Tuberculosis

foreign what's up Ninja nerds in this video today we're going to be talking about tuberculosis we're going to first go over the pathophysiology we're not going to go too crazy we're going to try to understand how tuberculosis actually occurs and what type of populations who are at high risk of exposure high risk of reactivation infection then what we'll do is we'll go over how does pulmonary tuberculosis look like and then in the scary situation where it spreads to other organs what does extra pulmonary tuberculosis look like then we'll go over kind of the step-by-step diagnostic starting off with screening then Imaging and then sputum cultures and then biopsy Etc and they'll finish off with how do we actually treat these patients who have something called latent TB versus active TB all right so first things first when we have a patient who has tuberculosis that we're concerned that they have that we got to think about the pathogen what's the pathogen that's responsible so the primary pathogen here is called mycobacterium tuberculosis so this is called Myco bacterium tuberculosis now this nasty pathogen is usually going to be inhaled so it's some type of Airborne pathogen that makes its way into the actual respiratory tract when it gets into the respiratory tract it moves its way down through the bronchial system finds particular areas of the lungs where it likes to invade you know what it usually likes to hit within the lungs it usually loves to involve particularly the lung tissue in the right middle lobe and right lower lobe first so generally what you may see in these patients is you may see this area of kind of a consolidation and usually it's very close to the pleura and so what happens is you kind of get this immune reaction that occurs here within the right middle lobe right lower lobes generally and it's an immune reaction that kind of is a very interesting process that occurs in the right middle or right lower lobe you know what happens here it's really cool kind of the basic concept we're not going to go crazy here but let's say that you have exposure to the actual mycobacterium when you're exposed to the mycobacterium you have particular macrophages here the macrophages generally what they'll do is they're within the actual Airway they'll find the mycobacterium and they'll engulf it and they phagocytose it and they put it into this little thing called a phagosome now normally what should happen is the phagosome should combine with these little vesicles these green vesicles that contain lysosomes and they break down the pathogen really really easily you know what tuberculosis does it inhibits the phagolysosome so tuberculosis is such a hearty pathogen that it inhibits the phagol lysosome process if you inhibit the phagolysosome now it can't break down the actual pathogen as easy and so then it multiplies and multiplies multiplies within multiple macrophages you know what happens though this dang macrophages they start releasing lots of cytokines like interleukin one interleukin six two monocratic Factor Alpha they really try to increase the production of these and the whole goal is that this is going to stimulate a lot of immune system cells to come to the area maybe it'll cause more macrophages to come to the area maybe it'll cause more lymphocytes to come to the area but the primary thing is that it's going to release these cytokines and it's going to try to get your lymphocytes to try to come to the area and then more macrophages to come to the area that's the goal and what happens is more macrophages will come to the area and lymphocytes will come to the area and encounter more of the actual mycobacterium they'll try to phagocytose that they won't do a good job with it and it continues to multiply what eventually starts to happen here is that you get a big kind of like interesting structure here of what's called a granuloma so in the center of it is where you had those original macrophages that phagocytose the tuberculosis it destroys them and it undergoes a cavitation and necrosis in the center you know what that's called whenever you have this kind of necrosis in the center here this is called Casius necrosis this occurs within the center of this big big kind of immune system structure around the edges of it you may have more macrophages so around the edges of it you may have some more macrophages and then around that you may also have lots of lymphocytes particularly what's called T lymphocytes and these are generally T lymphocytes what happens is is this is something called a casiating granuloma this is usually what forms within this right lower low right middle lobe with an exposure to mycobacterium tuberculosis the macrophages just aren't good at being able to completely break them down that they end up populating within the macrophage causes more macrophages more lymphasis to come to the area to try to wall the pathogen off and what it does is it forms this structure here called a granuloma and this granuloma really important here is a caseiating granuloma but it's a central necrosis within it it's really important now when this case eating granuloma forms here within the actual lung tissue usually it's really important to remember here that this is actually going to be something very interesting we call this a gone Focus and a gone focus is just basically this granuloma that usually occurs in the middle or lower lobes so it's usually in the middle or lower lobes okay the other thing is that it's subplural so it's usually going to be very very close to the pleura now here's what else happens sometimes these cases and granulomas will spread and they try to migrate to the nearby lymph nodes and as they try to migrate to the layer byte nearby lymph nodes it causes more Casio granulomas to form within these lymph nodes and then they get big and big and they cause a lot of higher lymphadenopathy what is this here called in now as we start having a lot of these granulomas and immune reaction occurring within the lymph nodes now we have Hyler lymphadenopathy the combination of a patient Who develops what's called Hyler lymphadenopathy and a gone Focus this combination here if you will is called a gone complex that is the combination so a gone complex is basically going to be very consistent with a patient having primary tuberculosis so what is this called here this is primary primary tuberculosis and it's very consistent for them to have what's called a gone Focus Acadian granuloma that forms within the middle or lower lobe subplural and a hilar lymphanopathy granuloma is forming within the nearby lymph nodes causing that to swell up the combination is called a gone complex and really this is just due to the macrophages not being able to completely break down the mycobacterium causing other immune system cells to come to the area and try to wall that off and protect it from spreading you know what else is really really important clinically as these T cells they're really interesting they love to cause more and more and more and more macrophages to try to come to the area to form a better granuloma and so they release a very important molecule called interferon gamma lots and lots of this molecule is released from these T cells so I would remember this potentially because it comes in later when we talk about the Diagnostics but the T cells will try to recruit as many macrophages as they can macrophages will try to recruit more macrophages and more T cells to wall the actual mycobacterium off and form these granulomas now my question to you is put this together a patient gets primary TB with a gone complex how did they get it they had to be exposed to it what patient populations are at high risk of exposure to the TB they can get primary TB and then from here a lot of things can happen my question to you is how do they get exposed to it so you need to know the patients are the patient population who has high risk of exposure this may be something that they present in the vignette so think about this in a patient population who are in prisons so patients who are in prison who are health care workers so Healthcare is a really big one because they definitely have exposure homeless um I would also remember patients who are immigrants immigrants would be another potential big one because if they're coming from a very high prevalent population so immigrants as well these would be the real big things that I would remember so patients who again have a high risk of exposure another one could be IV drug abuse if you want to add that one in there as well so exposure could be prison settings Health Care homeless immigrants and another one to maybe add in here is IV drug abuse but this prevents the op that presents the opportunity for the TB to be actually entered into the patient's Airway so once they have that here's the thing just because