DIP Episode 198 - Clutch Hypertensive Integrations

Okay, welcome my name is Devine. I'm a resident. This is episode 198 of the Divine Intervention Podcasts. And in today's podcast I'm going to be talking about like just high yield anti-hypertensive integrations for the USML Step 1, Step 2, Siegians, Step 3 exams. I will say this is this podcast should be relevant to pretty much anyone taking any of the USM Ls. At the same time as I'm recording this podcast I'm also trying out this video format. I'm trying to record actually record this video at home, believe it or not. I just want to see how it works and then I'll probably put it on the You Tube channel and see if this is a format that people are also interested in because hopefully in this new year we really want to make a lot of videos that hopefully people should find to be helpful. So let's just jump right into it. So what if they give you a question about a person that's pregnant and they ask you to recommend an anti-hypertensive. So I mean this is just going to be a game. Kind of like my podcast right. It's just going to be like a regular discussion. So what kind of anti-hypertensive would you want to give in pregnancy? Well I hope you're seeing something along the lines of like hydrozene, right? So remember you can give like hydrozene, you can give alpha methyl dopad, right? You can give labidolol, right? In fact and then you can also give my therapy.

In fact there is this nomonic that I learned back in the day when I was studying for step one that's hypertensive moms love my therapy. So hypertensive moms love my therapy to essentially help you remember the anti-hypertensive that has even pregnancy, right? So hydrozene is one of them. Alpha methyl dopad is another labidolol is another and my therapy is. One thing that your friends at the NBM love to test pretty commonly actually is how you should never give an ACE inhibitor or an ARB to a pregnant female. You do that. You're putting that baby at risk, right? Because those anti-hypertensives are heterogeneous, right? They can cause renal dysfunction in the fetus so you don't want to do those. Now what if they give you a question about a patient you know that has hypertension and you know potentially has stable lunges at the same time. Is there a drug you want to add to his anti-hypertensive regimen? Well I hope you're thinking in terms of a nitrate right? Nitrates are amazing right for treating anginal right because they dilute your coronary vessels, right? Although that's a minor effect the predominant effect of nitrates is that they have venodiliders and if you dilute veins right that will decrease the preload that the heart is facing and if the heart is seeing less preload then the heart is going to not have to use as much oxygen. So the myocardial oxygen demand goes down.

When a person is sticking a nitrate that's the primary mechanism behind nitrates being useful for the treatment of anginal because many people think oh it's because they're predominantly coronary vessel dilators that is actually not true. The thing they do is they decrease the myocardial oxygen demand so by decreasing the myocardial they do that by just putting less preload so your end astolic volume actually goes down when you're replaced on a nitrate right? So your heart does need to expand as much energy. Now what if they give you a question about a person that is hypertensive and the person has migrates? Is there a particular kind of drop or drop class you're going to give that person? Well I would hope you're telling me something along the lines of like a bit of blocker right? So bit of blockers they're pretty good for the treatment of hypertension. They work really well but they also I mean they're not grateful hypertension but they're good for migrates right? And again by migrating therapy I mean like chronic migrate therapy right? So obviously if a person has an acute migraine you're going to go ahead and give them a trip time you're going to give them like so much return, rise a trip time something like that right? But if a person is having like eight or more migraine episodes in a month right then you want to give them something a little better right?

Something that can profile out against migrates so that they have fewer migraine attacks and you'd want to use something along the lines of like a non-dihydroperadiene calcium channel blocker right? Alternative so something like verapinilodil tyazine those are pretty help with migraines but another thing you also want to use is you want to use a bit of blocker like a non-selective bit of blocker like perprone long those are also pretty good in terms of perphylaxis for migrates. Now what if they give you a question about a person and they tell you that this person has a histral hypertension but they also have a histral like systolic heart failure any heart failure for that matter and they have like peripheral edema. Then what drug class would you want to give those people that would also help with your hypertension and the edema? Well I hope you're telling me a lube diuretic right? So remember your lube diuretics so drugs like ferozomide, fumetanide, torsomide, ethycrinic acid. And remember if the chrynic acids clip to thing is that it doesn't have the sulfur allergy that's associated with the other lube diuretics right? The other lube diuretics contain sulfur groups so the person has a bad sulfur allergy, the lube diuretic the other lube diuretics with the exception of ethycrinic acid probably not the best idea in the world. Now what if they give you a question about a person that has hypertension?

