Cram The Pance - S1E46 MSK Rheumatology Part 1 of 2

Episode Date: June 28, 2022

MSK Rheumatology part 1 of 2 review for your Pance, Panre, and Eor's. Merchandise Link: https://cram-the-pance.creator-spring.com/►Paypal Donation Link: https://bit.ly/3dxmTql (Thank you!)Included in review: Fibromyalgia, Gout, Calcium Pyrophosphate Crystal Deposition Disease (Pseudogout), Juvenile rheumatoid arthritis, Osteoporosis, Polyarteritis nodosa, Polymyalgia rheumaticaBecome a supporter of this podcast: https://www.spreaker.com/podcast/cram-the-pance--5520744/support.

All right, so let's go ahead and get started with rheumatology. This is going to be a one of two-part podcast, 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 yield topics for rheumatology, and that's fibromyalgia. This is a chronic disorder of widespread musculoskeletal pain accompanied by other somatic symptoms.

So you're looking for fatigue. cognitive disturbances, psychiatric symptoms. Etyology is unknown and the pathophys 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, 20 to 55 years of age. It's much more common in women.

And like I said, generally in the age range of 20 to 55. So in the vignette, be looking for a young or middle-aged woman. On physical exam, 11 of 18 defined tender points. Now let's talk about that because there's a little FYI for that. So on physical exam, person with fibromyalgia, they're very often going to have tenderness. This is going to be at multiple soft tissue sites throughout the body. But with that being said, you likely have heard of this criteria, this 11 of 18 defined tender points. This was from 1990 diagnostic criteria for fibromyalgia, so it's been around a while.

Basically stated that if a patient had symptoms of widespread pain was tender in at least 11 of 18 different areas when you poke them, essentially they had fibromyalgia. This is what I was taught when I was in school. It's still in a lot of the literature. But if you go to 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 1990 ACR classification criteria.

Performing such a tender point examination has proven to be impractical and clinical practice. So in reality, still around, you 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 of the 2010 American College of Rheumatology Diagnosto criteria, which you don't need to memorize. I just want to make you aware of that. And then just kind of, I had to bring up the 11 of 18, tender 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 fibromyalgia in patients with three months of widespread or multi-site 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 you'll 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 in fibromyalgia.

Treatment, you start with your conservative measures, 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 fibromyalgia, it's going to be your TCA's. So tricyclic antidepressants, amatryptylene. So in most patients, you're going to initiate therapy with a low dose of a tricyclic antidepressant.

Amitryptylene's the main one. There's some other options, cyclobenzaprine, SNRIs. For your exam, though, I'd really focus on your TCA's, in particular, amatryptylene. So in conclusion, little to know for fibromyalgia. Just know the diagnosis should be considered in any patient with great. greater than three months of widespread or multi-site pain, accompanied by other somatic symptoms, no evidence of another condition accounting for the pain. Patient very likely is going to be a 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 TCA's, 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 hyperuricemia and deposition of monosodium urea crystals causing attacks of acute inflammatory arthritis.

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 in 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 pain, swelling effusion. And just so you know, hyperuricemia, while it's a, necessary predisposing factor for gout. The majority of people with hyperuricemia actually never developed gout. So it's just a little extra knowledge. You don't need one for the other and et cetera and whatever.

So you can have hyperurisemia and never developed gout. 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 gout. Male sex, gout has a male predominance. 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 uricosuric effect.

So it actually promotes the excretion of uric acid. So gout is very unusual in premenopausal women. So male sex is a big non-modifiable risk factor. Another one is advanced age. So that's another non-modifiable risk factor. So you're generally looking for an older man in the vignette. And then we have our modifiable risk factors for gout. So these are the ones you should be familiar with because this is more often tested

The two important ones to be familiar with is diet and medication. So let's start with your diet. So purine-rich foods is what you're looking for. So diet can be a triggering factor for gout, increased consumption of purines, which are found in seafood, red meat, organ meat like liver, alcohol is another big one. They can all increase the formation of monosodium uric crystals. So be aware of these foods. And the reason why it happens with purine-rich foods is because when purine,

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 urea lowering meds like allopurinol, diet really doesn't play such a big role anymore. Since these meds do such a good job of keeping the uric acid levels under control. But prior to the diagnosis and proper treatment diet's definitely a key factor to be aware of. And then there's medications. They can increase serum urate levels and can increase the risk of a gout flare.

