DIP Episode 66 - Pulmonary Pharmacology For The USMLE

Okay, welcome to episode 66 of the Divine Intervention Podcast. This podcast is going to be devoted to pulmonary pharmacology. Basically, if you're not in this podcast, you know everything you need to know about pulmonary pharmacology for the USML Es, right? So, and I'm going to cover all the drugs in this one podcast. So, let's go ahead and begin. So, let's start with allergies, right? So, we know that allergies are type 1 hypersensitivity reactions, right? So, like asthma, for example. And I mean, how do allergies work? So, basically the first thing that happens is you have like your first exposure to an allergen, right? And these allergens are taken up by, you know, like antigen presenting cells like macrophages, B cells, the endritic cells. And then they present these things to CD4 positive T-helper two cells. Okay, remember, T-helper 1 deals more with cell mediated immunity. T-helper 2 deals more with antibody mediated immunity. Okay? So, and then you make IGM, okay? And then remember into looking for, very high you to know this, into looking for, it helps you class switch to IGE, right? As long as you have those pesky CD40, CD40 ligand interactions you talk about in an immunology podcast in the future. Remember, without those interactions, you get a hyper-IGM syndrome, right? So, and then the FC epsilon receptors are mass cells, right? They combine the IGE, okay?

And if you have cross-linking of those immunoglobulins and those FC epsilon receptors are mass cells, you have the granulation, your release system in bradykining, and then you have the allergic response. And remember that histamine can cause bronchoconstruction, right? And it also increases vascular permeability because it can cause a contraction of cells known as parasites, okay? Parasites are the surrounding duphilial cells, so that allows for more space for flu to flow into the interstitial around blood vessels, right? And histamine also causes viso-dialition. Contrast this with bradykining, bradykining is a pyrogyne, right? So, it causes fever, that's one, two. It actually also increases vascular permeability because this viso-dialition just like histamine, right? But one high-althe, you kind of want to remember is that bradykining, right? There are certain things that can break down bradykining, right? So, to like inactive metabolites, one of this is ACE and you're tensing convertine enzyme, and another is another enzyme known as C1 S3 inhibitor. The thing is, if you have a deficiency of C1 S3 inhibitor, right? You have a disease known as hereditranger right? These people should not take ACE inhibitors because if they already have a deficiency of one enzyme that breaks down bradykining, and then you give them an ACE inhibitor, you kill the other enzyme that breaks down bradykining, they can get some very, very nasty, nasty stuff, right?

And remember that for bradykining to do its job like every molecule in the body, there's a receptor, it binds to there's a bradykining receptor. So, that leads into the first drug I'm going to talk about is known as IKATIBANT, I-C-A-T-I-B-A-N-T. It's not in first state yet, but I can foresee this coming to first state, or the USM is at some point in the very near future. So, this drug is a bradykining receptor antagonist, okay? You can actually use it to treat hereditranger a D-My-Gain, because it blocks those bradykining receptors. Now, let's talk about the anti-histamines, right? So, the anti-histamines, basically for this case we're talking about the H1 blockers versus G Iway, dealing with the H2 blockers, right? Then the thing is, for these H1 blockers you have two generations, right? There's the old school kind, there's the first generation, and then there's the new school kind, the second generation. So, the first generation, these ones, they have an awesome ability to cross the blood green barrier, okay? But the thing is, these drugs are also powerful muskonic receptor antagonists, okay? And some of them also blocks aerotonic receptors, I'll talk about that in a short while. But the classic drugs you need to know here are drugs like bifinhydramine, okay? Remember bifinhydramine, right? It is a powerful muskonic receptor. It's a benadural, right?