Well this person also has a histral osteoporosis what kind of drug would you want to give those people? Well I hope you're telling me you want to give them a thiazide. Remember lube's luce calcium, but thiazides retain calcium right? So if a person is placed on a thiazide and the mechanism behind this already described it in my renal podcast I think that's like an episode in the 50s on my website and the website by the way is the Vine Intervention Podcasts with an sdm.com you can find all my podcasts there so this is episode one I eat and basically right thiazides they help you reabsorb all calcium in the nephro right? So they're actually good for a person that has like a histral like nephrolethyases right? And they also go for a person that has a histral osteoporosis because they're essentially causing a hypercalcemia but at the same time they are causing a hypocalcyory so they are good from that perspective they are very very good at you know raising your blood calcium level so they are helpful if a person has a histral hypertension and osteoporosis right? Now just going off of that nephrolethyases business that I talked about remember thiazides are good for nephrolethyases because they reduce the amount of calcium that's in your urine but your lube diuretics are bad for a person that has a histral nephrolethyases right?

Because by giving a lube diuretic remember again lube smic you don't calcium in the nephro if you don't want calcium in the nephrored right then you have a higher risk of having that calcium precipitate and cause like a calcium nephrolethyases right? So lube diuretics are maybe not the best idea if a person has a history of nephrolethyases and they have hypertension. Now what are the anti-hypertensives that are decent in a person that has a histral heart failure? Well basically they are essentially asking you the question what are the drugs that improve survival in heart failure right? You want to think about about drugs that are more along the lines of like your beta blockers in fact there's some specific one there's specific ones there's like metoprolol right there's the cavidilol and then there's extended there's like the subprone law right? So like MCB right? so like metoprolol cavidilol and the subprone law those drugs they have all been shown to improve survival in heart failure right those are your beta blockers remember your ACE inhibitors and your AR Ps have also been shown to improve survival in heart failure right? So drugs like your lysinopril or your condesartan or your telnesartan those drugs improve survival and then you are those from a receptor antagonist right? So like spermolactone, plerinone right?

those are also improve survival and then if you're looking at a person that has a history of like an African American with heart failure you can also give the drug known as bideal bideal is like a combination of isosobide and nitrate and hydrozine it helps quite quite a lot to actually control our symptoms with hypertension but it also helps with heart failure symptoms right? So again the basic construct I'm going after in this podcast is for person has hypertension and certain other chromorobility that may guide the kind of therapy that you're going with with regards to hypertension and then if a person for example has a history of hyper thyroid is it right? And they have a history of hypertension what drug can you give to kill two birds with one stone? Well I hope you're telling me that you're gonna give those people a beta blocker right? You give those people beta blockers because beta blockers right? Especially for Prano long remember it inhibits the 5-prime diodinase that converts T4 to T3 in the periphery right? You remember it's one of those drugs you can use for thyroid storm right?

But again beta blockers yes they are not first line for treating hypertension but for presence hypertension and this chromorobility of having the chromorobility of having like hyper thyroid is a more thyroid storm blah blah blah blah blah then yes those people they'd be reasonable to go ahead and give them give them a beta blocker especially like a Prano long now what if they give you a question about a person that has a history of hypertension? Well this person at the same time also has a history of BPH what drug class would you want to consider in that person? Well I hope you're telling me that you want to give them an alpha one blocker right? Remember you alpha one blockers are drugs like Prano sin, Terazo sin, Doxazo sin by blocking alpha one receptors you decrease systemic vascular resistance and that should lower a person's blood pressure right? But also by blocking those alpha one receptors you open up that bladder neck right and the person's bladder will be able to drain better right? So if a person has a history of BPH and you have a history of hypertension then an alpha one antagonist is not a terrible idea and just as an offset remember when if a person has you know just BPH and you don't want to tank their blood pressures then it may not be a bad idea to give them the alpha one blocker times ulose. Remember times ulose is an alpha one AD receptor antagonist right?