important to know these meds because you may get a question like I did. It describes a patient with gout and they list a bunch of meds and basically say which meds should you discontinue in this patient. So should know your meds that can lead to hyperuracemia and a potential gout attack. The ones that you need to know, the ones that get tested on, are pyrozinamide. That's a tuberculosis med, loop diuretics like furocide, aspirin, but low dose. Aspirin's odd one because it really only triggers gout when it's taken in low doses like less than 325 milligrams. like a lot of people take for cardiovascular prophylaxis. Higher doses of aspirin actually have the opposite effect and decrease urea levels.

Another one is thiasides like hydrochlorothyside, and then Phambutal, 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, P-L-A-T-E, you'll get gout. So plate is the word that you need to remember. And plate stands for the P stands for pyrazinamide. The L in plate stands for loop diuretics.

The A in plate stands for aspirin. The T stands for thiozytes. And then the E. Athambutal. So remember that sentence. You remember the common meds you need to know. If you put too much seafood on your plate, you'll get gout, pyrozyndy, lupythiotics, aspirin, thysm, and athambutal.

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 80% of initial flares involved just a single joint. And then it's most common for it to involve the lower extremities. In particular, the most common area is going to be your first metatarsal phalangeal joint, so the base of the great toe. And this is known as Podagra. So if you hear Podagra mention, it's gout of the big toe.

So remember that term. It's, of course, possible to have it in other areas, the knees, another common area, ankles, but focus. on that first toe podagra. That's a really important one. All right. So as a recap, clinical manifestations of a gout flare, be looking for a description of severe pain, redness, warmth, 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. Arthurcentesis, that's the main one. And then you have your imaging. So arthrocentesis, this is your best test. Definitive diagnosis can be made with Arthur synthesis.

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 bedsheet makes them scream. It's questionable, but if they ask you the best diagnostic test on the exam, arthrocentesis is 85% sensitive and 100% specific for gout. And what you're looking for under microscopy when you perform an arthrocentesis is negatively biopharyngeant 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 biopharyngeant. It's really important to know it's negatively biopharyngeant because it differentiates it from pseudo gout, which we'll go over next. And pseudo gout is positively biopharynge. So again, negatively biopharynge. Needle-shaped crystals, you have to know that. All right. So I mentioned that gout is negatively biorefringent and pseudo-gout is positively biorefringent.

I do have a trick, not really a trick, but just an easy way to remember one is positive, one is negatively biorefringent. So pseudo-gout has a p, gout does not. So pseudo-gout is positively biorefringent, positive with a p, pseudo-gout with a p. Gout was negative to the biorefringent. So if you can't remember which one is negative or positive, just remember which one has a p in the name. Only pseudo-gout, therefore it's the one with positive with a p-biofringent, 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 in a vignette, they mention anything about overhanging edges or margins with a punched-out appearance. These are characteristic findings of the erosive appearance seen in a joint with a patient with gout. Normally, this is long-standing gout. So if you see that, in the back of your mind, just kind of remember that overhanging edges or this a rosa of appearance on x-ray that can be long-standing in a patient, long-standing findings and a patient with gout on imaging. So really, I would just focus on your orthorescentesis, 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 in the exam. There's even a diagnostic rule chart if you want to look that up. Not important to know for the exam, but just basically a point system that helps make the diagnosis in the absence of an arthrocentesis. 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 increased uric acid, hyperurisemia. Why aren't we checking the uric acid levels? So it turns out that up to 43% of patients with acute gout flares, they're actually going to have normal or even low serum urate levels. And part of the reason is because the cytokines that are released during an acute attack, they can actually lower the uric acid 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. You 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 your 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 of the meds, always make sure you address lifestyle changes, less beer, less meat, seafood, lose weight. Not so much tested 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. Enseds, steroids, and colchicine. They all work,

And quoted from up to date, we suggest oral glucocorticoids, nsets, and colchocene 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 nsets first. So insides, naproxin, endomethcin, those are some commonly used ones. A potent oral insid like naproxin or endomethicin, they work really well for gout. they're generally pretty cheap, so they are used very frequently. But you have to be careful in using these in certain patient population. So they're going to give you a patient with an acute gout attack.