But it probably has the most powerful muskonic receptor blocking properties of all the first generation anti-histamines, right? So, because it can block muskonic receptors, it's very sedating, right? It actually kind of works like scopolamine, right? Because again, being a paffelenthymoschronic, it can actually help with motion sickness. And again, please, because this drug has anti-cholenergic activity, right? You certainly do not want to use this in the elderly, right? It can cause delirium, and it can cause like urinary retention, right? And another awesome thing about bifinhydramine, coming shop on a site question is about a person that's taking a drug for schizophrenia, right? Like an anti-psychotic, and then they ask you about like, like acute dystonia, right? You can actually treat that acute dystonia, right? And some of the Parkinsonism features by giving diaphinhydramine, okay? Again, taking advantage of its anti-muskonic properties, right? Because remember, one of the ways you can treat one of those extra pyramidal symptoms is to give bench tropine. Bench tropine is a muskonic receptor antagonist, right? So, you can take advantage of all that, you can take advantage of all that stuff by giving diaphinhydramine because it has those anti-muskonic properties that you're looking for, right? And then another high yield, first generation anti-histamine is super-hyptidine, right?

The main reason I'm talking about this is it's a serotonin receptor antagonist as well, so you can actually use it to treat a serotonin syndrome. And then there are other high-yield anti-histamines that are H1 first generation, drugs like diamond hydrinate, like clofeniramine, like promethazine, right? Promethazine, I'll say it's probably used primarily for its anti-emetica properties, but it's also pretty sedated. Now, again, these are first generation H1 blockers, they're used primarily for allergies, but one thing that has actually come out from studies, fairly recently, is that these drugs are really increased this risk for Alzheimer's, so I know there are people that take this just chronically to help with sleep, I will encourage you to probably stay away from these drugs, at least you don't want to use them all day, every day, for weeks and weeks and weeks and months on end. It's probably not a good life strategy because again, kind of think about it, kind of makes sense, right? For Alzheimer's, we use acetylcholine esterase inhibitors, right? So like the Nepezel galantaminin-reverse stigmin, to boost acetylcholine levels. So if you're chronically taking a drug that blocks acetylcholine receptors, you can see how that could potentially spell trouble for a person in the future. Now, now that I've talked about the first generation, I'll just talk about the second generation real quick, these drugs, they cannot cross the blood-brain barrier, right?

So because they cannot cross the blood-brain barrier, right? They act primarily in the periphery, and they do not block most screening receptors, so the key drugs you want to know here are drugs like aluratidein or satyrzine or faxofenidine, and again, these drugs are used for allergies. If a presence chronic allergies probably makes more sense to take these drugs chronically than to take the first generation, until he's the means, given all the side effects they have. Now, the next drug I'll talk about here is a dextromethorphen. Dextromethorphen is, it has many properties, so first thing's first, it's an MMD receptor blocker, and it's also actually a weak, opioid receptor agonist. The main thing this is used for is used as a cough suppressant, and the thing is, if you take a superficial logic dosage of this drug, you can actually have a profound respiratory depression, because again, it activates opioid receptors, and you could actually reverse this with meloxone, it's just one of those weird high-ealted bits you want to know for your step one example. And then, the next drug I'll talk about is Guafenacine. Guafenacine is a mucolytic, right? It's used mainly in cystic fibrosis patients, because all that mucous they sort of cough up, right? It can help you break up that mucous. Now, please, please, please, do not confuse Guafenacine with Guafacine. Guafacine is a totally different drug. It's an alpha-2 agonist that actually works kind of similar to colonidine, okay?

And it's high young to remember, right? I've talked about this in a previous podcast, but high young to remember that one vaccine is used primarily for Tourette syndrome, right? It's used for Tourette's, because think about it, right? If you release like less norepinephrine, right? Because remember, alpha-2 agonist, the alpha-2 receptor is a GI-copyriceptor, so when you activate it, you release less norepinephrine, right? So, if you release less norepinephrine, that can potentially calm down someone that's kind of agitated, right? So like, Tourette syndrome, or even in ADHD, Guafacine is actually also used for ADHD. And while I'm on this tangent, please also don't forget that colonidine is used to treat opioid withdrawal, right? Because it basically works like an opioid, right? Opioids by binding to new receptors, they prevent the release of caracolomins, well, cloning them by binding to alpha-2 receptors, it prevents the release of norepinephrine, which is a caracolomine, right? So, cloning them is actually beginning to become a street drug in a many locales. Okay. And I guess while I'm on this, Guafana-Singuan-Fasim business, don't forget Prazosine, right? Prazosine is an alpha-1 blocker, right? It's used to treat the nightmares associated with PTSD, right? And then don't forget metasapine, right? It's an alpha-2 antagonist, it's used to treat depression, but it can cause weight gain, right?

