¶ Introduction to Emergency Medicine Concepts
Welcome. My name is Divine. This is episode 571 of the Divine Intervention Podcasts. And in today's podcast, we're going to be discussing a topic that I like to call Quick and Dirty Emergency Medicine for the USMLE exam. Quick and dirty emergency medicine for the USMLE exam. My goal today is to discuss a series of scenarios and thought processes
on questions that are kinda difficult to prepare for. Some of them are gonna be classic things you're probably aware of, but I'm gonna discuss quite a number of things that you're like, what? So these may not be things that again you see in any resource or you're like how do I ever prepare for stuff like this? But these are things that uh you absolutely need to know for your exam.
So we're gonna talk through these things so that you can feel very comfortable with them. So this podcast is certainly attuned to anybody taking step two CK or taking step three or taking level two or level three. But also this podcast I will see is certainly very helpful for a person studying for a surgery shelf, an emergency medicine shelf, or an internal medicine shelf. So let's jump right into it. So
¶ Initial Trauma and Airway Management
First thing I'm gonna say today is that if you have a trauma patient, you know, during a car accident or they fell from a height or whatever. What is one thing you should always keep in mind on your exams? You should always keep in mind the possibility of a C spine injury, a cervical spine injury. And I'm telling you this, our friends at the MBMEs. They sometimes write these questions to be very nondescript. You don't think too much about them.
But there are things that are actually pretty high yield to know for your exams. So I'll just really encourage you, if you see an answer that talks about like assessing for a C spine injury, then you should really be thinking of that answer. Just ask yourself, is there any reason why I should not pick that answer?
Again, be careful. I'm not saying oh it's always the right answer, but it's very common for it to be in an answer. Right? And if you really think about in a trauma situation uh like that, a person should Probably be immobilized in a collar, in a neck collar, until the C spine injury has been rolled out. Alright, so what if you give you a question about uh Ten year old child and this child comes to the is brought to the emergency room by his parents.
Because he's struggling to breathe for the last like six hours. He's been struggling to breathe. He has very high fevers. They tell you that you can hear audible strider without a stethoscope and whatnot. Um, what should you be thinking about? And they tell you that he's like drooling and whatnot. Well I hope you're saying, ooh, divine, this is epiglotti. So they then say, oh, what's the most appropriate next best step in management? Well your next best step in management is to intubate.
I can almost promise you they will give you an answer choice that says to give antibiotics. Don't do that. Right? The thing is, is the respiratory failure, the airway closure that's gonna kill this child and kill this child quick. So
you should go ahead and intubate. So they can then explain to you in the question that oh you know uh or they can make it a two-part question. They can say, you know, those questions where you click and then you can't uh once you click and submit, you can't go back to it and then it's a two part question.
And then they give you like some follow up that oh, you know, endotrecheal intubation was carried out in the operating you know, endotracheal intubation was attempted in the ICU or whatever, but it was unsuccessful. And then you're told, uh, what is gonna be your next best step in management? Well If you try endotracheal intubation and it doesn't pan out so well uh on your exam,
Then the next thing you should consider on your test is a surgical airway. You should consider a surgical airway. You should consider a cricophyroidotomy. A cricophyroidotomy. Right? Because again these people that have epiglottitis, I'm pretty sure I've had a patient like this actually. Person did not require a surgical airway, but that airway was probably one of the smallest airways I've ever seen uh in my life.
So I would just really encourage you if intubation fails, then you really should consider a surgical airway. You should consider a cricothyrodotomy, right? This is uh something you definitely want to keep in mind. So I just want to give you a general principle for your exams. If a person needs intubation and you're kinda worried and concerned that that person may have a kind of difficult airway.
You should probably try to do those intubations in a controlled environment where other interventions could be done if the classic method of securing an airway. Endotracheal intubation fails. Just a nice principle to keep in mind for your exams. All right.
¶ PPE Protocols in Critical Situations
Now, what if they give you a question about a twenty-five year old male and, you know, this person is in the emergency room or is in the ICU and this person has been diagnosed with COVID. This person has a severe COVID infection.
And you're told that this person is going into like immediate respiratory failure. The person's autosaturations are extremely low. Uh oxygen pastoral pressure in their blood is really, really low. You know, the person is crashing and burning. The person is very unstable. And then uh they didn't say, Oh, what's the most appropriate next best and they say that, oh, that there is a physician or a nurse or whatever that is um right outside the patient's room and the patient is under
um, you know, like the appropriate precautions and whatnot. But they tell you that oh that the physician is just wearing his scrubs or whatever. And then they ask for your next best step in management. So let me
Tell you what answer they will put. They'll put an answer that says that oh you should run in and they'll put something along the lines of you know running into bat the patient, see if the patient blah blah blah blah blah. But then you'll see another answer that says that uh personal protective equipment must be done first. So you must you know, put on your P P E, your personal protective equipment, you know, like your surgical masks. I mean, sorry.
