the glucocorticoids and when you're adrenaline sufficient it means you're basically adrenals are not making these glucocorticoids and mineralocorticoids or both of them all right and remember for the for the cortisol the way that happens is you've got acth that comes from the pituitary that tells the adrenal to make cortisol right so the pituitary tells the adrenal to make cortisol all right so that's our friendly adrenal let's talk about problems of the adrenal now unlike the thyroid remember when the thyroid it's usually a thyroid problem with the gland itself with the adrenal it's usually not the adrenal itself it's not usually primary adrenal problem it's usually something wrong with the hypothalamic pituitary axis so secondary or tertiary sort of thing okay and what's the most common cause of somebody being adrenal insufficient just think about it somebody comes into your emergency department they have adrenal insufficiency what's probably one of the most common reasons that you'll get that for yes probably steroids right so somebody was on chronic steroids they were on it for a long time their adrenals kind of shriveled up and they abruptly stopped their steroids someone stole their steroids when they stole their vicodin i don't know it happens i guess right um so they lost their steroids or whatever it is so they get a cro of sudden they'll come in adrenal insufficiency all right so that's probably that's the most common sort of thing now let's talk about the rarer stuff the adrenal itself what things will mess up the adrenal itself less common ones let's go through some first addison's disease addison's is an autoimmune disorder so it's autoimmune destruction of the cortex okay so basically idiopathic autoimmune destruction of the adrenal and so therefore they get adrenal insufficiency that makes a lot of sense infiltrative disease anything that infiltrates in these or infections in the adrenals tb sarcoid fungus amyloid all these sorts of things that get into your adrenals that can cause primary adrenal insufficiency you can bleed into your adrenals right from over anticoagulation from trauma remember that thing called water health friedrichsen syndrome where you've got meningococcemia and then you also get bilateral adrenal hemorrhage right vital adrenal infarction and hemorrhage waterhouse friedrichsen syndrome so you can bleed into your into your adrenals tumors so primary tumors of the adrenals mets to the adrenals can cause it as well drugs including atomidate you know our friend automate great drug we love using it for intubation you probably remember that if you took a normal person measured their serum cortisol and intubated them with automate and measure their serum cortisol later they would drop their serum cortisol it interferes with cortisol metabolism fortunately a single dose of automate while it drops your level it almost never really has important clinical consequences okay however multi-dose automate or in the old days when autonomy was first coming out they used to put people on atomic drips in the icu for sedation that'll give you a frank adrenal insufficiency that'll that'll knock the adrenals right out okay so single dose don't worry about it and i know there's the controversy in sepsis and that sort of stuff personally i don't worry about it okay but multi-dose atomic or atomic drips that could definitely cause adrenal insufficiency talked about waterhouse friedrichsen syndrome okay let me talk for a moment about the hyperpigmentation thing so there's a picture here of president kennedy here because he had addison's disease uh and you know you tend to get hyper pigmented when you have primary adrenal insufficiency who remembers why that happens what's going on what is it msh right melanocyte stimulating hormone so here's what happens when your adrenals themselves are messed up they're not working because something has messed them up your body tries to get them to work and it tries to get them to work by making a bunch of acth right so it'll make cortisol it says let's make a bunch of acth and try to get these adrenals to work well when acth is made it's actually made as a pro peptide that is cleaved into acth and msh melanocyte stimulating hormone and that melanocyte stimulating hormone does just what its name says stimulates melanocytes and it makes you hyperpigmented okay you'll have darker skin by having that extra msh and so it's only patients who have primary adrenal insufficiency where the adrenals themselves are messed up that are going to get the darker skin the hyperpigmentation because they're making too much hgth and too much msh does that make sense if it's a pituitary problem you're not going to get hyperpigmented because the pituitary means you're not making the acth that's the whole problem right so you're also not making msh so they don't get hyperpigmented primary adrenal insufficiency will get hyperpigmented okay how do you do the test to figure out whether it is primary adrenaline sufficiency you you know somebody came in they look a little hyper pigmented they're a little weak and all this sort of stuff and you're like oh i think maybe they've got adrenal insufficiency the way you do the test is that corticotropin stimulation test you basically