DIP Episode 217 - Family Medicine Shelf Review Series 6 (Pulm)

Okay, welcome. My name is Divine Amma resident. This is episode 217 of the Divine Intervention Podcast. And in this podcast I'm going to be commenting the Family Medicine Show for a View series. Like I said, it's going to ultimately be very comprehensive but for now I'm going to focus on the highest the topics. I know I've talked about GI so I'm going to talk about poem, right? Because in all the COPD asthma and all that stuff, it's going to high you to know for your exam. So the thing is you don't need to know like as much about pulmonary physiology for the shelf as you needed to know for a step one of the medicine shelf but you still need to know some things, right? So don't forget your spirometry values, right? I mean for the most part, if for example you're trying to diagnose some with asthma, with COPD or any of those obstructive restrictive lung diseases, the prudent thing usually you don't want to start with on an exam spirometry, right? And we know like you know the classically described FVV1 to FVC ratios. If the FVV1 to FVC ratio is less than 0.7 on your test, the person has some kind of obstructive lung disease, right? And then if you tell you that, oh you know what? After they give a bronchidylator persons FVV1 or FVC increases by like 12% right or by more than like 200 males like 200 C Cs, then that person essentially has like some kind of reversible airway obstruction. In this case we're probably looking at asthma, right?

And then if the FVV1 to FVC ratio is like normal or mildly increased, usually greater than 0.8, you know you want to think about restrictive lung disease under those circumstances. And in general, right? Don't forget, right? Like obstructive lung disease in general tends to have increased lung volumes, but restrictive lung disease in general tends to have decreased, sorry. So obstructive lung disease tends to have, yeah, increased lung volumes, restrictive lung disease tends to have reduced, so remember that R is matched. So restrictive lung disease reduced lung volumes, right? And don't forget like this thing called DLCO. DLCO just basically is a measure of how good your liver is and not liver your lungs are. And how good your lungs are at allowing oxygen to diffuse, right? So if you have like a diffusion problem, right? That will cause a decrease in DLCO, right? So for example, they love to make up questions where they talk about like obstructive disease or restrictive disease and you don't have to pick them all by which one has a normal DLCO, which one has a decreased DLCO, right? So for example, if you think about it, if a person has like restrictive disease and they tell you that this person's DLCO is decreased, right? You want to think about things that are intrapaginary and chimer, right? You want to think about like pulmonary fibrosis, right? If a person has some kind of normal conelosis and what not, right? Those because is obstructive disease will decrease DLCO.

And the reason the DLCO is decreased, right? If you remember from step one, right? The diffusion, the diffusion equation for the lungs, right? Is directly proportional to area available for the fusion and inversely proportional to the thickness of the membrane, right? So think about it. If a person has pulmonary fibrosis, the lung parankham is super thick, like the diffusion membrane is super thick, right? So because the thickness is going up, the diffusibility will be going down, right? So that's a fairly the mechanism of hypopsemia in a person that has pulmonary fibrosis, right? And that will be associated with decreased DLCO, right? But if they give you an example of restrictive disease on your life, this person's DLCO is normal in the question. Then you want to think about along the lines of a person having like some kind of neuromuscular disease, right? So say for example, a person has like Guillem-Barris syndrome or a person has myastinia graves or a person has ELS or a person has, you know, any of those neuromuscular things that can make essentially diaphragm not work as well as it should, right? Because there's nothing wrong with the ovular membrane. It's the mechanics that are, it's the mechanics of the lungs that are screwed up, not the actual lung parankham. So even obesity, right? Because again, if you have no, remember like your body is like kind of like a fixed space. If, if you have no cavities too big, right?