So AD as an Anthony Davis you can probably tell at this point from my podcast that I'm a Lakers fan but basically an alpha one AD receptor blocker. The alpha one AD receptors are found predominantly in the bladder and if you don't really find them in the vascular tree so they can essentially work specifically on the bladder right but they will not necessarily work on the bloodstream okay but again the big picture thing here the other history of BPH have hypertension they're getting put on an alpha one antagonist and then what if they give you a question about a person that is hypertensive and the person has a drug cough what kind of side effect at the experience what drug class is causing that side effect well I hope you're telling me that it's an ACE inhibitor right?

Remember ACE inhibitors the incubator is a transient converting enzyme right and ACE the enzyme is also something that helps you bring down really kinding so if you're not able to bring down really kinding the unfortunate thing that will happen is you have elevations if you're not able to bring down really kinding because ACE has been taken out of the equation then your levels of really kinding will go up and now potentially precipitate the dry cough now we see usually your next step in management on in-beaming exams for those folks is to go ahead and switch them to an ARP to an under-tensing 2 receptor blocker and something just came to my mind there is one question by your friends at the in-beaming occlusion law to test and they may ask you where is the site of action of an ACE inhibitor right and then they may put kidney as an answer choice again you don't want to make that kind of mistake because think about it where do we find a potential convert in enzyme we find in predominantly in the lungs right in the along the endothelial cells that constitute the long capillaries right so the site of action of an ACE inhibitor believe it or not is in the lungs you may say oh definitely that's kind of obvious but that's not something that people think about all the time so it's just something again to keep in mind as you're taking these exams now what kind of anti-hypertensive will be contraindicated in a person that has a history of hereditary dima or bilateral and all other stenosis well I hope you're telling me an ACE inhibitor and ARB right because again if you think about it if a person has hereditary dima they have a deficiency of an enzyme known as C1stres inhibitor and the thing is again C1stres inhibitor helps you break down really kind so the thing is it's bad enough you're already inhibiting ACE which helps also not superdumbed kinding if you're conquering them y

ou have a deficiency of C1stres inhibitor then you're not able to break down really kinding and then that patient gets in trouble for sure right there their throat closes up and all that badmits right so you know you don't want any of those things right so that's why ACE inhibitors ARB is baddened people that have a history of hereditary dima but they also baddened people that have a history of bilateral or in a lot of stenosis because again if you think about it if a person has been a lot of stenosis what is happening to the proficient of the afrin atyrus?

it's not great right so the hydrostatic pressures in your glomerular capillaries are in the toilet they're terrible right so your body is like okay since my hydrostatic pressures in the glomerular capillaries are in the toilet let me try to fix this by revving up the ring in and retention of the sterling system making more and retention too and then causing a constriction of the effrin atyr well if that happens you know that raise the hydrostatic pressures in your glomerular capillaries that would be great and at least you will try to you essentially maintain your renal profusion and your glomerular profusion pressures but if you take an ACE inhibitor and ARB and you take and you tend to out of the equation you'll blunt that body's like response to try to fix that problem then the thing that will ultimately happen is that the effrin atyrial will not be constricted anymore so that will tank the pressures in your glomerular capillaries some more and then the patient gets into big big big trouble right so that is why primarily if a person has bilateral renal otters to know if they should not give those people ACE inhibitors or AR Bs the classic way that tends to show up on MDM exam is they will give you a question about a person and they will tell you that oh this person has a histone hypertension area area and then they will tell you that oh this person was placed on lysinopryl or something right and then they will give you a lapse like one month ago when the drug was started and labs now maybe like yeah this person's kidney function is not doing well like the creatinine was like 1.2 back then that's like 2.1 what's up with that right and they will have like hyperchylenia because they are retaining potassium and hyperphosphatine because they are not retaining phosphory because the kidneys don't work if you see that think that's essentially a back hands wheel of your frie

