DIP Episode 287 - The Ultra HY USMLE Urinalysis Podcast

Okay, welcome. My name is Devine. This is episode 287 of the Divine Intervention Podcasts. In this podcast, I'll be talking about your analysis and the USM Ls. For whatever reason, your analysis is a big thing that many people seem to struggle with a lot on USML exams. So I'm going to talk through the classic your analysis scenarios so that when you get questions on these things, you feel very comfortable and you get them right. I would want to present ambivalence towards your analysis to be the reason why they get the question wrong. And then for those of you that are going to be taking the Step 2 CK exam anytime soon, feel free to shoot me an email through the websites to sign up for the MBME Testicking Strategies course and the Comprehensive Step 2 CK course. It's a 16.5 hour course. But again, the goal is to cover the vast majority of the high-yields you see on the exam. Bio stats, ethics, the new stuff that's been tested since November of last year and then expanded content in internal medicine, in peeds, in psych, surgery, OBGYN, neuro. I held the, you know, it's always been a 10 hour course, but again, with all these changes that the USML putting to place, I expanded the course to 16.5 hours and the first iteration of the course was a big success, big, big, big success. Definitely heard a lot of very good feedback from the course. If you're interested in signing up, just shoot me an email through the website. The course takes place via Zoom.

Okay, so let's just jump right into it. So what if they give you a question about a person that has SIDH? What do you expect that person's urine to look like? Well, if you think about it, if a person has SIDH, right, the syndrome of inappropriate age secretion, right? Obviously, it can pop up in a couple of ways on exams. It can pop up in the setting of small cell lung cancer as a panioplastic phenomenon. It can pop up in people that are taking SS Rs. Remember SS Rs, if a mom is taking, are the most common pharmacologic agents that are implicated in an etiology of SIDH? It can be a person that has pneumonia on an endemic exam that has SIDH. It can be a person that has a brain process meningitis or whatever, right? Like cryptococrom meningitis that has SIDH. In general, like any brain process, any pulmonary process can actually cause SIDH, right? So these are just all things to watch out for. It's obviously anti-directic hormone is going to reabsorb a ton of water from your urine, so your urine will be very concentrated, right? So your urine of smallality will be really high, right? It will be really high, at least relative to your serenose malality will be higher. Now, one if to where your friends at the MBME go after your inconsecientation of these days is to focus on the specific gravity, right? So focus on the specific gravity. Now, the thing is the magic number I think I'll encourage you to remember is 1.012.

Okay, for purposes of your serenose malacemate exams, remember the number 1.012. If your urine specific gravity, basically, is a measure, remember specific gravity, if you remember from college physics, is a measure of relative density, right? So if your urine specific gravity is less than 1.012, it means the person's urine is diluted. But if the urine specific gravity is more than 1.012, it means that the person's urine is concentrated, right? So what are some things that can cause concentrated urine? Again, if your volume, if your person has SIDH, right? For persons has SIDH, that's going to cause an increase in urine specific gravity because again, the urine, they are sucking out a ton of water from the urine, so the urine is very, very concentrated, right? So the urine specific gravity will be way higher than 1.012, usually it will be more than 1.02 on the exam, right? If a person is volume depleted, let's say for example, they have like pre-renown acute kidney injury, right? Then those people, right? Obviously, again, their body will be like, okay, let's try to conserve some fluid. So the urine will be very concentrated, super, super concentrated, right? So the specific gravity in that case will be more than 1.012, right? And if whatever reason the person's urine is super hypertolic, right? Again, that's also going to cause an increase in urine specific gravity. So let's say for example, the person is going through like some kind of diabetic crisis, right?

Like decay or HHS because they can make these questions, our own questions on the exam. In those cases, right? Like the person's urine specific gravity will be high because there's just a ton of stuff in it, right? It can be glucose in the case or the person that has diabetes. In fact, one actually unusual scenario is a person that is getting contrast, right? If a person is getting contrast for an imaging procedure, that contrast is a very big isotonic. It's a very big hyper tonic load, not isotonic, sorry, hyper tonic load on the kidneys, right? That's going to cause an increase in the person's urine specific gravity. Again, this is one of those reasons why contrast like a really tanker person's, a can really scrub a person's kidneys, right? That's why they tell you, give these people lively fluids, let them have big time hydration whenever they are taking contrast. I remember these people should not be a metformin at the time because again, contrast could potentially torch your kidneys. So if you're taking a metformin on top of that, right? That can potentially cause a fetal lactic acidosis in those circumstances, right? And then we know that in terms of a low specific gravity again, that means your urine is not very concentrated, right? That means the specific gravity of your urine is less than 1.012, right? So what are the things that can cause that? Well, again, for pressing has this super hydrated, right?

Let's see, they have like psychogenic polydipsia, for example, right? You drink a ton of water, that's going to dilute your serum, osmolality, so your body is going to be like, okay, we can't get hyponitremia here. So let's get rid of some extra fluid, right? So as you get rid of that excess fluid, that's going to dilute your urine. So urine specific gravity is going to be low. It's going to be less than 1.012, right? If a person has diabetes in symptoms of any sort, right? Basically, that's like the opposite of SIDH. You basically have, you can either have no ADHD at all, that's a central diabetes in syphilis, or you can have EBEH and it's not effective, that's an effort, genetic diabetes in syphilis, right? Like a person can get from lithium, or a person can get from a demyclocycline, for example, right? So in those circumstances, what happens? EBEH is not working, so they're not going to be able to anti-diaries your urine. So you're going to keep a ton of water in your urine, so your urine is going to be very dilute, so this specific gravity is going to be less than 1.012, right? And if a person also has this classic thing, they love to test, right? A person has like sickle cell disease, right? Remember, sickle cell disease can cause an effraperty, right? Those people have a lot of problems with concentrating the eye urine, right? So if you can concentrate your urine, your urine specific gravity is going to be high, right? It's going to be greater than 1.01.