Because the person is obese, then the pulmonary cavity will not be able to descend as much as it should. That will cause restrictive lung disease. A person has like some kind of an atomic problem, right? Like chifuses, colliosis, pectosexcavada, right? They can have restrictive lung disease for those reasons, right? So again, those are just things to keep in mind. Like, those would be examples of restrictive lung disease with those would be examples of restrictive lung disease with a normal, with an normal DLC, right? And then if we're going into the realm of obstructive disease, obstructive disease, right? Again, think about emphysema, right? Emphysema, you're literally having all those pretty eases just show up your avial membranes, right? So you have a decreased surface area for diffusion, right? So if you decrease the surface area, right? Then you're going to have less defissibility. So emphysema is one of those classic MDM exam causes of obstructive lung disease with a decreased DLC, right? But consider all the things like bronchietuses, for example, like bronchietuses, bronchietuses, right? Like, the lung parankham is not really that screwed up, it's the actual bronchiet, right? So the thing is, that'll be an example of obstructive lung disease with a normal DLC. And then you see the one you're kind of harping on, this DLC will crap like a lot. I promise you it's kind of high, it's not kind of high, it is high, you know? And you may think of family medicine, shall we?

Can never test these? Well, thankfully, I actually have experienced tutoring like, you know, a ton of people for set shelf, so believe whatever you want. Okay. And then this one is probably more so step two, but I'll just throw it in since I'm talking about DLC. If you see a person that has increased DLC, they want to think about people that have like police, say, female, or they have like blood in the lungs, right? Like they have like pulmonary hemorrhage, for example, the mechanisms behind that I'm not necessarily going to talk about those because they're kind of low yield. They just email me, I'll be happy to explain to you, right? And then so all the things with this, all this pulmonary testing, I think I should kind of mention is if a person has like, carbon monoxide poisoning, right? Or a person has like cyanide poisoning, right? It would make sense that, I mean, cyanide and carbon monoxide, the primary problems they cause is that they bind to hemoglobin and kind of screw up its oxygen carrying capacity, right? So the thing is the P little AO2, right? The partial pressure of oxygen is completely fine, right? So if you do post-oxymetry, it will actually be normal. And people that have like cyanide poisoning or carbon monoxide poisoning, it's the SAO2 that is abnormal, like the actual saturation of oxygen on hemoglobin that's all screwed up in a person that has cyanide poisoning.

So this one of those cyanide or carbon monoxide poisoning, this one of those things you want to keep at the back of your mind. So don't be fooled by a normal post-oxymetry. In fact, if you suspect that a person has a carbon monoxide poisoning, instead of doing post-oxymetry, do cooxymetry, right? Or you measure the levels of caboxymoglobin, whatever, right? And then one of the tests you may see, right, is this method, calling challenge test, right? The method calling challenge test essentially is a test where, you know, you're like, oh, this person I think you've got asthma, you do spirometry, stone code normal. You're like, oh, you know what, I'm already brining, I still think you have asthma. You give those people metocalling, right? Metocalling is a most grainy receptor agonist. So technically, it's supposed to cause like bronchospasm, right? So if you give a very dilute amount to normal people, they won't cause any problems. But if a person has like touchy touchy areas, right? Like, you know, hyper-responsive areas, they will have like, you know, like a decrease in the FVV1. So whenever you see stuff like that, right? You know, think about asthma. And a person has a positive and metocalling challenge test. So again, don't forget that post-oxymetry business with, with sunlight poisoning and a couple monoxide poisoning. So let's go talk about asthma, right? So the thing is asthma and embankment exams, you know, let me give you a person that wishes at night.

Let me give you a person that, you know, has cough, that seems to be a worst of night. Or let me give you a person that has a lot of like nasal polyps. Nisol polyps tends to have like this big association with like a aspirin or other end sets, right? So like, there's this thing called aspirin exacerbated respiratory disease, right? Basically, if you see a person that has asthma and nasal polyposis, you want to consider making that diagnosis. Let me see, what if I was the mechanism behind that? Well, if you think about it, if you remember back to step one, you know, like, membrane phospholipide, you can convert them with phospholipisi to our erycanonic acid. And then that our erycanonic acid can go down the prostaglandine pathway with cox, or can go down the lucotrain pathway with locks, right? Lightbox, eginics. So the thing is, if you take aspirin or an end set and inhibit cox, well, when cox is inhibited, then you have increased flux through the locks pathway. And you produce a ton of lucotrains, right? That can begin to cause problems, right? Because lucotrains, they can increase vescular permeability and all that stuff, they can cause bronchospasum. So those kind of, all those things can potentially cause, all those things can potentially cause symptoms of asthma, right? And usually that kind of asthma tends to respond extremely well to lucotrain inhibitors, right? So like those lucotrain receptor antagonists, remember the lucotrain receptor is the CYSLT1 receptor.

