DIP Episode 630 - 2 High Yield Integrated Cases (Step 1-3)

Welcome, my name is Divine. This podcast, I'm going to call this a series of related interesting mechanisms, a series of related interested mechanisms. Into this podcast, my goal is to go over some things that have a lot of relationships, just some common relationships that are frequently tested on step one, on step two CK and on step three. As I go through the podcast, you're going to see why I'm emphasizing certain things in this podcast. So the first thing I'm going to go over here is what if they give you a question about a patient that has a history of celiac disease and then they tell you that over the last six months, the patient has had mencise twice and that when she had mencise, she had very heavy flow. And then you're told that the longest she went between mencise was like 93 days. And then you're also told that this individual has just, they give you some vital signs, you notice that her blood pressure is like 120 over 90. I noticed that a heart rate is 49 beats per minute. And then they ask you which of the following is the underlying mechanism behind the patient's presenting symptoms. I would really hope that you pick an answer that talks about autoimmune cell destruction. Right? The thing is, if I'm being completely honest with you, the USMLE is they're not going to come out and say Hashimoto's. No. This is something that I emphasize a lot in my review classes that these days straight answers are like dinosaurs on the USMLE exams.

They have largely evaporated from the exams. These days, they will give you something that is correlated with, but not exactly what you expect in as an answer choice. So let's put the facts of this case together. What exactly is going on here? Well, the thing that's going on here is first, the USML Es have this habit of giving autoimmune diseases to people that have a history of autoimmune diseases. And honestly, that's just like a general truth of life. When you have one autoimmune disease, you have a very high risk of having another autoimmune disease. So in my experience with the USMLE exams, many times when they give somebody an autoimmune disease, just check their past medical history more than at least in my experience, more than 50% of the time, approximately. Most people tend to have a history of an autoimmune disease. So what autoimmune disease does this person have? This person has Hashimoto's thyroid diabetes. This person likely has Hashimoto's. Again, Celiac is an autoimmune disease where you have the anti-glyadin or the anti-indomisial or the anti-tichotransmitter terminus antibodies. So it starts to reason that if you're beginning to see signs and symptoms of hypothyroidism, it makes sense that the person likely has Hashimoto's. And even if the person does not have a past medical history of an autoimmune disease, epidemiologically, the most common cause of hypothyroidism in the US is Hashimoto's thyroid diabetes, right?

Where you have these anti-thyroglybulin or these anti-thyroproxidase antibodies. So the next question is, how exactly does having Hashimoto's feed into this person's presentation? Well, the first thing is, if you have these autoantibodies that destroy the thyroid gland, are you going to be making thyroid hormone? You will not, right? So that tells you that, oh, this person's T3 and T4 is going to be low. And let me ask you this, what do you think is going to be true of their thyroid globulin levels? Or the thyroid globulin is going to be low as well, right? Remember, thyroid globulin is like the CPEP Tide of the thyroid gland. I'm going to say that again. Thyroglybulin is like the CPEP Tide of the thyroid gland, just like in the pancreas, when insulin is released, CPEP Tide is released at the same time, when thyroid hormone is released, thyroid globulin is released at the same time. So you can use a person's thyroid globulin levels as a good surrogate for how their thyroid is functioning. So if these people's thyroid gland is not making thyroid hormone, T3 T4 is not being made because the thyroid follicular cells have been destroyed by autoantibodies. Then their thyroid globulin levels should also be low as well. Kind of high you to know that for your exams. So now the next question is, if your T3 T4 is low, what happens at the level of the anterior pituitary? What happens at the level of the hypothalamus? Well, you're not going to have negative feedback.

And if you don't have negative feedback, you're going to make a lot of thyroid tropin release in hormone, and you're going to make a lot of TSH, right? So you're going to have very high levels of TSH. And TSH, the tropin release in hormone, one thing it does is that it stimulates the anterior pituitary to produce prolactin. Okay? TSH is a very potent stimulator of prolactin production, right? So hypothyroidism is a cause of hyper-prolactinemia, right? So why would a person have irregular mences when they have hyper-prolactinemia? Well, the thing is, prolactin is a very strong inhibitor of gonadotropin release in hormone. It inhibits gen-RH, right? And if you inhibits gen-RH, your HPG axis is basically turned off. So it makes sense that this person should have irregular mences. Okay. Now the next question is, why does this person have a heart rate of 49? Why is this person ready cardiac? Well, don't forget one of the jobs of thyroid hormone. One of the jobs of thyroid hormone is to place beta-one receptors on the surfaces of the person's cardiac myocytes. So if a person has hypothyroidism, they don't have enough T3. Because remember, T3 is like the big, metabolic-lyactic form of thyroid hormone. Then they're not going to be sticking beta-one receptors on the surfaces of the cardiac myocytes. And if you're not sticking beta-one receptors on the surfaces of the cardiac myocytes, they're not going to be very responsive to cardiac coolant means.