someone has an exposure to the TB doesn't mean that they'll actually develop the disease process of active TB they may clear it they may go into a latent period or they may actually progress but the exposure is the key thing for them being at risk of actually being having the exposure to the bat the pathogen now once the patient has this primary TB what can happen is and about 90 of cases so greater than or equal to 90 percent of the cases they will go into this phase called the latent phase and we'll talk about that one first so the latent phase later we'll also talk about in about less than 10 percent of cases they may progress and we call this primary Progressive tuberculosis okay and that's a really scary one that we'll talk about all right so now let's actually come down and talk about how now the patient has primary tuberculosis do they develop a latent phase how do they develop a primary Progressive and then what's the complications that can happen as they continue to progress in other words Prime Progressive continues to get worse and cause more damage or a patient with latent tuberculosis reactivates and develops secondary tuberculosis and continues to cause destruction of the lung tissue let's come down and talk about that all right so if a patient has latent tuberculosis what happens is remember they start off with that gone complex right what happens is sometimes when they get that gone complex which affects like that right you know but generally the middle or lower lobe subplural and then again may give some type of like higher lymph node involvement called that a gone complex right generally what happens is some patients May completely clear this right they may completely clear the infection that's gone some patients though will keep it dormant and what they'll do is they'll have a lot of fibro calcifications that'll form around it lots of fibro calcifications that'll form around these areas and just basically try to keep this kind of tuberculosis within a dormant kind of shut down state their immune system is good enough to say hey I'm going to wall you off I'm going to keep you dormant I'm going to shut you down I'm the gatekeeper you ain't going to continue to keep replicating here baby and so it keeps it into this dormant phase where the bacteria is still there but it's in a dorm of phase it's not multiplying it's not dividing it's not causing destruction of the lung tissue causing symptoms you understand what I'm saying it's very important here so because of that when it causes fibro calcification here sometimes that fibro calcification we actually give it a special name it's the gone complex when a fibro calcifies you guys want to know what that's called yeah you probably do this right here whenever it fibro calcifies is called a ranky complex it's called a ranky complex so remember that if you really want to but what I really want you to understand is that once they have this latent phase the pathogen goes into this I want you to kind of remember dormant it's not causing any kind of damage it's just kind of in a period where it's not doing anything now here's where it becomes a problem if a patient is immunosuppressed all right so now you have immunosuppression decreased immune function now we got a problem because now these patient populations are not going to be able to keep this bad by dormant anymore if they can't keep this bad boy dormant anymore now it can continue to replicate grow and start spreading to other areas of the longitation causing destruction we need to think about what patient population if they have an exposure are at very high risk of this becoming reactivated or just going straight and primarily progressing through that tuberculosis for these two patients when it goes out of dormant into a reactivation or the primary TV continues to progress this is the patient population that you have to think about what are those patient populations it's not hard HIV right they're immunosuppressed status post transplant that's a big one on immunosuppressive medications you know what else is interesting as they get older elderly individuals malnourished have you really wanted to you can even go down the laying of saying diabetics CKD alcoholics who are malnourished you can the list goes on and on but these are the primary things the big one that I would really really try to remember here I think is the first three HIV status was transplant immunosuppressants because in those it's likely the easiest one to pick out on the exam but patient working a Health Care system when they're in a prison system they're homeless they're immigrant they're IV drug abuser and they have HIV or they're immunosuppressed or they just had a transplant they're at high risk of primary TB and then reactivation of TB or primary Progressive TB so what does that mean they're no longer going to stay dormant these bad boys are going to start replicating and as they start replicating they'll start here in that kind of like lower lobes and they'll move upwards into the actual upper lobes and they'll start kind of causing more casiating granulomas to form within the upper lobes because they love the oxygen the upper lobes they're aerobes you know what they do they start causing a lot of necrosis fibrocases necrosis of the upper lungs lots of consolidation of the upper lungs this is a problem because now we just reactivated the TB in this situation we have secondary tuberculosis why because what happened from this point here to this point here is the patient at a decreased immune function they had the TB dormant but then their immune system was depressed that it couldn't kind of wall it off act like the gatekeeper anymore and the problem here is reactivation okay and then now this son of a gun this gone complex that was here a ranky complex if it was fibro calcified then spread through the lungs through the lymphatics to other areas of the upper lobes and cause fibrocasius necrosis of the upper lobes and that's one of the classic types of presentations here so secondary TB could be a result of a patient with primary TB they had a gone complex they tried to keep it dormant maybe they undergo out of fibro calcified kind of structure there called a ranky complex or they just kind of shut it down it's Dormer for a while their immune system gets depressed for a temporary period of time they can't kind of contain it anymore it comes out of dormancy reactivates starts multiplying growing spreading through the bronchi spreading through lymphatic channels through the upper lobes causing fibrocaseous necrosis so what happens in this situation of secondary TB they form what's called fibro Cassius necrosis of the upper lobes upper lobes that's one of the big things whenever you reactivate lower lobes middle lobes primary reactivation secondary TB upper lobes cavitary fibrocavitary lesions okay big thing to think about now in this other situation here in the less than 10 percent of patients who have primary TB they have that gong complex it then decides to maybe not go into a dormancy it just says hey I got no immune function that's preventing me from continuing to replicate continuing to go crazy and so in this situation the decreased immune function it just goes right into primary Progressive TB your immune system isn't strong enough to contain it and keep it dormant from the get-go so in these patients who get primary TB and they also have hivs their status post transplant their own immunosuppressants diabetic CKD alcoholics malnourished whatever from the get-go they're automatically at risk of just progressing from primary TB just to Progressive primary TB and so the same kind of presentation happens in secondary TB where maybe they had a gone complex right right here in the lower lobes plus maybe they had a Hilo lymphanopathy then what does it do it gets activated when it gets activated it spreads to the upper lobes when it spreads to the upper lobes it forms more casiating granulomas that cause fibrocavitary lesions and these fibrocavitary lesions primarily form within the upper lobe so you see how primary Progressive TB and secondary reactivation TB kind of look the same it's just in these patients they either went from primary TB and progressed thus the name or they went to a latent period they had an immune system kind of depression and then they reactivated it but either way you get to the same kind of concept here where they still get these fibrocavitary lesions so fibro Cassius lesions where in the upper lobes very very important guys now here's the thing once this happens there's complications pulmonary TB that you actually see Within These patients so obviously the classic presentation is the fibrocabatory lesions within the upper lobes but you can get a lot of consolidations and what can happen is this fibrocabatory lesions they can extend imagine it cavitates