So drugs like Monte-Lucas, that's after Lucas, right? They work pretty well. Well, remember Monte-Lucas is preferred over Zaffer-Lucas because it has fewer side effects. And then there's also this, like, oxygenation inhibitor like xyloton, again, that's kind of hepatotoxic. So usually, Monte-Lucas will be the right thing you should select on your test, right? So asthma, again, like I said, if a person has the most inflammatory, doesn't mean they don't have asthma, right? You need to put your next step in diagnosis on the test, we'll be to consider getting a metacolina challenge testing, which already explained already, right? Now, one thing I just want to say since we're kind of talking about asthma, they give you a question about a person that, and usually whenever a person has asthma, they'll have like a storied family history of like all these allergic problems, right? That happens in like 90% of MDME questions, the detail asthma. But another thing to keep in mind is if they give you a question about a person that seems to have like asthma, and like, man, this person also has like some kidney swibles going on, right? And they tell you that the PNK is increased, you want to think about stroke strokes, right? Like, EGPA. EGPA stands for eucyrophilic granulomatosis with polyngelitis, right? And then if they give you a question about a person that seems to have like these chronic asthma stals symptoms, and then like, man, this person's EG is like crazy high.

And then we tell you that all this person has a history of like past TB, or this person has like, um, like, you know, you see like infiltrating the upper lobes of the lungs, think about like allergic bronchopominary as pergenosis, right? Allergic bronchopominary as pergenosis. In generally, you just do like some skin testing for as pergenosis to establish to establish the diagnosis. Now, asthma, right? The thing is asthma, you need to be able to classify asthma your test, right? And there are four wrongs on the lotter of asthma, right? And I know that people find this kind of hard to remember. So to be honest with you, here's how you learn this thing. There are essentially four wrongs in the lotter. And the smart thing to do is to learn the ends of the lotter, right? And then the stuff in the middle, you can usually like decipher what it is on the test, right? So for the most part, the least severe form of asthma is like mildly intermittent asthma, right? So they have symptoms less than like twice a week or less. Let me put it that way, twice a week or less, right? So they have symptoms like B times symptoms like twice a week or less, maybe a half a night time symptoms twice a month or less, right? So you just remember twice for mild intermittent asthma, right? And these people just give them a sabah, that's it, right? Sabah, so like a bit of all stuff like that, right?

And then the most severe is these people have just daily continuous symptoms, they can't do any physical activity because of the asthma, that's severe persistent asthma. I'll say that again, that severe persistent asthma, those people need to be placed on oral corticosterates, right? They need to be placed on oral corticosterates. And then in the middle, in the middle on on NV Me exams, right? You know, we have like mild persistent, basically mild persistent is just typically in the question, tell you that all those percent of the emblazion asthma and the symptoms are not very well controlled, right? Then just go ahead and add an inhaled sterile, like a ludo in a ill corticosteroid, right? And then if for example, the person is having symptoms like, you know, they're taking like a sabah, they're taking like an inhaled ludo corticosteroid and it's not really quite in it, then go ahead and add an lava, that's the third wrong in the latter, right? And then obviously, if a lava is not working, right? And you go to like oral steriles, right? And I'll say some things about oral steriles that your friends at the NV Me can integrate with other concepts on an exam, right? So again, mild intermittent again, symptoms, daytime symptoms, you know, two, twice or less per week, twice or less per month for nighttime symptoms, mild persistent is the second wrong in the latter, they have symptoms more than twice a week, right? Or more than twice a month for the nighttime symptoms.

