So we're about to get started for the afternoon session. I want to announce one or two schedule changes. Chris Kading will be giving his knee ligament talk today in the time slot that was previously occupied by the elbow. So we'll have Dr. Best give the talk on medical issues. It'll conclude that series of talks. And then Chris Kading will give his talk on knee ligament and follow up with his talk on test taking strategies. And then my talk on sports medicine research will be tomorrow, the last session where Dr. Kading was initially scheduled to be. So we'll go medical, knee ligament, test taking strategies for the rest of the day today. And so I'd like to call up Dr. Tom Best from University of Miami who will give the third medical session of the day. All righty. Thanks Bruce and thanks to Chris as well for inviting me back again this year. So we've got about an hour to finish up what Dr. Borcher started this morning on the medical side of things and sort of appropriate topics here as you can see. So just to kind of set the stage here, what I want to talk about is we'll do a little bit on the PPE, focus a lot on the cardiopulmonary issues, talk a little bit about environment, altitude, nutrition, exercise and eating disorders as well as exercise and pregnancy. So just to kind of set the stage, the pre-participation evaluation that we're all familiar with, you know, what's its real purpose? Well first of all, it's to detect medical conditions that may interfere with sports participation, determine any contraindications to participation, discover predisposition to injury including previous injuries that may require rehab, as we all know the major risk factor for injury is previous injury, fulfill legal and insurance requirements, that's perhaps debatable. What I want to draw your attention to is in the fourth edition there was a recommendation regarding use of functional testing and the most recent one, the fifth edition which was just released a couple months ago, there's a tremendous focus on mental health issues as well as the female athlete and transgender athlete. So just to be aware of that, I think down the line we'll probably see many of these issues coming to the forefront and that'll reflect what we need to know as team physicians. But like everything else in medicine, it always starts with the history, right? So when you start with the pulmonary system, we look at issues such as asthma, allergies, we see a lot down in our, I was just telling Bruce, part of the country, kids coming in from California and they for some reason develop seasonal allergies, so it's something to really be aware of. We'll talk a little bit about the paired organs and the ADA Act of 1990. Visual problems, remember in certain sports you must have a certain visual acuity in order to compete and of course that necessitates protective goggles. Immunizations, I've seen a question recently, think about the dorms and particularly meningitis, right? So you want to make sure that they're up on their immunizations. Heat illness, we'll talk a little bit about that. There's not a lot of ways to predict if something's going to happen other than perhaps sickle cell trait. Nutritional issues is a big one and then of course the final one with particular to the female athlete. And as we all know, the problem with the last two is it's by self-report. There's a lot going on right now looking at the electronic pre-participation evaluation and its accuracy versus the one that most of us are familiar with, which is the 10-page form that we have our student athletes fill out. So that'll be coming down the pipeline as well. This is really an important slide because this really drives our thinking and what we'll talk about in terms of screening for cardiovascular disease in the young athlete in particular. So in 2014, right, the recommendations changed, okay? So this is the so-called 14-point American Heart Association. And as you can see here, again, a lot of questions which I suppose you could debate particularly in a younger student athlete, for example, or say a high school athlete. What is going to be the accuracy of looking at these kinds of questions? And from a research standpoint, a lot of us are trying to get at that right now. Nevertheless, draw your attention to a couple of things. First of all, with heart murmurs, remember if it's a diastolic murmur, probably that should go to a cardiologist. None of us in this room should really be dealing with a diastolic murmur. And we'll talk about the systolic murmurs, which are potentially worrisome as well. Obviously, elevated blood pressure, I actually think this is undertreated, particularly at the Division I level. I know at our university, for example, we probably have at least 10 or 15 percent of our student athletes in certain sports that have probably stage 1 hypertension. And you know, sometimes they're treated and sometimes they're not. And then obviously any family history of genetic problems such as so-called HOCUM, we'll talk about long QT, marfans, and then certain arrhythmias. Here's another important slide, right? The Bethesda Guidelines. So why is this important? Well, as you can see, you have an X and a Y axis here. And what this, to make a long story short, this really drives our decision making when we're counseling athletes about their eligibility. So for example, if you have an athlete that has the so-called HOCUM or hypertrophic obstructive cardiomyopathy, that necessitates putting you probably down in the 1A category, which is things like bowling and cricket, for example. So the Bethesda Guidelines, what you need to know there is this is what drives our thinking when we talk about decision making. And I'll draw your attention to some of the newer literature talking about informed decision making and where that's leading us. So this is something I'm not sure it's going to hit the test yet, but I really think you need to be aware of, right? And that's this whole idea about shared decision making. So how did we operate for a long time? Well, if you look at the Bethesda Guidelines, it's a very binary thing. It's yes or no, right? If you have HOCUM, for example, you're disqualified. So it may not be that simple moving forward. And we probably have done a disservice to our student athletes with some of the decisions that we've made. So traditionally, it's been a very paternalistic decision making process, right? Doctors, schools, athletic organizations, we sort of make the call, and the kids and their parents have to live with it, as they say. Well, in 2001, there's a landmark paper that came out. It's called Crossing the Quality Chasm. And really, that took us forward into, you know, patient-centered care, if you will, and informed decision making. And here's a very specific example. So in 2015, the American College of Cardiology and American Heart Association, they really sort of turned this upside down on us in sports medicine, right? So now we have Class 1, so that means you're good to go. Class 2A and Class 2B, eligibility is reasonable or may be considered. So there's the gray zone, right? And then, of course, Class 3, which is not recommended. And what you're going to see more and more moving forward is there will be very few conditions where we'll have a quote, unquote, Class 3. And this has been, as we all know, has been contested legally several times, and certainly will probably not go away. And a specific example that we'll talk about is long QT syndrome. That used to be, if you had long QT syndrome, that was an immediate disqualification from anything but the 1A Bethesda sports, right? That's no longer the case. And there's a great paper that Aaron Baggish out of Harvard put out in circulation last year, which presents some really interesting data to show that a lot of these people can safely participate in sport. So stay tuned. That's going to be changing. Another one to be aware of, of course, is the single solitary organ. When many of us trained, this was, again, you could disqualify an athlete if they had, say, one kidney. No longer is that the case, right? And that's based upon the American Disability Act from 1990. So again, we're moving towards a trend of shared decision making. And really, it's become more and more