and it extends and starts eating and destroying some of the tissue of the pleural way it eats into the actual parenchyma and into the pleura and then that cavity opens up into the plural space Oh that's an opportunity for air to just leak right into the pleural cavity what is this called when you get air in the pleural cavity a pneumothorax the other thing here is that as you get kind of like these fibrocaseous necrosis and a lot of like this kind of situation here it can kind of lead to a lot of pneumonia being formed here so this fibrocases necrosis can also lead to a lot of pathogens not being able to be easily cleared and so because of that these patients May develop Broncho pneumonia okay Bronco pneumonia so watch out for a lot of infection within the bronchi around the area where the fibrocases necrosis is so you can develop Bronco pneumonia the other thing here is that whenever a patient has TB it's subplural usually right so it's usually in the upper lobes where you get these fibrocavatory lesions or you get the actual gong complex in the lower lobes right right you know lower middle lobes either way in this situation there is a massive amount of inflammatory cytokines that massive amount of inflammatory cytokines is going to cause increased capillary permeability vasodilation and proteins and fluid in cells and stuff like that to leak out and this will lead to a plural a fusion so also look for possible pleurisy TB pleurisy which is just basically a pleural effusion so these are some of the pulmonary signs that you can see now oftentimes a patient won't just say oh I got a pneumothorax so I got bronchod ammonia oh I got a pleural effusion these are just potential complications that they can have from the pulmonary system due to these fibrocases and lesions consolidations gone complexes Highland lymphanopathy Etc the oftentimes these patients who have TB especially primary TB they're asymptomatic sometimes even in secondary TB they're you know or active TB they don't even have any symptoms if they do present with symptoms it's usually secondary reactivation TB or primary Progressive TB and there's one other way that they can present but if they do present usually the pulmonary symptoms that you would want to think about Within These patients is because they have these fibrocavitary lesions that they're forming they're eating up at tissue lung tissue my friends and if they're eating up at lung tissue guess what could be near these lung tissue bronchial blood vessels and if they eat at the bronchial blood vessels and then the blood gets into the actual bronchial system now you can just start coughing up blood what is this called when you cough up blood due to the cavitation of those actual lung curriculum this is called hemoptysis so look for this relatively rare but something to think about the other thing is as you have these fibrocabatory lesions and you have a patient to increase the risk of like having Broncho pneumonia right so you have these fibrocavitary lesions what they're doing is they're starting to compress onto nearby bronchial systems they're not clearing secretions as well and so then they can end up with a really nasty type of inflammation of the Airways they can end up with a productive cough you know that as you inflame Airways what does that do as you inflame Airways it's pretty straightforward you have a lot of cough receptors you know different types of sensory receptors that pick that information up and trigger a cough reflex and so look for patients to have maybe a cough maybe a productive cough the last thing that actually would be somewhat helpful and I would actually remember this is when all these cytokines are being released from these granulomas and this fibrocasius necrosis what were some of those cytokines interleukin-1 interleukin-6 tnf Alpha these have somewhat of a profound effect on the hypothalamus and the hypothalamus controls are eating it controls our temperature and so what happens is these patients maybe have some dysregulation of their hypothalamus and have fevers here's a big one night sweats look for this one as well if they're complaining of night sweats and also weight loss so the features of pulmonary tuberculosis whether it be secondary reactivation TB or primary Progressive TB oftentimes can be complications such as pneumothorax bronchod ammonia pleural effusions think about those in each one of the individual lectures that we've already talked about with these and then look for hemoptysis look for a cough here's the big one look for fevers night sweats and weight loss oftentimes in primary TB they're completely asymptomatic latent TB completely asymptomatic and usually have no idea of any symptomatology now here's the big thing what's the problem when now this TB instead of it spreading into other areas of the lungs it decides I'm going to be a bad boy or a bad girl and I'm going to get into the bloodstream and I'm going to start spreading into the bloodstream and infecting other organs then we get something really nasty we can get systemic military TB or extra pulmonary TB let's hit that all right my friend so now we got a patient here who has that nasty fibrocasius necrosis of the upper lungs maybe it's going to even involving some of their middle lobes lower lobes they've got those gone complexes it's just really starting to affect multiple areas of the lung tissue right so we already talked about how that happens with the primary Progressive TB which just forms these nasty fibrocabatory lesions or the secondary reactivation TB we already know that what's the concern is when these actual pathogens like mycobacterium start saying hey I'm going to be a little interesting one I'm going to get into the bloodstream and I'm going to go ahead and spread to other different organs of the body and cause disease there that's when you get this systemic military TB or extra pulmonary TB so the primary organs that I want you to remember there's so many but the big ones that I want you to remember here first one is the meninges so if it kind of infiltrates the meninges what are you going to have that's not hard to think about meningitis so look for meningitis so I'm not going to go through every clinical feature that I would be particularly with each one of these diseases obviously when we talk about these in individual videos meningitis thinking about them having headaches and focal neural deficits and potentially like nausea vomiting Etc photophobia but meningitis would be one of the potential concerning signs we call this TB meningitis the other one is convey of your lymph nodes but you know which lymph nodes it loves to hit the cervical lymph nodes and cause a lot of swelling lymph and optic lymphadenitis they got this weird name for the dang thing they call it cervical Infinitis but if you really want to be an understanding of it they actually call it a scrofula scrofula okay it's just cervical Infinitis or cervical lymphadenopathy particularly of the upper lymph nodes the other thing is it loves to involve the pericardium of the heart if it hits the pericardium with a heart it causes it to become very very fibrotic and calcified what kind of disease causes an intense like shell calcifications of the pericardium what is it called constrictive pericarditis so watch for pericarditis which type constrictive pericardize I know that GS probably remember that from the cardiac lectures right so pericarditis so pericardite is particularly constricted pericarditis it also can involve the liver cause injury damage to the liver if it inflames the liver and causes things like asts and alts and all those things to bump up within the actual blood we could see that there may be some degree of hepatitis so look for hepatitis specifically maybe some abdominal pain right upper quadrant hepatomegaly as well as increasing their lfts the other thing is it loves to hit the kidneys I would not forget this one so out of these the really really big ones please don't forget scrofula this may be a big one that they actually present on the exam another one is they love to hit the kidneys the kidney is a very common location for the TB to infiltrate and when it infiltrates the kidneys what it does it cause a lot of white blood cells to end up in the urine lots and lots of white blood cells and what do we call that when you have lots of white blood cells within the urine pyuria so they have a very intense pyuria but it's a sterile pie area so there's not a lot of pathogens if you were to culture it so you don't actually get the TB in it it would just be a lot of white blood cells in their urine okay another one this is actually a pretty big one too is it attacks the adrenal gland you know adrenal glands if you attack it and you damage it then you lose the ability to make cortisol you lose the ability to make aldosterone what is that