DIP Episode 271 - The NBME and COPD (+ 2CK Courses 11/12-14)

Okay, welcome. My name is Divine. This is episode 271 of the Divine Intervention podcast. In this podcast I'm going to be covering COPD and the USML exams. Again it's a super high-yield topic. If you're taking pretty much any of the USML exams step one, step two, see key step three. You're gonna get COPD questions so you might as well just go ahead and understand it now. But if you listen to what I'm saying today you pay attention to this. You should be able to answer pretty much every question that you see. I'm going to be covering pretty much everything you can see about COPD in this review. So I mean obviously right we know that COPD typically on MBME exams you want to be able to compare to asthma and we know that an appristen has a COPD right they have like like an air flu limitation that is not reversible right or is not fully reversible. Compay that with asthma right in a person that has asthma the air flu limitation they have is absolutely reversible right but in COPD it is not reversible right and really for the most part there are two big conditions you want to think about when you're thinking of COPD right you want to think about chronic bronchitis right we want to think about infosima and really chronic bronchitis the big thing with this is this people are just having a ton of productive cough. I mean the official definition is you have a person has productive cough for at least three months every year in two consecutive years.

For present has that kind of problem they definitely have a chronic bronchitis right and the thing is it's actually very important to remember that a person that has chronic bronchitis for the most part you know it affects not most is name is chronic bronchitis so that means it affects the bronchitis right so for the most part the long parincoma parincoma for MBME purposes is spirit this is why the DLC is roughly normal person chronic bronchitis right but contrast this with infosima right so in the present has infosima there always a enlarged right they have like loss of long parincoma right so because they've lost office area for the fusion those people tend to have a decrease in the DLC that's a very high-yield distinction between infosima and chronic bronchitis right so a person that has COPD will have increased lung volumes for the way to tell infosima apart from chronic bronchitis on MBME exams is the decrease in DLC that accompanies infosima right so really in infosima you lose a lot of the elasticity of the lungs and the thing is the elasticity of the lungs is what keeps your earways open right like your bronchitis or bronchios and stuff so when you lose elastin right then you're not able to keep your earways open so your earways begin to collapse that's why those people begin to retain a ton of CO2 right so very in expiration this very high-yield to know very in expiration those people have collapse those these people have collapse of the earways right so that's again important to know and the thing is because they retain a lot of CO2 they begin to have all this lung hyperinflation you know they begin to have this lung hyperinflation the lungs are very compliant so their lungs become bigger and bigger and bigger so the thing is because their lungs are bigger right if you think about it it's much easier to blow balloon when it's you know not completely distende

d to a distended position than trying to blow balloon even further that is already distended right so because their lungs are already hyperinflated you know these people have like increased work or breathing and their respiratory muscles are not particularly efficient right and then don't forget right infosima chronic bronchitis actually the biggest risk factor for both of those right is smoking right cigarette smoking is the biggest risk factor for COPD but don't forget right of all antitrips in deficiency can absolutely cause COPD as well right can cause panasinar and fizema remember of all antitripsin basically it's it's an enzyme right that pretty much neutralizes the elasties that comes from neutrophils right so the thing is if you lack of all antitripsin right then you're not able to neutralize the elasties that comes from neutrophils and that elasties will basically elasties right it's an ease that destroys elastin right so that will destroy the elastin in the lungs right so usually these people get like very early on set the COPD right and usually when people have all four antitrips in deficiency they usually like have like liver problems because all four antitripsin is also found in the liver and they also tend to get skin problems as well right so you just want those big fins when you keep at the back of your mind now just some fins I will say because some fans they throw these on the exams to try to you know mess people's heads up remember if a person has like air flow limitations and you give them a bronchordi later and the air flow limitation gets better those people have asthma that's it if the air flow limitation does not get better they do not have asthma right and then remember bronchiectasis is also another common condition that me pop up on exams basically for whatever bizarre reason right these people have like abnormal dilation of their airways ri