They're going to list a bunch of meds, and they're going to ask you which you'd pick. You have to look at the comorbidities the patient has. You don't want to use nseds in a patient with poor renal or gastric ulcer, even in some types of cardiovascular disease like heart failure. There's some other contraindications, obviously allergies and insides, It's concomitant use of anticoagulants. But the three that I'd focus on for the exam, bad kidneys, bad heart, bad GI tract. Don't get tricked in a vignette when they give you a patient with gout, ask you which

men to pick. Before you pick neproxin, make sure their GFR isn't like 20. So again, Ns are a first line agent for acute gout as long as the patient doesn't have chronic kidney disease, generally a GFR less than 60, an 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 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 insides and steroids in the answer choices, make sure you're choosing your steroids and not insets. All right, so who should you be careful prescribing steroids to? Obviously, you're poorly controlled diabetics. This is really important. Steroids can and will cause a pretty significant spike in blood sugar. So be really careful with your brittle diabetics. I work in and the chronology, I see this all the time. Patients come in, their blood sugar is perfect. They get,

they get some prednisone and their blood sugars through the roof. So be really careful in patients with diabetes. It's not an absolute contraindication. You just want to be careful with that. Also be careful in patients that have an ongoing infection or post-stop patients because glucocorticoids 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 that's really important. You can use this in patients with kidney disease because that's likely the question you'll get. Let's talk about colchicine next.

So this is probably the least used option of the three. Colchicine 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 med 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. So just know that.

Really just two things I would know for Colchicine. One, like I just remember, you can use it for acute and chronic gout. And if they mention an adverse drug reaction with colchicine, it's going to be diarrhea. Colchicine 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 the diarrhea starts.

You know we're getting close. It should start working soon. So anyways, remember Colchene 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 alipurinol.

It's part of your xanthine oxidase inhibitors. If you remember only one medication for chronic gout men, management, let it be alipurinol. So it is your first line prophylactic treatment for gout. Like I said before, is a xanthine oxidase inhibitor. What the heck does that mean? So Xanthane oxidase is a enzyme that helps purine break down 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 allopurinol, the one that I would remember is Stevens Johnson syndrome.

So this one always seems to come up. Alperinol's, one of the medications, one of the many medications that can cause Stephen Johnson syndrome. And I went over this mnemonic before in the seizure lecture, but if you can remember, this demonic, it'll help you remember the common meds that can cause Stephen Johnson syndrome. So the sentence that I remember, as soon as I see Stevens Johnson syndrome,

I think of the first few letters in Stephen Johnson, and the first few letters of Stevens Johnson are also in Steve Jobs. And that helps me remember Steve Jobs. created Apple PCs. And then Steve Jobs created Apple PCs. Apple PC stands for the main meds that can cause Stevens Johnson syndrome, allopurinol. There's your alipurinol. Fenitone, phenobarbital, lomotogen, ethosuxiomy, penicillins, carbamazepine, and sulfonamides.

So those are the main ones. Allopurinol is obviously in the A there. So you remember, as soon as you see Stevens 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 xanthinoxidase inhibitors is one called phoboxistat. So this is another xanthianoxidase inhibitor. There's really nothing high yield to know about this meant except for the fact that it's a xanthionoxidase inhibitor.

We don't use phoboxysat as often as alipurinol because it has some adverse effects that alipurinol just doesn't have. In particular, an increased cardiovascular risk. So be aware of it. But remember, alipurinol 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 the Xanthinoxidase inhibitors, because I did get a question on this, they basically asked which of the following is a Xanthinoxidase inhibitor. And right away, I was like, oh, okay, where's alipyranol?

The answer choices, that wasn't there. It would obviously be too easy. They put Phobuxusat. So the way that I remember these two meds were Xanoxidase inhibitors was by remembering the sentence. In February, I get all of my XOs because it's the month. of Valentine's Day. In February, I get all of my XOs, like XOXO, XO, Hugs and Kisses. I get all of my XOs because it's the month of Valentine's Day. So in February, February is for Fubuxistat. All is for alipurinol, and then XO's stands for Xanthine oxidase,

as in Xanthin oxidase inhibitor. So just a quick way to remember the two drugs and their mechanism of action. All right. So our Xan antioxidase inhibitors help decrease production of uric acid. But what about medications for our patients that are just under excreting uric acid? They're building up uric acid. They're just not peeing enough out. What do you do then? That's when you use our uricosuric medications. So uricosuric medications, probenicid, is really the only one that you need to know because it's the only drug in the U.S. approved by the FDA for the specific purpose of promoting renal uric acid clearance. The other two, sulfimperzone and lisenurad. they're no longer marketed here in the U.S., so really just focus on probinicid.