called Addison's disease or adrenal crisis so watch out for these patients causing Addison's disease their ability to not produce corticosteroids so Addison's disease or some type of adrenal crisis pretty scary one there the next ones that I want you guys to remember here so remember Addison's I'd say this is a really big one to think about as well remember pyuria sterile pyuria remember scrofula here's another really big one just because it has a name to it anytime it has a special name to it they love to add things that's why scroful is one of them but here's another one if it invades the lumbar vertebrae hits the lumbar vertebrae and causes damage of the lumbar vertebrae can produce a disease called POTS disease so POTS disease so don't forget this one when it's hitting that lumbar vertebrae so here I'll just put like L1 L2 L3 L4 and you guys know we got an L5 in there yeah crack it I'll do it all right ready boom L5 but I want you guys to be thinking about this particularly if they present oh they got like you know a lot of back pain they have some degree of back pain plus they have some of the other features of pulmonary tuberculosis think about POTS disease so don't forget this one and the last one I want you guys to think about here as well is if it attacks the actual long bones it can actually cause necrosis long bones and what's that called osteomyelitis so watch out for Osteo myelitis but I would really really not forget POTS disease sterile pyria Addison's disease and astrophylla okay that will be the features of extra pulmonary tuberculosis now let's go on to Diagnostics all right my friend so when we have a patient that we're concerned has TB right so generally most patients when we're concerned that they have TB we look at the high exposure rate so patients who are working in a healthcare Society are working in a healthcare operation they're working in a prison they're homeless they're IV drug abusers they have again some type of immigration history from areas or populations where the TB is relatively prevalent and those situations they're they're high risk for exposure to TB we also have to think about the patient population who has high risk for actually the infection because their immune system isn't functional to keep it dormant or prevent it from primarily progressing right anything like I did that there so we think about HIV AIDS right you're thinking about a status post transplant immunosuppressed patients who are on immunosuppressive medications of some particular form diabetic CKD alcoholics malnourish whatever it may be in those patient populations you really should start off by saying okay I think that the patient could have tuberculosis right generally the way that we look for this is we screen patients doing something called a PPD a purified protein derivative a tuberculin skin test a man toxest there's so many different names I'm just going to call it the tuberculin skin test and the reason why I like that one is because you take a little needle and you inject into the dermis just a little bit of this molecule called tuberculin now tuberculin is kind of like one of the components of the TB bacterium and generally once you inject the actual tuberculin to the skin and patients who have had exposure what do you think is going to happen their immune system will recognize some of these proteins and mount an immune response against it and cause a localized inflammation not hard to think about so if they have had some exposure it'll cause a localized inflammation to the tuberculin so this is called a tuberculin skin test a PPD and mantox test a TB test they get a lot of different names for it but basically you introduce tuberculin and then tuberculin if it produces an immune response if you will in other words it caused like a little localized area of inflammation or induration this means an exposure exposure is present but we don't know if this patient has latent TB in other words they they went into a dormant phase we don't know if they have active TB or we don't even know if they've cleared the infection we just know that they've been exposed to TB that's all that we know okay now what's really important is is when we have this exposure because it produces an immune response the immune response will cause swelling and duration right so it'll produce a swelling all right or in duration of the skin that we can measure and use this as a threshold for certain populations to say oh that's a positive PPD they definitely had an exposure they could have cleared it they could have latent they could have active it could be one of these generally latent and active is the easiest way of looking at it so if they have a positive PPD it could be latent it could be active TB that's the easiest way of looking at it now how do we determine that we look at the swelling so we measure we inject them with the tuberculin and then generally about 48 to 72 hours so generally about 48 to 72 hours we look to see how much swelling there is and we measure it if a patient has five plus millimeters of swelling on their skin after the tuberculin skin test this could be a positive test and very specific populations what are those populations these are the ones with the decreased immune function so look for those I think that's easy to just remember decreased immune function population and the easiest ones to remember here are going to be HIV immunosuppressed oh you know what else would be a good one to think about as well I would also remember immune function decrease immune function and close contact with active TB patient so if someone actually had active TB and you had close contact with that patient and you have five plus millimeters of swelling after the tuberculin skin test that's a positive test that's a pretty you need to have a low degree of threshold for these patients so if they have swelling you want to have a low degree of threshold that's why we only go with five plus patients who are a little bit not as high risk they have a decent immune function but they have a lot of exposure risk so you see how decreased immune function puts you at very high risk that's why for these patients we have a very low threshold for them having primary Progressive TV or you know secondary reactivation TV if we go to the next one where the patient has 10 plus millimeters of in duration or swelling that's a positive test not for the decreased immune function like HIV or is the immunosuppressed the close contact with active TB this is more for the high exposure populations so this is going to be the high exposure population so this is going to be your prisons health care workers this is going to be you know the homeless individuals your IV drug abusers your immigrants Etc so you guys get the point here for this it's now they don't necessarily have a decreased immune function but they got an exposure risk so they could have primary TB and then go into a latent phase and only a very small percentage of them if they have a good immune function will go onwards to make a primary Progressive TV that's why we can relax the goal a little bit and do 10 plus millimeters of swelling and the last one here we can say that this patient population if they have 15 plus millimeters of swelling then I can say that's positive for really anybody else anyone else who doesn't have decreased immune function close contact with an active TB patient or high exposure risk so really this is everyone else besides the ones all the way to the left so if you have swelling of 15 plus millimeters that's a pretty significant swelling and that is concerning for that this patient population that they definitely could have some type of TB whether it be latent or active I can't tell you off of the tuberculin skin test let's write that down because I want to make sure that that gets into the head it does not tell active versus latent that's where you use other tests that's why the patient has a positive PPD you then go onwards to get an image chest x-ray CT scan and then sputum samples if the patient has a positive PP if they have a negative PPD you don't necessarily even have to go on to chest x-ray and CT scan so that's the reason why it's important to be able to understand this this is kind of a screening tool to determine who are at risk of latent being active TB and what's the next step Imaging so one of the things I really want to talk about though here really quickly is that sometimes this test can give what's called a false positive and in those patients who get a false positive PPD it's really important to ask them did they get What's called the BCG vaccine which if they got the BCG vaccine you really can't tell a PPD then you need to do something else and this is why I talked about it before and these patients you actually have to do what's called the interferon gamma release asset interferon gamma