difficult to DQ somebody. I mentioned heat intolerance earlier. This is a big problem. Bruce and I were just talking about before the lecture and sort of, you know, what our threshold is, for example, for starting IVs. And here's the problem. We really don't have good data that predicts, right, other than some of the factors we'll talk about. Genetics may play a role. There's been a couple papers in the literature, but that hasn't really been substantiated. That came out of the South African literature. We do know that sickle cell trait and certainly disease increases your risk, right? And we take specific precautions. So at least at our university, what we have is we have a color chart for our football team. And so we carry that on the sidelines so we know we have asthma, we have sickle cell, and we have a few other conditions, and they're all color coded. So it's easy to recognize so you get to know your student athletes. And then, of course, return to play guidelines are not well established. So if you have an athlete, for example, that suffers from heat stroke, what should you do? When do you return them to sport? Do they need to be evaluated? It's still a very gray area. The physically challenged athlete, if you will, the spinal cord injured patient, right, we all know about autonomic dysreflexia, so a lesion that's T6 and above. So this is an interesting situation, right? They have decreased cardiac output, and it's manifested as a decreased stroke volume with a minimal compensatory increase in heart rate. And this is a so-called clamp catheter boosting technique that a lot of these athletes will use to actually increase their blood pressure. So something else to be aware of. And then, of course, the Downs individuals and their risk for C1, C2 pathology. So just kind of wrap this up then. If we talk about the PPE, you know, we talk about screening, disqualifying, whatever. Very few athletes really get disqualified, right? If you look at it, for example, some of the data that's in the literature says it's probably around 1%. It may even be less than that. You know, who needs further evaluation, at least in my hands on the medical side, usually it's undetected. Stage 1 hypertension is probably the most common thing that we see, as well as some of the cardiopulmonary problems and certainly some of the cardiac murmurs. And then, of course, at the end of the day, we know that we're still not really good at screening for a lot of these problems that we see. So let's look at a couple of questions. First one, the PPE is designed to, A, substitute for a routine health exam, B, protect the institution from medical legal issues, C, identify athletes with CAD, D, detect any medical or musculoskeletal conditions that may predispose the athlete to injury or illness during competition, and finally, exclude athletes from participating with preexisting conditions. So as we mentioned earlier, one of the primary goals, right, is really to look for, particularly in the musculoskeletal section, these youngsters that have had, say, an ACL tear, Bankart lesion, whatever, so that doesn't necessarily, often we don't disqualify them, but maybe it's a rehab issue, so it comes to the forefront that way. Football, PPE reveals that an athlete has a normal functioning solitary kidney. After appropriate consultation and discussion with the parents and athlete, what should you as the team physician recommend? Participation after explaining the risks of playing contact sports. Participation in non-contact sports only. Participation avoiding NSAIDs and seeking nutritional counseling. Participation with the addition of special padding to protect the athlete's kidney. And finally, participation after modifying the weightlifting program, emphasizing core strength. And again, it's answer A, as we know, right? So in the old days, we actually had a couple of cases of this, very young in my career, of the single kidney, and we used to, we would say, you have to pad the other one, and actually the attorneys said that was probably the worst thing to do, because you're actually arguing that they shouldn't be playing by doing that. So bottom line is, again, think about the American Disabilities Act, if you have questions along the lines of DQing athletes with a single solitary organ. Final one, this kind of gets at the Bethesda guidelines, you're evaluating the cardiovascular risks of a certain sport, physician must consider the static and dynamic demands of the sport. We saw that with the Bethesda slide. So what is an example of a sport with both high static and high dynamic demands? Rowing, distance running, sprinting, baseball, and American football. The answer is, surprisingly, rowing. All righty. Take a deep breath. So here we go now. We're into the specific cardiopulmonary problems that you want to be aware of as team physicians. So again, what's our goal, right? Well, obviously, it's to prevent sudden cardiac death and allow these athletes to continue participation. The American Heart Association and the European Society for Cardiology, they both recommend screening. Okay? So now we're going to talk about screening. So in this country, at least our high school and collegiate athletes are probably our top priority, though age to best screen and frequency of screening is still unknown. And that's an important issue, right? So for example, we'll talk about HOCUM in a couple of minutes, hypertrophic obstructive cardiomyopathy. We know that one in 500 carries the gene. So that means at the University of Miami, we have about 450 student athletes. We have at least one student athlete, based on statistics, that has the HOCUM gene. But it's variable penetrance, and we really have no idea, do we, is it when it's expressed? Okay? So when should you screen? Do you screen the 10-year-old student athlete? Do you screen the college athlete? These are all very important questions. What we do know, at least in this country, that it's the 14-element screening. That's the important, okay? That's where you have to focus your efforts, is on the AHA guidelines. We also know that less than 35 years of age, HOCUM is the most common cause of death during sports and physical activity, and over 35, of course, it's coronary artery disease. I'd also draw your attention, and we have a slide looking at ARVC, the incidence for some reason is increasing in this country, and we don't understand why. It may just be a detection phenomenon. So let's talk about screening, because this is something you need to know about for the exam, right? What are the pros and cons? And Ben Levine gave a great talk at the Advanced Team Physician course a few years ago that really kind of highlights, you know, why screen and why not screen? First of all, it's a highly visible event, right? Somebody who goes down on the sidelines, the Hank Gathers story, for example, that people like to play back once in a while, it's a tremendously emotional event. There's loss of numerous years of life. We do know that there's an association between exercise and sudden death, and there may be interventions such as defibrillators that can help. What is against screening for cardiovascular disease? Well, first of all, it's extremely uncommon, right? It's extremely uncommon. There's only been about 350 cases at the NCAA level in over 50 years. Most of those have occurred in African Americans and in the sport of basketball. So when you start talking about cost effectiveness of screening, you really have to, you know, you really have to think about these issues. It's been estimated in this country alone, if we wanted to screen with just an EKG, it would cost about $2 billion a year to screen all of those who participate at the high school and collegiate level. So here's what you need to know. What are the current best practices? Well, in the U.S., the U.K., and the Canadian models, it's still the pre-participation evaluation, which is the history and physical. The Italians, on the other hand, as many of you may know, they also demand an ECG and an echo, and we'll look at why that's the case in a minute. We know that 80% of athletes who die from sudden cardiac death are asymptomatic with a normal physical examination. So that high school student athlete that dies on the field, if