severe persistent is just again, they have symptoms all the time, that's the fourth wrong in the latter. The third wrong is just they have symptoms almost every day of the week, right? That's just again, rough ideas, but I feel like if you're just, if you kind of remember these rough things I'm giving you, you should be able to answer like 99% of the questions you've seen. So the only thing is if you have never truly set up on exams, so like, ooh, I gotta memorize this, these are asthma, guidelines, like, oh, mild, they're spout that, I've just never found it to be helpful on exams, and I've taken many exams with this concept that's been tested. Just remember the wrongs in the latter. Is that what a sabah, like a bit or all? If that's not according to other ludes in Hild, clinical steroid, if that's not according to other lava, although instead of, let's say you don't see a lava as an answer choice for the third room in the latter, you can consider adding like medium dose of an inhild clinical steroid that's fine, or you can add like a luchotrain antagonist, that's another thing you can consider, and then again, the fourth wrong in the latter, like severe persistent, you again add oral steroids, right? So again, don't forget, there's mild intermittent, mild persistent, moderate persistent, and severe persistent. Basically, I just remember the three M's, and then the S, and the only one that has intermittent in it is the first one.

So mild intermittent, then mild persistence, then moderate persistent, and then severe persistence, and the all going alphabetical order, like mild intermittent, that's an M and an I, and then mild persistence is an M and a P. Yes, moderate persistence is also an M and a P, but if you look at the word mild, M, I, I comes before when the alphabet moderate, and then severe persistent, S is much later than M in the alphabet, so everything follows alphabetical order, so it should be said pretty much from that perspective, right? And then, you know, the wrongs on the latter are kind of different for COPD. So COPD, you started like a Saba, or like a Saba, or I'll talk about this in a bit, but you know, like Saba Sama for COPD, and then after that you add a, you add a lava, that's the second wrong on the latter, and then the third thing is you then add the inhild clinical steroid, and then oral steroids as the fourth wrong on the latter for COPD. So there's kind of a difference there compared to Asma, right? And again, remember certain drugs that can trigger Asma's symptoms on exams, right? Like like a non-selective beta blocker, or even a beta blocker, because they can give you a question about a person that has Asma and glaucoma, and maybe the stat treatment for glaucoma and then the Asma gets worse, because remember, it can give beta blockers for glaucoma, right?

So, you know, don't give those things to people that have Asma, that's probably not a, not a pretty good idea, because again, beta blocker, I mean, there's a reason we give beta against Asma, so if you give it a beta blocker, you're like saying, ooh, you know what, let's go some more brinkel spasit, right? You don't want to do that to your patients, that's probably like, you know, like ill-advised, right? So, you don't want to do that. So if you really need to use beta blockers in the presence of Asma, you know, try to avoid it, but if you can't, you know, use the selective beta blockers like those that go from letters A through M, right? Like a tenon long metoper-lost of like that, right? And again, remember Asma, sprained induced Asma, NSAD induced Asma stuff like that, I already explained the mechanisms behind those and how you could try receptor blockers are probably pretty good for those people like Monte-Locast, right? And then, if they give you like a weird, bizarre question about a person that has Asma, and they have like very high IG levels, you can, and they say, oh, which of the following medications is shown to decrease the incidence of attacks? Now, you can give them like a drug that is, especially if they have like very high IGE, you can give them like anti-IGE preventive meds like, like a, like a homalysium up, right? Homalysium up is a monoclonal antibody against the IGE, right?