Because it's COVID, right? So you're gonna wear respirator, so like an N ninety five, gown, gloves, eye protection and stuff like that. And then they say, oh, you know, place uh wear PPE before going to save the patient. What answer should you pick? I will encourage you to actually wear PPE before you save the patient. Um, I know this may seem crass, but that's actually what you're supposed to do on your test. And think about it: this patient has severe COVID.
Do you want to become just like that patient? Do you want to get a bed next to that patient in the in the emergency room? Right? So proper stewardship as an individual means you take care of yourself first, and then after that you can take care of others. It's a very high old thing to know for your exam. This is a very classic, bizarre ethic situation you may see on your text.
If a patient, if taking care of a patient requires you to wear PPE, you should wear especially in an emergency situation because they like to throw these kinds of questions with emergency situations because think about it, right? Why make it a benign situation where it's like, no, make it an emergency situation where you you're forced to make like a tough, hard decision. So don your PPE first before you go in and save the patient. All right.
¶ Advanced Intubation Indications
And then, you know, I'm sure many of you have heard of this thing that, ooh, if a person has a GCS less than eight intubate, I'm sure many of you have memorized that, you know, the Glasgow Comer scale, right? GCS less than eight incubate. Fine. All right. I'm sure that you've memorized that. I'm sure it's in all every Anki deck known to mankind.
It's kind of a little problem though. The USMLEs, they don't really deal too hard in GCS because again, it's something everybody knows. It's like memorizing some algorithm. The US MLEs these days, and many people do not believe me when I say this, until you then take your exam and you're like, Oh shoot, this is actually true. The USMLEs these days they focus on people that can understand concepts. And people that can integrate concept.
You notice that many times even memorizing an algorithm, like algorithm from QBanks and stuff. They're beginning to have less and less utility these days on the USMLEs. This is something I actually talk about quite extensively in my test taking strategies class. Right. So again, don't just be a person that is giving to memorizing algorithms.
or giving to memorizing uh oh acronyms and all those things. Those things have much less utility and the utility is getting smaller and smaller every day on the exam. Right. But what are some classic situations where our friends at the MBMs want you to intubate besides the G C S less than eight intubate?
Well, think about it. If a person has a stroke, like a severe stroke, let me tell you this. That person, they have a very high risk of like drooling and, you know, aspiration and all those things. Those people certainly deserve endotracheal intubation. Or think about a person that has altered mental status from like a drug overdose
or drug intoxication or like really bad sepsis and you're like, hmm, this person is like drooling, they can't protect their airway. Like the person that has epiglottitis, you should probably go ahead and intubate that patient as well. Another kind of weird situation of intubation that you may see on your exam is a person that is in status epilepticus. I can promise you, a person that's in status epilepticus certainly does not have a good Irwin.
So uh I mean cannot protect their airways, right? So those people that are in status, you absolutely positively need to intubate those people on an exam. And the good thing is you're already giving those people like IV benzodiazepines, right? So that can certainly help in kind of knocking them.
¶ Altitude Physiology: Oxygen & Acid-Base
All right. Now, one thing I want to talk about here is this concept of FIO2, right? FiO two, right? Um FIO two. Because you know, many people know that oh in the atmosphere we have about 21% oxygen.
But the thing is, our friends at the MBM is there are many different ways they can kind of manipulate this. Uh just to see if you actually really understand pathophase. And then I'll talk about it from an email perspective. So let me ask you this. If you go to the top of Mount Everest, what happens to your FIO2?
What happens to your FIO2? Hmm. It actually does stay the same, right? So I know some people may be like, oh, divine, the FIO2 must drop. No, no, no, no, no, no, no, no, no, no, no, no, no. No, your FIU2 does not drop. If you're at sea level, your FIO two is still about twenty one percent. If you go to the highest heights, right, go to the top of Mount Everest, your FIO2 is still gonna be 21%. So why is it that your blood oxygen content goes down as you go to higher elevation?
Well, the thing is as you go to higher elevations, atmospheric pressure plummets. So you're taking 21% of a smaller number. That's why overall the oxygen that's coming into your lungs is actually lower. So let me explain this. I believe atmospheric pressure is like seven hundred and sixty millimeters of the earth. Right. So if you take 21% of 760 millimeters, let me see if I can do this math real quick here. So 10% is 776. Another 10% is 76. So that's 152.