And if that happens, you're going to become pretty cardiac. Okay. You're going to become pretty cardiac. All right. Now let's go to the next mechanism. Again, these things have just discussed these interrelated things frequently tested on the exams. Now the second thing I want to discuss is what if they give you a question about a patient? And they tell you that this man, you know, has had his commercial driver's license suspended because he has fallen asleep on the job and was recently in an accident. And then you're told that this patient, you know, when it comes into your office, you know, you check his vital signs, his blood pressure is 150 over 100. His heart rate is 92 beats per minute. And then you notice that his respiratory rate is 8 per minute, right? And then they ask you which of the following lab abnormalities will be expected in this patient. I would really hope you're looking for the answer that shows hypercarpnea, right? Hypercarpnea. So what exactly is wrong with this person? This person has a really significant severe variant of obstructive sleep apnea known as obesity hypoventilation syndrome, right? Obesity hypoventilation syndrome. So what's going on here? Like let's put this all together. And then I want to discuss a series of arrows that are friends at the USMLE's love to throw on exams. So first things first, this person, right, we see this, you know, this person fell asleep on the job.

That's a very, very common issue in people that have obstructive sleep apnea or this variant obesity hypoventilation syndrome, right? Because they're very, they don't get very good sound sleep at night. So during the day, they are like extremely tired, right? They're extremely tired, right? And you notice these people, they can fall asleep on the job. In fact, this is one of the reasons why when a person is being, you know, if you're a commercial driver within the US, you know, you need a medical card to be able to practice your craft. And that medical card is usually given for two years, right? One of the things that is evaluated in that process, in you getting your medical card, you know, that is timely limited for two years is that, you know, you're evaluated, you know, they look at like your mal and party scores, they look at your BMI, they look at things like that just to make sure you don't have sleep apnea, right? Because if you're a commercial driver, that is a safety sensitive position. You can kill people if you have an accident because you're literally carrying like thousands and thousands of pounds of cargo, right? So this person has obesity hypoventilation syndrome, right? And why can we say that is because of the person's daytime symptoms, right? If the person did not have daytime hypoventilation, daytime hypercapnea, then we will probably reserve the diagnosis of obstructive sleep apnea for this person, right?

But if you see a person that has signs and symptoms of obstructive sleep apnea, and then you notice that they also hypoventilates during the day and they have hypercapnea during the day, then you'll want to think of this person having obesity hypoventilation syndrome, daytime hypercapnea, daytime hyperventilation, think of obesity hypoventilation syndrome, right? So why will this person have hypercapnea? Well, this person is going to have hypercapnea because they're not breathing enough, they're not ventilating enough, right? So they're going to retain a lot of CO2. So they're going to have hypercapnea, right? So what acid-based labs would you expect? Will you expect their pH to be low, right? They're going to have a respiratory acid doses, right? And what would you expect to be true of their bicarb? Their bicarb is going to be high. The kidney is going to try to make more bicarb, right? It's going to try to create like a metabolic alkylosis to counterbalance the respiratory acid doses that they have. So this person's serum pH will very likely be in the acidotic range, but it will be close to normal actually. So just something you want to keep in mind. So now my next question for you, what would you expect to be true of this person's AA gradient? Well, the AA gradient should be completely normal because if you think about it, when a person has obesity, hypogen, ventilation syndrome, there is nothing intrinsically wrong with the lungs, right?

There is nothing intrinsically wrong with the lungs. The actual lung parankoma works just fine, right? So oxygen can diffuse very fine between the persons of your life and the person's pulmonary vessels, right? Remember AA gradient just means the spread between your PBGAL to your viola oxygen tension and your P little ill to your arterial oxygen tension. There is nothing wrong with diffusion in your lungs, so these people should have a completely normal AA gradient. Now my question for you is what should be true of the ideal seal? What should be true of the diffusion capacity for carbon monoxide in these people? It should also be completely normal. Again, as long as you have a normal intact pulmonary architecture, you are not going to have an abnormal DLCO for the most part on the US semily exams. So this person's DLCO is going to be pretty close to normal in terms of percent predicted. All right. Now what should be true of this person's lung volumes? Well, I hope you're saying that divine, this person's lung volumes should be diminished, okay? This person's lung volumes should be diminished. Well, why is this person's lung volume diminished? Well, the lung volumes are diminished because obesity, hypogenitilation syndrome, obstructive sleep apnea, when they present with lung disease, they present with a restrictive pattern of lung disease, right? They present with a restrictive pattern of lung disease. So why do they cause a restrictive pattern of lung disease?