And then, one other thing you want to keep in mind is people that have Asma, because the family medicine shelf has a big preventive medicine component. You want to remember that those people should get the anal flu vaccines, right? And they also, actually, are one of those people that the pneumococcal vaccine is relevant for, right? And then, they may also just ask you like all these weird questions where the persons Asma symptoms are not well-controlled because they're not using gang healers properly, right? Or if a person is taking like an in-hield corticosteroid and they start having like dysphysia or like odenophysia, you know, you want to think about throsh, like candidly suffogitis, right? Especially again, if they're, that's why if a person is using ill corticosteroids, you tell them to like drink water or something, right? So that they can kind of like decrease the contact time between the ill corticosteroids and the esophagus, right? And the thing is, if a person is on chronic steroids, right? For like Asma, you want to put them on like PPI, it's really prophylactic PPI is because steroids can cause a peptic ostrich disease. I also want to put them on like prophylactic like dysphosphonids or like calcium vitamin D supplementation, because remember corticosteroids can cause osteoporosis, right? And then these are all things to keep in mind for tests. And then sometimes on the family medicine shelf, they love to ask about like some drug interactions, right?

So the first one is remember you cannot give a lava like some mineral foam or mineral as like a singular therapy in Asma like monotherapy that actually increases morbidity and mortality, so you want to avoid that. And then a fluoroquino loans and or like marcoilids, those drugs because remember one of the drugs you can use to treat like Asma, or even really bad COP Ds, the Ophilin, although same also Asma. So the thing is the Ophilin has a ton of drug interactions, right? So the thing is if they give you a question about a person that you know comes in for a COPD like an Asma or COPD exacerbation and the Ophilin at home, right? Remember when people have like Asma or COPD exacerbations and let's say there is an infectious component to the asymptoms, they tend to get like a fluoroquino loan or a marcoilid, right? And then they tell you that all these persons that's having like these nasty dangerous arrhythmias, you want to be super careful, right? It's they're likely suffering from like the Ophilin at toxicity on the exam, right? So don't forget those don't forget those things. And then if for whatever reason they give you a question about a person that has like a bad Asma exacerbation in the emergency room, mean when they come in, you essentially need to give them like a bit of roll, like you know like a continuous like nebulizer, um, and then you give them like IV steroids, right?

And typically when they're living the hospital you need to give them like three to four days worth of like oral clinical steroids so that you don't have like a quick return of symptoms, um, you can also give like a dual nebulizer, right? Like you give a a bit of agonist like a bit of roll and then a most chronic antagonist, right? Like like a hypertrophy, right? You can give them combined and then let's say you're giving everything and it's like, oh, this person is not getting better. You can give IV mag, like IV magnesial, um, and if a person is not like doing well, right? Because normally, in fact, let me take a step back here. During an asthma exacerbation, it should be hyperventilating, right? So your PCO2 should be low. If the PCO2 is beginning to normalize and a person that's undergoing an asthma exacerbation, this bagging is right there, right? Um, that's why you obtain like routine like regular AB Gs or people going through like an asthma exacerbation or a COPD exacerbation. Um, but especially asthma exacerbation, this is how they test it. You see the person's PCO2 is like 40 in an asthma exacerbation. That's bad news, right? Means the person's beginning to, the person's respiratory muscles are tiring out. Uh, your next step is to go ahead and to be that person like yesterday, right? If not the whole crap out on you and die, you know, pretty quickly, right? Um, so you're again, just keep all those things at the back of your mind with asthma.

Again, COPD, um, I've kind of talked about like some of the testing. But again, COPD is going to be in a smoker, right? If you see a person less than the age of 45, even if they've smoked on an MBA meeting with COPD, you want to begin to think about like an alpha one anti-trapsin deficiency, right? And again, don't forget that again, if you want to have you see less than 0.7, that's it. Presidents are destructive lung disease. And if a person has hemophysi amazement, the cause of the COPD, the DLC is going to be decreased, all right? And again, if you see a person that has like multiple family members with COPD, that's very likely going to be alpha one anti-trapsin deficiency on your test, right? And, um, there are some other things, right? That can cause a destructive lung disease. Like I'll give you a COPD like picture, like for example, if you give your question about a person that has like cystic fibrosis or catatonic syndrome or a person has like, um, you know, like a ton of sputum production, like the cough up a lot, like superproductious sputum, they have like episodes of hemoptysis. And they tell you that, oh, you see like these like linear streaks on a chest x-ray, um, think about bronchic the way you ultimately make the diagnosis of bronchic diseases with a higher resolution CT scan. Um, you'll see like the tram track pattern of the presence of bronchic on a, on a, on a higher CT.