they've had an exam, chances are it's been a normal exam, okay? So that's important. We also have to know that the EKG, it does add value, but again, at least in this country, when you look at the people that have been screened, we do have a fairly high positive false rate, okay? And there's an interesting editorial coming out now that looks at screening for cardiovascular disease in athletes and compares it to, say, breast cancer screening. And we're actually better at things like breast cancer and colon cancer screening if you really look at the purpose of screening than we are with sudden cardiac death. The other thing, and I'll show you a slide in a second, you need to understand what's actually normal, right? What's a physiologic adaptation? What does an athlete's heart or athlete's EKG look like? That's entirely normal. So here's a slide that you want to know, right? You need to remember, of course, that with exercise, what happens, you have an increased vagal tone. So what can you see on that resting electrocardiogram? Often these athletes have sinus bradycardia. They can have a first degree AV block, which simply means they have a prolonged PR interval. They can have an incomplete right bundle branch block. They can have early repolarization changes, and finally, isolated QRS voltage changes. What are abnormal findings? T wave inversion, ST segment depression in at least two to three consecutive leads, pathological Q waves, et cetera. So as you can see, there's some things that are normal, right, that are very specific to that so-called athlete's heart. And we're actually looking at our data now. We have a cardiologist by the name of Dr. Meyerberg, who's about to retire, and he's got 12 years of data that we're looking at now. We're trying to establish some parameters for what we think is the normal EKG, particularly in the African-American. It turns out that they have a lot of changes in the left ventricle. Their left ventricles are a lot more thickened. So for example, you may think they have hypertrophic obstructive cardiomyopathy, and they simply have a normal athlete's heart. So let's look at some of the specifics, right? So the first one is the so-called HOCUM. This is what we need to know. As I mentioned earlier, it's got an incidence of about 1 in 500. It's autosomal dominant, right, with variable penetrance. So we don't know the expression of this gene pattern. That's a real issue when you start talking about screening. Their physical exam can be normal. The key testable question here, remember, is that systolic ejection murmur, right? So if you have an athlete with a systolic murmur, the first thing you want to do is have them squat down and repeat that exam. If that murmur increases in intensity, I encourage you to call a cardiologist, because that's when you need to start thinking about HOCUM, right? So HOCUM, systolic murmur, systolic ejection murmur that increases with a Valsalva maneuver. The other thing you need to know is how they die. Well, they die from ventricular arrhythmias. So again, it gets tricky, right? The EKG findings can be variable, all right? ECHO, we used to say that was the gold standard. It was diagnostic. Now, of course, it's the cardiac MRI and even genetic studies. So if you have an athlete with so-called HOCUM, we're typically now getting MRIs and looking at gene studies as well. The treatment has traditionally been the beta blocker and the implantable defibrillator. Again, we get into this whole issue, does that allow them to participate, okay? At this point in time, I think the question would still go back to they're disqualified, but I'd be very surprised if they put a question on about that, because that one could be contested, right? This is one of those, as I mentioned earlier, where, and there are cases that are out there right now, one that I'm very aware of where there's an athlete that has HOCUM, has an implantable defibrillator, and is probably going to be allowed to compete at the Division I level. Another condition is comedial cortis, right? So that's the result of blunt, non-penetrating chest trauma. They get ventricular fibrillation from a blow that's delivered during the vulnerable period of the cardiac cycle, just prior to the onset of ventricular contraction. Mean age is about 13, as you can see here, sports, contact sports, or sports where, for example, such as baseball, getting hit by a ball in the anterior chest, can produce this problem. Dave Janda, when he was at University of Michigan, showed that the breakaway bases, for example, and some of these protective gears, or chest protectors, did reduce the incidence of the problem. They like to ask about myocarditis. I think I've only seen it once in my career, which probably means it's zombie, and I didn't see it, but in any event, this is something they like to ask about. Many different causes here, right? The big thing to remember is the EKG findings. So they present with nonspecific, diffuse ST and T wave changes across the precordium. If they're going to ask anything about this, I would bet that's what they'll ask you. The treatment's a little bit debatable. We say restrict them from activities until their ECG normalizes, and that can take up to six months. Again, not a lot of evidence for it, but that's the question would read something like that. So I mentioned RVC, or arrhythmogenic right ventricular cardiomyopathy dysplasia. It's a lot easier just to say RVC. So this is, as I mentioned earlier, this is a condition which is quite interesting. So this is the one that the Italians, there's a much higher prevalence, particularly in the Sicily region, about 20% of athletes. So that's why they recommend or demand now ECG and echo screening. So they see a different incidence of this problem. Now as I mentioned, we're starting to see this more in this country, and we don't know if it's a detection, but nevertheless, as you can see, it's got a familiar occurrence in 30 to 50%. The key here is the so-called epsilon wave, which you can see down on the bottom right on the ECG. It's an autosomal dominant condition, and again, generally speaking, we disqualify these athletes from all but 1A sports. Long QT I mentioned earlier, right? This one's really quite interesting. I think what you need to know there is the medications. So if you have an athlete, for example, that has been on, say, erythromycin for acne, for example, and they come in with some sort of cardiac ectopy or complaining of tachycardia or whatnot, I would get an EKG, and I would be looking for long QT syndrome. So that's how they'll probably get at it on the test. The treatment here, again, is beta blockers to control their heart rate, and again, there's a nice study that was published in 2013 out of the Mayo Clinic where they looked at all of these cases and showed that at least in a third of them, they were able to continue in sports, and really, there was no risk. So again, that's that paradigm shift I mentioned earlier. So long QT, we used to disqualify these people without any question, and now many of them are being allowed to participate under certain conditions. Marfan's is another one they like to ask. You know about the musculoskeletal factors or things that you can find in a physical exam that tip you off. So let's focus a little bit on the medical side. So it's the aorta. That's the key. So these are these tall African-American athletes, typically. They've got the long limbs. You get a little bit suspicious about it. You look for it. Typically, we'll get an echo, and the reason you're getting an echo is you want to look at the aorta, and specifically, the aortic root. Now, again, generally, no contact sports, although, again, I think this is debatable with this paradigm shift I mentioned earlier. So Marfan's, you need to know a little bit about as well. All right, let's do a couple of questions to kind of highlight some of the cardiac issues. 