nds at the MDM asking you essentially testing you about a person having renal otters bilateral renal otters to know how to get the potential cause of the hypertension to start with right so again those are I know you may see all the money you've been superspeed here but I promise you these things are very high you to know for purposes of the US Emily exams now what if they give you a question about a patient that's on a diuretic for hypertension right like a thiazide like hydrochlorothiazide for hypertension and in detail that this person is hypokivemic and then the S for your next best step in management what do you want to do well I hope on that those circumstances you're thinking about adding a potassium sparing diuretic right so from something like an outdoor receptor antagonist like spurnolatone or pleurin or remember spurnolatone causes the big big boobies right so the ganycomastia where the pleurinone does not because the pleurinone does not have the added mechanism of action of being able to block androgen receptors right and also your inachinal blockers like amelorite and triamterine right those also potassium sparing diuretic so you're taking advantage of your hyperkalemia side effects to temper the hypokillemia side effect that's associated with taking a regular diuretic like a loop or a thiazide again that's a high yield concept to know for example now what if they give you a question about a person that is hypertensive because they have con syndrome right remember con syndrome is also known as primary hyper-adosteronism what kind of drug would you want to give those people I hope you're telling me again you want to give them an aldosterone antagonist right because again you're essentially attacking the primary pathophysiology of what those people have right because again by taking an aldosterone receptor antagonist right you're essentially blocking aldost

erone receptors so the con syndrome the adrenov critical adrenoma that's making a ton of our aldosterone you're essentially taking that out of commission right because again you're essentially limiting the ability of that aldosterone to function in the presence but by blocking those receptors now what do they give you a question about a patient that was recently studied on an anti-hypertensive and then they develop a Miller rash what should we be thinking about well I hope you're thinking about like drug-induced lupus right remember drug-induced lupus can be caused by like yourself phonomites can be caused by hydrozine which will be the answer in this case and then isonize it which is a TB drug phenetoin can also cause drug-induced lupus right proquinamide can also cause drug-induced lupus so they could also just make a question about a person that has a history of WPW it's now been well controlled and then the person develops a Miller rash again think of drug-induced lupus and then in tonn recept that's a decoy receptor against the TNF alpha can also cause drug-induced lupus right but in this case person be treated with an anti-hypertensive and then they develop a Miller rash think about drug-induced lupus from hydrozine okay think about drug-induced lupus from hydrozine and this idea just again kind of popped into my mind so I don't forget if a person has a erotic dissection given hydrozine is a terrible idea you always get that in the question wrong if you do that hydrozine actually worsens outcomes if you use it to lower persons blood pressure in the setting of an erotic dissection again very high you to know that for purposes of the years and the exams now and remember that you're drug-induced lupus right as result like anti-hystolantiba that's just a factor you're doing to commit to Miller now what if they give you a question about a patient you know that has a

history of hypertension but also has a history of like bipolar disorder right and is there a particular kind of anti-hypertensive it's sort of kind of a diuretic that can help with like lithium toxicity from bipolar disorder so see for example like a nephrogenic diabetes insipidus or they have the tremors or whatever from lithium how what drug can we use specifically to help with the nephrogenic diabetes insipidus that's also an anti-hypertensive well I'll hope you're telling me about the in-external blockers right again like amelioride and triumtory remember lithium if you remember from genchema also tuberculosis or college courses if you sort of think back to general chemistry remember that lithium is in group one of the periodic table kind of like sodium I think lithium is like element three and then sodium is like element eleven right so they all use the same because they have like one ultra-most shell you like you know like a low-linked electron that's reactive right the you know they have very similar chemical properties so that in a channel you find that the level of the principle cell of the collecting duct believe it or not lithium also uses that to get in and screen the second second messenger system of of EDH right so that's how it causes nephrogenic GI so the thing is if lithium is using that in-external to gain access and cost problems then it would make sense that one thing you could potentially do is to you know just go ahead and give something I'll block that in-external like amelioride triumtory and those are really the drugs of choice in treating very high in treating the nephrogenic diabetes insipidus associated with the use of lithium now what if they give you a question about a patient that is being treated for a hypertensive emergency right and then this patient now develops like a lactic acidosis has like altered mental status what are you think