And then if you add a one percent on top of that, that's seven point six. So that's one fifty nine point six, right? So you have about a hundred and fifty nine point six millimeters of mercury of oxygen in in the in the air around you at sea level. Right? Well let's say you go to Mount Everest, the top of Mount Everest. Let's assume it's six hundred there. I'm just making up this number. But I think sometimes using actual examples can really help people understand certain
You go to the top of Mount Everest. Well, let's say the atmospheric pressure there is 600. Again, the FIO2 is still going to be 21%. But 21% of 600 is what? 10% is 60, another ten percent is sixty, that's one twenty, one percent is six, so it's one hundred and twenty six millimeters of mercury. So literally by going from sea level to the tippy top tippy top of Mount Everest, you've gone from one fifty one fifty nine point six to one twenty six, right? That's kind of a big draw.
It may not seem like much to you, but that's actually a big drop, right? So as you go to a higher elevation, the FIO2, again, I can easily see them giving this as an arrow question on your exams. Your FIO2 does not change. But what happens to your PBGO2? The partial pressure of oxygen within your alveola, your PBGO2 is going to go down because, again, there's less oxygen in the atmosphere.
Right, so because there's less oxygen in the atmosphere, there's less oxygen entering into your alveoli, so your pbgO2 is going to go down. Now, if your PBGO2 goes down, what happens to your P little AO2? Again, what is P little AO2? P little AO2, so lowercase A, is the oxygen partial pressure within your capillaries, within your blood vessel. It's gonna go down as well because the feed stock which is your PBG O two is smaller.
So the P little AO2 this time is going to be smaller as well. Okay. Now what should happen to that person's SAO2? SAO2. Remember, SAO2 refers To your hemoglobin saturation with oxygen. Again, where does hemoglobin get the oxygen that it is saturated with? It gets it from the oxygen that has been dissolved in your plasma within your blood vessels. So if the oxygen dissolved in your plasma, the oxygen dissolved in your blood vessels has gone down precipitously. Guess what?
The oxygen that is going to be saturating hemoglobin is going to go down as well. So your sao2 is going to go down. So what should you expect these people's EPO to look like? What should the erythropoietin look like? The EPO should increase. because of hypoxia, because of tissue hypoxia, the EPO should increase. And if the EPO increases, what should you expect to happen to your hemoglobin and your hematocrit? Well that should increase. Remember, EPO comes from
The kidneys, right? Comes from the kidneys and then you're you're you're you're gonna make a you're gonna make a More red blood cells. Now, what would you expect this person's P Little A CO2 to look like? What should their P A CO2 look like?
The partial pressure of carbon dioxide. I would really hope you're saying, oh, divine is gonna be low. Man, I'm telling you all these hours I'm talking about. You may think I'm joking. I'm really not joking. This stuff I'm talking like this is no joke. Like this is no joke. Like I'm pretty fired up talking about this right now. This stuff is pretty high yield to know for your exam.
Your PACO2 is gonna drop. You know why? Because you're hypoxic. When you're hypoxic, how do you think your body responds? Your body's gonna respond by hyperventilating. So it can blow off CO2 and bring in more oxygen. So your p little ACO2 is gonna go down. Now, what's gonna happen to your pH? What's gonna happen to your pH? Well, if you're blowing off a lot of CO2 because you're hyperventilating, you're gonna have a respiratory alkalosis.
If you have a respiratory alkalosis, guess what? Guess what? Your pH is gonna go up, right? Now what's gonna happen to your bicarb? What's gonna happen to your bicarb? Well, think about it. Your kidney is gonna try to be compensating for the respiratory alkalosis. So your kidney is gonna try to do that by excreting more bicarbonate.
Right. So as you excrete more bicarb, you're losing more of a base. You're gonna develop a metabolic acidosis. So your bicarb is gonna go down, right? You're gonna try to compensate for the respiratory alkalosis with a metabolic acidosis by losing bicarb in the kidney. This is why when a person has high altitude sickness, one thing you can do is to give them acetazolamide. As we know acetazolamide is a carbonic and hydrase inhibitor. When you inhibit carbonic anhydrase is is uh
Uh is going to prevent you from reclaiming bicarb at the level of the proximal convoluted tubule. So you're gonna dump it in your in your urine. So you kind of speed up that bicarb loss to compensate better with the metabolic acidosis by giving acetosolum.
Please know this stuff. I'm begging you, please know this stuff. All right. So one thing I want to discuss, they can literally make that an AM question, right? But uh you you you know, like there there there are questions you may see uh student asked me a question recently that hey, uh You know, what what's the order in which uh, you know, like almost like escalation of oxygen therapy? This is almost certainly something that you will maybe not see on a USMLE exam or on a shelf exam.
¶ Progressive Oxygen Delivery Methods
But I guess it's kind of useful information to know. So let's kind of talk about it. I'm not gonna spend more than a minute at best on this. But in terms of methods of delivering oxygen to patients, which basically from lowest FIO2 delivery possible to
highest FIU to delivery possible, which was the gradation in terms of like lowest to highest. Well, lowest obviously is gonna be you just breathing in room air. If you're breathing in room air, you're getting that oxygen that's in the atmosphere, the 21%. No big deal.