Probenicid works by promoting renal clearance of uric acid by inhibiting the proximal tubule that mediates uric absorption. So there's not a lot to know here. Just remember probenicid is the one that makes you pee out uric acid. It's not used very often. One other thing to know about it is you want to avoid this drug in patients 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 other 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 piglodicase. It's really only reserved for patients with severe cases of gout who have failed to previously mentioned therapies like gallopurinol. 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 colchicine, because remember, colchicine can be used for acute and chronic management of gout. All right, so to wrap up treatment, I would know your acute treatments, your acute meds, your acute meds, well, insed steroids colchicine.

For 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. Pseudogout, the name isn't really used that much anymore. It more accurately describes the acute attacks, which clinically resemble acute attacks of gout, but I'm going to call it pseudogout 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 pyrophosphate dihydrate. So in gout, we had accumulation of uric acid. In this case, we have an accumulation of calcium pyrophosphate depositing in the joints in the soft tissue. The knee is going to be the most common joint to be affected. The knee is affected in over 50% of all acute attacks. So in gout, it was all about the first toe, podagra, pseudogout, 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 gnomonics are sometimes the best. So instead of remembering pseudo gout, I used to remember sumo gout, as in sort of. 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 stance, apparently. So anyways, as soon as I see pseudo gout, I think of sumo gout and a 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 knee. All right. So the knees most common. Other areas, of course, can be affected to the wrist, the MCP joints, the hip, shoulders, elbow, spine,

all fair game. Just an FYI, an acute attack of pseudo gout. while it can be very similar to gout, and that's why they initially came up with the name pseudo-gout because the close resemblance to gout attacks, the intense pain, redness, warmth, swelling. But the thing about it is that in pseudo-gouts, 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 pseudogout. If you forget everything else, remember this, positively biopharyngeant crystals on synovial fluid analysis. Oftentimes they're going to be rhomboid shaped. This is the key difference between pseudogout and gout, because remember gout was negatively biopharyngeant.

And again, remember that because pseudogout has a p, gout does not. So pseudogout is positively biorefringent. Remember, on pseudogout, you're looking for positively biopharynge. 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 pseudogout. If they mention on X-ray these punctate or linear radio densities 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 their name for pseudo gout. So if you see anything mentioned about punctate or linear radio densities or if they use the word chondrocalcinosis, be thinking pseudo gout. All right. And then one last thing to know when we were talking about the treatment for acute attacks of pseudo gout, it's the same as in gout. So the treatments are essentially the same. The only slight difference is there's more of an emphasis on intraarticular steroid injections. So when two or less joints are involved, intracicular steroid injections are generally going to be your first line in these patients.

Otherwise, treatment for acute attacks in pseudo-gout, it's identical to the treatment of a gout flare. So just as we went over before in gout, Nseds, P.O. steroids, colchicine, there's really nothing new to know here except for a slight emphasis on those intracicular glucocorticoid injections. So five things to know for pseudo-gout. This is a calcium deposition disease. Knee's going to be your most common joint to be involved. Remember, your sumo wrestler.

positively biorefringent calcium crystals on x-ray, be looking for chondrocalcinosis, those little white lines on x-ray in 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, systemic oligal articular, polyarticular. I wouldn't focus too much on that. This is a chronic pediatric inflammatory arthritis, onset before 16 years of age, and presence of arthritis for at least six.

six weeks. So juvenile adiopathic arthritis, it's this blanket term that covers a bunch of different types of chronic pediatric arthritis. Pathos really not well understood with this condition. It's ultimately a diagnosis of exclusion. 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 16 years old is the cutoff for this disease. So if they're any older, if the onset is after 16 years of age, it's no longer called juvenile idiopathic arthritis. It's then going to be called adult onset stills disease. Remember, they're going to be younger than 16 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. That's going to be fever, arthritis, rash, uveitis. All right, so let's talk about them. So the fever. This is primarily seen with a systemic subtype, but it's not just any fever. The fever is unique and you need to remember its 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 quotient 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 a 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 chordium pattern to the fever, and it's how they're going to describe it in the vignettes. 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 oligal 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 oligoarticular and polyarticular subtypes. It's most prevalent in patients that are ANA positive. So children who are positive for antinuclear antibodies, they're screen more often than those who are ANA negative since they're at a higher risk.