19-year-old female basketball player born in Indiana presents for her college PPE. She has all negative findings on her 14-point AHA history and exam. Which of the following is true about further evaluation for college athletes in the United States? Number one, ECG should be done on all college athletes. Number two, echoes should be done on all college athletes. Number three, ECG and echo should be done, and number four, no further testing is necessary. So we talked about this earlier, right? The standard of care still in this country is it's the history and the physical. This is, I think, an evolving field. At our institution, we're very fortunate, as I said, because of a cardiologist who is one of the leaders in the world in this field, and we're actually, as I said, looking at our data now to really see if we've made a difference or not. In my three years at the University of Miami, we have not disqualified one athlete. We have certainly had some what we thought were abnormal EKGs, but we haven't found anything yet. So knock on wood. But from test-taking purposes, and they'll try to trick you with this, right? A lot of us think that all of these people need to get echoes or EKGs, and that's still not the case in this country. Second one, whether a 12-year-old baseball player has heard about another young boy dying while being struck by a baseball in the chest. So what condition are we talking about here, right? We talked about comedial cortis. It produces fatal inflammation, including pericarditis, damages the heart valves, leading to heart failure, occurs when the chest is impacted at a vulnerable period in the cardiac cycle, leading to a fatal arrhythmia, can be prevented with chest protectors if worn correctly, and finally, is usually related to an underlying congenital heart problem. And the answer is C, right? So these baseball, these protectors really haven't helped reduce the incidence of this problem. Again, the other thing they may ask you is, have a defibrillator on the sidelines, right? So that's another question that could come up. What's the single thing that we can probably do most to prevent sudden cardiac death is having a defibrillator on the sidelines? All righty. So now we'll get into some of the pulmonary issues, and the first one that we see a lot of, of course, is EIB, or exercise-induced bronchoconstriction, a little bit of a differential diagnosis here. Obviously, you have to think about cardiac disease, right? So that's the so-called cardiac wheeze, right? So we think about arrhythmias, hocum, et cetera. Vocal cord dysfunction is another big one, and we'll spend a couple of slides talking about VCD. Exercise-induced anaphylaxis, we see that a lot. GERD, that can be concomitant with vocal cord dysfunction. And then finally, some of the rare problems such as tracheomalacia and a vascular ring. So EIB is probably, again, one of those conditions that saw you and it didn't see us, and maybe they're doing okay or they're using somebody's inhaler, but it's probably a lot more common than we think. So what do we need to know? Well, first of all, you know, typically we think about cough, wheeze, shortness of breath, chest tightness. Remember, it occurs after exercise. That's a key point, right? It's after exercise. It's estimated to be 12 to 15% of the population, and it's reversible, right? It's like asthma. Remember, the definition of asthma is reversible airways disease, as opposed to, say, restrictive lung disease or COPD. It's caused by bronchial smooth muscle constriction, airway inflammation, cytokine release, and mucus production. The other thing that I like to ask is, you know, what's the diagnosis? How do you make it other than a clinical examination? And it's a drop in the FEV1 greater than 10%, right? So we often order PFTs in these individuals, and that's now become the standard of care best practice. It used to be when I started, if we thought we had an athlete with EIB, we just put them on a short-acting bronchodilator, and if they got better, we empirically thought that was the diagnosis. The reason you have to really document that carefully now is for drug testing, all right? Some of the drugs that we use, such as corticosteroids and so on, you have to be very careful. So I would encourage you, if you have an athlete that you suspect EIB, you should really do PFTs to document it. Some of the newer tests that are out there, such as the EVH and mannitol, that's more at the national and international level. So what are the presenting signs and symptoms of EIB? Well, the common ones we all know, right? Cough, shortness of breath, chest tightness, wheeze. But it can be often more subtle, and that's why I say it probably saw us and we didn't see it. People who suffer, for example, of poor performance, they're out of shape, for example, avoiding certain activities, and then symptoms in specific environments. Again, you get a lot of these kids who probably it's more allergic than it is true, you know, asthma or EIB. Again, their exam is usually entirely normal, right, unless you see them during an exacerbation. And again, make sure that you objectively confirm this with pulmonary function testing. The treatment of EIB is still pretty much the same as it was 25 years ago. We typically start with the short-acting bronchodilators, right? So that's your beta-2 agonists, such as albuterol, 2 to 4 puffs about 15 minutes before exercise. That should give you up to 4 hours relief, except in certain situations, say, in a sport like hockey, if you're inside, for example, with the cold air, sometimes they'll take a puff, you know, between periods or whatnot. Other things to consider in terms of the treatment algorithm, you can use chromalimb sodium and the leukotriene modifiers. They are permitted by WADA. Remember, if you use inhaled steroids, that you've got to document that very carefully, right? Any athlete that goes on steroids, you've got to document that very carefully. And then some of the practical issues, again, such as adequate warm-up, avoiding triggers, and then a cold air scarf and mouth cover. One final plug for carbon monoxide poisoning. Again, this is probably something not necessarily poisoning, but if you have athletes that play, say, in a hockey rink, the Zamboni and so on, they've shown in many states, such as Minnesota, that without proper ventilation, there can be problems due to CO. I mentioned earlier VCD. So this is the big masquerader, and they like to ask this on the test, right? So what's the difference between vocal cord dysfunction and EIB, or exercise-induced bronchospasm? It's when this occurs. Remember, we talked about asthma, for example, is a disease of expiration, right? So when you do pulmonary function testing, peak flow volume loops, asthmatics can take a deep breath in. They can't exhale. So that's why, for example, on a chest X-ray, they have hyperinflation, okay? So asthma, reversible, it's a disease of expiration. VCD, or vocal cord dysfunction, these are the kids that present, or the athletes that present, you'll see them, for example, clutching their throat, right? They say, I can't take a deep breath. That's not asthma. That's something else, and you want to think about vocal cord dysfunction. Flow volume loops can be helpful, but really the best way to do this is send them off to your ENT surgeons. They'll spray the back of their throat, have them say, ah, and you can see if the vocal cords abduct or not, okay? The treatment is interesting. You may go, wow, speech therapy? It actually works, all right? So speech therapists are very good at helping these young people with breathing techniques to avoid symptoms related to VCD. Often, and I'll do this myself, we usually put them on an H2 blocker as well because they often have concomitant reflux, which will exacerbate things. So there's just a real quick slide showing you with normal expiration, right, the vocal cords abduct. If they have VCD, they just sit there. So again, remember the difference between VCD and asthma. So a couple of questions here. We have a 20-year-old swimmer who reports coughing, chest tightness, and shortness of breath after completing a 1,000-meter freestyle event, what should be the next step in evaluation? Arterial blood gas, electrocardiogram, PFTs, and echo or bronchoscopy? The answer is C, right? We want to get pulmonary function tests to confirm that this athlete has exercise-induced bronchospasm, which again is manifested, as I mentioned earlier, by at least a 10% drop in their FEV1, and first-line treatment, again, is the beta-2 agonists. Previous athlete