release assay so do you remember I'm not going to draw the whole diagram here but do you if you guys remember we had that caseiating necrosis here and then we had some macrophages that were around here and then I told you that we had a bunch of lymphocytes that were also mixed around here remember I told you that the T lymphocytes they released a lot of a very specific type of molecule what was that called interferon gamma that's why we use this release assay and patients who have been vaccinated because it's very very good so really this is even better than the PPD test because it'll rule out a lot of your false positives and false negatives we could also do this test if the patient has a false negative test so a false negative test I would really think about these patients who don't have a good immune response Maybe and so they may not produce enough induration to be able to have significant swelling for us to be able to get that five millimeters because they don't have the immune system able to do this and so think about those patients with HIV and think about patients who have sarcoidosis this is due to what's called Energy so in these patients I would again do and interferon gamma release assay it's going to be way more uh like specific and also less chance of false positives with false negatives so that's an alternative to the diverglin skin test if they have a BCG vaccine HIV or sarcoid okay so patient test positive for the PPD or the interferon gamma release assay then what do you do so here's how I want you guys to think about this step by step in your head have a systematic or goal for the stuff you first start off PPD positive or interferon gamma release assay is positive in this situation you go on to Imaging okay that's the next step so let's talk about that I have a patient test positive I can't tell if they're positive if they have active or latent so I don't know if they have primary Progressive secondary reactivation or dormant latent TB so it was a primary TB that got shut down and kind of put into a dormant phase I don't know the only way I can do that is if I look and see if their Imaging suggest active type of TB so do you guys remember just a quick start off here you have a patient usually lower lobe middle lobe around these areas they have a gone Focus then Hilo lymphoninopathy What's this called this is called a gone complex usually indicative of primary TB what happens is generally in patients about 90 percent of the time what will happen is this can get completely cleared or this can undergo a lot of fibro calcification fibro calcification so we either can clear it or we can cause a lighter fibro calcification essentially kind of like shutting down and kind of keeping this into a dormant phase so sometimes you can see what's called a ranky complex a lot of fibro calcifications around the gone complex what's really concerning and really positive imaging signs because this isn't really the case here if you have a gone complex or ranky complex it doesn't necessarily mean that you have positive active type of TB what really is the case here is these next two if I see those fibrocaciating necrosis I see any of this or I see a lot of consolidation in those upper lobe areas so here's some fibrocaciating necrosis is a really really big big big sign here for this active TB whether it be secondary reactivation TB or a primary Progressive TV if I see these fibrocasius kind of like lesions that definitely makes me think about active TB so active TB okay because it's fibrocases necrosis a lot of upper lobe consolidation upper lobe involvement generally these are big big things to take away the last one is if I start to see a lot of that Millet C type of appearance it's spreading so diffusely throughout the actual lung tissue maybe I still have some fibrocaciating necrosis up here but I have so much of these kind of like spreading or nodular opacities and bilateral lung fields and it's involving so much lung tissue What's this called miliary TB so this is called miliary TB which is usually when it starts to spread to the extra pulmonary system so generally when I have a patient I'm concerned that they have active TB versus latent TB how do I kind of use this if they have a positive PPD and an interfering gamma release assay one of the two they get the Imaging if the Imaging shows chest x-ray or CT is positive for active kind of like findings then it's active TV if the chest x-ray or CT is negative for any types of active disease then it's latent TB it's not too complicated to think about that right and really the way that we're looking for this is the upper lobe involvement fibrocases necrosis if they have like a Gong complex that could be primary DB well if you're looking for again them to clear it generally they may clearly and have a little bit of scarring there present or a lot of fibro calcifications they're present that could be still latent TB so it doesn't mean that it's an active tuberculosis really I think the big thing to remember here is the patient is having some of this upper lobe fibrocases necrosis consolidation infiltrates that are being involved there or military involvement the military appearance bilateral small nodular opacifications there all right so like we talked about on the actual whiteboard particularly with the Imaging it's really important to again think about the particular findings so if you have a chest x-ray and the chest x-ray is completely normal and there's no abnormalities present then it could be potentially a patient who is either resolved or cleared the infection has like a latent TB but in a patient who has like a primary tuberculosis remember I talked about how they get those cases and granulomas that can be sub plural in the middle or lower lobes and then they can all they're just called the gone focus and then on top of that some of the actual cases and granulomas can spread to the nearby hilar lymph nodes and so if you have a patient who has a higher lymphat or not but the plus they have some of these gone focuses and the right middle over right lower lobe what is that called again a gone complex so that could be somewhat suggestive of a primary tuberculosis all right let's take a look at another chest x-ray here we have another chest x-ray of a patient right so let's say that they started off they had primary tuberculosis where they had that gone complex now the gone complex right could be indicative of primary TB now they may completely resolve that infection clear it out cause to become a fibrocalcified type of structure which is called what a fibro calcified gong complex is called a ranky complex right now what can happen is is that a patient may have a healed up lung so they may have latent TB and then what happens is they have a reactivation of the TB so they develop secondary TB or they ended up with primary ptb and they continued to cause Progressive lung damage primary Progressive tuberculosis and what happens is they spread from like the right middle lower lobes or left middle lower lobes and then they move upwards to the top parts of the lungs the upper lobes of the lungs where they start to form a lot of granulomas that KCA and cause fibrocaseous necrosis of the upper lungs and so you see how in the upper lungs you have like this consolidation and opacities up here but you know what else you can see it's kind of fable you see this like little circular and like cavity here that's really dark this is a fibrocasius necrosis here of the upper lungs this is indicative of a primary Progressive TB or a secondary reactivation TB and it's just causing consolidation it's causing fibrocasius necrosis of the upper lobes this is big things to think about in patients with tuberculosis now we'll take a look at a CT to really get an idea of what that fibrocases necrosis looks like it's actually pretty nasty take a look at this so here on this CT you can see as we come down we're going to move into the lung Windows oh my gosh look at this you see these big big cavities with a lot of fibrous tissue around it and calcification this is a big fibrocasia is necrotic cavity here due to secondary reactivation tuberculosis or primary Progressive tuberculosis that just really damage up those lungs and cause an Associated kind of like cavitation there and a lot of consolidative lesions there that can increase the risk of bronchial pneumonia if that cavitates near the pleura can cause a pneumothorax and cause a lot of exudative pleural effusions to form as well so think about that in these particular patients right so definitely interesting to be able to see these fibrocases necrotic cavities here and the upper lobes here in patients with TB okay now the last one that I want you to take a look at for this image is a patient to us what's called miliary TB all right so here's another image and this is actually the worst