All right, so let's go ahead and get started with rheumatology. This is going to be a one of two part podcasts only because rheumatology is just too dense to make this into one podcast, I broke it up into two before we get started. Thank you, as always for the really nice comments the support. I really do appreciate it. All right, let's go get started with rheumatology. We're going to start with probably one of the lowest heel topics
for rheumatology, and that's five romyalgia. This is a chronic disorder of widespread muscular skeletal pain accompanied by other somatic symptoms. So you're looking for fatigued cognitive disturbances, psychiatric symptoms. Etiology is unknown, and the patho phiz is uncertain, so there's really not a lot to know here. Just know that they're going to have some kind of chronic, widespread MSK pain combined with other somatic symptoms. So who you're going to be looking for in the vignette is going
to be women twenty to fifty five years of age. It's much more common in women, and like I said, generally in the age range of twenty to fifty five, So the vignette be looking for a young or middle aged woman on physical exam eleven of eighteen to fine tender points. Let's talk about that because there's a little fyi for that. So on physical exam person with fibromiologia, they're very often going to have tenderness. This is going to be
a multiple soft tissue sites throughout the body. But with that being said, you likely have heard of this criteria. That's eleven of eighteen to fine tender points. This was from nineteen ninety diagnostic criteria for fibromylogist, so it's been around a while. Basically stated that if a patient had symptoms of widespread pain, was tender and at least eleven of eighteen different areas when you poked them, essentially they had fibromylogia. This is what I was taught when I was
in school. It's still in a lot of the literature, but if you got up to date and you look at their latest information, their latest quote from up to date, they state quote, we no longer recommend palpating specific tender point locations or enumerating the number of tender points. The presence of such tender points was part of the nineteen ninety ACR Classification criteria. Performing such a tender point examination has proven to be impractical and clinical practice, So in reality
still around may honestly still get tested on it. And that's why I bring it up. It's an easy thing to make an exam question out of. But there's newer criteria, the twenty ten American College of Rheumatology Diagnostic Criteria, which you don't need to memorize. I just wanted to make you aware of that, and then just kind of I had to bring up the eleven of eighteen ten or points just in case you're testing on it, but just be aware of the more up to date info as well. All right, moving
on diagnosis, this is very much a clinical diagnosis. You're going to have normal lab tests. So that's the hard part about fibromyalgia is there's no confirmatory tests or biomarkers. It's a clinical diagnosis. You suspect fibromylogien patients with three months of widespread or multisite pain without another identifiable cause, so you get lab
tests, but this is just to rule out your differentials. You mainly want to exclude systemic inflammatory diseases, so get a CBC and esr C reactive protein. This is really just to rule out another underlying inflammatory cause. Key thing to remember here is that all of the labs and imaging are generally going to be normal and fibromyalgia treatment you start with. Your servative measure is patient education
including cognitive behavioral therapy. Exercise. Low impact aerobic exercise actually has been shown to improve not only the pain, but improves the sleep disturbances these patients may have. You also want to address any comorbidities, so these things aren't always often tested on. What they're likely going to ask you is the pharmacologic treatment. So if they ask you which medication you're going to give a patient with
fibromylogya, it's going to be your TCA. So tricyclic antidepressants AM a trip DeLine So when most patients, you're going to initiate therapy with a low dose of a tricyclic antidepressant and a trip delane is the main one. There's some other options cyclobenzoprene a cent arise for your exam, though I'd really focus on your TCAs in particular am a trip DeLine. So in conclusion, little no
for fibromyology. Just know the diagnosis should be considered in any patient with greater than three months of wide spread or multi site pain companied by other somatic symptoms, no evidence of another condition accounting for the pain. Patient very likely it is going to be female normal labs. Treatment's going to be conservative initially, exercise, patient education, cognitive behavioral therapy, and if you're going to give them meds most of the time, it's going to be your TCAs. That
is fibromyalgia, all right, Moving on to gout. So gout it's a very dense topic. I honestly could have made a whole podcast just on gout, but I try my best to condense this and focus just on the high yield stuff. So there we go. Gout is a condition characterized by hyperurasemia and deposition of monosodium ura crystals, causing attacks of acute inflammatory authoritis. So
I'm sure most of you are already somewhat familiar with gout. It's a common condition, but essentially, you have too much uric acid and the blood from a number of causes will go over and this results in the formation of these sharp needle shaped crystals that can deposit in the joints, leading to severe pains, swelling, effusion, And just so you know, hyper eurasemia. While it's a necessary predisposing factor for gout, majority of people with hyper eurasemia actually
never developed gouts. It's just a little extra knowledge. You don't need one for the other and etc. Whatever, So you can have hyper euraseemia never developed GAUT. All right, let's talk about risk factors. So there's a few different things that can trigger a GOUT attack. There's certain people that are more susceptible to gaup male sex. GAUT has a male predominant, so very
likely in the vignette it's going to be a man. Part of the reason it's more common in men compared to women is estrogen actually has a mild euricosuric effect, so it actually promotes the excretion of uric acid. So GAUT is very unusual in premenopausal women. So male sex is a big non non modifiable risk factor. Another one is advanced age, so that's another nonmodified I can't say that word nonmodifiable risk factor. So you're generally looking for an older man
in them. Yet, and then we have our modifiable risk factors for GAUT. So these are the ones you should be familiar with because this is more often tested on. The two important ones to be familiar with is diet and medication. So let's start with your diet. So puring rich foods is what you're looking for. So diet be a triggering factor for gaut increase consumption. Consumption of purings which are found in seafood, red meat, oregon meat like
liver. Alcohol is another big one. They can all increase the formation of monosodium urate crystals, so be aware of these foods. And the reason why it happens with puring rich foods is because when puring that's founding these foods is broken down when it's metabolized in the body, it's actually broken down into uric acid. So you can see why the problem happens with these types of foods.
So once the patients are actually on urate lowering meds like gallopurinol, diet really doesn't play such a big role anymore since these meds do such a good job of keeping muric acid levels under control. But prior to diagnosis and proper treatment, diets definitely a key factor to be aware of. And then there's medications they can increase cerum urate levels and can increase the risk of a Gaut
flare. And it's important to know these meds because you may get a question like I did it describes a patient with GAUT and they list of buns of meds and basically say which med should you just continue in this patient? So should know your meds that can lead to hyperurosemia and a potential gout attack.