does not have PFTs consistent with asthma. During her next episode, you are present and notice that she is clutching her throat and has inspiratory stridor. What is true about this condition? So this is classical for VCD, right, or vocal cord dysfunction. It's more common in men, characterized by abduction of the vocal cords during inspiration, effective treatment by consultation with a speech therapist and stress management, never seen in conjunction with asthma, and diagnosis often made with full-volume loops. The answer is C, they have vocal cord dysfunction, right? So again, remember the differences between vocal cord dysfunction and exercise-induced asthma. All righty, so we'll switch gears. We're right on time here. We've got 30 minutes left. Let's start with heat, cold, and altitude. So one of the things that they'll sometimes ask you is, what is it, you know, what are your responsibilities as a physician, team physician or whatnot if you're running a mass participation event? So always have to remember, right, you approach this as a planned disaster. Remember, as the medical director, what are you really responsible for, like everything else, like being a team physician, the health and safety for your participants, your athletes, and decisions, right, regarding their medical care. Things that you need to have available, obviously, these are pretty straightforward, IV fluids. Remember, 3% saline, right, exercise-associated hyponatremia that we'll talk about in a second. So you want to have 3% saline available. Some of the medications are listed. Point of care, you want, ideally, if you can get a serum, sodium, BUN, potassium, accrete, glucose, and oxygen saturation. The final one, I cannot emphasize enough, they like to ask, right, if you start talking about heat problems, make sure you have a rectal thermometer. That'll be the number one problem that gets you into court, right, if you have an athlete that goes down with heat stroke. The two things are rectal thermometer and ice, okay. Any lawsuits that occur are typically related to absence of either one of those. So let's talk about the collapsed athlete, all right. What's the differential diagnosis of the collapsed athlete? So, obviously, cardiac arrest, exertional heat stroke we'll talk about, hyponatremia we'll talk about, hypoglycemia is pretty rare unless you have a diabetic, right. Again, remember, you have to have a rectal thermometer if you're running a marathon, for example, and you're the medical director. Always think about seizures. And then, finally, another condition we see called exercise-associated collapse. They like to ask you about that. So this is the high school girl, for example, that runs 400 meters. She comes to the finish line, she stops, and she drops. Is that a serious condition? Most likely not, right. What is it? Well, why do we tell athletes to keep walking? They stop, they get all that venous return just sitting down in the bottom of their legs, and they become hypotensive, right. So the testable part here is if you have an athlete that stops at the finish line and then goes down, that's not as worrisome as the athlete that's still exercising and goes down. So that's how they like to get at exercise-associated collapse. Physiologic adaptation to the heat, another very testable here, right. So what do you need to know? Well, first of all, it takes about 10 to 14 days, right. So when you're providing recommendations and guidelines, just keep in mind it's about two weeks before they're optimally conditioned, if you will. And that's really important, and we'll talk about that in a second, for example, with the sicklers. When do the sicklers run into problems? It's usually the first couple days, right. There's very good data now looking at these heat stroke issues. They tend to occur within the first couple of days of starting fall football camp. And if you look at the incidence, after about two or three days, these conditions tend to go away. You do need to know the adaptations that occur in response to heat. First of all, there's a decreased heart rate, and that's a resting heart rate. The increased plasma volume, that's how you can sweat more and dissipate heat. They start to sweat earlier, so that makes sense. There's an increased sweat volume and skin distribution, again, so that you can dissipate heat. And finally, a decrease in the amount of sodium that's lost. So adaptations are important to heat. Mechanisms of thermal regulation. So what do we need to know there? Bigger athletes produce more heat, right. The exercising skeletal muscle likes to produce a lot of heat that we need to dissipate. And how do we do that? The blood is shunted to the periphery. So evaporation accounts for about 85% of heat loss with heavy exercise. And one of the things I like to tell the fellows when they cover the Miami Marathon, the first thing you always look at when somebody goes down is, are they sweating or not? So the athlete that goes down and is not sweating, that's problematic. What do you need to think about? You need to think about heat stroke, right, because they've lost their ability to dissipate heat. A number they like to throw around is the average 70-kilogram athlete sweats about one to two liters per hour. So a lot of fluids are lost. Another important point here, why are children at greater risk for heat problems? Well, they have a smaller surface area to body mass ratio and a lower sweat rate. For some reason, they like to ask that. So what are the risks, then, for heat illness? Well, obviously, the first one is the environment, right, the hot, hazy, humid day. We're all familiar with that. Again, thanks to Randy Eichner, who's now a retired numericist professor at the University of Oklahoma, he had a lot of data to show us that it's the first couple days of football camp is when things are going to happen, right? We also know the so-called double sessions was a problem, right, and the NCAA has certainly helped us out by doing away with that. One thing you need to keep in mind is the so-called wet bulb globe temperature, right? So that's the kind of measure that a lot of us use from a medical decision standpoint when we're saying, for example, can the Chicago Marathon occur this year? The other thing you have to be aware of is you can still have a cool day and have heat stroke and heat illness problems. Bill Roberts at the University of Minnesota has a great talk that he gives all the time and he's got data now from the Twin Cities Marathon and they've had heat stroke problems even in the, say, when the ambient temperature is 60 or 65 degrees. So it's not just a hot, hazy, humid day. All right, so some of the specific conditions. Most serious one is exertional heat stroke. By definition, it's a rectal temperature, again, rectal temperature greater than 40 degrees centigrade. The problem is some of the symptoms are nonspecific early on, right? They can be fatigue, they can have impaired judgment, for example. It's great if you know your student athletes, but if you're covering a marathon and don't know individuals, that can be very problematic and you can see some of the other nonspecific changes. One thing that I'll draw your attention to, they like to test this. If there are CNS changes, they're confused or whatnot, you need to think heat stroke, okay? The ones who just have, you know, heat cramps, for example, or anything like that, typically, they're not disoriented. So if they have mental status or CNS changes, think heat stroke. Always remember that contact sports, it can be mistaken for head injury, right? That's a so-called lucent interval. Another important point, seizure is not common in exercise heat stroke problems, okay? So if you see a seizure out there, think of two things. If it's a short duration seizure, think cardiac arrest. If it's a longer duration, that's so-called hyponatremia and we'll talk more specifically about that. And then finally, remember what's the treatment and they'll test you on this, right? If you have an athlete, you suspect heat stroke or any heat illness, what's the first thing you do? You put them in an ice tub, okay? You put them in an ice tub. And again, Bill's got a nice paper that's in current sports medicine reports. I mentioned earlier