And then CF, again, CF is actually the most common cause of bronchic diseases in this country. I remember CF ultimately causes a restrictive kind of lung disease, not obstructive or restrictive kind of lung disease. Um, but again, they may have bronchic diseases alongside with that. And again, obviously for cystic fibrosis, again, you do the sweat blood test, right? And don't forget CF, right? Like they can have pneumonia on exams, right? If they're less than 20, right? It's stuff-or else that's causing it. You give them like the drops that cover stuff-or else, right? Like vancomycin, especially like mercer, like vanc, um, lignisolid, um, your tigacycleans, you can give safe taro lind, that's a fifth gen cephalosporin, um, you can give that to my say, right? But if you're more than 20, it's probably pseudomonas aeroginosis that's causing their, their pneumonia, right? So you want to give those rooms that cover pseudomonas, pneumonia, right? So like, um, you can give like a third gen cephalosporin, so tazidine, the fourth gen cephalosporin, sythepine, right? Or you can give, um, your carbapenem, like meropenem, imipenem, gorypenem, eropenem. I know one of those penems though, doesn't cover pseudomonas, but I'm not gonna go into which one. That's the one for the, um, also as sure number, I can cover pseudomonas, um, your fluoroquinolones can cover pseudomonas, right? Uh, there's one more drug class, I think I'm forgetting, um, your amino glycosides, right?

It can also cover pseudomonas, in fact, for people that have cystic fibrosis, you can actually try to decrease the, uh, risk of like pulmonary infections by giving them inhaled to bromide set, as per if you're an access to remember to bromide set, is one of those amino glycosides. Um, so, if I'm bursting as COPD again, like I said, go ahead and start them on a, um, a short actin, beta agonist or a short actin most chronic antagonist. If they give you both as answer choices on a test, go with the short actin most chronic antagonist, uh, those are slightly preferred over the sabers in a COPD management, and again, if that's not quite in it, if that's not controlling symptoms, um, you just need to go ahead and, um, add, uh, add a lava or a llama, right? A llama is something like some mineral for motor oil, uh, uh, a llama. So a long actin most chronic antagonist is something like, um, it's something like, um, tyotropia, right? Tyotropia. I think that's what's called spirivine, the hospital, right? And again, COPD, you know you're going to see COPD questions on your shelf, right? So you better pay attention on to this part. And one thing I'll just go ahead and say is never give a summer an llama together. So a person should not be on epiretropium and tyotropium at the same time. To be honest with you, I really don't know why, but that's just one of those weird things that really shows up on exams, if you showed up on exam on an exam, almost everyone will get it wrong.

But thankfully, you won't get it wrong because you paid attention to the spot cast, right? And then indications for home oxygen therapy in COPD, right? You want to know those? Like, if a person's p little ill too is less than 55 or yeah, all too sad, so less than 80% or they have like polysiphemia, right? You want to consider, like, your person has like polysiphemia, like the hematocryt is like crazy high. And remember to go from hematocryt to hemoglobin, divide the hematocryt by three, right? Or if they have like pulmonary hypertension or signs of right-sided heart failure, those people certainly need a continuous home oxygen therapy. And you know, like, the thing that has been, that's actually one of the things that I've been shown to improve survival in COPD, continuous homo-two therapy, but the best intervention to improve survival in COPD is to, you know, like stop smoking, right? So that's one thing I want to keep at the back of your mind for tests. And if a person comes in for a COPD examination, right? And you know, they're having trouble breathing, obviously they're going to give them like the short-acting stuff, but in addition, you can place them, you don't just go straight to into beating those people, right? You usually try like, like, like, like, buy-pap, right, before you tube into beat those folks. And the thing is on your MDM exam, right? You know, they'll probably want to put buy-pap, that's too easy, everyone will crush the exam, they did that.