case of TB like a milliary TB so again we said that how patients can start off they can have primary TB with a gone complex it can become fibro calcified and completely clear stay latent right so they could either completely resolve the infection or they could actually stay until late inferiorate period and so they could have if it's a fibro calcified necrosis there it can actually be what's called a ranky complex sometimes if it reactivates or they have primary Progressive they can cause fiber cases necrosis of the upper lobes and then consolidation right things of that nature but then here's where it gets really really bad sometimes what can happen is you can have that kind of pathogen spread and cause increased nodular kind of opacities in the bilateral Airways because it spreads through lymphatic channels it spreads through the bronchi into other parts of the lungs and you get this like little Millet seed kind of nodular opacities in the bilateral lung Fields this is really nasty miliary TB and usually at this point some of the actual kind of infection is seeding into the circulation and spreading to other areas of the body where it's affecting the vertebrae the meninges the kidneys the spleen the liver uh the adrenal glands Etc so at this point this is a really bad case all right so that would be military TB all right let's get back to the Whiteboard okay after we've done this and we think that the patient may have active TB and then we can move onwards and really kind of add on to the next part here which is saying I need to get sputum plus or minus biopsy to truly kind of have a some degree of confirmation that this patient has tuberculosis let's come down and talk about that all right so you think that the patient may have active TB okay so what you can do is if you have some degree of Suspicion the other thing that you could be doing at for this patient is let's say that you have again that Consolidated lesions or infiltrates of the other fibrocaseous necrosis here or maybe have kind of like a gone Focus here here whatever it may be let's say that you want to aspirate or obtain some of the actual contents of this infiltrator consolidation or fibrocases necrotic area what you could do is is you could pull some sputum from their airways and you can do this via induced so sometimes you can actually kind of like take like a nasotracheal suction or you can have them kind of cough it up sometimes you can do what's called a Bronco alveolar lavage where you send a bronc down and you kind of suck some of the actual mucous secretions up and what you do is you obtain some of the sputum then what you do is you take the sputum and you put this you actually have to do this at least three of them so you have to obtain at least three cultures generally we like them to be at least eight hours apart sometimes we just do them every morning so you do three days of student culture generally right in the morning and you'll do this via again like some type of induced sputum what we're going to do is we're going to take the pathogens that we abstained from the sputum and put them into a very specific type of culture medium and we test them so what we do is we take all of these and here's the gold standard I can't stress this enough you take these three samples and you do something called an acid fast bacillus smear and a culture and this here together is the gold standard okay so if this comes back positive in combination with imaging findings in combination with the positive PPD and the patient has symptoms this is a rip roaring active tuberculosis that's really important to be able to remember oftentimes that's a big big thing that I want you guys to be able to understand so we take three sputum cultures at least more than eight hours born but generally just doing the morning and then we test them via the acid fast bacillus mirror and culture sometimes nucleic acid amplification tests may also be another one like a PCR test sometimes if you really want to and you're doing a bronc as you're going in and trying to suck up some of the sputum and you find the area of where the fibrocases necrosis is you can biopsy a piece of tissue if you're already down there so if you already are bronching them you can just pull a piece of that fibrocasis necrosis out and then send it to the lab and then this could also be another thing if you send that off to the lab what they'll do is they'll look at that under the microscope and what do you think they're going to find so I told you this term over there before Casey eating granulomas so casiating granulomas kind of one of those buzzword terms all right my friends if a patient who has positive BBD or interference gamma really sad States positive they get Imaging it's positive they also have symptoms and they have a positive sputum particularly via the acid fast bacillus smear and culture then this is a very significant or they have granulomas they have the case eating granulomas these are all pointing towards rip roaring active TB okay just kind of additional things to support it all right my friends now that we've done that let's talk about the treatment of TB and some of the quick adverse effects of the medications they may ask you about on the exam all right my friend so now we're going to talk about the treatment of tuberculosis so we'll talk about the two types latent active right so just to remind yourself right if a patient if I'm concerned that they have some type of latent tuberculosis so let's say that this is in the category of latent tuberculosis if I think they have latent TB what did I already kind of go through all right I told you that the chest x-ray CT finding should be negative for any kind of active disease so chest x-ray CT should be negative of any active type of TB PPD will or interfere on gamma release acid will be positive or negative it'll be positive so that'll be positive the other key feature here is do they have symptoms what I tell you about patients with latent TB or primary TB they are usually completely asymptomatic no cough no hemoptysis no fevers no night sweats no weight loss no features of pneumothorax bronchod pneumonia pleural effusions extra pulmonary TB all of those things so because of that look for features of no symptoms no symptoms my friends all right so we're treating a patient with latent tuberculosis what are the regimens well there's two particular regimens here the first one that I would want you guys to know here is primarily isoniaism we call this inh so in this situation you know ionized that ironh causes B6 division CB so because of that we just like to give B6 with it to prevent the actual incidence of B6 deficiency so oftentimes we give inh and we give B6 which is paradoxine and we do this approximately in like nine months okay so for approximately nine months that's a long time for latent TB but that's how we'll generally do it and we do this based upon if a patient has a positive PPD they have a negative chest x-ray CT they have no symptoms but here's the other thing we would do this if the patient has a high exposure risk so if the patient is has HIV they have immunosuppressant immunosuppression of some kind they are working in a Health Care System they are working in a prison they have IV drug abuse you see what I'm saying so really try to risk stratify your patients and think about which ones you're going to put on this medication for that long the other one which is a shorter regimen which sometimes is preferred by some people is you can do Rifampin so Rifampin generally we actually prefer its brother rifampicin erythromycin I apologize just because a lot of these patients may have HIV and rifampins a cyp450 inducer so it decreased the effectivity of HIV drugs so we prefer the brother which doesn't do much of that kind of problem called rifamycin but we're going to put Rifampin and generally that's a less like long time so four months now because you're putting patients on medications this long you may want to consider some directly observed therapy for patients who are concerned that they're not going to be complying with these medications for that long time so sometimes we consider dot therapy so directly observe therapy for people who are concerned they won't stick with it especially if they have active TP we really need dot therapy all right but that's how we'll kind of go through this all right now for the next one active TB you think that they have active TB whether this be secondary reactivation TB or primary Progressive TB in these situations what do we know about their chest x-ray CT is going to be positive for active disease okay upper load fiber capillary lesions military TB nasty consolidations things of that nature pbd interfering gamma release acid positive or negative positive and then symptoms yes that's kind of the big thing there as well right so they