So it's very good for, like, depression in a patient with anorexia nervosa, for example. So again, Guafana-Singuan-Fasim is a mecholetic, but don't confuse it with these other drugs that have somewhat similar sounding names, but totally different effects. Now, next drug I'll talk about is Dorni's alpha, okay? Dorni's alpha, it's used in cystic fibrosis primarily. It sort of breaks up DNA, right? That's made by inflammatory cells in the early again, to also help with clearing up secretions. But on Guafana-Sing, right? That on Guafana-Sing, Dorni's alpha actually works by breaking up phosphodiester bonds, okay? Now, the next pulmonary drug I'll talk about is like ridiculously high, right? Anacidocystine is almost like a wander drug because it does so many things, right? Basically, anacidocystine is an analog of glutathione, right? It's like reduced glutathione, essentially, right? So it helps a lot with dealing with oxidative stress. So what are the things we use anacidocystine for? And again, I promise you, you need to know all these things for your exam. First thing is, you can use it to treat acetaminophen toxicity, right? Because it helps you deal with like NEPQI toxicity, right? I've talked about that pathway in a prior podcast. You can actually also use anacidocystine as profile axis against the contrast nephropathy, right? Because again, you'll mop up free radicals in the kidney from contrast.

And then in cystic fibrosis patients, because anacidocystine can break disorfide bonds, right? You can actually use it to break up mucus plugs in CF patients. And then another thing that anacidocystine actually does is it can actually be used to treat the hemorrhagic estytis that's associated with cyclophosphamide, right? Remember that hemorrhagic estytis is mediated by a metabolite of cyclophosphamide known as acroline, okay? So cyclophosphamide metabolite to acroline, acroline is a bad vasocan, it can scrub your bladder, right? So you can sort of prevent that by giving an acetylocystine to mop up all those free radicals. And while we're on the topic of hemorrhagic estytis, don't forget that hemorrhagic estytis can be caused by adnovirus, right? Which can also cause a faringo conjunctivitis, right? So like pink eye and soft throat. And don't forget that she's to somahematobium, right? So if they give you an Egyptian with pinless hematoryria exam, think about hemorrhagic estytis with she's to somahematobium. Now one way thing I'll just see here since I'm sort of diving into that topic now is if step one asks you about the first immunoglobulin that is made when you're exposed to an allergen, resist the temptation to pick IgE, it is actually IgM, right? You need to class which would IL4 for you to make IgE but again, if you're exposed to an allergen, the first immunoglobulin you make is IgM, that is like super super super super super high yield to know.

Now but after you have like say for example the second exposure, right, to the allergen and then that's where you have IgE already, right? Because you've had all that class switching and all that fun stuff happen. And the thing is IgE, right? Again, IgE can not just work on it's own, right? It needs to bind the allergen and then bind to the FC epsilon receptor and mass cells, right? When allergen binds to that IgE, you have cross-linking of those FC epsilon receptors that causes degranulation of mass cells, right? So if you want to basically prevent that mass cell degranulation that can cause a lot of allergy symptoms, right? Or inflammatory reactions that you can see in asthma for example, you can try to actually block the constant region of IgE by giving a drug like Umalizumab or you can essentially, you know, and again, this is more for prophylaxis, right? Because obviously if you've been exposed to the allergen already and you don't have the drug on board, you already kind of screwed, right? But if you have that constant region of Ig already bound, you can use it as prophylaxis, right? You can use it as a, you can use it as prophylaxis. Now alternatively, right? You can also actually like, this is like a teleological explanation, but it works. You can actually try to almost, I guess, like a suture mass cell membranes together with drugs like a neocromyl or chromolyne sodium.