So remember UVitis, really oligal articular and polyarticular subtypes that you'll see it in. treatment, mild to moderate symptoms, nseds are going to be your initial treatment option. More severe disease, you'll start the amount of biologic like actemra, even glucocorticoids, but for the exam, focus on your n-says, that will likely be the answer. And that's really it for juvenile adepathic arthritis. Remember, your daily spiking and remitting fever, your salmon-colored rash, some uveitis in the oligo and polyarticular subtypes, and n-sets for your treatment, and you're done. Let's move on to osteoporosis.

Like gout, this is another very dense topic. Let's just focus on your need to know stuff. So osteoprocess 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 patho 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 stand 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. factor, 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 decreased 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 consumption, some other ones, and physical inactivity, just to name a few.

There's a ton more, some secondary causes like celiac disease, Cushings, diabetes. It's more common in Caucasians, with 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 osteoporotic fractures. This is the one that you need to focus on. What's really interesting about this type of fracture is that,

two-thirds of vertebral fractures in 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 fact that they've shrunk in the past few months from the fracture and the result in disc space narrowing. So remember, vertebral fractures are the most common type of osteoporotic fracture and just be aware they may not be complaining of any pains in the vignette be looking for them just to mention maybe a patient complaining of shrinking or maybe you'll notice some kifosis on the exam that hunchback appearance which can also come from this. Another common one

it would be hip fractures 15% of women, 5% of men by the age of 80 will have an osteoproducture and then distal radius fractures your collies 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 the dexas scan because this is your best test, your gold standard for osteoporosis. That's what you really need to focus on for your exam. So dexas scan or dual energy x-ray absorptiometry is how you check the bone density of a patient. It 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 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 2.5 or less so that means there are 2.5 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 2.5 or less, that is diagnostic of osteoporosis. And then negative 1.0 to negative 2.5 would be osteopenia or low bone mass is 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 osteopenia, which one classifies osteoporosis. What I want you to remember is pen is 10, poor is less than 2.4. Penn is 10, poor is less than 2.4. So a little rhyme there. So what does that mean? So osteopenia,

like P-E-N, is negative 1.0 or less, aka pen is 10, 10 being 1.0. And then osteoporosis, poor is less than 2.4 because remember, osteoporosis is negative 2.5 or less. Another way of saying negative 2.5 or less is less than negative 2.4. So remember, pen is 10 as an osteopenia is negative 1.0 or less. And then poor is less than 2.4 as an osteoporosis is less than negative 2.4. 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 has osteoprotic. 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 osteoporosis in that patient. Most common sites of fragility fractures are going to be the spine, so your vertebral compression fractures, the hip, the wrist, they can also occur, the humorous, ribs, pelvis. So again, for diagnosis, really just two things that you have to remember, negative 2.5 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 frax 10-year probability that can be used for diagnosis, but for the exam, focus on your dexia inner fragility fractures, and you're done. All right, let's move on to treatment. Start with your lifestyle. I won't go too depth into that. because the bulk 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 prevention, etc. All right, let's talk about meds, which is where the high-yield stuff is at. So let's start with your bisphosphonates, olendronate, rysynate, those are your first lines. Bisfosphonates are going to be your first-line treatment for most patients. They're very effective and expensive 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, Lenrinate, which is Phocimax, Residronate, which is Actanil, 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 meds in this class have the word drone in them, allendronate, zolodronic 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 Lendronate to build strong bones. So when they give you a vignette, clear-cut osteoprocessant, they list a bunch of meds, ask you which is the first line med 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 for your bisphosphonates, they inhibit osteoclastic bone resorption.