ght and usually they will give you like some image in finding in the question that oh this person has like very thick airways or you see like a tram track pattern in the distal airway right so they'll tell you that the person's airways thick they'll tell you that the person's airway looks a cystic that's why it's called bronchiectasis right is almost like ecstasia of the earlys right whenever you see stuff like that right you definitely want to think about it definitely want to think about bronchiectasis and usually these people have like a ton of spudum production although some people may actually not have that ton of spudum production if you may right and the thing is sometimes your friends at the Mb me especially for those taking step one they love to go after like the things you may see on his stology right or grossly in a person that has your PD if you're looking at their airways right remember these people they have like met a pleasure of their airways right so instead of having that the pseudo stratify column epithelium that you find in the early actually becomes squamous epithelium right so they have like a metaplesia to squamous epithelium that's high or to know right and then remember all that Celia that helps you move your mucus around those things actually begin to not work properly in a person that has COPD right and then they have like a ton of like elastic smoke muscle ton of connective tissue that begins to proliferate so again just the their airway dynamics becomes a becomes abnormal right the airway dynamics become becomes abnormal and remember if you want to reduce mortality in COPD I'll talk about some other interventions but the big thing you want to keep in mind is stop smoking right if you stop smoking I mean it's not like you're gonna recover a long function but your long the decline in your long function will basically go back to the exact sam

e level as a person that does not smoke right so that's very high or to know right so smoking is the is basically the most cost effective the most clinically effective solution right to slow down the product progression of COPD and if you also want to improve survival right remember the MBMD love to ask questions on what improves survival right what improves survival and then one thing I just want to mention is if you see a person on an MBM exam that has like COPD symptoms in their 40s right you absolutely want to think about alpha-1 antitripsin deficiency right and usually for those people just go ahead and check the alpha-1 antitripsin levels if it's less than like 80 milligrams per deciliter they pretty much have a alpha-1 antitripsin deficiency right now what are some things that the MBMD threw in a in a COPD question to kind of tell you that oh okay this person has COPD right they may tell you that oh the person has a loud P2 right or a loud S2 right because remember when a person has COPD right they become chronically hypoxemic right and when you're hypoxemic right that's gonna cause a pulmonary vascular constriction and if that happens right that will increase the pressures on the right side of the heart and that can cause pulmonary hypertension right so if you see like a loud S2 allow P2 you absolutely want to think about COPD on an MBM exam right or if you tell you that all the S2 is split right if you see like a split like all the time right because remember you can have a physiologic split on inspiration because you know when you inspire your venus return increases more blood goes to the right side of the heart so if that happens right you know it will take a while for all the blood to leave your right side of the heart and for the pulmonic valve to close so the urethic valve will close before the pulmonic right so you have that physiologic split but it doe

sn't happen under every other circumstance right but if you notice that the person has like that split on the inspiration and the expiration right then you absolutely want to think about like a persistent list of S2 that's path of the money for a person having like pulmonary hypertension which you know again can be caused by can be caused by COPD or sometimes they can tell you that all the person on imaging the person has a all physical exam the person has a parasternal lift to the heart if you see that again that tells you that this person's right heart is not working well right the parasternal lift just means that the person has some kind of right ventricular hypertrophy right and again because the person has pulmonary hypertension right if a person has like really bad COPD really bad pulmonary hypertension from COPD they are going to have decrease a decrease in the pulmonary vascula markings on image right remember those pulmonary vascula markings is an indication of the p-tancy of your of your pulmonary vessels right so if you have a decrease in pulmonary vascula markings that means the person very likely has some kind of pulmonary hypertension right and also don't forget right obviously the diaphragm is going to the diaphragm is going to be flat in a person that has a COPD right because again of that long hyperinflation right so the diaphragm just kind of like settles down and then don't forget the big big big thing you're looking for FVV1 to FVC ratio if it's left that if it's less than 70% you're done the person has COPD right so again I'll say that again if the FVV1 to FVC ratio is less than 70% the person has COPD okay and remember that usually in COPD all the long volumes are going to go upright like your total long capacity FRC all that stuff is all going to go up in a person that has a COPD again remember I said those big high-eal things about the DLC the