ing about well I hope you're thinking about like cyanide toxicity right remember classically when a person has a hypertensive emergency or urgency on an embankment exam the drug you would want to use is something like nitro-perside right now the thing with nitro-perside is that nitro-perside contains cyanide groups so for person has like a long nitro-perside in future that would potentially cause issues with cyanide poisoning right which is bad right and how do you treat cyanide poisoning well you can take one of two routes on an embankment exam you can give hydroxocobalamine it's like a vitamin B12 derivative alternatively one other thing you could do is you could go ahead and give sodium amelonitrate amelonitrate is a pathology that is an agent so we convert the hemoglobin that person has in the body at least some of this to methemoglobin remember hemoglobin has iron in the two plus form but methemoglobin has iron in the three plus four right methemoglobin is a very powerful binder of cyanide so if you give amelonitrate remember it's a nitrate so so pathology that is an agent so you give that you know the person will have an a very level of methemoglobin that bind of the cyanide and then give like sodium thiosolvite and then your form is complex known as thiosyanides that they can then pee and poop out successfully right so again high old stuff to know right and one of the usual questions your friends at the MDM could set up again this is just popped again you may notice from my because I feel like you know I've not really done much in real videos but if you listen to my podcast you may see me take all these side bars maybe see me take side bars is because of an idea just drop in my mind as I'm kind of like talking on the spot of the moment right so the thing is amelonitrate can I pretty see and the MDM you're writing a question where amelonitrate will be contraindi

cated in person that has a history of like G CxPD deficiency right because people that have G CxPD deficiency they cannot do an oxidative stress very well right so you don't want to give them something that is a powerful oxidizing agent like amelonitrate that'll actually be a genius of MDM question who knows maybe they're listening to this and they'll probably write a question that tests that concept in the future now what if they give you a question about a patient that has a history of hypertension and has PTSD is there a anti-pretensive that's actually great for PTSD well I hope you're telling me something along the lines of like Prasocin remember people that have PTSD they think to have like these nightmares these flashbacks Prasocin we know that our phone blocker is actually pretty good for helping with those nightmares that accompany PTSD so that will actually be a good drug again to treat that comorbidity I can totally see that being like a psych question on the USM Ls or a psychshop question in 30 now what if they give you a question about a patient that has a history of hypertension but they also have some kind of visospastic disease like Reynolds phenomena what kind of drug would you want to give those people well I would hope you're saying to give those people a dihydroproedic calcium channel blocker right so drugs like amelone the pain fellow the pain my favorite pain right those are dihydroproedic calcium channel blockers right they cause visodilation right so if a person has like a visospastic disease right so they can make it like a scleroderma question or they can even give you a question about a person that has a what's the name of this disorder burgers disease right that vasculitis that's found in smokers right so those people if they have hypertension a dihydroproedic calcium channel blocker may not be the worst idea on that those circumstances and the

n what if they give you a question about a person that has a hypertensive emergency or urgency what are the drugs you can give when an endemic exam already mentioned one you can give sodium nitropercyte right but on that role you can give you can give labella law you can give my cardipine or you can give clay VBP you see the one you're giving for specific things I promise you this for specific means that the only answers that will be correct from the exam I'll say that again my cardipine clevidapine labella law and sodium nitropercyte those are the anti-hypertenses that are safe in the treatment of a hypertensive emergency or urgency where again a person has like really high blood pressures and they have like end organ damage do not give hydrozine do not give my fedipine you give those you will get the question wrong and I'm literally promising you that right so you don't want to get into those kinds of troubles on exams now there's some drops that are some anti-hypertenses that are contrary to you when a person has like an acute decomposition of CHF well I hope you're thinking along the lines of like a bit of blockers or so again if a person's heart is acutely like you know kind of like in the toilet no working very well it would not make much sense to give them drugs that can depress the cardiac function even more like a negative vinyl drop like a bit of blocker or a non-dihydroperidine calcium channel blocker like Vera Pamele or the Othaisa now what did they give you a question about a person that has a history of hypertension but they also have a history of e-fib is there a particular drug class that will be reasonable for those people well I hope you're telling me that you could potentially give them like again a bit of blocker right or a non-dihydroperidine calcium channel blocker right so basically your class two and your class four anti-rhythmics right you're