hyponatremia. This is a condition, again, that probably saw us and we didn't see it, right, for years. And the South Africans taught us a lot about this problem. First of all, thirst is not a good indicator of overall hydration status. What's the best indicator? It's body weight. So for example, in Kona, I'm the medical director there once every five years. And we've been able to implement a policy where the athletes are not allowed to participate unless we have a body weight within one hour of starting the competition. The reason that's important is if we take them off the course, the first thing we try to get is a body weight. Now sometimes that's difficult, of course, if they're disoriented. But body weight is really the best way to follow their hydration status, right? That's why we check it every day at football practice. So if they have a serum sodium in that sort of low normal range or just below normal, 131 to 135, you don't see much, all right? And then you can see the progression here as the serum sodium starts to fall. So who are the athletes that are at risk? This is something else I'd like to ask you, all right? So it's not the winner of the Boston Marathon that finishes in two hours and 15 minutes. It's that runner that's out there for four or five hours. They've had a body weight increase amazingly, right? So that should make you suspicious. I have some, if somebody weighs 100 kilos before the race and they come in weighing 100 or 101 kilos, you should think hyponatremia. They're fluid overloaded, okay? They're fluid overloaded. The treatment of hyponatremia is what? It's 100 mils of 3% saline. Now theoretically that can cause central pontine myelinitis, but that's actually never been reported in the literature. So think about exercise hyponatremia. These are the athletes that are out there the longest. They often can gain body weight as well, which is pretty hard to do if you're running a marathon. I mentioned sickle earlier. Let's talk a little bit about that, right? Because sickle cell trait is something that's always out there for us. And why is that? Well, first of all, we know, for example, that at least 10% of African Americans are sickle cell trait positive. Okay, what does that cause? That's that so-called log jam effect in the blood vessels. And of course, they can be at risk for a lot of problems including rhabdomyolysis. Think about this, right? When does sickling occur? It usually occurs early in exercise. So these are the athletes, and we watch ours very carefully. We have about 10% of our African American athletes at the University of Miami that are sickle trait positive. And the ones that start cramping right away during practice, those are the ones that we get rid of right away, so to speak, meaning they're off the field and treated appropriately. So again, what are other risk factors? If you have heat, dehydration, altitude, don't forget altitude is a problem for sicklers, right, and that increases their risk for problems. Again, informed consent screening at the NCAA level. We can't mandate it, right? So they have to sign a release that they do not want to be tested, but I've never actually seen that occur. Shift gears a little bit. Let's talk about hypothermia, problems related to these conditions. So by definition, it's a core temperature less than 95 degrees Fahrenheit or 35 degrees Centigrade. So remember, hyperthermia, usually over 40, hyper is under 35 degrees Centigrade. Here it's a little bit different, right? Heart rate, respiratory rate, cardiac output, they all decrease. Everything slows down. It's the easiest way to remember that. Remember, you need to know the difference between mild hypothermia, that's 90 to 95 degrees, and then moderate to severe is less than 90 degrees. And why is that important? Once the core body temperature falls below 90 degrees Fahrenheit, the myocardium is at risk for problems. Okay? So just remember that. Less than 90 degrees, severe hypothermia, think about the heart. Treatment, again, we won't spend too much time here. Mild to moderate is pretty straightforward. Big thing is just to get them out of that environment, obviously. They can usually just be treated with oral fluids, okay? So if they have a rectal temperature greater than 90 degrees, they're probably going to do okay by just getting them out of that environment, getting rid of their wet clothing, for example, and just orally hydrating them. Moderate to severe is a different beast altogether, right? Once the core temperature is below 90, as I said, think about that irritable myocardium. So they're at risk for atrial and ventricular tachycardias, and that's when things start to get more interesting, obviously. And these are the people that we obviously typically transport, right? So if you're running the Twin Cities Marathon, for example, like Bill Roberts does as the medical director, they actually have microwaves right there on the sidelines so that they can warm up IV saline and stuff if they have that condition or are at risk. I need to talk a little bit about skin problems. First one to think about is frost nip, right? So that's a superficial vasoconstriction without tissue freezing. So you have burning followed by numbness, and that's the gray or pale skin on the face and extremities. And remember, do not rub that skin, right? You can damage it very quickly. That's in contrast to frost bite. So now we have something a little bit more, right? It's not superficial. This is when you have tissue damage. They like to ask about this. Remember, it takes up to six weeks to determine the level of tissue damage, if you will, or the depth of tissue damage. Once they're thawed, if you will, that's when the blisters start to occur, and you can see the yellowish or red, as well as they have purple fluid. If they have no blisters, of course, that's severe. That's gangrene, right? They like to ask you that question, too. So an athlete who's at risk or if you're suspicious of gangrene, these are the ones that don't have blisters, okay? Initial treatment is protective clothing, but they need to go to the hospital. I mentioned earlier altitude. A couple slides on altitude. The first thing we'll talk about is high altitude illness, if you will. Most common reason for that is rapid ascent, right? So you're climbing Mitrapichu, and you go up too quickly, okay? So it's due to the decreased barometric pressure and partial pressure of oxygen. Again, symptoms can be nonspecific early on. Most people who climb that probably experience this. They can get some headache, nausea, anorexia, insomnia, fatigue. It's usually mild and self-limit. You just slow down their ascent, right? You just slow down their ascent. Now, they like to ask about this. What's the treatment, right? So the first thing is, as I mentioned earlier, slow ascent, okay, acclimatization, obviously, and obviously avoiding things like alcohol and stay hydrated. So that's a relatively easily manageable condition. In contrast, we have two other problems you need to be aware of. The first one is HAPE. That's high altitude pulmonary edema. These people are sick. So they're dyspneic at rest. They have severe hypoxemia, and they have non-cardiogenic pulmonary edema. So these people are sick, right? The same as the so-called HACE. That's the high altitude cerebral edema. These people are ataxic. They're vomiting, and they have decreased level of consciousness. So these are severe, life-threatening conditions and need to be recognized quickly. The one thing they like to test on sometimes is steroids, okay? Steroids are good for HAPE, all right, for high altitude pulmonary edema. They do not treat HACE or high altitude cerebral edema. All righty. So a couple of questions now. The first one, which of the following is true for children? Mentioned this earlier, right? Are they at equal risk for heat illness as adults exercising in the heat? They can acclimatize to heat faster than adults. They have a higher sweating capacity than adults and can dissipate heat more effectively. They have a smaller surface area to body mass ratio. Encourage them to use sport drinks rather than water for rehydration. So before we get to the answer, one thing about E from a practical standpoint, if you have athletes that are