DLC is roughly normal and a person with chronic bronchitis but the DLC is decreased in a person that has and FISIM right because remember the diffusion capacity like the ability to diffuse right there's a pulmonary equation that relates that right so the diffusion ability the basically diffusion ability right is equal to the area divided by the thickness right the area divided by the thickness so if the surface area so the area is directly proportional to the diffusion capacity the thickness is inversely proportional to the diffusion capacity right so if the surface area available for diffusion is low then that means the diffusion capacity will be decreased right so a decreased surface area for gas exchange right is the mechanism behind the hypoxemia that characterizes a COM FISIM right and then if a person has pulmonary fibrosis for example right which is more an example of a restrictive lung disease the thickness in the walls of the long schools up right so because there's an inverse relationship between the thickness and the diffusability right because the thickness is up and the diffusion ability goes down right that's the mechanism behind the hypoxemia and a person that has like some kind of fibrosis in the lungs right so again very high you to know these things for example right so the thing is for the most part right like let's talk about how you manage COPD remember COPD for the most part you always want to start with a with a short actin bronchodyte leader right so you can start with like a bit of twiginess like a bit of raw you can also use like a short actin muscarinica antagonist right so something that blocks those muscarinica M3 receptors right something like epitopeum for example if that's not putting it then you then go the next step the next step is to go ahead and add a long actin agent right so you can add a lava right a long actin beta twiginess so

mething like salmeterol or formolero or you can add a long actin anti-cool energy agent right again a long actin like muscarinica receptor like tiotropium remember epitopium is the short actin anti-cool energy tiotropium is the long actin anti-cool energy right and then if those things are not working right then you go ahead and add an helicorecosteria if that's not working then you want to begin to make sure you know you're adding like home oxygen we'll talk about the criteria for that in a bit right and you can also begin to consider things like surgery right like there's this common surgery that sometimes you mission an in-beam example right like it's called long volume reduction surgery right but remember before you do that stuff you've got to check the presence of the reward the presence of the one is less than a liter that's a contraindication to any kind of longer-sective surgery right because the person will not have enough long remaining right to to participating gas exchange so they're going to die on the operating table right you obviously do not want that so remember the so remember the stepwise provision of COPD treatment right so short actin stuff first long actin stuff first in helicorecosteria and then oxygen therapy plus or minus surgery right contrast that with asthma asthma you start with a short actin stuff first right a sabba right like a a bit or all right and then after that you go to an in-beam corticostero so it's almost like the second and third places are swapped between COPD and asthma management right so you do the in-beam corticostero second for asthma third you do the lava right like some matter off or more they're all and then fourth you would then do oral steroids right you can do oral steroids and the thing is they are just some weird unusual questions your friend that's the in-beam you love to you know test in terms of like managing

people that have COPD again obviously again you're going to tell these people stop smoking stop smoking stop smoking right these people should get the the influenza vaccines every year right that's very very important right and remember people that have COPD also candidates for the normal coco vaccine right especially those that are over 65 right I mean obviously if you're less than 65 you still want to give them the regular vaccine you give them the PCB 13 first if we give them the PPSV 23 right what the thing is if they're over 65 and they've gotten the got their vaccines like more than five years ago right go ahead and re-vaccinate them against the pneumococcus this is absolutely important to know for example right and then remember that there are many different ways you can give those inhaled agents to a person that has a that has COPD right you know you can use like a meter dose inhaler right you can use a spacer you can use an abuser the thing is sometimes on mbim exams they try to get it to pick one over the other for a person right now the thing is if a person has like a lot of physical limitations like they have like really bad arthritis or for some reason like the coordination is not great lessons you have they've had a stroke or something and an abuser is the agent of choice in those people right the thing is for you to use a me third dose inhaler you need to have like good body mechanics and stuff like that right and then obviously the thing that is the best of the best is a spacer right but usually they'll try to get it to pick between an m like a meter dose inhaler and an abuser again use an abuser in people that for some reason just have like weird body mechanics pomodal activity to allow them to inhale those things right but an mdi if you have good instructions and you know you're able to use it properly right I mean it's equivalent to an abuser in how