The ones that you need to know, the ones that get tested on are piazenamide that's a tuberculosis med, loop diuretics like ferosamide aspirin, but low dose aspirin's odd one because it really only triggers GAUT when it's taken in low doses like less than three hundred and twenty five milligrams, like a lot of people take for cardiovascular prophylaxis. Higher doses of aspirin actually have the opposite effect and
decrease urate levels. Another one is thiazides like hydrochlorothiside, and then a fambuta, which is another tuberculosis med So those are the main meds to be aware of the ones that are commonly tested on. The way that you're going to remember those meds is by remembering this sentence. If you put too much seafood on your plate, you'll get gout. If you put too much seafood on your plate plat, you'll get gaut. So plate is the word that you
need to remember. And plate stands for the P stands for piazenamide, the L and plate stands for loop diuretics, the A and plate stands for aspirin, The T stands athisides, and then the E a Thambutall. So remember that sentence, You remember the common medas you need to know. If you put too much seafood on your plate, you'll get gallup, pure zenemie, loop diuretics, aspiranthisides, and a thambutall all right. Clinical manifestations, they
are going to have severe pain, redness, warmth, swelling. That's very common. Usually this is going to be isolated into one joint. Around eighty percent of initial flares involved just a single joint. And then it's most common for its involve the lower extremities. In particular, the most common area is going to be your first metatar sophalangial joints, so the base of the great toe, and this is known as podagra. So if you hear podagram mentioned
it's gout of the big toe, so remember that term. It's of course possible to have it in other areas the knees and other common area ankles, but focus on that first toe podagraph. That's a really important one, all right. So as a recap clinical manifestations of a gaut flare, be looking for a description of severe pain, redness, warm swelling, likely going to
be the lower extremities most often the base of the first toe podagra. All right, So for diagnosis, there's two things that I would be familiar with for diagnosis, Arthur a centesis that's the main one, and then you have your imaging. So Arthur a sentesis. This is your best test. Definitive diagnosis can be made with Arthur sentesis in real life. How many patients are actually going to let you stick a needle in the toe that's hurting them so
bad? Even a vet she makes them scream, It's questionable, But if they ask you. The best diagnosis tests on the exam, Arthur sentesis is eighty five percent sensitive and one hundred percent specific for gaut and what you're looking for under microscopy when you perform an Arthur sentesis is negatively biofarringent needle shaped crystals, which is a characteristic finding of monosodium urate. So again I'll repeat that because it's very very important to know this. You have to know this.
They're going to ask it. So aspiration of the synovial fluid of the joint and a patient with gout is going to show negatively by your farringent. It's really important. It's negatively bierfarringent because it differentiates it from pseudo Gaut, which will go over next. And Pseudogaut is positively buy a furringent. So again negatively buyerfarringent needle shaped crystals. You have to know that, all right, So I mentioned that Gaut is negatively by a farringent and Pseudogaut is positively by
afringent. I do have a trick, not really a trick, but just an easy way to remember. One is positive, one is negatively buy a furringent. So Pseudogaut has a P. Gaut does not. So Pseudogaut is positively buyer farringent positive with a P. Pseudo Gaut with a P. Gaut was negative buyer furringent. So if you can't remember which one is negative or positive. Just remember which one has a P in the name only pseudo gaut. Therefore it's the one with positive with a P buyer furringeent. Just an
easy way to remember that, all right. So what about X ray? So I mentioned before imaging does play a role. Imaging isn't really super high yield except for the fact that if you see an a vignette they mention anything about overhanging edges or margins with a punched out appearance. These are characteristic findings of the erosive appearance scene and it joint with the patient with gout. Normally,
this is long standing gout. So if you see that the back of your mind, just kind of remember that overhanging edges or this erosive appearance on x ray that can be long standing in a patient, long standing finding sent a patient with gout on imaging. So really I would just focus on your author of sentesis, but just kind of have that in the back of your mind, all right. So those are the things I think you should know
for the diagnosis for the exam. In real life when you're practicing, very often the diagnosis of gout is just going to be a clinical diagnosis made upon the history of the exam. There's even a diagnostic rule chart if you want to look that up. Not important enough for the exam, but just basically a point system that helps make the diagnosis in the absence of an Arthur sentesis. All right, So one last thing that you might be saying to yourself,
what about measuring uric acid to help make the diagnosis. We're talking about diagnosis. We know, you know increased uric acid hyper eursemia. Why aren't we the uric acid levels? So it turns out that up to forty three percent of patients with acute gaut flares they're actually gonna have normal or even low serum urate levels. And part of the reason is because the cytokinds that are released during an acute attack, they can actually lower the urate levels. So
measuring uric acid levels not a good idea during an acute attack. So when are you going to measure uric acid? Best time is two or more weeks after the flare has completely resolved, and measuring uric acid levels it's a good tool to measure the response to treatment once you have them on a prophylactic agent like alipurinol. Obtain uric acid levels to make sure the treatment is working at suppressing the uric acid levels in the body. So to reiterate, don't measure
uric acid levels during an acute attack. All right, let's talk about our treatment. Let's start with acute first and then we'll talk about chronic treatment. So before we start with treatment and the meds, always make sure you address lifestyle changes less beer, less meat, seafood, lose weight. Not so much test it on, but just good to know for real life. All right, let's talk about acute attacks first. So for an acute attack,
there's three meds or classes that you need to know. End sets, steroids, and culture scene. They all work and quoted from up to date, we suggest oral glucocorticoids, end sets, and culture scene as equivalent first line options. So basically, you just have to decide which agent will be your best for a patient, considering the patient's comorbidities and other factors which I'll go over. So let's start with our end sets for US, so end sets,
neproxin, endomethsin. Those are some commonly used ones. A potent oral nd set like neproxin or intomethicin. They work really well for GAUT. They're generally pretty cheap, so they are used very frequently, but you have to be careful in using these in certain patient populations. So they're going to give you a patient with an acute GAUT attack, They're going to list a bunch of meds and they're going to ask you what you'd pick. You have to
look at the comorbidities the patient has. You don't want to use end sets and a patient with core renal function and active duad and ologastric ulcer. Even in some types of cardiovascular disease like hard fact failure, there's some other contraindications. Obviously, allergies and sets can combinatet use of antiquagulance. But the three that I focus on for the exam bad kidneys, bad heart, bad GI
tracked. Don't get tricked in a vignette when they give you a patient with gout asking which meant to pick before you pick the proxy and make sure their GFAR isn't like twenty. So again, end sets are a first line agent for a cute GUT as long as the patient doesn't have chronic kidney disease. Generally, a gfar less than sixty and acute ulcer or certain types of cardiovascular disease, but really focus in on the chronic kidney disease because that's normally what
they're going to give you in the vignette to try to trick you. Okay, let's talk about our glucocorticoids next. They come in a couple of varieties, oral, intraarticular, so like a steroid injection, all depends on how many joints are involved. They work really well, and what's really important, they can be used in patients with moderate to severe renal insufficiency. So keep
that in mind. If they give you a patient that has chronic kidney disease and they have nd sets and steroids in the answer choices, make sure you're choosing your steroids and not end set. All right, So who should you be careful prescribing steroids too? Obviously you're poorly controlled diabetics. This is really important. Steroids can and will cause a pretty significant spike in blood sugar, so it'll be really careful with your brittle diabetics that work and the chronology.