Those drugs are mass cell membranes stabilizers that can be used for the treatment of allergies or prophylaxis against allergies. Now, I'll say some more things about those drugs in a bit. Well, let me say some things about a bronchodilation, right? So there are certain things that can cause early bronchodilation, right? One thing that can do that is if you activate beta-2 receptors, remember, right? Beta-2 receptors, they are GS couples who cyclic AMP increases. Alternatively, you can just block most chronic receptors, right? So if you're sort of thinking and reverse with that, right? Think about methecoline. Methecoline is a most chronic receptor agonist. It can be used in a provocative test for asthma, right? And again, let me just stay this again. I was kind of mentioning it already, but again, let's just sort of make this very clear. If you increase cyclic AMP, that causes smooth muscle relaxation and bronchodilation. Another thing is if you actually increase cyclic AMP, you will also get smooth muscle relaxation and bronchodilation, right? And alternatively, if you also blocked lucotrain receptors, right? You can also get bronchodilation, right? That's something that's done, that's something that's done in asthma therapy as you'll see in a bit, right? So because the thing is lucotrain actually causes smooth muscle contraction, right? So you can get bronchod contraction under those circumstances. So what's the pathway to creating lucotrain?

The first thing that happens is membrane phospholipids, right? They are converted to arachidonic acid, but an enzyme known as phospholipase A2, remember phospholipase A2 is actually inhibited by corticosteroids, right? And then arachidonic acid can be converted to lucotrain by an enzyme known as five lipoxygenase, five lipoxygenase, right? And then those lucotrain that you've produced, then act on lucotrain receptors, right? And again, don't forget that the lucotrain receptor is known as the cis LT1 receptor, okay? Is known as the cis LT1 receptor, and you say, oh, divine, what are you saying? How can this be high yield for step one? Well, think again, there are actually some receptors that are very high yield to know that you have to like re-gurge word for word on exams. One is the cis LT1 right? That's the lucotrain receptor. Another one is the P2 Y2 receptor, right? That's a receptor found on platelets, and then another is the angeotensin 2 receptor on blood vessels. The angeotensin 2 receptor is known as the type one receptor, so you can see how confusing that is and how likely your friends at the MBMER to sort of test those on exams. So back to lucotrain, right? So I will say that one high yield lucotrain, you probably want to keep at the back of your mind, is lucotrain B4, okay? It's a chemotactic factor for neutrophils, right? Same thing with interlooking 8 and C5 A. Those are all chemotactic factors for neutrophils.

Now, another thing I like to do is I've talked about it, and again, I will mention drugs in a bit, but I just want to walk you through these pathways. Another thing I like to do is I can do instead of going down the lipoxygenase pathway to make lucotrainases, it can also go down the cycloxygenase of the cox pathway to fomperstaglandins, right? So the thing is, let's assume you irreversibly inhibited cox with aspirin, right? You can go something known as aspirin-exacerbated respiratory disease, right? Because again, by giving aspirin, you kill the cox pathway, so that will increase, that will increase a flux through the locks or the lipoxygenase pathway, so you make molecule trines, right? So that's the potential pathophysiology behind aspirin-exacerbated respiratory disease, and classically, this disease is associated with a nasal polyposis on exams. Now, some other high-youthins that associate with nasal polyps, are things like cystic fibrosis or like a wegnaz agranolumatosis. I believe that's the thing that's known as agranolumatosis with poly and G Itis, right? So that's kind of like one high-youthin you want to know, for exams. So think about this, if you know the pathophysiology behind aspirin-exacerbated respiratory disease, then that tells you that you know what, if increased flux through the lipoxygenase pathway can cause problems, then maybe you should block that lipoxygenase pathway to treat aspirin-exacerbated respiratory disease.