But the next thing that comes after that is is are those uh like nasal prongs, those nose prongs, those things that you just kind of stick in your nose, right, to give you some oxygen. Uh those things can give you a little more FIO2 than just breathing in room air. But if that's not giving you enough oxygen, what should you step up to next? Well uh next thing to step up to is a face.
Right, you know those masks that you can basically put over that covers like your nose and most of your mouth. That gives more FIO2 than those nasal prongs. Alright, so let's say you've given through the face mask and that's not giving you enough oxygen, you want to give even more FIO2. Then the next thing you should go for is a non-rebreather mask. A non-rebreather mask. A non-rebreather mask absolutely, positively gives more FIO2 than a face mask.
And then what if that is not working? If that is not giving you enough oxygen, you want to give even more oxygen. Then you want to go for a CPAP or BIPAP, right? Uh CPAP means I think continuous positive airway pressure. And BIPAP is uh bilevel whatever intermittent positive re pressure right those two things because they know that everybody that has the job description medical student has memorized
C Pap Bip. C Pap Bipop. What do they do? Sometimes on the exams they will call that non-invasive positive pressure ventilation. Non-invasive positive pressure ventilation. Those things can give you pretty steep levels of FIO2. Right. Pretty steep levels of FIO two. Why do you think it's called non-invasive? Because literally nothing is being stuck down your throat. Right? Obviously endotracheal intubation, like the GOAT method of delivering oxygen to people.
is is an a form of invasive because it's literally invading your airway. Is it's a form of invasive positive pressure ventilation, right? So again you go from room air to those nasal prongs to a face mask. To a non-rebreather mask, to the NIPPVs, to non-invasive positive pressure ventilation. like um CPAP and BIPAP. Although CPAP is used more like in a home setting, you know, like for like OSA, BIPAP is used more like in a hospital setting. And then after that we have endotracheal intubation.
¶ Trauma Shock: Hemorrhagic & Obstructive
Right. Um and then you probably get a little more invasive and do crackothyrodotomy, right? That that's like the uh like uh new new nuclear forms of uh oxygen delivery. All right. Now what if they give you an epidemiology question on your exam, right? And they'll frame it like They give you a patient comes to the emergency room. And this patient is in shock, right? Person is like extremely hypotensive, systolic blood pressures are like in the 70s or 80s. Um, the person is.
uh, tachypnic, person is tachycardic, you know, not doing very well at all. And then they say, uh, what is the most likely etiology of this? And this is a trauma patient, maybe car accident, fell from a height or whatever. And then they say what is the most likely etiology of this patient's uh Abnormal vital signs. And then they give you literally all the kinds of shockers and
They give you like septic shock. They give you neurogenic shock. They give you hypovolemic shock. They give you uh hemorrhagic shock or whatever. They give you all those things that you're like, oh my goodness, which one do I pick? Well, let me explain something to you. If they give you a question, because again, the USMLEs these days are critical thinking galore. Critical thinking galore, right? Uh galore is a real word. Trust me. You can look it up. G-A-L-O-L-A.
But different discussion. This is not an English lesson. But if they give you a question like that, the answer you want to pick is hemorrhagic. Really? Yeah. The most common kind of shock in trauma is hemorrhagic. I'm gonna say that again. The most common kind of shock in trauma is hemorrhagic shock. This is extremely high you to know. The most common kind of shock in trauma is hemorrhagic shock. Now, let me explain something here. Let me explain something here.
If however, so if they give you a question on oh trauma patient, shock, and they give you almost no clues, pick hemorrhage as the cause of. But if they give you certain clues, they should go in certain directions. Like for example, if the person's skin is like warm and flushed and the person has a very high fever, even if hemorrhage is the most common cause of shock in a trauma patient.
With that extra context that was given, you should probably be thinking more along the lines of a septic sharp. Right. Again, when they give you specific clues that lead you down specific directions, then you should go in those specific directions. If they don't give you clues, jump on what is common, right? The most common kind of shock in a trauma patient is hemorrhagic shock. All right. So let me ask you this. If a person has hemorrhagic shock, what happens to their prelude?
Well think about it, if you're bleeding out, you don't have enough blood within your blood vessel. Are you going to be sending more blood back to the heart? No. So your preload is going to go down. Okay. So since you're sending less blood back to the heart, what's going to happen to your cardiac pressures? What's going to happen to your pulmonary capillary wedge pressure?
Which is a surrogate for left heart pressure, or your central venous pressure, which is a surrogate for right heart pressure. What's gonna happen to those pressures? Again, this is not something you have to memorize. It makes perfect sense if you just think about Those pressures should be low.