I see this all the time. Patients come in, their blood sugar is perfect. They get some prednicess on on their blood sugars through the roof, so be really careful in patients with diabetes. It's it's not an absolute contriunication. You just want to be careful with that. Also, be careful in patients that have an ongoing infection or post op patients because gluca cortochoids can increase the risk of impaired wound healing. So remember steroids are another great treatment option
for acute flares. And I'll say it again because it's really important you can use this in patience with kidney disease, because that's likely the question you'll get. Let's talk about Culture Scene next. So this is probably the least used option of the three. Culture Scene is effective for acute flares. But what's unique about it that you really need to remember it can actually also be used for chronic management of gout. And it's the only men that can be used
for both acute and chronic cases of gout. Although it's certainly not the preferred agent for chronic gout management, but you can use it for that. To just so just know that really just two things that would know for Culture Scene one, like I just remember you can use it for acute and chronic out, and if they mention an adverse drug reaction with culture Scene, it's going to be a diarrhea. Culture Scene is notorious for causing this, and they,
for some reason often like to ask about it. On Apocrates, it actually says in the comments quote diarrhea will likely proceed pain relief, which I just thought was funny. You can tell your patients once a diarrhea starts, you know we're getting close. Just start working soon. So anyways, remember colch scene is another option for acute flares as well as chronic management. Most common ADR is diarrhea. All right, let's talk about our chronic treatment.
So for chronic treatment, there is one drug that absolutely runs the show, and that is lapieran al. It's part of your x anti inoxidase inhibitors. If you remember only one medication for chronic gout management, let it be lapper at all. So it is your first line prophylactic treatment for gout. Like I said before, is a xanthe and oxidase inhibitor. What the heck does that mean? So? Xanthe and oxidase is a enzyme that helps puring breakdown
into uric acid. So if we inhibit this enzyme, we stop the process and therefore we decrease the amount of uric acid that can be produced. And this works obviously very well. Adverse drug reactions for alla purnal. The one that I would remember is Steven's Johnson syndrome. So this one always seems to come up. Alpurnals one of the medications, one of the menu medications that can cause Stephen Johnson syndrome. And I went over thisnemonic before in the seizure
lecture. But if you can remember this demonic, it will help you remember the common meds that can cause Stephen Johnson syndrome. So the sentence that I remember as soon as I see Steven's Johnson syndrome, I think of the first few letters in Stephen Johnson and the first few letters of Steven Johnson are also in Steve Jobs, And that helps them remember Steve Jobs created Apple PCs, and then Steve Jobs created Apple. Piece sees Apple PC stands for the main
meds that can cause Stevens Johnson syndrome. Aliperan al, there's your alipianol, fennetin, pheno, barbital, lemotorgene, ethosuxomie, penicillans, cover mazipine and sulfonamides, so those are the main ones. Alipianil is obviously in the a there, so you remember as soon as you see Steven's Johnson syndrome, think of Steve Jobs and Steve Jobs created Apple PCs. Those are the main meds
for Stevens Johnson syndrome. And one of the men I wanted to mention the anthienoxidase inhibitors is one called Fabucks's stat so this is another X anthienoxidase inhibitor. There's really nothing high yield to know about this men except for the fact that it's ax anthienoxidase inhibitor. We don't use fabucks as SAD as often as aliperanol because it has some adverse effects that alipionol just doesn't have in particular and increased
cardiovascular risks, so be aware of it. But remember aliperonil is going to be the preferred agent. So there's only two meds to know for this class. But sometimes you're going to forget their mechanism of action. So if you want a way to remember there's anthienoxidase inhibitors, because I did get a question on this, they basically ask which of the following is a x anthienoxidase inhibitor, And right away I was like, okay, whereas all appear and all
the answer choices that wasn't there. It would obviously be too easy. They put fabucks is set. So the way that I remember these two meds were as anthienoxidase inhibitor as well was by remembering the sentence. In February, I get all of my exos because it's the month of Valentine's Day. In February, I get all of my exos like xoxo, hogs and cases. I get all of my exos because it's the month of Valentine's Day. So in February, February is for Fabucks's stat all is for all apperanol, and then
XO stands for xantien oxidase as an xanthienoxidase inhibitor. So just a quick way to remember the two drugs and their mechanism of action. All right, So, ours anthienoxidase inhibitors helped decrease production of uric acid. But what about medications for a patients that are just under excreening uric acid? They're building up uric acid they're just not peeing enough out. What do you do then that's when
you you use are uricosuric medications. So uricosuric medications. Probenicid is really the only one that you need to know because it's the only drug in the US approved by the FDA for the specific purpose of promoting renal uric acid clearance. The other two sulf in pyrozone and lesinurad, they're no longer marketed here in the US, so really just focus on probencid. Probenicid works by promoting renal clearance of uric acid by inhibiting the proximal tubule that mediates urid reabsorption. So
there's not a lot to know here. Just remember probenicid is the one that makes you pe out uric acid. It's not used very often. One of the thing to know about it is you want to avoid this drug in patience with the history of nephrolothiasis because it can increase urinary calcium excretion in patients with gout, so it can cause a recurrence, so just be careful in patients
with prior kidney stones. One of the medication to be aware of. I don't think there's much to know about it, or really anything to know about it. Just know that it's a treatment for chronic gout and it's called pick a lotic case. It's really only a reserved for patients with severe cases of GAUT who have failed to previously mentioned therapies like alipurinol. It's administered intravenously. I'm not really going to go any further into this, man, because I
really don't feel like it's important enough. And then, of course, remember another chronic med like I mentioned before, is culture scene because remember culture sting can be used for acute and chronic management of GAUT. All right, So to wrap up treatment, I would know your acute treatments, your acute meds, your acute med's well and said steroids, culture scene, if your chronic meds, just really focus in on alipurinol, and that is your treatment for
gout. All right. Next we're going to talk about gout's cousin. That would be calcium pyrophosphate crystal deposition disease aka pseudo gout pseudogaut. The name isn't really used that much anymore, and more acutely, more accurately describes the acute attacks which clinically resemble acute attacks of gout. But I'm going to call it pseudogaut the whole time because calcium pyrophosphate crystal deposition disease is just too long to
say, so there's way less to know here compared to gout. I've broken it down into just about five things that you need to know. First, it is a deposition of calcium pyro phosphate dihydrate. So in GAUT we had accumulation of uric acid. In this case, we have an accumulation of calcium pyrophosphate depositing in the joints and the soft tissue. The knee is going to be the most common joint to be affected. The knees affected in over fifty
percent of all acute attacks. So in gaut, who is all about the first toe, podagra pseudo gut, It's all about the knee. So about half of the cases are going to involve the knee. I used to have this weird way of remembering this, you know, but weird demonics are sometimes the best. So instead of remembering pseudo gout, I used to remember sumo gout, as in sumo wrestlers and anytime you see a sumo wrestler, they're always bent over with their hands on their knees. If you google it,
you'll see what I'm talking about, Like the sumo wrestler stands apparently. So anyways, as soon as I see pseudogaut, I think of sumo gout and the picture of the sumo wrestler bent over with his hands on his knees, and that just kind of triggered my memory to remember. This disease most commonly affects the need, all right, so the needs most common. Other areas, of course, can be affected to the risk the MCP joints, the hip, shoulders, elbow, spine, all fair game. Just an fyi
and acute attack of pseudogaut. While it can be very similar to gout, and that's why they initially came up with the name pseudo gaut because the close resemblance to gout attacks, the intense pain, redness, warmth, swelling. But the thing about it is that in pseudogauts, these acute attacks, they're much less common. Majority of patients with its disease with the calcium deposition in their joints, more often than not, are going to be completely asymptomatic,
So just kind of be aware of that. All right now, this is really important. Positively biofringent calcium pyrophosphate crystals. This is the thing to know about pseudogaut. If you forget everything else, remember this, positively biofringent crystals on synovial fluid analysis. Oftentimes they're going to be rhomboid shaped. This is the key difference between pseudogut and GOUT because remember GAUT was negatively by afarringent.