So bisphosphonates are what are known as antire sorptive agents. It's a little more complicated than this, but the general idea is that a patient takes a bisphosphinate. bisphosphonates plant themselves onto the bone onto something called hydroxyapotite. Osteo-class 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 osteoclast ability to resort 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 going to 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 asophagitis. So in patients that take bisphosphonates, you have to tell them to remain upright for at least 30 minutes and take with 6 to 8 ounces of water. To avoid esophagitis, you have to remember to tell all of your patients that stay upright for at least 30 minutes, have them take it with 6 to 8 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. Then you also want to try to avoid these medications in patients with the history of eccalasia, esophageal strictures, Barrett's esophagus, or really any of the esophageal problems, particularly with allendronate.

That's really important. So remember that about this class. They're going to ask you a question on it. Most commonly, they'll list a bunch of meds. They'll say which one of these medications should the patient avoid recumbency for at least 30 minutes. And then, of course, one of them will be a bisphosphonates. Remember, bisphosphinates can destroy your esophagus. So stay upright 30 to 60 minutes, take with 60 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 30 minutes or they have esophageal disorders, you can actually give them an IV bisphosphonate like zoolodronic acid as opposed to P.O. to circumvent this issue. Another adverse drug reaction is osteoencrosis 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 osteoenocrosis of the jaw, the incidence is anywhere from 1 in 10,000 to 1 and 100,000. And it was really only seen in cancer patients or in patients with a compromised immune system that were treated with high doses of IV bisphosphonates.

But it can still happen. So encourage 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 drug 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, osteoacrosis of the jaw, and your atypical femo fractures. All right, let's move on. There's some other classes of meds 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 99% of the time, it's going to be on bisphosphonate.

So focus on those, but at least let's mention the other classes. So first let's talk about your anabolic agents. these are used more frequently. They're really reserved for patients with severe osteoporosis, like a T score of negative 3.5 or less. The reason that you reserve these meds for your more severe cases is because these meds, unlike bisphosphonates, that really only preserve existing bone,

these anabolic agents actually have the ability to rebuild new bone. The meds in this class are teraparotide, abeloparotide, and then romo susamab. These are your anabolic. and teraparotide and abeloparotide are synthetic forms of PTH and PTH-P-RP respectively. And then when you take these drugs, these agents stimulate osteoblasts, which help rebuild bone. Like I said before, this is different than your bisphosphonates, which were antirestorptive agents that prevented bone resorption.

These anabolic 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 antirexorptive just to preserve that new bone that was built. The last one that I mentioned, Ramosuzumab, it's a fairly new med. It just got FDA approval in 2019. 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 anabolic agents. I gave you a little bit of extra info there. I don't think you should memorize all of that. Just be aware when it comes to your anabolic 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.

All right, so another medication for osteoporosis is another anti-resorptive drug like our bisphosphonates, and it's known as denosimab. So it's not as potent as the anabolic agents I just went over, but the nice thing about it is it's only administered once every six months. It's basically reserved for people who are, not good candidates for bisphosphonates. And it's particularly useful in patients with impaired renal function as it can be safe in these patients. And then one final med to be aware of is

raloxifine. So raloxifine is a selective estrogen receptor modulator or serm for short. It's another anti-reserptive agent. It does not work as well as bisphosphonates, 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 osteoporosis patients when there's also a need for breast cancer prophylaxis. And the way that you can remember that is raloxifine also sounds similar to another breast cancer prophylaxis treatment med that you've probably heard of, and that's tamoxifen. So it sounds very similar, right?

Roloxifen or raloxifine sounds similar to tamoxifen. So remember, this is the one that you use when breast cancer, breast cancer prophylaxis is also indicated. that's the unique thing to focus on here. So those are some additional options outside of your bisphosphonates for treatment of osteoporosis. I'll reiterate. Focus should be on your bisphosphonates, 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 bisphosphonates if they give you a farm question about osteoporosis. So remember, phoning your drones to build strong bones, lindrinate, residronate. Those are the ones you need to know. All right. So there's a lot to know for osteoporosis. if I had to give you a few top things to remember, it would be one. Remember your Dexas scan is your gold standard test and a negative 2.5 or less is

diagnostic of osteoporosis. Remember, vertebral fracture is your most common. Remember, bisphosphonates are first line treatment. And remember, esophagitis is an adverse drug reaction of bisphosphonates. So avoid recumbency for at least 30 minutes after taking them. Those are the highest skilled things to remember about osteoporosis. All right, but we're almost there. We just have two small topics to go over.