Why are they low? Because your preload is low. If you're not sending blood back to the heart, garbage in, garbage out. If you're not sending blood back to the heart, blood is not going to be collecting when you're doing your heart. So your cardiac pressures are going to be low. Alright. So what's going to happen to your cardiac output in this circumstance? Well again garbage in I'm not saying your heart is garbage, but I'm just using a
classic computer science description. Uh but i if you put in less blood in the heart Are you gonna put out much blood? No, your heart is not like a magic machine, right? You cannot put like 10 ml of blood in the heart, and magically your heart produces like 50. No, if you find that kind of heart, uh let me know, right? That doesn't happen, right? So the thing that's gonna happen is Because your preload is low.
Or your cardiac output is gonna be low. That's literally the Frank Starlin principle in a nutshell. In fact, let me ask you this: for this person, because they know that, you know. Quite a number of people have memorized many of these arrows. Oh, I know the arrow for preload, cardiac output, PCWP, C VP, you've memorized all those things.
But what can they do on your exams? They can just do a little bit of a step one throwback. So let me ask you this: what's gonna happen to this person's end-diastolic volume? Oh. Remember, what's end diastolic volume? End diastolic volume is the volume of blood that is left in the heart at the end of diastole, at the end of filling. Well, if your preload is low, you're not bringing much blood back to the heart. So your EDV, your end diastolic volume should go down. All right.
If your end diastolic volume goes down, what should happen to your end systolic volume? Again, literally, what is end systolic volume? N-systolic volume is the amount of blood. That is left in the heart after the heart has systoled, after the heart has contracted. Right? So because your EDV is low, the amount of blood that was in the heart after feeling was low. The amount of blood that's gonna be left in the heart after contracting is gonna be low as well. So your ESV is gonna go down as well.
So it should make sense that your stroke volume, which is the amount of blood that is ejected with each heartbeat, should go down, right? It should go down, it should go down. Your stroke volume also goes down. Now, let me ask you this: what happens to your
What happens to your heart rate? Well, your heart rate should obviously go up, right? Because your body's gonna try to maintain cardiac output in one way or the other. And many of you know that heart rate times stroke volume is equal to cardiac output. So if your stroke volume is plummeting, one of the ways your heart can try to respond is by jacking up your heart rate. So your heart rate is gonna go up in V
And then what's gonna happen to your systemic vascular resistance? Well think about it. Your blood pressure is extremely low. So your body's like, oh shoot, this is not great, right? So it's like, hmm, how can I try to maintain uh profission pressures in my in my bloodstream, you're gonna clamp down on your vessels. You're gonna increase your systemic vascular Again. Emergency medicine.
The USMLEs, they love their precious arrows. You gotta know these things for your exams. I promise you, these things I'm discussing, they are not low yield for your tests. All right. Now, that that was almost like a mini shock shock discussion there. Now, one thing I just want to say so that people don't miss out on this is is the following, right? So Um obstructive shock. You may hear the term obstructive shock. Honestly, I really don't like this term because it does not really
It's kind of confusing, right? Uh under the right circumstances, it can be confusing. But the thing is, it's something that you may see on your test. So let me explain something here. If you see the term obstructive shock on your exam, There's one of three pathologies that they're discussing. Okay? There's one of three pathologies they're discussing. They're discussing attention your thorax.
Or they're discussing cardiac tamponat or they're discussing a pulmonary embolus. Okay? Tension newothorax. Cardiac tamponat or pulmonary embellished. So let me try to give you some reasoning as to why these things may be called obstructive. Well, think of a tension hemothorax, right? You have a tension hemothorax, literally air is accumulating within your thoracic cavity and it has nowhere to go. So that air, because it's under high pressure, is gonna be compressing your heart.
So it's almost like you're s you're s clamping down on the heart from the outside. You're doing like an external compression of the heart. It's gonna make it really hard for the hearts to fill with blood. That's a problem. But also do not forget that you're also compressing the superior and inferior van a cave. If you compress the SVC and the IVC, your preload is going to drop like a stone. You're literally not going to be sending blood to the heart.
Right. So the combination of all these factors impairs the feeling of the heart. If you impair the feeling of the heart, guess what? Your cardiac output is gonna drop significantly. You're gonna be in shock. Now, why would cardiac tamponade be called an obstructive shock? Well, a reason why cardiac tamponat may be called an obstructive shock.
Unlike in a case of a tension pneumothorax, I remember in a tension pneumothorax you're gonna do a needle decompression, right? A needle thoracostomy first, and then after that you go for a chest tube, uh, which is a tube therocostomy, right? But for cardiac tamponat, it's not air that's compressing the heart from the outside.