So you can give drugs like xyloton, right? That's a lipoxygenase inhibitor, it inhibits the actual enzyme that converts arachidonic acid to luchotriens. Only problem is xyloton is not great for your liver, so it's not commonly prescribed. Alternatively, you can block those luchotriensis LT1 receptors with drugs like a Monte-Lucast and Zerfelocast. Those drugs are actually good for the treatment of AERD. Now, let's go to asthma, right? So asthma have talked about all the high-youth relevant receptors, right? So let's start with asthma treatment, right? So the thing is, for asthma treatment, obviously you want to cause bronchordialition, right? So you can do this in many ways. You can give a beta-2 receptor agonist, as I described already. And those beta-2 receptor agonist can either be short actin, right? Like a uterine or long actin, like just remember some Francisco, like SF, that's some meterine and formodero. These beta-2 agonists, right, they're used for asthma, albederol, right? You usually use it for like an acute asthma exacerbation because it's short actin versus some meterol, formodero, you can use them for chronic asthma therapy, right? They're not going to help you acutely. And then you can also use these beta-2 agonists for the treatment of COPD. And then don't forget that albederol, by being a beta-2 agonist, it also has the ability to activate the sodium potassium ATP espomp.

So you can actually use it as one of the treatments for acute hyper-kilemia, as soon as you throw that in there. Now, one weird thing you, they probably expect you to know for step one is if you're trying to treat asthma, right? First, you need to start with albederol as needed, right? If that's not controlling symptoms, you then add inhaled corticosteroids. If inhaled corticosteroids are not controlling symptoms adequately, then you add something known as a lab, a long actin beta-agonist, right? Or you can actually add a luchotrain blocker, right? Like Monte-Locasters or Félocaster. So what am I saying this? The thing is you should never use labas monotherapy. If you use them, actually, if you use them as monotherapy, there's actually an increased risk of a death when you use those drugs as a monotherapy. And then if labas and luchotrain blockers are not helping asthma symptoms, last-line in asthma, like the oral steroids, right? So like P.O. steroids. Now, for us, again, to cause bronchodilation, another thing you can do is you just block most grainy receptors. You can do it in short actin-faction, we drugs like epitopium or in long actin-faction, we drugs like tiotropium, right? Remember, can I easily remember that is that T is later than I in the alphabet? So T should be, tiotropium should be long actin, epitopium should be shorter and again, these drugs are used to treat asthma and COPD.

Alternatively, remember, I say that an increase in cyclic AMP causes smooth muscle relaxation and bronchodilation. So one thing you can actually do is you can try to both stop cyclic AMP in the smooth muscles of your airway to treat asthma symptoms, right? And one way you can do that is you can inhibit an enzyme known as PDE-4, FOSFODYSTORIS-4. FOSFODYSTORIS-4 is an enzyme that breaks down cyclic AMP, right? So you can do this with drugs like a fioffelene, right? So fioffelene, it can inhibit PDE for increase your cyclic AMP, right? You can actually use this to treat asthma and COPD. The thing is fioffelene also has the ability to block adenosine receptors, okay? Because again, it's a methylzane thing, right? Kind of like caffeine. So the thing is if a patient is on fioffelene chronically, you cannot use adenosine in V in those kinds of patients, right? To break a thaky arrhythmia because it will not work, right? Because you've essentially blocked those adenosine receptors so they will not respond. They will not respond. Okay. Now, another thing with fioffelene is that it can actually increase conduction through the AV node. So contrast this with, I sort of think of fioffelene as like the evil twin or the, I think of it as like an adenosine archrival or something like that. Because the thing is adenosine slows conduction through the AV node. That's how you use adenosine to break thaky arrhythmias. But fioffelene actually speeds conduction through the AV node, okay?