pretty good for the treatment of e-fib right like chronic therapy for e-fib right so if a person has a history of hypertension and they have those problems they may not be the worst idea in the world to give them those kinds of drugs now what's um uh there's a scenario that kind of popped up in my mind what kind of anti-hypertensive will be contraindicated in a person that has a history of like like second degree heart block like movies two or like third degree heart block what kind of drug would be contraindicated there well I would hope you're telling me that you don't want to give those people again bitter blockers or non-dihydroperidine calcium channel blockers for epimodal tires and right because the person has hard block yeah if you know this already walk going at a snail space right it would not make sense to like oh you know your good at a snail space then put you to a complete halt that's probably not a good idea right because you're again you don't want them to you know kind of like die of like a really last year uh a brilliant right so for person has a history of like uh hard block it's really like a really bad one like uh movie two or type like a third degree heart block well even a person that has a history of like WPW right where they have like that a sensory bundle of Kent you don't want to give those people an even noodle blocking agent right because we give them that even auto blocking agent then the thing that will happen is that they will then have more flux through that uh Kent bundle right and see for example let's see they have the WW and they have like a compliment if if you block their AV nodes right and then it's the Ken bundle that's the only thing that's available you will essentially convert that a fib that they have in their feature to v fib right and then they will die right and you know that's usually not a usually not a good outcome rig

ht so it's never a good outcome let's put it that way right so yeah so if a person has WPW do not give an AV node blocking agent because there's a hypertension podcast I'm advising again don't give a bit of blocker and don't give a non-dihydroperiodine consumption of blocker but one off-target off-putting thing that again you may not see mentioned all the time is if a person has WPW the juxtain is a bad idea right the juxtain many people just think of the juxtain as a positive and ultra-puch it is but the other thing that the juxtain does is the juxtain is also a most organic receptor agonist okay so it actually slows conduction down the EV node so the juxtain is not a good idea for a person that has a history of WPW because again that will encourage more flux through the bundle of Kent which is bad right now what if they give you a question about a person that you know is having because they've had like you know really bad nasty resistant hypertension and you'll find out that it's from a phyocromosyptoma right and then you're like okay we're gonna go ahead and take you for surgery what kind of pre-surgical anti-hypertensive planning would you want to go with well I would hope you're saying to give an alpha blocker first right so you can give like phenoxybenzamine right phenoxybenzamine is an irreversible alpha one blocker right and then you so you block out for receptors first before you block better receptors because again if you give a bit of blocker first then you have that on a post alpha stimulation and present can get a hypertensive crisis and die you don't want that right that's not again not an ideal outcome right so you give alpha blockade first after you give alpha blockade you then go ahead and give bit of blockade so hopefully that's something that makes sense to you now what if you get a question and actually a similar concept kind of applies to a person

that has like cocaine overdose right again if a person has cocaine overdose you don't want to give a beta blocker that's not a smart idea because again on a post alpha business but you can give an alpha beta blocker you can give like labeta law works great in a cocaine overdose you can give nitro-prosite just don't give a beta blocker and you'll be fine for the most part and usually people that also have cocaine overdose they actually tend to respond pretty well to benzoz benzoz are usually very good with treating many of the high-proud synergic symptoms that those patients are having and then if a person has nephrogenic diabetes in syphilis what kind of anti-hypertensine drug in general is good for nephrogenic diabetes in syphilis well I would hope you're telling me that you want to consider a thiozide right thiozides are good for nephrogenic DI again with the exception of a person having nephrogenic DI from lithium toxicity right again if you give a thiozide that will potentially worsen the lithium tox like the nephrogenic DI associated with lithium like as a lithium side effect because again I kind of said this in a prior podcast I'm not going to be able to that fact here but anything that would increase the activity of your reading under tensile dose-tron system will worsen the phium toxicity because and the reasoning behind that is if you're reading under tensile dose-tron system is working really well then our dose-tron levels will be high and when our dose-tron is high our dose-tron increases the activity of that in a channel that we find at the level of the principle cell of the collecting duct so if a person has nephrogenic DI from lithium toxicity the drugs of choice are your in-external blockers amylo-right triumtery not a thiozide right not a thiozide because thiozides will make you willing to plead it and then your response you're reading under tensile d