It's fluid that is compressing the heart from the outside. Literally fluid that's compressing the heart from the outside, right? Fluid that's within the pericardium. And what can cause that fluid? Well, if you have really bad urania, right? So let's say you've missed a bunch of dialysis sessions. or you have a erotic dissection, believe it or not.
cardiac tamponade is a very feared complication of aortic dissection, right? Or you have like viral pericarditis or whatever, and all the fluid has built up, right? You're going to be having this extrinsic compression of the heart. From the fluid that's in the pericardium, that can absolutely positively cause you to go into shock, right? Again, whenever the heart is being compressed by something from the alzheimer.
you should really think of some kind of obstructive shock. And obviously if a person has cardiac tampoco What should you be doing next? You should do a pericardiosynthesis, right? Many times a pericardiosynthesis is going to be done with echocardiography. You're going to do it under ultrasound guidance, under ultrasound guidance. And then uh why will a PE, a pulmonary embolus, be called an obstructive shock? You are you're literally obstructing flow of blood.
out of the right side of the heart, out of the right ventricle, because your pulmonary artery has been occluded. That's why those things are called obstructive shocks. Okay? So don't forget your tension emothora. Your cardiac tamponade and your pulmonary embolas. And obviously, if a person has a PE, you want to go ahead and give IV heparin. IV heparin. All right. Now.
¶ Autoimmune Shock: Addison's Disease
What if they give you a question about a patient and they tell you that this patient has a history of celiac disease? And then this person is in shock. This person is like extremely hypotensive, extremely tachycardic, right? What is going to be the likely cause of shock in this person? Well, on your exams, there are two corporates I want you to think about. The thing is, our friends at the MBMEs really love these two corporates.
And you're gonna see the link to celiac disease in a moment here, right? But I want you to think of Addison's disease, primary adrenaline sufficiency, and I want you to think of a myxedema copy. Coma. That's something you can have as a kind of a feared complication of really, really bad hypothyroidism. Right? So it's like you may be wondering: Divine, what in the world are you talking about with celiac disease and these causes of
Well, the first thing is you need to establish a principle in your mind. Our friends at the MBME. when they are testing an autoimmune disease more than 50 to 70% of the time, they will give you a past medical history of another autoimmune disease. Again, the USMLEs are not based on algorithms, they are based on context. It's a very it's kind of one of these things that people do not.
Think about, but again, it's really important. But basically, if a person has celiac disease, celiac is clearly an autoimmune disease, right? You have these anti-gliadin or this anti-indomicile or these anti-tissue transglutaminase antibodies that you make. When you make those antibodies, they'll destroy your microvilli, they cause malabsorption. All right. Well, the thing is, if you have one autoimmune disease, you're likely to have another autoimmune disease.
Well in Addison's disease, you're literally damaging the adrenal cortex. Remember, in Addison's the adrenal medulla is not affected. Please do not mess this up. In Addison's disease, it's your adrenal cortex that is messed up, not the adrenal medulla. Why is this the case? Well this is something many people do not keep in mind.
The adrenal gland is almost like two organs that were just smashed and made one organ, right? It's almost like you had a merger between like two companies, right? Those two let's say you're margin you're merging a company that makes soap and a company that Those companies have nothing to do with each other. They just happen to like merge, right? Kind of think of like a Bexhir Hathaway, right? Bekshair Hathaway, you know, many of you know I love Warren Buffett, right?
Uh Picture Hathaway has a ton of companies in their portfolio. They own Geico, they own uh Cs Candies, they own uh Tons of Coca-Cola, tons of apple if he's not completely sold out of that, right? Siri serious XML, a bunch of random things.
You probably like the how do you know all this stuff? Well, I do like the stock market. I'm a person that likes the financial markets, but that's a different discussion for for another day, right? But y you merge all these things together. Same thing with the adrenal gland. The adrenal cortex, believe it or not. is derived c from a completely different embryologic
angle than the adrenal medulla, right? The adrenal cortex I believe is actually derived from mesoderm. I believe, don't quote me on this, but I believe it's derived from mesoderm. But the adrenal medulla I'm pretty sure is derived from neurocrescel. Different different different things, right? So when you have autoimmune destruction of the adrenals, you're destroying the adrenal cortex.
You're not destroying the adrenal at dollar. That's a very important thing to keep at the back of your mind, for exams. All right. So why would Addison's disease cause a person to go into shock? Well, think about it. If you have Addison's disease, well, guess what? You're gonna be short on our doster. You're gonna be short on cortisol, you're gonna be short on DHEA.
But the one we're really worried about, I mean, obviously the aldosterone, if you're lacking that, you're not gonna be reabsorbing sodium and water from your kidneys. So that's gonna cause you the hypotensive. But remember, cortisol has a permissive effect on the sympathetic nervous system. Basically, your blood vessels do not respond very well to catecholamines if you're in a state of cortisol deficiency. If you're in a state of cortisol.