much medication that you get right and then sometimes they love to test side effects of these drugs right of the drugs that I used for COPD remember if a person has a COPD right and they're taking like a better two agonist remember those things can cause tremors those things can cause an increase in heart rate because literally those things are better to agonist right but the thing is they do have some better one activity so they can absolutely increase their presence of heart rate and then remember these anticholinergic drugs right you know again they basically block with allergic receptors almost on salivary glands right so these things can pretty much you know cause dry mouth right and then also remember if a person has like closed-angle glaucoma these most granic antagonists are not you know I'm not a great idea and also remember your parasympathetic system makes you pee right so if for example a person has like BPH right or a person has like urinary obstruction for any reason again these anticholinergic agents will be contraindicated in those people right then remember right you can also use the ophiline in some select patient so those theophiline it's a very toxic drug has like a supermyr therapeutic index right and remember it can cause a lot of like cardiac arrhythmias right it goes a lot of nausea a lot of vomiting right and remember basically the with the ophiline works basically it's a phosphodiester is inhibitor so by doing that it will increase the amount of cyclic AMP in the smooth muscle that aligns your earways and that will cause like a bronchidylation right that's also the same way there's this drug known as a roflu melast right roflu melast is a phosphodiester is foing inhibitor so by inhibiting phosphodiester is right again it will bump up your levels of a cyclic AMP and that will cause a phosphoryluxition and visodilation in your earways right an

d again remember when a person has COPD one thing that can improve survival besides smoking cessation right is oxygen right although they need this homo too they need this oxygen for at least 15 hours a day right they need it for at least 15 hours a day and there's some criteria you want to know for the purposes of example who should get homo too right so remember if the person's p little ill to the you know the partial pressure of oxygen they are in their arteries right if it's less than 55 you know 55 or less so 55 is included right so 55 or less millimeters of mercury right or they are otusats are like less than like less than 80% again 80% is included right then those people should get a homo too I mean like the criteria is a little higher I just remember this as the rule of mines right so just add mines to those initial numbers right so if your arterial PO2 is 59 or less or your otusat is 89% or less where you have pulmonary hypertension then you also eligible for home for homo too and also if the person has like evidence of like right heart failure you know like about corpomenality have like right heart failure their right ventricle is no working when on an echocardiogram or they have like a demon and all that stuff or even if you have like a very high hematocrit right telling you that oh this person has polisidemia these people are all in you know eligible for for homo too therapy right and then if a person has COPD exacerbations right the big thing you see on an MBME exam is these people they have a bad change from baseline right so they have a bad change from baseline what in the world do I mean by that basically like they are coughing more they are producing most put them stuff like that right and really the most common cause causes on MBME exam so for COPD exacerbation the first one should think about is infection right but also if you inhale a lot of air p

ollutants that can also cause a COPD exacerbation but the big big big one I want you to think about on MBME exam right is a is infection and usually you know if a person has a COPD exacerbation you're gonna you know give them like a short actin agent you're gonna give them IV like so like a short actin a bronchidyl leader right like a bitter role in protropium stuff like that right and then don't forget that these people if for some reason for some bizarre reason the MBME is trying to get it to pick between a bitter role aniprootropium as a short actin agent to treat COPD pick a bitter role first okay pick a bitter a bitter role is just generally preferred right over the um over like a protropium for example in those are circumstances right and again you're gonna give those people like IV steroids right and in addition to that if you know let's say your trying all these things is not working then your next step on an MBME exam is to give these people like knowing these if a positive pressure ventilation right so basically like by pap by pap or CPAP right the thing is uh that stuff actually reduces mortality right in a person that has a COPD exacerbation but again remember there are some high-yield contraindications for this stuff right so if for some reason just basically think of a person that can aspirate right a person that can aspirate the person that has like tons and tons and tons of secretions when you see people like that those people are not eligible for those right in those circumstances unfortunately you need to proceed to into beating those people right again you may see why it's divine making a big big force about all those stuff I promise you all the stuff I'm saying is fluently high yield to know for the exam right it's fluently high yield to know for the exam and usually when a person has a COPD like a COPD exacerbation one thing you usually try to do