Instead of doing that, they may put like NIPPV as an answer, right? So like non-invasive, positive pressure, ventilation, right? That's something I want to keep at the back of your mind for tests. So NIPPV, non-invasive, positive pressure, ventilation. And typically, the antibiotic of choice in people that come in for COPD examinations, on MDM examinations is it through my sin? Because apparently those marker leads also have like some anti-inflammatory properties, so that can help in a COPD examination. And if a person, you know, has like, ends the COPD, you know, like, yeah, this person is going to be dead soon. And you know, they're having like, seviationness or breath. The drop of choice will actually be an opioid like morphine. It actually helps with shortness or breath. And again, those people just like the asthma folks, you know, they need their unlawful influenza vaccine, they need the soup, they need the mokoko vaccine, right? And if a person has like, alpha-1 antitripsine deficiency, they need like IV, like, pulled alpha-1 antitripsine, that typically helps. And again, an exacerbation, right? You give them the short acting stuff, you give them IV steroids, you can do the NIPPV, if they're not responding to NIPPV, then you're into big them. And then you also give them oral steroids to go home, right? So that, like, you know, like a three to five a course of oral clinical steroids. Okay. Now, I think, yeah, I think I should probably consider like grounding obstinate.

But cystic fibrosis have already kind of talked about it, right? Like, you'll be a person that has low weight, and you have a ton of nasal polyps, recurring sinusitis, they usually have finger clobbing, and you have fat malabsorption, because remember, they're pancreas, essentially dead, right? So that's why you typically have to do like pancreatic enzyme replicelines in those people, or you may have like diabetes, right? Because, again, the pancreas is dead. So they have like an endocrine and an exocrine of pancreatic insufficiency, right? So that's something to keep in mind with exams. And remember, cystic fibrosis, the most common cause of bronchitis is in this country. And remember that if a person has a history of CF, and then they have like sodium onset, severe bumbinoping, you want to think about it into a perception. That's a video one of those rare NBM exam causes of into a perception, in adults, right? Think about an adult with cystic fibrosis, right? And again, what are the things you do for CF, right? You know, you just do things like, I've talked about the antibiotics, you can use it, you have like, like the stuff, or your infections, or whatever. And here's one thing, if a person has like really bad pneumonia, and they're like, like pretty advanced cystic fibrosis, unless you don't put MRSA's an answer, or should the monos as an answer, think about this bog Bocodaria's sepacia.

So it's like BIRK, like BURK, HOL, D-E-R-I-E, Bocodaria's sepacia, C-E-P-A-C-I-A, okay? And again, how do you treat to the CF? You know, you replace those pancreatic enzymes, you also need to supplement the fat soluble vitamins, right? Because the pancreas doesn't work, right? They know they have a fat-and-absorption, so they don't be able to reabsorb fat soluble vitamins like vitamins A, D, E, and K, right? You need to do chest physiotherapy for those folks. They may need like, bi-papal, sepapal, at night, if they're like superhypoxemic at night, you can give them like, like, dorniz alpha, like it's like a recombinant DNA, it's like, full-soda histra bonds, so you can break up those secretions, or you can give them like, anacetyl-sistine, right? Remember, it breaks like disulfide bonds and all that stuff. So, you know, you can help them coff up that nasty, guppy stuff in their lungs, right? So just, you know, kind of keep that at the back of your mind. And again, remember, it's sweat-chloric testing that you use for that. So I think I'm going to go ahead and pause, and I don't want this to be super long, because I do idea with a river podcast. I also want to want to run tier 1 for a ton of exams, step 1, 2 CK, 2 CK, and step 3, pre-clean cool med school exams, 30-ish-off exams, actually, you should have a ton of people for 30-ish-off exams.