Right. So that can cause the person to be profoundly hypotensive. Okay. So again, if you see a person that has an autoimmune disease and they're in shock. you really want to think about that person potentially having Addison's disease.
And they will try to hopefully give you more clues like hyponitremia, right? Because again, if you lack aldosterone, you wrap up you won't re-absorb sodium, so it'll be hyponitremic. They'll give you hyperkalemia. Because remember, aldosterone makes you excrete potassium in the kidney.
If you lack aldosterone, you will not be able to excrete potassium. You're gonna have hyperkalemia. And then they'll also have a normal anion gap metabolic acidosis because one of the jobs of aldosterone is to make you excrete.
Hydrogen ions in the kidneys. Well, if you cannot excrete hydrogen ions in the kidneys, you're gonna hold on to them. You're gonna have a metabolic acidosis. Okay, you're gonna have a metabolic acidosis. Although sometimes they can make it a higher anion gap acidosis, but classically, aldosterone deficiency, hypoaldosterone state.
should cause you to have a normal anion gap metabolic acidosis, right? In fact these hypoardosterone states they're the things that tend to cause uh type four RTAs, type four renal tribular acidosis. Again, different discussion for another day and I'm pretty sure I've made podcasts online. Nagmas on anarches, I think. I think. All right. So just kind of keep that at the at the back of your mind for for exams, right?
¶ Autoimmune Shock: Myxedema Coma & Adrenal Crisis
Now, what's another thing that can cause shock in a person that has a history of another autoimmune disease? You want to think about mixedemacoma, right? This is something that happens in people that are hypothyroid. So hey, what's the most common cause of hypothyroidism in the US? I hope you're saying, ooh, divine, Hashimoto's. Hashimoto's. Hashimoto's is the most common cause of hypothyroidism in the US. Okay. Most common cause of hypothyroidism in the US, right? So if you have Hashoto,
And you don't treat it well, right? In fact, mixedema coma may be your first presentation, all right. Again, you need thyroid hormone for metabolic stuff in your body. If you're super short on thyroid hormone, and obviously if a person has mixed edema coma, what do you expect their T3, T4 to be? It's going to be extremely low. So what should their TSH look like?
Well, it should be extremely high. Their TSH will be very, very, very high, right? And those people, again, they can be in a very, very, very just I mean, because you may wonder why why why may they be in shock? Why may they be hypotensive? Well, those people pretty much almost have like a cardiovascular collapse. Because many people do not think about this. But again, this is why having an understanding of pathophysiology is extremely helpful on the USML.
One of the jobs of thyroid hormone is to increase the insertion of beta one receptors on the surfaces of your cardiac myocytes. Hmm. Okay. So if you if you put more beta one receptors on the surface of your cardiac myoside, Well what do beta one receptors respond to this? They respond to catecholamines. So you're gonna respond to catecholamines better if you have Enough tired home on around.
So your heart will be like in a parasympathetic state almost. You won't have like good inotropy, you won't have good chronotropy if you're in a thyroid deficient state. But that's not all. Where else do we have beta one receptors in the body? We have beta one receptors in the kidneys. Mmm.
So just kind of keep those things in mind. But I will say that probably the primary effect you should keep it at the back of your mind for exams is that cardiac effect, right? Is that cardiac effect, right? You're gonna have less stimulation of the heart when you're in a thyroid deficient state. Those people obviously should be on IV level thyroxine. And if I'm not mistaken, those people should also get like.
some kind of uh like IV presser or something to kinda help them through those situations. And I think when people like Mixidima coma Right. You really need to watch those people because that thing can actually kill. It's not like some fly-by-night disorder. No, it can actually kill you. Right? And I guess since we're kind of talking about like an uh Addisonian crisis causing shock.
Just just be careful about adrenal crisis from people that are chronically using steroids, right? They can literally make this an emergency medicine situation. So this person may not necessarily have a history of an autoimmune disease.
But they may have a history of some disorder that's treated with steroids. So let's say they have like giant cell arteritis, temporal arthritis or whatever, and the on chronic steroids or a person that has like really, really nasty asthma, right? And the on chronic oral steroids. Well those chronic oral steroids you're taking is gonna literally suppress.