Well, think about it. I like to think of the region from the shoulder to your hips as being a fixed box with two tenons. Well, who are the two tenons that reside in that box? Your thoracic cavity and your abdominal cavity, right? It's a fixed-size box. So the thing is, if your abdominal cavity has too many contents, then the thoracic cavity has to be squished to make ample room for that expansive abdominal cavity, right? So if your thoracic cavity is squished, then you're going to become short of breath because you are literally compressing the contents of the thoracic cavity. Why do you think a woman that is heavily gravied, that is in her third trimester? Why do you think she struggles to breathe? She struggles to breathe because she has a temporary, she has a transient, restrictive lung disease. Why? Because that gravied uterus has overwhelmed the abdominal cavity. So the thoracic cavity has been heavily squished, right? Again, that's something pretty high you'll to know for your exams. When a person is pregnant, they have restrictive physiology or pretty with their lungs. That's a USMEL exam question right there, right? So let's not lose track of where we are, right? But this person is going to have restrictive disease. And when you have restrictive disease, the problem is that your lungs are restricted from expanding. If your lungs are restricted from expanding, then you're going to have reduced lung volumes, right?

And ask you this, what should be true of this person's p little a or two? This person's p little a or two should be low, right? Because again, this person has trouble getting air in, they have restrictive disease, right? Again, remember, you can have hypoxia, you can have it with a completely normal a ingredient as it is in this person, right? This person is not ventilated appropriately, so they are not bringing enough oxygen into the avial line. So the pbgeo 2 is going to be very low. Remember pbgeo 2 is the avial oxygen tension. Well, if your avial oxygen tension is low, guess what happens to your arteries? Your arteries like garbage and garbage out, if you're not bringing enough oxygen into your lungs, then you're not going to be sending enough oxygen to your vessels. So your p little a or two, which is your arterial oxygen tension, is also going to be low. And then let me ask you this, what do you think happens to the SAO2? Your SAO2 means your hemoglobin saturation with oxygen. Your hemoglobin saturation with oxygen is going to be decreased. Because remember, where does the oxygen on hemoglobin come from? It comes from the oxygen that has been dissolved in your plasma. But again, think about it, take it from the top. If enough oxygen is not entering into your avial line, enough oxygen is not going to enter into your arteries, enough oxygen is not going to hop on hemoglobin. So your SAO2 is going to be diminished under those circumstances.

So what can you tell me about the blood oxygen content in this person? Well, this person's blood oxygen content is going to be reduced, right? It's going to be reduced because again, a non-foxygen is not dissolving in the blood. A lot of oxygen is not dissolving in hemoglobin. So this person is going to have a reduced blood oxygen content. Now what should be true of this person's lipop? This person's lipop should be elevated. In fact, this person may actually have polycythemia. This polycythemia is a compensation for the problems that they have, right? You can see the same thing in anybody that has chronic hypoxia for any reason, like a COPD patient or whatever. These people are going to have an ipo-induced polycythemia. So this person's hematocrit can be high and their ipo is going to be high, right? Remember, you can have polycythemia with low ipo. For example, in polycythemia vera, right? In polycythemia vera, you have a high hematocrit from a non-ipo cause, right? From a non-ipo cause, typically from a jaqtu mutation on the exams, right? So this person is going to have an increase in ipo and that ipo is going to drive red blood cell production, right? So again, that's very high up to know for you exams because if you think about it, if you know that, ooh, you have a reduced blood oxygen content, well, why don't you put more red blood cells into service? If you put more red blood cells into service, then you have more carriers for oxygen, right?

Even if they are not fully saturated, at least you're putting more carriers. So you're going to be able to move more oxygen around in the body, right? You're going to be able to move more oxygen around in the body, right? But you can already begin to see that, huh? This polycythemia can begin to cause other problems for the patient, right? There is a reason why obstructive sleep apnea and obesity hypofintillation syndrome are really bad, right? You may think that there is nothing wrong with these disorders, but no, there is something wrong with these disorders because that polycythemia can make you more hyperquaglubal. Well, think about it. Why may that be the case? Well, if you become polycythemic, what happens to the viscosity of your blood? The viscosity of your blood increases. And when you have an increase in your blood viscosity, that's going to cause an increase in blood stasis. And when you have an increase in blood stasis, you're pretty much going with verkylstriad. Remember verkylstriad of hyperquaglability? Stasis? Hyperquaglability and endothelial dysfunction, right? So that is part, that's stasis. You're amping up that stasis. When you have blood stasis, you're going to have more interaction between your clotting factors and that's going to kick start. Your coagulation cascade and you can get in trouble, right? You can get in trouble. Again, that's why people that have polycythemia verkylstriad is because they have increased blood viscosity, right?