exercising less than 60 minutes, normal free water is probably absolutely fine. They don't need to spend money on Gatorade, okay? Over an hour is when you start to get into electrolyte problems. So it's a really simple way to kind of... Not everything is black and white, I realize. Most things aren't in medicine, but it's a good way to sort of practically manage these individuals. So again, we talked about this earlier, the answer here, right? These children are at greater risk for heat illness problems because they have a smaller surface area to body mass ratio, i.e., they can't dissipate heat, and they have lower sweat rates, right? So children have two reasons to get into trouble, which is probably why we see some of the problems in our high school athletes, right, as opposed to, say, our collegiate athletes. All righty. You're covering the marathon in Phoenix. It's a warm, sunny day. 30-year-old female collapses at the finish line. She's unconscious, but breathing with a good pulse. She's warm to touch, and she's not sweating. So what's the key point here? She's not sweating. Great. So what do we need to think about if she's not sweating? Probably something related to heat, right? She's lost her ability to dissipate heat. So what's the answer? Do we administer Dantrolene, measure oral temperature, give oral Tylenol or other antipyretics, encourage cool liquids, or immerse in ice water bath? And we know the answer, right? Answer E. When in doubt, get them in a tub, okay? That's going to hopefully save a life and obviously keep you from further problems as well. All right. Asked about the prevention of altitude sickness, what do you recommend is the best way to avoid symptoms? A, slow ascent. B, premedication with scopolamine. C, proper nutrition. D, optimal physical condition. And E, appropriate clothing. We talked about this as well, right? By far and away, slow ascent is the way to go. Now, one thing they like to sometimes ask about is acetazolamide, okay? Acetazolamide, there's not great data that says it does diminish, but it does not eliminate the risk, okay? Most of us will prescribe it, but it really isn't foolproof, if you will. All righty. Covered a marathon in August. Participants bring a friend to the medical tent. It's his first marathon. He's finished in four and a half hours. He was stumbling a little, somewhat confused at the finish line. They encouraged him to drink, and he subsequently consumed four liters of water. He becomes unsteady and confused. So where are we headed with this question? Great, right? We're headed towards probably answer D, hyponatremia, okay? So again, think about hyponatremia in the setting. These are the people that are out on the course longer, and sometimes they'll even gain weight, right? So that's something that's difficult to do in running a marathon. All righty. Now, let's switch a little bit to nutrition. So the first thing we want to talk about is what are the sort of energy storage requirements for typically, you know, exercising individuals, if you will. Well, first of all, it's the glucose and free fatty acids, right? That's what provides the majority of energy for the working skeletal muscle. Muscle and liver glycogen, that's how we store carbohydrates. Adipose tissue, we store free fatty acids, which again, provide, particularly in the longer events, are important for energy requirements. A couple of numbers to keep in mind, exercising males, typically 2,500 to 6,000 kcals a day. Exercising females is about half, and that's really just related more to body weight than anything else. Once you normalize it to body weight, the requirements are about the same. Carbohydrates, they like to ask you, right? It's the predominant fuel source beyond 65% of the O2 max, okay? And it's about two-thirds of daily intake. So just remember that. If you see carbohydrates, it's two-thirds, as I always tell the fellows. If you think that, you probably will get it, you'll get the question right. They like to ask you about protein, okay? They like to ask you about protein. So what are the numbers you need to know? Protein is about 10 to 15% of your total energy requirement for exercise. In strength-trained athletes, it's about 1.6 to 1.8 grams per kilogram. So it's a little bit higher than endurance athletes. But there's no benefit greater than 2 grams per kilogram body weight, okay? So these are the athletes. We know them all. They like taking lots of protein supplements. Probably most of them don't need to take them, though. And finally, as I mentioned, fat, right? About 20 to 35% of total calorie requirements. So what do you need to know about carbohydrates? Again, it's about two-thirds of the requirement for exercise in skeletal muscle, right? And carbohydrates actually improve performance. We know that from the so-called carbohydrate load for the marathoners, right? So what do carbohydrates do? They prevent the fall in blood glucose because you're using glycogen. They maintain muscle carbohydrate oxidation and brain glucose supply. They actually reduce the perception of fatigue. It's really interesting. There's some really nice studies that show that. And finally, they increase your exercise time to fatigue and total work. So carbohydrates work. That's why we take them and consume them with exercise. They also like to ask about timing of nutrition, okay? So pre-competition, what are the things you need to remember? So that's your high carbohydrate, moderate protein, low fat meal three to four hours before competition, okay? So the pre-competition phase, usually three to four hours beforehand, some carbohydrates, and you want to avoid fats if at all possible. In recovery, this is another question they like to ask, right? So first of all, carbohydrates, right? You've got to restore your glycogen, and it's about 1 to 1.5 grams per kilogram. Remember that protein is a significant as well, right? And the key point here is chocolate milk does work, right? You don't need to spend all that money on muscle milk. We all have it. I know our athletic departments love to have it, but for everyday people like most of us, chocolate milk actually works quite well, right, to restore our protein. So carbohydrates and protein together actually provide some advantage, okay? It used to be we just talked about, you know, at the Boston Marathon, for example, it's, you know, the pasta dinner two days beforehand. Well, now protein is part of that as well. And of course, don't forget hydration and fluids. So which of the following is not true about protein intake in athletes? Protein is the last fuel source used. Strength-trained athletes have greater protein requirements. Carbohydrate and protein should be ingested together after muscle-damaging workouts. Chocolate milk is as effective. Most athletes that participate in strength sports need protein supplements, and protein should account for about 15% of total energy intake. And the answer is D, right? Most athletes actually don't need a whole lot more extra protein, okay? All right, a 33-year-old triathlete comes to your office to discuss his training for an up-and-coming triathlon. He's trying to lose weight, but wants to ensure optimal performance as he continues to increase aerobic performance. He is interested in the ketogenic diet to help him meet his goals. How would you best describe a ketogenic diet? This is important, okay? This is actually starting to show up. So what is a ketogenic diet? High in protein, low in carbohydrate. Low in protein, high in carbohydrate. High in fat, high in carbohydrate. Or high in fat and low in carbohydrate, right? So the ketogenic diet is? Answer D, right? High fats, low carbs. And it does work. There's some very good data, particularly Jeff Volek at Ohio State's done some really good studies with triathletes. And we actually did a survey two years ago at the Ironman, and 25% of the top 100 finishers are actually using the ketogenic diet now. So it's quite interesting. So I think that's coming. That's going to show up on the test sooner or later. So ketogenic diet, right? High fat, low carb. Iron deficiency anemia, okay? So when do we suspect iron deficiency anemia? These are the female athletes, endurance athletes. And remember with vegetarians, they like to ask