Your HPA access, right? And that's not a big deal, right? Uh it's not a big deal as long as your level of stress in life doesn't go up. But if your level of stress goes up because you're like in trauma, Or you know, you're you're in mental trauma because you're studying for the USMLEs or whatever. Well, that's gonna suppress that access. If you suppress that access,
Your body is like, Oh, I'm stressed, I'm stressed, I'm stressed. I need to make more cortisol. But hey, you've literally suppressed your HPA axis because you're on chronic steroids, right? So, in those circumstances, it's kind of a bad situation you're in.
uh you need to give a stress dose of steroids to rescue those people, to rescue those people. Um so just keep that in mind, right? That adrenal crisis can also present as shock, right? And don't forget that in Addison's disease we're gonna treat those people with uh with uh uh fludrocortyzone and uh you know a steroid. You're gonna give them steroids and fluidocortisone. The flujocortisone is a mineralocorticoid analog.
the steroid is gonna replace the glucocorticoids that they're missing. All right. Uh we're gonna wrap this up shortly here soon. Uh this podcast is kind of running a little long. But uh I just want to say two more things, right? What if you're stabbed by a foreign object, right? You're literally stabbed with a foreign object.
¶ Acute Emergency Procedures
Um and the foreign object is like in the patient and the patient is like hypotensive or maybe stable or whatever. And then you know the person comes to the emergency room and you're told, ooh, what's the next best step in management? Now, here's one answer that you want to resist picking on your exams. The answer you want to resist picking on your exams is the answer that involves you removing the object in the emergency room. Don't do that.
Don't do that. Please, don't do that. That foreign object that is in the person that is lodged in the patient may be tamponadding a bleed. So just keep that in mind. It may be backstopping that bleed. Do not remove it. That foreign object has to remove under safe conditions, usually in an operating room. All right. Do remove in the emergency room. Not a good idea. All right.
Now, last thing I'm gonna say, what if a person has like an openly bleeding wound? Right? Literally they're like openly bleeding. Uh what should be your next step on your exams? You see the open one is like right in front of you. Your next step on the exam is gonna be to apply direct pressure. Apply direct pressure, right? They'll give you a bunch of answers that deal with like uh
Fluid resuscitation, blah blah blah blah. I'm not saying you shouldn't do those things, but the most appropriate immediate next step in management is to literally you're literally seeing the bleed right in front of you. Apply direct pressure to that bleed straight up.
¶ USMLE Preparation Resources and Outro
Okay, that's the right thing to do. So again, if you just love this lecture, you love the way I teach, you love the way I explain pathol phase, you love the way I make integrations. You're gonna be very interested in the classes I offer next week. Starting next week, Tuesday, the 18th of February. I have a bunch of classes that are starting for step one to step three. Okay, let me first talk about step one. Step one, I have a class uh in the first week of March. It's a 25-hour step one review.
That's a good class for both taking step one or level one. Or if you're taking step two or level two or step three or level three, and you have a poor basic science foundation because basic sciences are now becoming very heavily represented on the USMLEs. That's a class that you definitely want to take.
And then also for step one to step three, next week, Tuesday, the 18th of February, I have a two and a half hour test taking class. On the 19th, I have a four-hour biostats class. On the 20th, I have a five-hour social sciences quality improvement healthcare systems class.
um ethics class as well. You know, many people have taken these classes, found them to be extremely helpful for the exams. Therefore step one to step three. And then for step two and step three specifically, uh on the twenty first of February I have a Three hour last minute review. It's a very, very high class. Very, very helpful class for step two, step three. And then the week after that, um, I believe from the 20th.
4th to the 27th of February, I have a 20-hour step-to-step through review. Again, I've had many people take these classes, get 270s, do really, really well on their exams. I'm not saying everybody gets a 270. But many people have got in in the two seventies. I've had a lot of two sixties, a lot of two fifties, a lot of two forties. So people do pretty well.
Nob been passing practice exams, they take this 20-hour class, they take this series of classes, and they end up doing really, really well on their tests. They are doing 30, 40, 50 points higher than their practice test. So again, I think these are classes that are well put together that can really, really help you. And in the grand class is in the first two weeks of June, the 50 hour step two, step three review.
That class, I made a special podcast on it. Um, you can find it on the website. That class is gonna be so helpful to everybody that attends. I can tell you that. I'm the one that's gonna be teaching the whole class. I can tell you that. That's all I'm gonna. Now, uh, I also have these podcasts on Apple, Google, Spotify, so check those out. And I have a YouTube channel you can check out where I post all the podcasts that I meet.
And then I have another website called Divine Intervention Life Lessons dot com. Um Divine Intervention Life Lessons.com. Every week I post like two to three podcasts where from a biblical perspective I address a life lesson. There's actually an Apple podcast associated with that called the Divine Intervention Life Lessons Podcast. And then I also offer one I want you to learn for all the USMLE exams, all the Complex exams.
And I help with Eras applications, mock interviews, personal statements, and all those things. So if you're interested in any of those, uh shoot me an email through the website. If you want to sign up for these classes, shoot me an email through the website and I'll give you some more information. Thank you for listening to me today. Again, this podcast is pretty high yield. Don't throw it away. So I'll see you in episode 572. So God bless you. Bye for now. Thank you.