ose-tron system will get revved up that in-external work really well and then you get more lithium toxicity because the lithium will be reabsorbed at an accelerometer rate right that's also why NSAIDS are terrible ideas in people that are experiencing lithium toxicity because NSAIDS they will inhibit the synthesis of first-agglendants so if you inhibit first-agglendants synthesis then your afternoon arterial will be constructed right and if it's constructed you will hyper-prefuse those GG cells and then you'll freak out and start making a ton of reading now what are some anti-hypertensives that are contraindicated in a person that has a history of gaps well I hope you're telling me like your firesides and your loops right because your thighs and your loops interfere with the excretion of uric acid in the nephron so if you're taking a thiozide or loop as your body is trying to get rid of that thiozide or loop because drugs don't sting the body forever then you'll not lose as much uric acid in your urine and then you have a higher risk of precipitate those uric acid crystals in your body like maybe like your great toe your first NTP and then you get into troubles we got now what did they tell you that a person was really studied on a non-tie hypertensive or like a heart failure drug and then they have kind of comastia what are you thinking about what I'll hope you think it's an unactive right because again it blocks out of those some receptors but it also blocks androgen receptors and then if they give you a question about a person that has a history of hypertension and they have renal failure or history of hypertension and they have diabetes what is the preferred drug plus for those people to treat your hypertension and I hope you're telling me to go ahead and give those people like an ACE inhibitor or an ARB right remember ACE inhibitors again by mechanisms have descr

ibed their multiple podcasts right they decrease something known as intrablomerola hypertension right so hyper filtration injury does not happen right so that slows down the rate of the key of the person's kidneys right because if you remember from the GNC guidelines for hypertension you typically would not want to start with an ACE inhibitor and ARB in an African-American but this is the one key high-yield exception to that role for person has a history of hypertension and you have diabetes or you have renal failure ACE inhibitors or AR Bs at the preferred agents in that in those efficient populations now what did they give you a question about a person that you know what study on anti-hypertensive and demisadouths and their blood pressure just goes sky out what drug class are you thinking about well I hope you're thinking about like the alpha-2 agonist quantity right quantity it has this classic as a strong rebound hypertension and remember that colony also has like some very high-yield uses on endgames you can actually use it in a trick like opioid withdrawal right because again opioid is right by actually on those new receptors they decrease the synthesis the release of cadet colamine so they have dronegic synapse well guess what?

cloning by being an alpha-2 agonist also inhibits the release of cadet colamine like not repinephrine at the adrenergic synapse so cloning in essentially works unlike an opioid believe it or not in some localities in the US cloning is a street drug right because it makes your opioid withdrawal symptoms not feel as bad right in fact if you are if you're resident or you're doing like a rotation if you hear about opioid power plants opioid power plants that are used to manage like opioid withdrawal in the hospitals they almost always include cloning right so cloning can be this opioid withdrawal and that how you think you want to keep in mind with cloning is you can actually use it as first line for the treatment of Tourette remember Tourette's first line use your alpha-2 agonists like cloning in on one person second line use your atypical anti-psychotics third line use your typical anti-psychotics at least that's what the mb me kind of recognizes so i think i'm gonna go ahead and stop here this is going on for over 30 minutes and again this is my first like one video so let's see how this works as i do at the end of every podcast i don't for one or one children for many exams right so step one step two ck step two cs step three pre-canceric omega school exams 30-ish-elf exams if you're a medicine resident i need children if you're like your internal medicine treatment exam or your internal medicine ibi-informed exam or let's say you're a college student and you need children for like general chemistry or organic chemistry physics biochemistry histology physiology basically many of the m-cuts subjects or many of the pre-match subjects like again i do offer tutoring for all those stints and then if and the kind of terrain i do i mostly do one on one children with people but and that thing i also do is i also do like large group tutoring right so if you interested in any o