And again remember that because pseudogut has a P GAUT does not, in as pseudogaut is positively biafarringent. Remember on pseudo gaut you're looking for positively biafarringent calcium pyrophosphate crystals. Often they're going to be rhomboid shaped, all right now. On X ray, you can use X rays another diagnostic tool for pseudogaut.
If they mention on X ray, these punctate or linear radiodensities in the cartilage of the joint spaces, that's from the accumulation of calcium crystals in and around the joints, and they look like these little white lines on the joints. In the X ray and they're called it's known as like chondrocalcinosis, which is like another name for pseudo gauts. So if you see anything mentioned about punctate or linear radiodensities, or if they use the word chondrocalcinosis, be thinking pseudo
gaut all right. And then one last thing to know. When we were talking about the treatment for acute attacks of pseudo gaup, it's the same as in gouts. The treatments are essentially the same. The slight difference is there's more of an emphasis on intra articular steroid injections, So when two or less joints are involved, intra articular steroid injections are generally going to be your first line of these patients. Otherwise, treatment for a cute attacks and pseudo gaut
it's identical to the treatment of a Gaut flare. So just as we went over before in gout and says posteroids culture. See, there's really nothing new to know here except for a slight emphasis on those intraarticular glogal cortaicoid injections. So five things to know for pseudo gaut. This is a calcium deposition disease
needs going to be your most common joint to be involved. Remember your SSEUMO wrestler, positively buy your fringent calcium crystals on X ray BI looking for chondrocalcinosis those little white lines on X ray and the joints and intraarticular steroid injections are first line when two or less joints are involved. All right, let's move on to juvenile idiopathic arthritis. There's a few different subtypes. Isstemic, oligo,
articular, polyarticular. Wouldn't focus too much on that. This is a chronic pediatric inflammatory arthritis onset before sixteen years of age and presence of aarthritis for at least six weeks. So juvenile idiopathic arthritis, it's this blanket term that covers a bunch of different types of chronic pediatric authritis. Pathos really not well understood with this condition. It's ultimately a diagnosis of exclusion and there's really only
a few things to know for the exam. So peak incidence is between one and five years of age, and it's important to remember that less than sixteen years old is the cutoff for this disease, so if they're any older, the onset is after sixteen years of age. It's no longer called juvenile idiopathic authritis. It's then going to be called adult onset stills disease or remember they're going to be younger than sixteen years old. Let's talk about the clinical manifestations
next. These are fairly unique and you should be familiar with them. It's really four that you need to know, and that's going to be fever, authritis, rash uveitis. All right, so let's talk about them. So the fever, this is primarily seen with the systemic subtype, but it's not just any fever. The fever is unique and you need to remember it's unique characteristics for the exam. So first it's persistent at least two weeks to make
a definitive diagnosis of the systemic subtype. And then more importantly, it follows this diurnal or quotium pattern, meaning that every day they're going to spike a fever, but every day the fever is also going to dissipate. That's the key. The diagnosis is questionable if the patient's temperature is not spontaneously returning to normal on a daily basis. So fever during the day then return to normal each day. That's the diurnal or quotium pattern to the fever, and it's
how they're going to describe it in the vignette. So remember that arthritis arthritis has to be present for at least six weeks. The polyarticular subtype just means that specifically five or more joints is involved, and fewer than five joints would be the ollegal articular subtype rash, the salmon colored rash we see in the systemic subtype. It's another thing that they love to mention. It's this evanescent, macular salmon pink rash. So look out for that too, because,
like I said, oftentimes that comes up in the vignette as well. And then uveitis, this is really only seen in the oligo articular and poly articular subtypes. It's most prevalent in patients that are ANA positive. So children who are positive for anti nuclear antibodies their screen more often than those who are ANA negative since they're at a higher risks. Remember, uveitis really oligo articular and poly articular subtypes that you'll see it in treatment. Mild to moderate symptoms and
sets are going to be your initial treatment option. More severe disease, you'll start them on a biologic like a temera, even glucocorticoids, but for the exam, focus on your end says that will likely be the answer. And that's really it. For juvenile dowpathic authritis. Remember your daily spiking and remitting fever, your salmon colored rash, some uveitis, and the oligo and poly articular subtypes and end sets for your treatment and you're done. Let's move on
to osteoporosis. Like gaut this is another very dense topic. Let's just focus on your need to know stuff. So. Osteoporosis is a metabolic bone disease characterized by deterioration of bone tissue, leading to low bone mass and increased skeletal fragility. I don't want to dive too deep into the patheo because the pathos multifactorial, but basically, your osteoclasts are breaking down the bone faster than osteoblasts can rebuild them, so we get osteoporosis leading to these porous, brittle bones
that are susceptible to fractures. Just an fyi if you ever forget which breaks down bone and which builds new bone when it comes to osteoclast and osteoblasts. Just remember, osteoclast has a C, and that C in my mind stands for consume bone because osteoclasts are involved in the breakdown and resorption of bone. And then osteoblasts has a B, and the B in your mind should stands for build, as in build bone, because osteoblasts are involved in rebuilding and
remodeling bone. Let's talk about the risk factors next. Advanced age is obviously a really big risk fact Probably one of your biggest females are more at risk glucocorticoid therapy long term. One of the main reasons steroids put you at a higher risk for osteoporosis is that they actually decrease calcium absorption from the GI tract. They also cause osteoclast activation. They inhibit osteoblasts a lot of different reasons.