And then I do this longitudinal tiering, where, unless you're studying off med school, or you're studying off 30-year, and you know, just tier 4 for all your exams. And again, as I'm doing that, I'll be teaching you step 1 stuff, or step 2 CK stuff alongside. And most of the people I've done that with, again, be wildly successful, and then I also offer these booster courses, like it's 15 hours for step 2 CK, step 3, it's 20 hours for step 1, where, again, Q&E format, very rapid fire. And I also explain pathophysiology, like I talk about the high-yields, most notes for those tests. And then another thing that I also do is it also is pretty good at helping, like, flush out whatever weaknesses you have, and then we deal with them. And then, again, if you have, like, a problem in a specific subject, let's say, like cardiology for step 2 CK, or whatever, you can schedule like a 2 R tutorial with me. I do it one-on-one. And basically, after those two hours, that subject will not be a weakness for you in exams. I mean, like, it's really pretty striking when I hold those tutorials with people, and you see them, like, they took a practice exam, and they helped, like, the NBM, like, confidence bars all to the left for that subject. And then we do the tutorials, they take the next practice test, and for that's okay, it's all the way up to the right. So those are usually like two-hour tutorials.

And then, if you're a college student or an MCAT, whatever person, that needs to be done for like Gen CAM, O-CAM, Physics, Bio CAM, Histology, Physiology, Alpha Turion for all those things. And then, I also do, like, coaching, or consulting for, like, you know, if you're a medicine or a plant, to residency, so like an ERAS app, or a college student or a plant to med school, like an AMCAZ app, like, you know, like rec letters, personal statements, mock interviews, editing applications. Again, I've worked with many specialties, the vast majority of people have worked with, have all much that they're first, at their first choice. And again, I have admissions committee experience at our top two med school, like, I was literally on the admissions committee. So again, if you need advising with any of those things, or if you're a medicine resident, then you need to do it for like the internal medicine board exams, the internal medicine, the interim exam, feel free to reach out to me. And if you're like, PEEDS resident, I need to learn for the intramural exam for PEEDS, or the PEEDS boards, reach out to me as well. I'll probably start doing like mainstream tutoring for the surgery boards in the future. So, have a wonderful rest of your day. Thank you for listening to me. And I will continue poem, critical care in the next, in another family medicine podcast. So thank you for listening. God bless you. I'll see you next time.

FEV1/FVC ratio less than 0.7.

Neuromuscular disorders (e.g., Myasthenia gravis) or chest wall deformities (e.g., kyphosis).

Destruction of alveolar walls leads to a decrease in the available surface area for gas diffusion.

Cooximetry (to measure carboxyhemoglobin levels).

Montelukast (preferred over Zafirlukast due to fewer side effects).

Smoking cessation.

Coverage against Pseudomonas aeruginosa.

It suggests impaired gas diffusion. Mechanisms include increased membrane thickness (e.g., Pulmonary Fibrosis) or decreased surface area (e.g., Emphysema).

Neuromuscular diseases (Myasthenia gravis), obesity, or chest wall deformities (Kyphosis/Pectus excavatum).

Asthma treatment involves a stepwise approach using LTR As/ICS/LABA; COPD management emphasizes LAMA $\rightarrow$ ICS $\rightarrow$ Oral Steroids, and requires careful monitoring of oxygenation.

Vitamins A, D, E, and K.

It can be used as a rescue measure when the patient is failing standard therapy, helping to improve ventilation and reduce the need for intubation.

Non-selective beta-blockers (Beta-1/2 blockers).

It suggests impaired gas diffusion. Mechanisms include increased membrane thickness (e.g., Pulmonary Fibrosis) or decreased surface area (e.g., Emphysema).

Neuromuscular diseases (Myasthenia gravis), obesity, or chest wall deformities (Kyphosis/Pectus excavatum).

Asthma treatment involves a stepwise approach using LTR As/ICS/LABA; COPD management emphasizes LAMA $\rightarrow$ ICS $\rightarrow$ Oral Steroids, and requires careful monitoring of oxygenation.

Vitamins A, D, E, and K.

It can be used as a rescue measure when the patient is failing standard therapy, helping to improve ventilation and reduce the need for intubation.

Non-selective beta-blockers (Beta-1/2 blockers).