That's actually why fioffelene can cause thaky arrhythmias. That's why fioffelene is not a commonly prescribed medication. And then there are drugs that have the ability to raise your cyclic GMP. There is a drug known as a rio-seguat. Rio-seguat activates one little cyclase. You can raise your cyclic GMP. You can get smoth, muscle relaxation, and then bronchodilation. So you can actually use this drug to treat COPD. It's not really used to treat asthma. It's used more for the treatment of COPD. Now, the Lucotron receptor blockers, I've kind of mentioned those already, C-Celti-1 blockers, Monte-Locas, the fellow cast. These drugs, so they may be a weird thing in issue on step one, or you may read about in books, right? That these drugs associated with a truck-strel syndrome. So the thing is, it's not that these, and again, just to make ends clear, truck-strel syndrome, no one really calls it that anymore. Trox-strel syndrome is actually known as, excuse me, it's actually known as EGPA. So, it's a rio-seguat. Excuse me, wow. It's a rio-seguat, granulomatosis with polyangitis. That's where basically a person has like granulomas in the long, they have it, a rio-seguat, and they have asthma. The thing is, these drugs, they are usually given as steroids perine agent, right? It's like, oh, you can use these drugs to treat like inflammatory airway disorders so that you don't have to take steroids because steroids have all these bad side effects.

But the thing is, if a person was already on steroids, those steroids may have been suppressing whatever inflammatory disorder they may have as a sort of like a side benefit to treating whatever airway problems they have. So the thing is, if you then start taking luchotrain receptor blocker, like Zafelokas, Montelokas, you stop taking those steroids. Those other inflammatory disorders that a person may have had, like Chok-strel syndrome, that we're sort of treated as a side benefit without you even being aware of because we're taking the steroids, they may basically unmask themselves. So that's why there's this association between the luchotrain receptor antagonists, right, or like I guess, Zaluton, which is a lipoxygenase inhibitor, and Chok-strel syndrome. So you're sort of those weird things you just want to keep in mind, and that's the potential explanation behind why that is the case. Now, I've talked about the mast cell membrane stabilizers, right, so like Chromoline, Neidocromyl. Those drugs stabilize the mast cell membrane, you can use them as like asthma, prophylaxis, or like allergy prophylaxis. And while we're on the topic of like, stabilizing membranes of weird stuff, right, one important thing you probably want to know, right, or sort of correlate is a drug like calcium gluconeid, right, you can use it to stabilize the myocardial membrane, right, if a patient has a hyperchylemia, right. What am I seeing this? You're like divine.

This doesn't really, this is a, this is a, a, a, a, a, a, a, a, a, Reno review, anything like that. Here's one wasting time on that. The first thing is, the first thing is, step one may give you a question where they describe something, and then they can see which of the following drugs acts in similar fashion, or has a similar mechanism of action to whatever drug dimension in the Q-stem, right. You want to make that connection that, oh, stabilization of a membrane can be something that can be done by calcium gluconeid in the realm of Reno or cardio, versus neidochromyl and chromolyne that can do the same thing in the realm of terminology. So just one of those weird things you want to keep at the back of your mind. And then I've talked about umalizumab that is, you know, basically used for the treatment of asthma, especially as prophylaxis, especially in the pediatric population. Three of the kids that have like cystic fibrosis, right, you don't want them to get like a superimposed like asthma attack or something, right, that can kill them pretty quickly, right, so you can prophylax by giving them umalizumab. And then the last thing I will say on that terminology is, uh, is a pulmonary hypertension, okay, pulmonary hypertension. The classic case here is a young woman, maybe in her 30s, that's having like, you know, chronicly increased shortness of breath, and then you do an echocardiogram, you'll see like high pressures in the right ventricle.

Um, remember this is associated with a BMPR-2 mutation, I think it's like bone morphogenic protein receptor two, okay, uh, it's associated with a BMPR-2 mutation, right, so like pulmonary arterial hypertension. So the person has pulmonary arterial hypertension, well, you can try to treat this by dilating those pulmonary vessels, right, so you can do that with a few drug classes, right, one drug class, I like your prostaglandin at the logs, remember, prostaglandins dilates things in general, right, so they can dilate those pulmonary vessels. So drugs like epoprostinol or Iloprost or treprostinol can be used for the treatment of pulmonary hypertension. Those drugs all have prostin in the name, so they are easy to remember. Alternatively, you can give a PDE5 inhibitor, right, because remember, I told you that PDE4 breaks down cyclic AMP, right, but PDE5 breaks down cyclic GMP, so if you wanted to increase your levels of cyclic GMP and basically treat pulmonary arterial hypertension, you can give a PDE5 inhibitor, right, because by inhibiting PDE5 your cyclic GMP keeps going up, right, and that can cause spunt muscle dilation and vasodilation.