So polyartoritis nodosa, which 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. vessel to die and then we're left with these fibotic changes and due to all the fibrosis and

inflammation we have these blood flow disturbances so ischemia 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 and 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. In 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 Hep B or Hep C, but it's mainly hepatitis B that they'll talk about, which is more common. So we'll 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 on the renal arteries are affected, we have renal ischemia, which 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 purpera, levido reticularis, ulcers. It's even possible to get these tender nodules on the skin. Levitolidiluris, 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 net-like or web-like pattern, which is just due to vessel ischemia.

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 ischemia. But in this case, the ischemia isn't from the cold temperature. It's from the fibrodic changes we talked about before. Something else with your neurologic findings is known as mononeuropathy multiplex. So mononeuropathy multiplex or asymmetric polyneuropathy is another common finding in patients with pan. It's seen in up to 70% 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 mononeuropathy multiplex. So those are the main clinical manifestations 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. And 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, involuntary infarction, orchitis, abdominal pain from mesenteric arthritis. But the ones I listed above are the most common ones and the ones 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. It's really unique. It could absolutely be mentioned in the vignette. So if you see lung parankhamal 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. So remember that.

If it mentions lung involvement, be looking for something other than Pan. Diagnosis. Most important thing to remember about diagnosis is that this condition will generally be ANCA negative. So nothing is 100% in medicine, but most of the time, Pan is not going to be associated with the presence of antineutrophil cytoplasmic antibodies, or ANCA, for short, and so. So if you see the patient as anka positive, generally you should be thinking of some of the other vascular tides like microscopic polyangitis, et cetera. So remember that. You also need to know for diagnosis, if you do an angiogram of these patients, you're likely going to see numerous aneurysms of the vessels.

The reason this happens is from the fibrodite 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 anken 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. Your more severe cases, you can add on your immunosuppressive meds like cyclofosophomide,

but in general, glucocorticoids 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 ANCA. So no lung involvement negative ANCA. 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.

Polyartitis no dosa. So when you see polyartitis 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 ANCA positive? No, no dosa. So if they mention the lungs or positive anca, it's very unlikely to be polyartaritis, nodosa. So be thinking of some of the other vasculatides that don't have no in their name, like microscopa polyangitis, Shurg Strauss disease, which are generally anca positive and do involve the lungs.

Remember, if you see no and no dose, I'd be remembering no lung involvement, no anka, as this will likely be the only thing to differentiate from the other causes. All right, so let's move on to polymyology rheumatica. It's not a lot to know for this, but there's a few. high-yield things I 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 in multiple muscles. So you would assume that this involves the muscles,

but the muscle in PMR is histopathologically normal. And that's why on physical exam, you'll normally find normal muscle strength. PMR really involves the joints and the hairy articular structures like the bursa and the tendons. PMR is almost exclusively a disease of adults over the age of 50. The older the patient, the higher the prevalence. Peak incidence is going to be between 70 to 80 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 20 year old in the vignette, you know it ain't PMR. So move on, look for something else. Next thing, giant cell arteritis. 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 arduitis is associated with polymyalgia rheumatica. You have to know that. Anywhere from 5 to 30% of patients with PMR are going to have giant cell. So why is that so important to know? Well, giant cell arthritis can lead to blindness if it's not treated. So if you make the diagnosis of PMR in a patient, make sure you're asking the patient about headaches, jaw clotication, 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 arthritis. You don't want to miss that diagnosis.

It's really important. It's so important that I had this ridiculous way to remember it 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. myalgia rheumatica, Paul E. myalgia rheumatica. I want you to instead of remembering Paul E. my algebra romatica, remember Paul B. myalgia rheumatica, Paul as in the name Paul, P-A-U-L, and B as in the letter B, B as in boy. So instead of Paul E-Mialia-Mi-A-Milatica, Paul B, Miala-Mi-A-Malda. So forget about the name Paul E-Mialgia.

Forever, I want you to remember this as Paul B-Mialgia. 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 it helps you remember giant cell arteritis. So polymyalgia rheumatica is forever going to be known for you as Paul B, myelgia rheumatica, Paul B, as in Paul Bunyan, the Giant, to help you remember this is associated with giant cell arteritis. Let's talk about the clinical manifestations next.