Just remember steroids are another big risk factor for development of osteoporosis. Cigarette smoking and alcohol consumptions, some other ones, and physical inactivity just to name a few. There's a ton more. Some secondary causes like ciliac disease, Cushing's diabetes. It's more common in Caucasians worth other ethnicities. It's really a lot of difference factors, and I encourage you to look them all up if you're interested. But the ones I went over the more common ones to see,
so keep those in mind. Clinical manifestations, so osteoporosis really has no clinical manifestations until the patient has a fracture. So there's no weakness or other symptoms. There's really nothing, and that's why it's sometimes referred to as the silent disease. So let's talk about the fractures, because that's what you're going to talk about. You know, when we're talking about the clinical manifestations is the actual fracture. So the big one that is associated the type of fracture,
the main one that's associated with osteoporosis. Most common type of fracture you'll see in a patient with osteoporosis, by far, is going to be vertebral compression fractures. So these are your most common type of osteoprodict fractures. This is the one that you need to focus on. What's really interesting about the type of fracture is that two thirds of vertebral fractures and patients with osteoporosis are
painless. That's just crazy to me. And this is actually one of the many reasons why we assess for loss of height in patients at risk for osteoporosis, because the only indicator that in some patients that they've had a vertebral compression fracture is the pact. That is the fact that they've shrunk in the past few months from the fracture and the result in disk space narrowing. So remember
vertebral fractures are the most common type of osteoproduct fracture. And just be aware they may not be complaining of any paint and they vignette be looking for them just to mention maybe a patient complaining of shrinking, or maybe you'll notice some chyphosis on the exam, that hunchback appearance, which can also come from this. Another common one it would be hip fractures. Fifteen percent of women five percent of men by the age of eighty will have an osteoproduct hip fracture.
And then distal radius fractures your colleagues fractures, But again really focus in on those vertebral fractures. Now, diagnosis, there's two main ways to diagnose osteoporosis. It's going to be with a fragility, fracture, and then the other one. The main one you should focus on is with your DEXAS scan. So let's start with a dexas scan because this is your best test, your gold standard for osteoporosis. It's what you really need to focus on for your
exam. So DEXAS scan or dual energy X ray absorbed geometry is how you check the bone density of a patient. Uses low dose X ray to measure the bone density at different sites in the body, usually the spine, hip, forearm, and then we measure those areas we come up with this T score. So the T score measures how far away this person's bone density is from that of a young, healthy individual with normal bone density. And that's
why osteopenia and osteoporosis are represented with negative numbers. So that's how far they deviate from a normal healthy adult. So osteoporosis, for instance, is defined at a negative two point five or less, so that means there are two point five standard deviations below the average healthy adult with normal bone density. All right, So now that we have an understanding of the test, let's talk about the numbers you need to know for the exam. So the one.
We just went over t score negative two point five or less that is diagnostic of osteoporosis, and then negative one point zero to negative two point five would be osteopenia or low bone masses, the new term that they're using more often. Now, how do you remember those two key numbers for the exam? How do you remember which one classifies osteopenia, which one classifies osteoporosis. What I want you to remember is pen is ten poor is less than two point
four. Pen Is ten poor is less than two point four, So a little rhyme there. So what does that mean? So osteopenia like PN is negative one point zero or less aka pen is ten ten being one point zero, and then osteoporosis poor is less than two point four because remember osteoporosis is a negative two point five or less another way of saying, negative two point
five or less is less than negative two point four. So remember pen is ten as an osteopenia is negative one point zero or less, and then poor is less than two point four as an osteoporosis is less than negative two point four. All right, So I talked about this before. Bone density isn't the only way to make the diagnosis of osteoporosis. Another way is from fragility fracture. So a fragility fracture is just it's another way to make a diagnosis
of osteoporosis independent of the T score. So a fragility fracture is a fracture that occurs from minor trauma like a fall from standing height, something that wouldn't normally lead to fracture unless the patient is an osteoproduct. So if a patient tells they were casually walking down the street they had a trip in a fall, now they have multiple vertebral compression fractures. That's a fragility fracture, and
you've made a clinical diagnosis of asti process in that patient. Most common site of fragility fractures are going to be the spine, so your vertebral compression fractures the hip the risk. They can also occur the humorous ribs, pelvis. So again for diagnosis, really just two things they have to remember negative two point five or less for the T score or a fragility fracture. That's really
all you need to focus on for diagnosis. Technically, there also is the fracts tenure probability that can be used for diagnosis, but for the exam, focus on your DEXA in your fragility fractures and you're done. All right, let's move on to treatment. M start with your lifestyle. I won't go too depth into that because the book of your questions are going to come from your pharmacologic agents. But just make sure your patients have adequate vitamin D and
calcium intake. Encourage weight bearing, exercise, smoking cessation, counseling on fall prevent mention, etc. All right, let's talk about men's which is where the high yield stuff is at. So let's start with your bis phosphonates alendronate, recindronate. Those are your first lines. Bis Phosphonates are going to be your first line treatment for most patients. They're very effective, inexpensive in comparison to some of the other classes, and they've been around a long time,
so there's long term safety data available. So lendronate, which is fospimax, recindronate, which is actin. Now, these are the ones that you're going to hear about the most. There's also zolodronic acid abandronate. These both come in IV forms. So a few different agents in this class, a lot of different weird names, and how are you going to remember the drugs in this class? Well, luckily, all of the men's in this class have
the word drone in them alendronate, zoladronic acid. So as soon as you see a med that has the word drone in it, I want you to think of this sentence. Phone in your drones to build strong bones. Phone in your drones, to build strong bones. So what does that mean? Well, drones, we just went over all the meds have the word drone in them. Phone is because bisphosphonate has the word phone in it. So
if you can remember the sentence, you can associate the two together. So phone as in bisphosphonates, drones as in allen dronate to build strong bones. So when they give you a vignette clear cutost your process patient that lists a bunch of meds, ask you which is the first line men for this patient? You know it's a bisphosphonate, but you can't remember any of the drugs in the class. Remember, look for your drones. Phone in your drones
to build strong bones. All right, Now, the mechanism of action if your bisphosphonates, they inhibit osteoclastic bone resorption. So bis phosphonates are what are known as anti resorptive agents. It's a little more complicated than this, but the general ideas that patient takes bisphosphonate. Bisphosphonates plant themselves onto the bone, onto something called hydroxy appetite. Osteoclasts begin to resorb that bone that's impregnated with
bisphosphonates at these binding sites. Once they do, this leads to a couple different things that ultimately leads to the destruction of the osteoclast. What happens, the first one is that it disrupts the osteoclass ability to resorb bone, and then the second thing is it leads to osteoclast apoptosis. Once the osteoclast absorbs these bisphosphonates, so the cell dies. So in the end we have less bone breakdown or resorption, which is pretty nice and simple if you just think
about it that way. Like I said, it's a little bit more involved than that, but that's just the general idea. Now adverse drug reactions, this is probably the most important thing about bisphosphonates that they always test on always, I mean, there's always gonna be a question on this, whether it's in your clinical medicine class on your pants. You need to remember this about
this class. They can cause pill induced esophagitis. So in patients that take bisphosphonates, you have to tell them to remain upright for at least thirty minutes and take with six to eight ounces of water to avoid esophagitis. You have to remember to tell all of your patients that stay upright for at least thirty
minutes them take it with six state ounces of water. If you take one of these meds and you lay down to bed right after, you don't drink enough water, they remain in the esophagus and they can lead to esophagitis. You have to remember that in these patients you have to tell them those instructions, and then you also want to try to avoid these medications and patients with a history of echalasia, esophageal strictures, barretts esophagus, or really any of
the esophageal problems, particularly with allandronate. That's really important to remember that about this class. They're going to ask you a question on it. Most commonly the list a bunch of meds. They'll say which one of these medications should the patient avoid recumbency for least thirty minutes, and then of course one of them will be a bisphosphonates. Remember, bisphosphonates can destroy your esophagus, so stay upright thirty to sixty minutes, take with six state ounces of water,
and just a heads up. If you really need a patient to be on a bisphosphonate and you know they're not going to follow the rules and stay upright for thirty minutes, or they have esophageal disorders, you can actually give them an IV bisphosphonate like solodronic acid as opposed to PO to circumvent this issue. Other adverse strug reaction is osteoocrosis of the jaw and atypical femur fractures. I
list these not because they're common, it's quite the opposite. They're actually quite rare, but just because they do come up in questions from time to time. So austegnocrosis of the jaw, the incidence is anywhere from one in ten thousand to one and one hundred thousand, and it was really only seen in cancer patience or in patience with a compromise immune system that were treated with high doses of ibiv bisposphonates, but it can still happen, so encouraged dental hygiene.