So you can use drugs like cell dynaphyl and tadala phil, okay, remember those drugs are used for erectile dysfunction, we can also actually use those drugs as well for pulmonary hypertension, right, so but don't forget though, you don't want to give these drugs along with nitrates or with hydrozene or like alpha-methodopa or prazocin, right, because remember that all those drugs are viso-dialiders, right, so you can cause like life threatening if you give those two drugs together, and then I guess the last drugs I'll talk about are the endothelian receptor blockers, endothelian is probably the most powerful viso-constructor in the body, right, so you can try to treat pulmonary hypertension by giving an endothelian receptor antagonist, you can block, I mean there are multiple endothelian receptors, there's like endothelian A, there's endothelian B, so you can block endothelian A receptors by giving a drug like ampersentan or you can block both endothelian A and B receptors by giving both sentan, okay, those drugs actually used to treat pulmonary hypertension, but they're like super expensive, so I guess that's the end for me with this pulmonary pharmacology, I hope you find this helpful and useful for your exams, if you have any questions please don't feel free to send responses my way, some people have actually suggested that I try to make my podcast available on like a podcast app or something, trust me I've tried, I don't know for some reason, I don't know if it's a software issue or what, but I've tried multiple times and I've not really had any progress with that, like I always get like some error message or something, when I try to add it to like Apple podcasts, so I'll try again when I'm off my I see rotation, and then I just want to throw this out there, I offer tutoring for many exams, like step one, step two CK, step two CS and step three, and also offer tuto

ring for the internal medicine, training exam, and also for the MCAT for certain subjects, not all subjects, and then I also prepare applications, right, so like ERAS applications or like AMCA's applications for med school, and I do like mock interviews, I help with preparing like personal statements, and all that stuff, so feel free to reach out to me if you want to do if you want to tutor in for any of those things, I have tons of experience, I've worked with thousands and thousands of students, so just reach out to me and I'll be happy to work on that with you, so I wish all the best, have a wonderful night, and I will see you in episode 67, God bless.

IgM. Remember that IgE requires class switching (mediated by IL-4).

Deficiency of C1s inhibitor, leading to uncontrolled bradykinin levels.

It is an $\alpha_2$ agonist that reduces norepinephrine release from sympathetic nerve endings.

Second-generation antihistamines (e.g., loratadine, cetirizine). This limits their central side effects.

They inhibit phosphodiesterase type 5, preventing the breakdown of cyclic GMP (cGMP), thus causing smooth muscle relaxation and vasodilation.

Cromolyn or Nedocromil.

It acts as a glutathione analog, helping detoxify the toxic metabolite NAPQI and reducing oxidative stress.

ACE inhibitors break down bradykinin; since HAE patients already have impaired breakdown via C1s inhibitor deficiency, adding an AC Ei can dangerously elevate bradykinin levels.

$\beta_2$ agonists stimulate adenylyl cyclase to increase cAMP; PDE-4 inhibitors (like roflumilast) prevent the breakdown of existing cAMP, thereby increasing its concentration.

Prazosin.

Aspirin-Exacerbated Respiratory Disease (AERD). The mechanism involves COX inhibition leading to increased LOX flux.

It acts as a glutathione analog, helping detoxify the toxic metabolite NAPQI and reducing oxidative stress.

ACE inhibitors break down bradykinin; since HAE patients already have impaired breakdown via C1s inhibitor deficiency, adding an AC Ei can dangerously elevate bradykinin levels.

$\beta_2$ agonists stimulate adenylyl cyclase to increase cAMP; PDE-4 inhibitors (like roflumilast) prevent the breakdown of existing cAMP, thereby increasing its concentration.

Prazosin.

Aspirin-Exacerbated Respiratory Disease (AERD). The mechanism involves COX inhibition leading to increased LOX flux.