These patients are going to 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 manifestations in almost all patients 70 to 95%. 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, they're going to be worse in the morning or after any period of inactivity. Up to date 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 achiness to aching to be worse than the morning. They also may mention the patient has difficulty arising 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 your acute phase reactants, erythrocyte sedimentation rate, and your C-reactive protein, which are your inflammatory markers, they're going to be. elevated in 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 differential. So you'll check your rheumatoid factor. You'll check your anti-CC. This is to rule out late onset rheumatoid arthritis. You also check

your muscle enzymes like creatine kinase to rule out polyomyocitis. So with PMR, there's really no pathonomotic test or labs to make a definitive. diagnosis, you're essentially just looking for a few different factors. Is this patient over 50? Check. Do they have the classic presentation? Bilateral shoulder or pelvic girdle aching? Worse in the morning. Check.

Are my acute phase reactants 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, 100% steroids. So low dose glucose corticoids is recommended for all. all patients diagnosed with polymyelial rheumatica, anywhere from 15 to 25 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 meds 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 glucoricoid dose. Majority of patients experience 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 glucocorticoids strongly suggests an alternative diagnosis.

Now, of course, this isn't 100%. Some patients may take longer to respond, but in general, a rapid response to prednisone is very characteristic of this disease and is actually included 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. 52-year-old man presents to the emergency department complaining of severe pain in his first metatarsopulangial joint. He denies trauma to the area and states it started suddenly. Arthrosincese is performed, which displays negatively birefringent, needle-shaped crystals.

Medical history includes hypertension, type 2 diabetes, hyperlipidemia, and current medications include hydrochlorothyside, metformin, glypid, and resubostatin. 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 meds, those were hydrochlorothyside, metformin, glypozyde, and resubistatin, which medsum, likely led to the clinical manifestations, that would be hydrochlorathyz. So this is about as clear cut a case of gout as you can get, severe pain in first toe, negatively biophringenetal-shaped crystals on arthrosynthesis, ring the bell, that's your answer

You just have to remember which meds can cause gout flares. And in this case, it's hydrochlorothyside. Just remember your thyside diuretics, like hydrochlorothyside, can increase urate reabsorption of the proximal renal tubule, which can elevate your uric acid levels and precipitate gout flares. So remember they're one of the many meds that can cause gout flares. Remember the way that you remember that is you remember, put too much seafood on your plate and you'll get gout. Plate again stands for pyrazinamide, loop diuretic, aspirin thyside, like your hydrochlorothiaseide.

that helps you remember the main meds that can cause your gout flares. Question two, a 72-year-old female presents to the office today for a routine checkup. Past medical history includes hypertension, hyperlipidemia. She states she has concern about osteoporosis as her mother was diagnosed with it in her 60s and wound up with a hip fracture. A dexas scan is order, which reveals a T score of negative 2.6. It is a sign that the patient will be started on the first line medication class for osteoporosis. what important instructions should be provided to the patient before taking her first dose. So that would be to avoid recumbency for at least 30 minutes and take with 6 to 8 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 30 minutes, takes the medication with at least 6 to 8 ounces of. water. It's actually a contraindication if you look at all of the bisphosphonate meds listed under the contraindications to give this to any patient who can't remain upright for at least 30 minutes. So remember that. It's really important. Question three, 63-year-old female presents to her physician's office complaining of pain and stiffness in 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 creatin kinase are normal. The patient is diagnosed with polymylogeromatica and started on corticosteroids. A clinical assessment for the presence of what other associated condition should be considered in this patient. You 100% need to know this and that will be giant cell arthritis. So remember, giant cell artery. is associated with polymyelioramatica, you have to know that anywhere from 5 to 30% of patients with PMR will have giant cell arthritis.

Need to remember the two are associated together. Always remember, instead of Paul E myelioramatica, remember Paul B myelioramatica, Paul B as in Paul Bunyan in the giant. Remember, this is associated with giant cell arteritis. Question four, what is the most common type of osteoporotic fracture? And that is going to be your vertebral fracture. 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 63-year-old male presents to 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 change is 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 colchicine. So it seems like a very simple question. But just remember that because I definitely got a question on this in school. Colchicine, most common adverse drug 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 panery. and your EORs.