And then the atypical femur fractures is another rare complication, so just be aware of those in real life, very uncommon. Really, just focus in on your esophagitis. So those are the main adverse strug reactions to focus on. Of course, there's a laundry list of others, but again, focus on what's likely going to be tested, which is burning a hole in your esophagus, austeinocrosis of the jaw, and you'r atypical fema fractures. All right,
let's move on. There's some other classes of men's to treat osteoporosis. I'm going to mention them, but I'm not going to go really that into depth because if you're going to get an exam question nine of the time, it's going to be on bisphosphonates. So focus on those, but at least let's mention the other classes. So first let's talk about your antibolic agents. These are used more frequently, they're really reserved for patients with severe osteoporosis,
like a T score of negative three point five or less. The reason that you reserve these meds for your more severe cases is because these meds, unlike bis phosphonates that really only preserve existing bone, these antibolic agents actually have the ability to rebuild new bone. The meds in this class are terraparatide, a belloparatide, and then romo suzumab. These are your antibolics, and teraparatide and a belloparatide are synthetic forms of PT and PTRP, respectively. And then when
you take these drugs, these agents stimulate osteoblasts which help rebuild bone. And like I said before, this is different than your bis phosphonates, which were antiresorptive agents that prevented bone resorption. These antibolics are actually rebuilding new bone. What you do is you take these meds for a year or two, you
build your new bone, and then you discontinue these meds. They can really only be used for a max of one to two years, and then you start them on a bisphosphonate or another anti resorptive just to preserve that new bone that was built. The last one that I mentioned Romo suzumb it's a fairly new med It just got after you approval in twenty nineteen. Same idea, though it builds bone. Just does it a little bit differently. It's actually
a monoclonal antibody that inhibits something called sclerostin. Don't worry too much about that. So those are your antibolic agents. I gave you a little bit of extra inflo there. I don't think you should memorize all of that. Just be aware when it comes to your antibolic agents. Have some familiarity with the names of the meds that are involved, and know they're generally reserved for your more severe osteoporosis and that they can build bone. And that's really it,
right. So another medication for osteoporosis is another antiresorptive drug like our bisphosphonates, and it's known as dinasim mAbs. So it's not as potent as the antibolic agents I just went over, But the nice thing about it is it's only administered every six months. It's basically reserved for people who are not good candidates for bis phosphonates, and it's particularly useful in patients with impaired renal function as it can be safe in these patients. And then one final men to be
aware of is reloxophene. So reloxophene is a selective estrogen receptor modulator or SERM for short. It's another anti reservative agent. Does not work as well as bis phosphonates. But the unique thing about this drug in addition to treating osteoporosis is that it also reduces the risk of breast cancer, so it's usually reserved
for osteoprosis patients when there's also a need for breast cancer prophylaxis. And the way that you can remember that is reloxophene also sounds similar to another breast cancer prophylaxis treatment met that you've probably heard of, and that's tamoxifen. So it sounds very similar, right, reloxofen or reloxophene or sounds similar to tamoxifen. So remember this is the one that you use when breast breast cancer prophylaxis is
also indicated. That's the unique thing to focus on here. So those are some additional options outside of your bis phosphonates for treatment of osteoporosis. I'll reiterate focus should be on your bis phosphonates, your drones, the other ones I went over. Just be familiar with them. But I wouldn't waste any more than a minute because you're likely going to get a question about your bis phosphonates if they give you a farm question about osteoporosis. So remember phoning your drones
to build strong bones, willindronate residronate. Those are the ones you need to know, all right, So there's a lot to know frosteoporosis. If I had to give you a few top things to remember, it would be one. Remember your DEXIS scan as your gold standard test, and a negative two point five or less it's diagnostic of osteoporosis. Remember vertebral fracture is your most
common Remember bis phosphonates are first line treatment. And remember esophagitis is an adverse drug reaction of bis phosphonates, so avoid recumbency for at least thirty minutes after taking them. Those are the high sealed things to remember about osteoporosis. All right, we're almost there. We just have two small topics to go over. So polyardorized night polyardoritis no dosa wich is also known as PAN to keep
it short. So this is a systemic vasculitis characterized by necrotizing inflammatory lesions that primarily affect medium sized arteries, with occasional involvement of small arteries. So in this condition, the immune cells attack the endothelium. This causes transmural inflammation of these arteries. Transmural meaning all of the layers of the vessel are inflamed.
Eventually this causes the wall of the vessel to die. And then where we're left with these fibrotic changes, and due to all the fibrosis and inflammation, we have these blood flow disturbances, so a schemia infarction, which causes a
lot of the clinical manifestations will go over in a minute. Basically, this disease screws up your arteries, which screws up your blood flow, and whichever organ is supplied by the artery that's affected is going to lead to your clinical manifestation so kidney, heart, intestine, etc. Then Remember, mainly is going to be affecting your medium sized arteries, but occasionally can involve the small
ones as well. Hepatitis, So what about hepatitis. The etiology of most cases of PAN is going to be idiopathic, but hepatitis B and hepatitis C infection are important in the pathogenesis of some cases, and one study from France they found that hepatitis B virus accounted for one third of all the cases, so look out for that in the vignette. It can be HAPPY or C, but it's mainly hepatitis B that they'll talk about, which is more common.