give them a little dose of acth and you see if the adrenals respond okay you're giving them a dose of acth and seeing if the adrenals respond so you measure a baseline serum cortisol you give them a little dose of iv acth and then you measure the cortisol it's like at 30 minutes and an hour and two hours something like that some serial measurements pretty soon after and you're looking for that cortisol to go up if the adrenals are normal they should right it should go up a certain amount or a certain percent or a certain level again you can look up the thresholds but if it's going up normally then the adrenals are fine but if it's not going up normal you've got a primary problem with your adrenals okay that's a corticotropin stimulation test you're giving a little dose of acth and watching the cortisol go up okay um so that was primary adrenal insufficiency the adrenals themselves messed up secondary or tertiary means you've messed with something in the hypothalamus or pituitary stroke tumors things like that but also could be just prolonged steroid use and then abrupt withdrawal lab abnormalities in adrenal insufficiency sorry folks just a little trivia you got to know hyponatremia is the most common electrolyte abnormality you don't have mineralocorticoids you don't have aldosterone so you don't hold on to your sodium anymore so you get hyponatremic and you might get hyperkalemic and if you see that combination of low sodium and high potassium either in real life or on the board exam particularly on the board exam go for adrenal insufficiency okay because they're probably showing you that combo for a reason most patients don't have the full combo but if you see it i really want you to think about that so low sodium high potassium they can have a low glucose because you don't have a cortisol and they can have a lot of eosinophils as well all right how do patients with adrenal insufficiency present if you remember they are weak and they tend to be have hypotension they have orthostatic hypotension when it's really bad they have refractory hypotension so they're in front of you they've got sepsis they're hypotensive you're giving them fluids they're not getting better you're giving them pressures they're not getting better it's because they need the steroid okay they need the steroids so refractory hypotension think about adrenal insufficiency and they can have fever from adrenal insufficiency itself it's not always sepsis all right so nausea vomiting weak things like that okay how do we treat adrenal crisis some fluids some normal saline or maybe even d5 normal cell and fetal extra sugar and give them some steroids you can either give them 100 a hydrocortisone right which certainly works works just fine or an alternative is just to give them four milligrams of dexamethasone now why would you ever pick the dexamethasone instead of hydrocortisone when it's so easy to remember the 100 hydrocortisone all right well it turns out that hydrocortisone will interfere with that corticotropin stimulation test it interferes with the cortisol assay so if you know this person's got adrenal insufficiency it's the third time this year they've come in with that you know what's going on by all means give them the 100 hydrocortisone because you don't need to do that fancy test you know what's going on if you're really not sure and you want to be nice to your internist upstairs you know and you don't want to ruin their day you know mess up their corticotropin stimulation test for an internist right that's not fun i mean that was their whole day right definitely a lot of fun right so in that case you might just give them four dexamethasone and that way they can still do the test upstairs all right so either a hundred hydrocortisone or four dexamethasone that'll work and of course they might need pressers for their hypotension but the bottom line here is you can give them fluids you can give them pressures if they have adrenal insufficiency you have to give them the steroids if you don't give it they will die end a story period they will die you got to give it to them all right so that's that let's do hyper adrenalism this is too much cortisol going on right too much cortisol so it could be too many steroids at a tumor of the adrenal cooking out cortisol a pituitary microadenoma making too much acth there are some cancers that will secrete an acth-like substance like small cell or bronchial carcinoid cancers signs of this remember too much cortisol they get obese they get overweight but it's a truncal obesity it's in the middle the central truncal obesity it's not the extremities as much truncal obesity they can uh get this buffalo hump in the back there they get these purple stria okay they get the moon faces right too much steroids you've seen that the round moon faces so buffalo hum moon faces purple stria all these sorts of things as well you got to get rid of the cortisol or whatever is causing the problem so either get the tumor out stop the steroids whatever that's cushing syndrome too much of that okay

Channel: The Center for Medical Education

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Keywords: emergency medicine

Id: HwPd_kJPRCI

Length: 60min 4sec (3604 seconds)

Published: Sat Jan 02 2021