this, what do you need to look out for in vegetarians? It's zinc, B12, and vitamin D deficiency. How do we screen for iron deficiency anemia? We look at ferritin and hemoglobin. I don't think you'll get a question on this, but the best evidence out there says if ferritin's less than 30, you can supplement with iron. The big thing with iron is the side effects, right? It tends to slow the gut down, and a lot of these athletes don't tolerate it very well. Menstrual dysfunction, all right? So let's start out. You need to know the difference between primary and secondary amenorrhea. So primary amenorrhea is the absence of menstruation by age 16 in girls with secondary sex characteristics or females without secondary sex characteristics and no menarche at age 14. Secondary amenorrhea is the absence of at least three consecutive cycles after menarche or less than three to six cycles a year. The key point here is it's not due to estrogen, right? It's due to the so-called energy drain hypothesis. So these athletes, they expend more energy than they consume, and it leads to a disruption in their luteinizing hormone pulsatility. So amenorrhea and oligomenorrhea are both associated with low estrogen. So why is that important? Well, first of all, we know that the effects of low estrogen on bone mineral density are not reversible. There's that window of bone accretion, which is from the early adolescence until the mid-20s, right? So that's why this is so important, particularly in our high school and collegiate athletes. Return of menses without medications is optimal for bone health. We used to treat this routinely with oral contraceptives, and we probably did a lot of our younger athletes a disservice, right? What you need to do is increase their caloric intake, decrease their so that's that energy drain hypothesis. So a real testable point here is that amenorrheic athlete, what's the first thing you do? You need to look at their caloric intake and caloric expenditure. It's not putting them on oral contraceptives. Some of the pharmacological interventions, calcium, right? We know that the requirements, they do like to ask this sometimes to the prepubertal children, requirements of calcium 12 to 1500 milligrams a day and vitamin D is 800 international units. If you do have athletes with menstrual dysfunction and or eating disorder, what do we need to know? Well, first of all, estrogen prevents further bone loss but has little effect on bone mass. And that's why I said earlier, we probably did these athletes a disservice. Oral contraceptives really should only be considered if there's no menses for six months at least and a history of a stress fracture. Again, think energy drain or energy hypothesis first, right? Look at their caloric intake and expenditure. Nasal calcitonin, minimally infective, and as we know, the bisphosphonates and selective modulators are contraindicated under age 18. Anorexia nervosa, by definition, what is that? It's a refusal to maintain body weight at or above the minimally expected normal body weight for age and height. Weight loss leading to body weight less than 85% of affected. One percent of the population, I think that's debatable. My guess is it's actually higher. It can occur in all sports. We know that it's increasing in males. And obviously, the treatment is multidisciplinary approach. The female triad, what's the definition? Well, we have disordered eating, amenorrhea, and abnormal bone loss. So you need all three to actually make the diagnosis of the female triad. And again, take-home message here is you have to start with the energy, right? So it's low energy availability treatment is the first thing to look at. So with menstrual dysfunction, there's a decrease in the release of GnRH, which leads to a decrease in luteinizing hormone. They have decreased bone mineral density, so we obviously got to address those issues as well. Exercise and pregnancy, just a couple of slides to kind of finish that up. So the majority of healthy pregnant women, they can exercise, right? They can exercise. That was a long myth that we've dispelled many years ago. We do know that about 80% of exercising women will experience diastasis recti. Most of that can be treated non-surgically. They do like you to know what are the physiological changes that occur with pregnancy. So there's obviously weight gain, ligamentous laxity, increased lordosis. We have an increase in estrogen, prolactin, and relaxin. And then some of the cardiovascular changes as well. You actually see a 50% increase in plasma volume, all right? You have increased heart rate, stroke volume, and cardiac output. Respiration, increased tidal volume, respiratory rate, oxygen consumption. So basically everything speeds up with pregnancy, right? They do want you to know the absolute and relative contraindications to exercise. And I won't spend a lot of time with these slides. You can review these. Probably the biggest one that they'll talk about is premature labor or ruptured membranes. And the relative contraindications as well. You can read these at your leisure. So just a couple of questions to finish up. First of all, which of the following is true about exercise during pregnancy? Number one, should it be gradually increased in intensity during the second and third trimester? Well, I think it's when things start to slow down, right? It should not involve weight training because of detrimental effects on maternal fetal circulation. There's an increased maternal cardiac output and uterine blood flow. Maximum oxygen consumption at term is greater than in the non-pregnant female and finally results in increased maternal resting blood volume and increased resting heart rate. And the answer is E, right? Things speed up with pregnancy. Another question, 25-year-old female long-distance runner presents to your office complaining of fatigue and poor performance. This is a tough one, by the way. I like to throw it in though. History and physical exam are consistent with anemia. Almost all lab work including peripheral smear, serum iron and TIBC are consistent with iron deficiency anemia. The one exception is that the ferritin level is normal, right? We're used to seeing ferritin levels are low so we put them on some iron. So what is the most likely explanation for a normal ferritin in this athlete? They have sickle cell trait, vitamin D malabsorption, they have hepatitis, volume depletion or malaria. And it turns out the answer is hepatitis and I'll let you read about this as well. So iron deficiency is something to know about. If they have a normal ferritin, think something else is going on. 33-year-old female runner has increased her running regimen for an upcoming marathon, has a history of three menstrual periods in the last six months, her pregnancy test is negative. Remember, always check that pregnancy test first. The most likely etiology of her menstrual dysfunction is which of the following? We talked about the energy drain, right? Is there increased testosterone, increased luteinizing hormone, decreased GNRH or increased prolactin? And the answer is C, right? So it all starts with that GNRH and leads on to luteinizing hormone problems. I think one final question here, 19-year-old female athlete with secondary amenorrhea for six months, no history of prior stress fracture or concomitant eating disorder, which of the following is not appropriate? Increased her nutritional uptake, we talked about that's important, right? Evaluation including pregnancy and other tests, you're going to look at that. Evaluation of her caloric intake, both quality and quantity and assuring appropriate calcium and vitamin D. Initiating bisphosphonates or continuing with regular exercise, right? So pregnancy should be excluded and additional labs are necessary to exclude other causes of amenorrhea. All righty, I've got about 56 seconds left, so got through everything. Thanks very much for your attention and do we have time for questions? One question, Bruce, or we're going to move on? Okay, thanks very much. Thanks very much.

medical conference

schedule changes

pre-participation evaluation

pulmonary issues

nutrition

cardiovascular diseases

vocal cord dysfunction

exercise-induced bronchoconstriction

proper nutrition