Talk about our clinical manifestations next. So renal disease. Renal disease causing hypertension, So the kidneys are going to be very commonly affected. In autopsy studies, they actually found the kidneys to be the most commonly involved organ And I mentioned hypertension as a clinical manifestation under renal disease because remember the kidneys control blood volume and in turn are blood pressure. So when the renal arteries are
affected, we have renal eschemia, which you can lead to hypertension. So they may mention hypertension because of the renal arteries being affected. So let's talk about our dermatologic findings next. So there are some skin manifestations of PAN that can include purpora, levid or articularius ulcers. It's even possible to get these tender nodules on the skin levito articularius. If this is the first time you're
hearing this term, it's just this blue purple discoloration of the skin. It almost has this netli or web like pattern, which is just due to vessel eschemia. If you've ever gotten really cold and you notice your skin was kind of turning blue, that's what this is. It's just when your blood vessels constrict in response to the cold, which leads to a schemia. But in this case, the eschemia isn't from the cold temperature, it's from the fibrodict
changes we talked about before. Something else with your neurologic findings is known as monneuropathy multiplex. SO monneuropathy multiplex or asymmetric polyeuropathy is another common finding and patients with PAN. It's in up to seventy percent of patients. The neuropathy is usually asymptomatic at the start, but later on, as it involves additional nerve
branches, it can lead to a more systemic neuropathy. So just kind of remember that term mono neeuropathy multiplex, So those are the main clinical benifestations I feel like you should try to focus on. In reality, though virtually any organ of the body can be affected in patients with PAN, then you can have a wide number of clinical manifestations, so I'm obviously not going to go over all of them. But you can also have breast and uterine involvement,
splenic infarction, orchitis, abdominal pain from esenteric arteritis. But the ones I listened above are the most common ones and the ones that you should try to remember. But I said, it can involve almost anything, but there is one really important exception that you need to know. So it has this tendency to spare the lungs. So I said that PAN can affect almost any organ. But what's unique about this form of vasculitis compared to the others is that
it has this tendency to spare the lungs. That's really unique. It could absolutely be mentioned in the vignette. So if you see lung perinchomal involvement by vasculitis, this strongly suggests a different disease, not PAN, because PAN has the striking tendency to spare the lungs for whatever reason, which is quite different than the other forms of vasculitis. To remember that if it mentions long involvement, be looking for something other than PAN diagnosis. Most important thing to remember
about diagnosis is that this condition will generally be ANCHA negative. So nothing's one hundred percent medicine, but most of the time PAN is not going to be associated with the presence of antineutrophil cytoplasmic antibodies or ank UP for short. So if you see the patient as anchor positive, generally you should be thinking of some of the other vascular tides like microscopic polygitis, et So remember that you also need to know for diagnosis. If you do an androgram of these patients,
you're likely going to see numerous aneurysms of the vessels. The reason this happens is from the fibrotic changes we talked about before. Those fibronic changes weaken the vessels, which make them more susceptible to aneurysm. So just kind of be aware of that as well, but really focus on that ANCHA negative. That's the important takeaway here. Now for treatment, it's pretty easy. It's going to be glucocorticoids pretty much all patients with PAN are going to be treated
with glucocorticoids. You're more severe cases, you can add on your immuno suppressive man's like cyclophospha mind, but in general, gluca corticoids is going to be what you need to remember for your treatment of PAN. All right, So the most important thing to remember about PAN is not what it does have, but what it doesn't have, and that's really the best way to differentiate it from the other forms of vasculitis. And what it doesn't have is lung involvement
in ANKA, so no lung involvement, negative anchor. And the way that you're going to remember that is PAN is the only vasculitis that has the word no at the start of its name, polyardoritis no dosa. So when you see polyardoritis no dosa, I want you to remember the no in its name and think, this is the one doesn't involve the lungs no no dosa. Is this the one that's anchor positive? No no dosa. So if they mentioned the lungs or positive ANCA, it's very unluckly to polyardoritis no dosa.
So be thinking of some of the other vasculitides that don't have no in their name, like microscopa, polyangitis, shirt strauss ease, which are generally anchor positive and do involve the lungs. To remember, if you see no and no dosa, be remembering no lung involvement, no anchor, as this will likely be the only thing to differentiate from the other causes. All right,
So let's move on to polymyalgia rheumatica. It's not allow to know for this, but there's a few high old things I've picked out for you to focus on. So this is a chronic inflammatory condition of unknown etiology leading to pain and stiffness in the shoulders, hip, girdle, and neck. So the name may throw you off because polymyalgia rheumatica polymyalgia basically, when you break it down, means pain and multiple muscles. So you would assume that this involves
the muscles. But the muscle in PMR is histopathologically normal, and that's why in physical exam you'll normally find normal muscle strength. PMAR really involves the joints and the periarticular structures like the bursa and the tendons. PMR is almost exclusively a disease of adults, over the age of fifty. The older the patient, the higher the prevalence. Peak incidence is going to be between seventy eighty years old, and women are affected two to three times more common than men.
So the vignette be looking for an older patient, likely a woman. If you see a twenty year old NA vignette, you know it ain't PMR, so move on, look for something else. Next thing, giant cell ardoritis ring the alarms. This is the most important thing to know about PMR, probably the top five things to know in all of rheumatology. You're going to be asked about this at some point. Giant cell arduritis is associated with
polymyalgia rheumatica. You have to know that anywhere from five to thirty percent of patients with PMR are going to have giant cell So why is that so important to know? Well, giant cell ardoritis can lead to blindness if it's not treated. So if you make the diagnosis of PMR and a patient, make sure you're asking the patient about headaches, jaw claudication, transient vision loss, which can all be found in a patient with giant cell So you want to
make sure that they don't also need a workup for giant cell ardoritis. You don't want to miss that diagnosis. It's really important. It's so important that I had this ridiculous way to remembered in school, and so to this day I remember the two are associated with each other. So I want you to remember instead of the name Paul E. Mayaljo roumatica, PAULI mayalgio romatica. I want you instead, instead of remembering PAULI mayalgio romatica, remember Paul B.
Mayalgio rumatica. Paul as in the name Paul Paul and B as in the letter B, B as in boy. So instead of Paul emyalgo romatica, Paul B Mayaljo rumatica. So forget about the name Paul mayalgia forever. I want you to remember this as Paul B. Mayalgio romatica. Why Paul B. Because Paul B is going to help you remember Paul Bunyan. And if you remember those stories you read as a kid, like in elementary school, Paul Bunyan was that giant who held that big axe and then helps you
remember giant sell artritis. So Paully mayalgio romatica is forever going to be known for you as Paul B Myalgia romatica Paul B as in Paul Bunyan the giant to help you remember, this is associated with giant cell artortis. Let's talk about the clinical manifestations next. These patients are gonna have aching and stiffness involving the shoulders, hip, girdle, neck, and torso that's going to be
worst in the morning. So this is the general presentation. You're looking for pain in the proximal joints, with bilateral shoulder pain being the most common presenting menifestations in almost all patients seventeen to nine. You can also remember that because if you think back to Paul Bunyan, remember he carried that big axe over his shoulder all day. Definitely had some shoulder pain, at least that's how
I remembered it. And like I said, these symptoms that they're going to be worst in the morning or after any period of inactivity up to day. Goes as far as to say morning stiffness in PMR is invariable. Its absence excludes a diagnosis of PMR, So look for that in the vignette to describe
the stiffing or acheness to aching to be worse in the morning. They also may mention the patient as difficulty rising from a chair, turning over in bed, raising the arms above shoulder height, but in general be looking for stiffness aching in the shoulders most common, as well as the neck hips worst in the morning. Let's talk about our laboratory findings next. Increased ESR and CRP.