do have symptoms so obviously in this situation cough fever night sweats weight loss hemoptysis features a bronchod ammonia pneumothorax plural effusions extra pulmonary TB of all those organs that we talked about case and I have a patient who has active TB how do I treat them so we do something called The Ripe regimen so the ripe regimen is consisting of four particular drugs right so generally we'll do something first so the first two months first two months will do something called Rifampin there's a bunch of these dang things plus isoniazid plus paracetamide Plus Ethan butal now here's the thing there's another drug that we can use or streptomycin it's one of those two so you can kind of like substitute as you see but generally the most common one is going to be Rifampin isonized it perazenamide and Ethan butyl but you can potentially substitute streptomycin for FM butyl especially if they have underlying eye disease because we'll talk about later Ethan butol causes optic neuritis so generally we do this particular regimen and we do this for at least two months okay so for at least in this patient population two months then after we do that we do something else we follow it up so we continue and we do something else after that so the second thing that we'll follow up with is after they finish this regimen for two months we do something else for four more months so then we just do Rifampin Plus isoniazine and then you do this for again how long four months so we'll do that for four four months now one of the big things I already told you is what should we add on to isoniazide if we're ever anytime you're giving isomizer what do you have to give with it B6 so just remember we already put it up there but add B6 to the regimen so that you don't get a B6 deficiency but that's kind of how we'll do this we call this The Ripe regimen we generally give r-i-p-e usually not streptomycin it's not very common but we usually do this for two months and then we follow up with Rifampin nice and eyes of performance so a total of six months and then again because there's such a long duration you may need to have dot directly observed therapies for patients that you're worried about compliance all right my friends that's how we treat Laden TV active TV the last thing here that I want to quickly touch on because they may actually kind of try to sprinkle this into the exam is if patients have these medications and they're taking these medications what are some of the things that you could observe they say oh patient has active TB you put them on the ripe regimen and they started to develop this particular thing which one of the medications could be due to if they say patients coming in freaking out losing their mind saying I have like red orange urine what's wrong with me this could be due to Rifampin so look for any kind of red or orange colored urine that could be a feature of the Rifampin the second thing here is that Rifampin is also a cyp 450 so a sip 450 inducer it's an inducer what the heck does that mean that means that it helps to be able to stimulate the cyp 450 system to rapidly metabolize drugs so that means if I take this drug and I chew it up I'm going to have less of this drug and more of the actual metabolite if you will so less active drug it decreases the actual concentration of drug so it decreases the concentration of active drug why would that be a problem my friends if I had patients who are already very high risk for TB like HIV they're taking HIV medications which interact with the cyp450 system they take rifamp because now they have TB what does that do TB will inhibit the actual um well I'm sorry we'll accelerate the metabolism of the HIV meds what happens to the concentration of their active HIV meds it goes down are they going to be able to treat their HIV now effectively no so that's why in certain situations if we are concerned that they have HIV we switch things to like rifamycin orifibutin in those patients who have HIV all right but that's the big thing to think about really really don't forget this one for a phantom for isoniazide I already kind of talked about it it's peripheral neuropathy in the peripheral neuropathy is usually due to B6 deficiency so I really just want you to remember this one there's a lot of these things that can happen but B6 divisions is going to be the big one that's why we give B6 if they present this they say they have neuropathy the neuropathy is likely due to the B6 deficiency there's so many other features but I don't think it's worth mentioning them because you're not likely going to see them on the exam the other one here is that it can cause hepatotoxicity so it can kind of injure the liver so they may say you're on this type of medication regimen what should you monitor on these patients lfts so monitor their lfts because isonized pairs into a minor minor degree of hampin have a padotoxicity so monitor lfts that's another big thing so pure xenomide what's the problem with this one what they may say is you have a patient who's putting on the ripe regimen and they have gout you know what Pierce nmi does it increases uric acid if I increase uric acid and I cause more uric acid to go into that big toe and I just cause it to kind of deposit there what am I going to do I'm going to exacerbate that gout and that person is not going to be happy with me so watch out for patients who have gout because it can cause hyperuricemia and again we already said this it can cause piercingamide hepatotoxicity so monitor the patients lfts we often do this anyway for The Ripe regimen in general so monitor lfts because of these two primary watch out for HIV medications with Rifampin and watch out for gout with pyrizinamide watch out for B6 deficiency with isonized Ethan butyl it loves to damage the optic nerve so it just jacks up the optic nerve and causes inflammation of the optic nerve what is this called optic neuritis look for color blindness maybe Vision like decrease in visual Acuity as well so optic neuritis oftentimes these patients need to get frequent eye exams all right streptomycin we don't often use it so I'm going to briefly go through this one I'm not even going to write it down but it loves to attack the ear and the kidney so nephrotoxicity nephrotoxicity watch their BMP being creatinine and also loves to attack the inner ear so it may cause Oto toxicity so decreased hearing so watch out for any ototoxicity decrease hearing and nephrotoxicity kidney injury all right my friends that covers tuberculosis all right Engineers let's do some cases here so we got a 45 year old male who's homeless recently released from prison presented in a journal Clinic with night sweats weight loss and hemoptysis medical history pertinent for HIV and IV drug abuse so given these types of information here we can definitely see some particular risk factors for this patient for tuberculosis right so we see a lot of risk factors risk factors for exposure being homeless recently released from prison IV drug abuse and we see a potential risk of again the progression of the disease that being HIV and even again IV drug abuse so if we look here at the physical exam findings we see that the vitals nothing really kind of pops out super obvious other than one thing but BP's normal heart rate normal respiratory rates normal spo2 is normal but the temperature is just a slightly bit elevated so there's a low grade kind of temperature here now the question that I have for you guys is if this patient does have tuberculosis right they definitely have the risk factors they definitely have the risk factors for exposure and for progression of the disease my question to you is what would be some of the pulmonary complications of TB if you got into the lungs what could it actually do well the big thing to remember here is it can actually cause you know consolidation to form within the lungs and that consolidation can definitely increase the risk of pneumonia so that's one thing second thing is it can actually chew away at some of the actual vasculatures that kind of necrotizes through the tissue and can actually cause hemoptysis the other thing is it can actually necrotize through the pleura and cause the pneumothorax and on top of that can even necrotize through the pleurine cause air to leak into it causing again I'm sorry a little fluid leak into it causing a pleural effusion so you can see things like pleural fusion pneumothorax and bronchopneumonia primarily now the question is is once the actual kind of like tuberculosis starts kind of eating and really becomes either secondarily you know reactivated um because it's in a latent stage and it becomes activated because of their disease process they have something that actually kind of weakens their immune system um or they have the primary infection and then it continues to progressively cause more