So this person can become hyperquaglubal, right? And that hyperquaglability can make them have an increased risk for myocardial infarctions, for strokes, for mesenteric ischemia and things like that, right? And then also, let's not forget that this hypoxia can ultimately lead to heart failure, right? It can ultimately lead to heart failure because again, think about it. These people have a chronically reduced blood oxygen content. When your blood oxygen content goes down, what do you think happens to cardiac output? Your cardiac output is going to increase. In fact, this is probably why this person's heart rate is elevated. It was not like over 100 in the case when I started it, but over time, this person will develop high-up or heart failure if this is not taking care of, right? Because when you're hypoxic, your tissues are stopped for oxygen. So they start telling the heart, hey, heart, we want oxygen, we want oxygen, we want oxygen. So what will your heart do? The thing your heart will do is that it's going to, your heart is, the thing your heart will do is that your heart will start increasing its output, right? So that you can send more blood around the body, right? So that you can send more oxygen, more blood around the body, right? So your cardiac output is going to rise. But again, the thing is your heart, your cardiac muscle is straighted muscle, right? It's going to get tired after a while, right?

We cannot keep working at that elevated level of cardiac output, right? Over time, that chronically elevated cardiac output will cause the heart to fail. That is what is called high output heart failure. That is what is called high output heart failure. So again, and how we're going to diagnose this person's disorder, we're going to do a sleep study, right? We're going to do a polysomnogram, right? And then this person certainly needs weight loss. And then this person also certainly needs C-PAP, right? C-PAP on your exams, they could call it positive, non-invasive positive pressure of ventilation, right? Because again, they know that everybody has memorized the term C-PAP. So I use the term C-PAP, you know, continuous positive airway pressure. When you can just use the term non-invasive positive pressure of ventilation, C-PAP is an example of non-invasive positive pressure ventilation. And then if they're asking for pharmacotherapy on your exams for a person that has obstructive sleep apnea, I will encourage you to pick the answer choice that talks about terzepotype, right? Terzepotype is one of these GLP1 agonists, but it also has activity on the GIP receptor. All right. So I think I'm going to go ahead and stop here. Again, these are two interesting cases we've discussed today, but look at how much integration there was with these two cases. You love the way I teach, you're going to love my classes. Imagine going through this for like 25 hours.

You're going to get something similar with my 25 hours step one class that begins tomorrow. And to be honest with you, it's a step one class, but honestly, it works very well for people studying for step two and step three, right? It works extremely well for both studying for step two and step three. So if you're interested, shoot me an email. You can still sign up the class. It's going to be held live over Zoom. And I'm the person that's going to teach that class. And then also, if I also offer one on one tutoring, I also help with your applications and personal statements and mock interviews and things like that. And then I have these podcasts on Apple, Google and Spotify, you know, and then I have a You Tube channel. You can also check out Divine Intervention, USMD podcasts and videos. And then I have another website called Divine Intervention Lifelessens.com. Divine Intervention Lifelessens.com. I am a Christ follower. I am a Christian. So every week I produce about, I produce one or two podcasts a week. We're from a biblical perspective. I do address a life lesson. There's actually an Apple podcast associated with that called the Divine Intervention Life Lessons Podcast. So thank you for listening to me today. God willing, I will see you in episode 631. Have a wonderful week. God bless you and bye for now. Thank you.

Hashimoto's thyroiditis (or simply "autoimmune thyroiditis").

Because the low circulating T3/T4 removes negative feedback on the anterior pituitary, causing excessive TSH release.

High TSH stimulates prolactin release; elevated prolactin then inhibits GnRH, shutting down the HPG axis.

Beta-1 ($\beta_1$) receptors. Low T3 leads to fewer $\beta_1$ receptors and bradycardia.

Respiratory acidosis, compensated by renal bicarbonate retention.

Because they present with a restrictive pattern of lung disease; abdominal contents restrict the thoracic cavity volume.

Polycythemia (increased red blood cell count) to increase oxygen carrying capacity.

Hyperprolactinemia (due to high TSH).

The gravid uterus occupies space in the abdominal cavity, compressing and restricting the thoracic cage.

Both should be normal (normal $\text{DLCO}$ and normal $\text{A-a}$ gap).

High output heart failure, due to the chronically elevated cardiac output required to compensate for low blood oxygen content.

Polycythemia (increased red blood cell count) to increase oxygen carrying capacity.

Hyperprolactinemia (due to high TSH).

The gravid uterus occupies space in the abdominal cavity, compressing and restricting the thoracic cage.

Both should be normal (normal $\text{DLCO}$ and normal $\text{A-a}$ gap).

High output heart failure, due to the chronically elevated cardiac output required to compensate for low blood oxygen content.