So you're a cute phase reactance, orthrocyte sedimentation rate and your c reactive protein, which are your inflammatory markers, they're going to be elevated and virtually all patients with PMR, so keep that in mind. That's really important. And then really the only thing otherwise to focus on for labs is you're going to order other labs, but it's just to rule out your differentials. So you'll check your rheumatoid factor. You'll check your anti CCP. This is to
rule out late on set a rheumatoid arthritis. You also check your muscle enzymes like creating kind as to rule out polyumyocytis. So with PMR, there's really no path etemonic test or labs to make a definitive diagnosis. You're essentially just looking for a few different factors is a patient over fifty? Check do they have the classic presentation bilateral shoulder or pelvic girdle aching horse in the morning?
Check? Are my cute phase reactance elevated? Your ESRCRP check? And then finally, one of the most important keys to the puzzle to say whether or not this is indeed PMR is their response to treatment. So first, what is the treatment for PMR. It's steroids. One hundred percent steroids, So low dose gluco corticoids is recommended for all patients diagnosed with polymiologial romatica anywhere from
fifteen to twenty five milligrams daily. The thing about PMR, unlike a lot of things in medicine that we treat, where most of the time it takes a while for the METS to make an impact, PMR is one of the few diseases that responds super quick to treatment. Some patients report dramatic symptomatic relief after just a single corticoid dose. Majority of patients experienced substantial improvement within just
a few days of starting treatment. Now, I mentioned before when I was talking about diagnosis that steroids can be part of making the diagnosis, and that's because the lack of response to initial therapy with glucal corticoids strongly suggests an alternative diagnosis. Now, of course, this isn't one hundred percent. Some patients may take longer to respond, but in general, a rapid response to pride zone is very characteristic of this disease and has actually include in some diagnostic criteria.
All right, so that was part one of the rheumatology section, Part one of two. Let's do five quick questions and we will wrap it up. Question one, fifty two year old man presents the emergency department complaining of severe pain in his first metatarsulphalangeal joint. He denize trauma to the area and states its started suddenly. Arthur synthesis is performed, which displays negatively by a
fringent needle shaped crystals. Medical history includes hypertension, type two diabetes, hyperlipidemia, and current medications include hydrochlorothizide, metformin, glyposide, and resuva statin, which medication that the patient is currently taking is the most likely culprit leading to his current clinical manifestations. Again, I'll tell you the mens. Those were hydrochlorothiside metformin, glyposide and resuvastatin, which men likely led to the clinical manifestations
that would be hydrochlorothiside. So this is about as clear cut a case of gout as you can get severe pain first toe negatively by a fringine needle shape crystals on Arthur synthesis. Ring the bell your answer right there. You just have to remember which meds can cause Gaut flares, and in this case it's
hydrochlorothiside, So remember your thyside. Diuretics like hydrochlorthiside can increase urate reabsorption of the proxymoorhinal tubule, which can elevate your uric acid levels and precipitate Gaut flares. So remember they're one of the many meds that can cause Gaut flares. Remember the way that you remember that as you remember, put too much seafood on your plate and you'll get gaut played again. Stands for pierrezenamide, loop
diuretics, aspirin, thisides like your hydrochlorothyside, and a thambutol. That helps you remember the main meds that can cause your Gaut flares. Question two seventy two year old female presents to the office today for a routine checkup. Path medical history includes hypertension, hyperlipidemia. She states she has concern about osteoporosis as her mother was diagnosed with it in her sixties and wound up with a hip fracture. A dexas scan is order which reveals a T score of negative two
point six. It is designed that the patient will be started on the first line medication class frosteoporosis. What mordant instructions should be provided to the patient before taking her first dose, So that would be to avoid recumbency for at least thirty minutes and take with six D eight ounces of water. So first you need to know what's the first line medication for osteoporosis. That, of course
is bisphosphonates. And one of the most important adverse drug reactions, like I went over before from bisphosphonates, that you have to know is esophagitis, and that can be avoided by making sure the patient stays upright for at least thirty minutes, takes the medication with at least six D eight ounces of water.
It's actually a contraindication if you look at all of the bisphosphonate meds listening under the contraindications to give this any patient who can't remain upright for at least thirty minutes, So remember that that's really important. Question three. Sixty three year old female presents to her physician's office complaining of pain and stiffness and her shoulders,
hip and neck. She states the symptoms are very severe in the morning, sometimes limiting her activity, and as the day goes on there is moderate improvement. Physical exam reveals normal strength and slightly reduced range of motion. Labs reveal elevated erythrocyte sedimentation rate and C reactive protein serum rheumatoid factor as well as creating kinase are normal. The patient is diagnosed with polymyodro romatica and started on
cortico steroids. A clinical assessment for the presence of what other associated condition should be considered in this patient. You hunt one hundred percent need to know this and that will be giant cell ardoritis. So remember giant cell ardorius is associated with polymyogio romatica. You have to know that anywhere from five to thirty percent of patients with PMR will have giant cell ardorritis. Needs to remember the two
are associated together. Always remember instead of Paul emylgier romatica, remember Paul b mylgi romatica, Paul b as in Paul Bunyan the giant. Remember this is associated with giant cell ardortus. Question four, Who is the most common type of osteoporotic fracture? And that is going to be your vertebral fractures, So
your vertebral compression fractures are the most common type of osteoporotic fracture. These type of fractures can sometimes be asymptomatic, so remember assessing for loss of height and chyphosis. These are important because sometimes these can be the only indicator of a vertebral compression fracture in an osteoporotic fracture. Question five, last one. A sixty three year old mail presents at the office today complaining of diarrhea and abdominal
cramping for the past few days. He denies recent dietary changes, no recent travel, he states. The only changes he was recently diagnosed with gout and started on a new medication. Which medication did this patient likely start on for the treatment of gout? So that is going to be culture scene, so it seems like a very simple question. But just remember that because I definitely got a question on this. In school culture scene, most common adversdrug reaction
is GI problems, specifically diarrhea. They do like to ask about that, so remember it, all right. So that was the first part of Rheumatology, part one of two. I really hope that was helpful. Thank you so much for listening, and good luck in PA school, your pants, your panory, and your ears.