prankimal lung damage and then again it starts actually seeding it starts seeding into the lymphatic system seeding into the circulatory system and getting to other areas of the body where can it go we can go to the brain and cause meningitis and go to the cervical actual like uh lymph nodes and cause what's called a cervical sclerophila it can go to the pericardium because pericarditis and go to liver it can cause hepatitis and go to the kidneys and cause pyuria it can go to the adrenal glands and cause Addison's disease or adrenal failure it can go to the actual lumbar vertebrae and cause POTS disease and go to long bones and cause osteomyelitis so there's a lot of different types of things that we can see with this particular disease now the next question that we have to think about is when we have a patient who we are concerned has tuberculosis how do we go about diagnosing these patients well first off we should start off with kind of a screening test which is that PPD or TB or montauks test and so we'll start off with that first when we do that we actually find that it measures about six millimeters after giving the patient about 48 to 72 hours of that tuberculin exposure and you can see here we're just injecting a little bit of the tuberculin intradermally now after they had that they had a lot of swelling they have a lot of induration but generally theirs is six millimeters which may not sound very big but it's big to a person who has a history of HIV IV drug abuse in these types of situations here especially is if we have a greater than five millimeters with a patient who's HIV positive that's actually considered to be a positive PPD and so I think that's important to be able to remember that if they have a history of HIV they have a recent active exposure to TB that puts them at high risk and so we would kind of make their threshold very very sensitive that being five millimeters or greater now patients who actually have exposure high risk of exposure and in an infected population we can go up to 10 millimeters or greater and then those who don't have any kind of exposure no risk factors for TB that would be generally everyone else and so that's important to be able to remember these but this patient is definitely going to test positive because they're HIV positive or immunosuppressed and based upon that they're also going to be six millimeters of induration after this so they're five plus so we would consider than a positive PPD and then if you look this patient does have particular symptoms which is concerning so when we have a positive pbd it doesn't mean that the patient has like active TB they could have a latent TB they could have an exposure to TB they could have active TB it could be any of those so it doesn't really tell us exactly what kind of TB they have or if they have it but what is concerning is the patient's features they have features of they have generalized features of tuberculosis night sweats weight loss and hemoptysis so that's concerning so with that being said I definitely want to get a chest x-ray or CT scan of the patient's chest one thing to note though is that impatients who have sarcoida have HIV you want to be careful remember I told you that there is a chance of a false negative on their PPD test and the reason why for those is just because kind of a lack of an immune response and so that's really really important is that they might not actually be able to generate a strong enough immune response to actually produce any induration so sometimes that's important to remember because of what's called Energy um and just remember if a patient did get a BCG vaccine they can have a false positive so in those patients you actually want to do what's called an interferon gamma release assay test which is important to remember as well all right my friend so with that being said I see positive PPD I see a lot of risk factors I see a lot of exposure factors and I have a positive PPD in a patient is symptomatic I'm going to move now on to a chest x-ray or CT scan but we can while we're doing that we can go ahead and we can obtain some sputum samples it is important to be able to obtain sputum samples generally do this we do it three days in a row um and you'll attain three sputum cultures and what you'll do is you'll run these through What's called the acid fast bacillus mirror and you'll run it through a particular kind of culture because if you culture off the actual mycobacterium tuberculosis generally we do at least three of them at least eight hours apart it's actually easy just to do it every single morning so three days of sputum cultures every morning but generally that's what we're going to obtain on this patient the next thing is that we're also going to get a chest x-ray and CT of their chest to see what's kind of going on and we look at the chest x-ray we definitely see some type of like lower lobe type of involvement here on the left side and then if we go ahead and get a CT we can actually see like some you know fibrocavitary lesions and Consolidated lesions here this is definitely supportive of an active TB whether this be a primary Progressive TB or whether this be a secondary reactivation TB likely more the primary Progressive but nonetheless this patient definitely has tuberculosis and it's active tuberculosis which is concerning because they're symptomatic they have a positive PPD they have chest x-rays T findings and they have three positive stains so all very concerning for this patient all right so how do we go about treating these patients well they have active TB active TB you treat with the ripe regimen so you start off with Rifampin isonize it perazenamide and FM butyl and you do that for how many months two months and then you follow up afterwards after the two months with Rifampin and isolation for another four months after that and just remember that whenever you put a patient on isoniazid it can cause B6 deficiency which can cause a lot of problems like neuropathy and seizures and lactic acidosis and Etc so it's important to put them on B6 or paradoxine during that process if a patient for example had a positive PPD they had no symptoms they did have some type of risk factors that were concerning for TB but their chest x-ray CT scan showed no you know features of TB again all they had was really a positive BPD and some possible exposure to TB then you could think that this patient may have latent tuberculosis if that's the case you can treat latent tuberculosis with isoniazide or Rifampin now the duration that we treat them isonize it can be up to nine months and then if you're doing Rifampin by itself it can be up to four months so important to be able to remember that all right my friends last thing that I want to take you guys through here is how to be able to think about if we're going to put a patient on one of these medications the exam questions may come up what are the adverse drug reactions what are the contraindications what are things that you want to watch out for when you put a patient on one of these anti-tb medications and so I want you to think about that refer a refam first which one of these does it match up with it's important to tell the patient when you take this you may see red orange colored kind of discoloration in your urine your tears and it is very important if they have HIV and they're taking any kind of nrtis to really try to avoid this medication because what happens is where fampin is a cyp450 inducer so if you give it and they're taking an HIV medication what it'll do is it'll actually rapidly metabolize their HIV medication decreasing the concentration of it so they won't have as much of that medication and so that could worsen their HIV disease so I would say red orange urine cyp450 inducer is going to be the answer here the next one that we're going to go on to is isoniazide which one fits this one remember I told you take it with B6 because it can cause B6 deficiency which can increase the risk of seizures neuropathy cideroblastic anemia lactic acidosis and again hepatotoxicity you can see with this disease as well so don't forget that the next one is pyrizinamide remember causes hyperuricemia so be careful and avoid this in patients with gout and it can increase those lfts so make sure to monitor the lfts in these patients Ethan butyl make sure that you get regular eye exams because it can cause optic neuritis and cause visual changes and then lastly any type of aminoglycoside is both nephrotoxic and ototoxic such as streptomycin alright my friends that would cover this kind of lecture and all the information that you guys would need to know about tuberculosis I hope it made sense I hope you guys enjoyed it and as always until next time thank you [Music]

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Length: 69min 29sec (4169 seconds)

Published: Tue May 02 2023