is you try to actually um you try to actually give those people like you know like anti-biotics because usually people that are going through COPD you know again like I said infection is one of the most common causes of a COPD exacerbation right so the thing is what are some bugs that can cause problems in a person that's you know going through a COPD exacerbation the most common one that you absolutely absolutely want to think about on exams is um the one you you know definitely want to think about on exams I would say for sure is you want to think about um H flu right he more flows influence on nmdm exams is probably the most common cause of pneumonia in patients that have COPD right although you can also see like more axella or like stripping him or what again the big big big one I want you to think about is he more flows influence right so usually when a person has like a COPD exacerbation if you're trying to give them like anti-biotics right one thing should consider is give them like a third generation self-low sparring you know like uh like um safe triaxone and then you can add like um a microlyde like is it through my cell right so you can do safe triaxone plus is it through my cell but if you don't see that as an option you can also just give them monotherapy with like an IV fluoro flueno right and remember to reduce the risk of those people coming back to the hospital right you need to give them like like a three to five day course of oral steroids right that's actually one of the things that actually reduces the risk of re-admission again you may see why is the fine making all these foresee points I promise you the stuff is florida high you to know for purposes of the USMLA exams so I think I'm going to go ahead and stop here today um again uh if you're studying for step 2ck and you need uh like an nbm testing strategy scores or the 10 hour comprehensive re

view course um i'm going to be holding those next week right so the 10 hour comprehensive review course i'm splitting it into two days the 13th and the 14th it's five hours each day it's from like 11 a.m to 4 p.m mountain standard time on both of those days and then the testic in strategy scores um is on the 12th right from 2 to 4 30 p.m.

mountain standard type so again if you're interested in any of those just shoot me an email through the contact button on the website and I'll be happy to provide some more information and again please subscribe to the podcast or an Apple podcast on Google Play on Spotify um I also have these podcasts available on um um you know on the website obviously again if you sign up on the website then you you'll be getting emails when i make uh when i make new podcasts and uh please also subscribe subscribe to the youtube channel that's where you can find many of my videos although again you can also find those on the website so thank you for listening to me Rambo for a bit I hope you have a wonderful day and i am praying for peace in America so thank you for listening i will see you next time god bless you have a wonderful day thank you

Asthma airflow limitation is absolutely reversible; COPD airflow limitation is not fully or easily reversible.

Chronic bronchitis.

Emphysema is associated with decreased $\text{DLCO}$ due to loss of alveolar surface area, while chronic bronchitis maintains a relatively normal $\text{DLCO}$.

Loud P2 heart sound or a persistent split S2 (split on both inspiration and expiration).

Haemophilus influenzae.

Anticholinergic agents (Muscarinic antagonists).

Loss of elastin leads to decreased lung elasticity, causing airway collapse on expiration and resulting in a decreased $\text{DLCO}$.

Loud P2 sound or persistent split S2.

Smoking cessation (it is the most cost-effective and clinically effective measure).

Short-acting $\beta_2$ agonist (SABA).

$\text{PaO}_2 \le 55$ mm Hg OR $\text{SpO}_2 \le 80\%$.

An abuser (spacer).

Loss of elastin leads to decreased lung elasticity, causing airway collapse on expiration and resulting in a decreased $\text{DLCO}$.

Loud P2 sound or persistent split S2.

Smoking cessation (it is the most cost-effective and clinically effective measure).

Short-acting $\beta_2$ agonist (SABA).

$\text{PaO}_2 \le 55$ mm Hg OR $\text{SpO}_2 \le 80\%$.

An abuser (spacer).