f those stints either reach out to me through the website or you send me an email divine intervention podcasts with an s at the end at gmail.com and if you're a college student of lunch or med school so like an amcass application or a med student of lunch or residency so like an airs application i do offer again like one on one like coaching one on one advising for those things so like personal statement smock interviews editing applications and all that stuff again i have like admissions committee experience i've worked with the admissions committee on the top two med school like a year so again i have experience reviewing high quality applications and i've also worked with tons of people that have successfully matched into residency so um yeah so that's it pretty much i hope you enjoyed this video um for those of you that are listening please subscribe to the podcast and subscribe to the youtube channel as well it's called divine intervention podcasts and videos um you know subscribe hit subscribe and i guess we'll see how things go but yes this year my game plan is to make a crap ton of podcasts especially from like uh like more from a step to seek a perspective but also pretty heavily from a step one perspective and then also expanding to all these specialties like um like internal medicine make more internal medicine podcasts um you know make some podcasts for some other specialties that peripherally related to internal medicine so that's just he's just time that's my biggest um almost like my biggest and immediate factor if i had more time i would make more podcasts uh because most of my days end up being extremely busy so i was seeing the next podcast thank you for listening and again just give me feedback in the comments if you have any questions or you having any topics like one podcast meetup again just reach out to me um either in the comment section or you

can send me an email i'll be more than happy if it's a reasonable request i'll be more than happy to make a podcast on that topic because there's many podcasts i have in my hand i just don't have time to meet those so i'm one of the rest of your day i'm glad the leakers are on the winning streak now and i hope they continue that tomorrow when they plead their game so i'll see you next time but bless you thank you

Labetalol, Hydralazine, and Methyldopa. (Remember: Hypertensive Moms Love My Therapy).

They cause venodilation, decreasing preload and thus lowering myocardial oxygen demand.

ACE Inhibitors or AR Bs, because they blunt the body's compensatory mechanisms to maintain glomerular filtration pressure.

Alpha-1 blockers (e.g., Tamsulosin), as they decrease systemic vascular resistance and improve bladder drainage by blocking alpha-1 receptors in the bladder neck.

Any AV node blocking agent (Beta-blockers or non-dihydropyridine CC Bs), because this can shunt conduction through the accessory bundle, potentially causing fatal ventricular fibrillation.

ACE Inhibitors or AR Bs, as they are protective agents that slow the rate of kidney decline by reducing intraglomerular hypertension.

Labetalol, Hydralazine, Methyldopa.

They can cause fetal renal dysfunction.

ACE Inhibitors and AR Bs.

Potassium-sparing diuretics/Aldosterone antagonists (e.g., Amiloride, Triamterene), because they block the epithelial sodium channel (E NaC).

Beta-blockers and non-dihydropyridine Calcium Channel Blockers.

Alpha-blockade first (e.g., Phenoxybenzamine), followed by beta-blockade.

Thiazide diuretics and Loop diuretics, because they interfere with uric acid excretion, increasing the risk of crystal precipitation.

Labetalol, Hydralazine, Methyldopa.

They can cause fetal renal dysfunction.

ACE Inhibitors and AR Bs.

Potassium-sparing diuretics/Aldosterone antagonists (e.g., Amiloride, Triamterene), because they block the epithelial sodium channel (E NaC).

Beta-blockers and non-dihydropyridine Calcium Channel Blockers.

Alpha-blockade first (e.g., Phenoxybenzamine), followed by beta-blockade.

Thiazide diuretics and Loop diuretics, because they interfere with uric acid excretion, increasing the risk of crystal precipitation.