I mean, it's going to be low, sorry, so urine specific gravity is going to be less than 1.012, right? And also, again, when a person has the other kinds of EKI, right? Like post, like an intrarino, I feel like when it begins for the most part, the focus for the most part on the pre and the intrarino, in the intrarino-li-ki, the tubular epithelial cells are dead, right? So because the person's tubular epithelial cells are dead, they're not going to be able to concentrate urine, right? So again, the person's urine specific gravity is going to be really low, right? It's going to be less than 1.012, right? So, again, be able to tease apart these EKI's, right? Remember, cyclosporin causes a pre and a liquefied, does the mechanism behind it's nephrotoxicity, right? It causes a constriction of the afran arterial, right? So again, if a person's digging cyclosporin, for example, they can give you a urine specific gravity question, the urine specific gravity should be elevated, right? Because again, if you concentrate the afran arterial, you're going to be high-poo profusing the kidneys, right? Again, the body's going to be like, oh, okay, let's start conserving fluid, right? So in those circumstances, your urine specific gravity will be elevated, or they can give this to you in the context of a person that has an inset nephropathy, especially when they have like pre and a liquefied from an inset, right?

Again, insets, they give it cycloxygenase, so you're going to be making less prostaglandins, so that's going to cause a net constriction of the afran arterial, right? Again, whenever your hyper-prefusing the afran arterial, that is usually going to be associated with an increasing urine specific gravity, because the body is like, okay, let's conserves fluid, right? So it will suck up a ton of water from the urine. Okay, and again, the mechanism there, right? Obviously, if you're not profusing the afran arterial, then your GG cells will start to freak out, they start freaking out, they will secret a ton of, of a reigning, right? And then that reigning, right? We'll convert angiotensinogen from the lever into angiotensin-1, and then when that angiotensin-1 gets to the pulmonary arteries as it traverses the pulmonary couplers, it'll get converted to angiotensin-2. One of the things angiotensin-2 does is that it goes to the super optic nucleus of the hypothalamus, and it causes you to release the ediage, right? So when you release that ediage, it's going to cause you to suck up water from your urine, when your urine is going to be very concentrated, right? Remember, another job of angiotensin-2 is that it goes to the zonal glomerulosa of the adrenal cortex, and it causes you to release melaroloporticoids, in this case, our duster, right? And our duster in helps you reabsorb most sodium and water from your urine, right?

And again, I remember that, again, angiotensin-2 is also a very powerful viso-constructor, just a little show through that in by the side, right? So, in a present that is hypoperfused, again, they can give you all these physio-like people think that for some reason, when you get to steptusic, when you get to stept 3 physiological scenarios, disappear on these exams, that's not true, right? They can give you like a systemic vascular resistance question with angiotensin-2. If a person, again, for whatever reason, right, they give you that, oh, this person has a CHF exacerbation. Well, what do you think will be true of the SVR? The systemic vascular resistance will be increased, right? Because, again, if a person has CHF, right, their heart is not working, or cardiogenic shock, their heart is not working, they're not able to pump blood forward, right? So, the effective arterial blood volume is decreased. So, those people are hypoperfusing the afran arterial, right? So, again, the GG cells freak out, go through the serenin-1-10s in our duster-1 system, cascade. So, 1-10s in 2 is produced in great measure. That's going to cause a constriction of the vessels in the body, right? So, because you have a net constriction of vessels in the body, that ultimately is going to cause an increase in systemic vascular resistance, right? When it causes an increase in systemic vascular resistance. Okay.

So, now that we've hit specific gravity, well, let's see, I mean, I guess maybe this podcast may be a two-part podcast, because I have a quite a bit of stuff I actually want to want to talk about, right? So, let's talk about urine peach. Let's talk about urine peach. So, what are some classic ways your friends at the MBME go after urine peach? Well, I will see probably like one of the most obvious ones is in the setting of an RTA, right? It's in the setting of an RTA. So, remember, there are many kinds of RT As. There's a type 2 RTA, which is the proximal RTA. There's a type 4 RTA, which is the RTA that's associated with low-dosterone states. And then there's a type 1 RTA, which is the distal RTA, right? That's the offer intercalated cell RTA. Remember, the type 2 RTA, you can think about it as a proximal convoluted tubular RTA. The type 1 RTA, you can think of it as an alpha intercalated cell RTA. And then the type 4 RTA, you can think of it as a low-dosterone state RTA, right? So, let's head up the one where this is the most, I guess maybe any, since I'm talking about this, my mother's will give you a good algorithm for RT As. Again, how do you answer RTA questions on your exam? First thing you do is look at the potassium. Is the potassium high? If the potassium is high, the pressure has a type 4 RTA, the end, right? Because remember, again, I type 4 RTA, I said it's a low-dosterone state RTA.

So, if you have low levels of our dosterone, well, what is the job of our dosterone normally? Well, if you look at the level of the principle set of the collecting duct, our dosterone's job is to make your RTA absorb sodium and to peel our potassium. So, if you have low our dosterone for any reason, right? You're not going to be able to reabsorb sodium, and you're not going to be able to peel potassium. So, if you cannot peel potassium, you're going to hold on to that potassium. So, your potassium will be high. That's the hyper-calemic RTA, right? So, look at the cause of type 4 RTA. If your person is taking an our dosterone receptor antagonist, right? Like Spirano-Lactone or Eplereonone, that can cause a type 4 RTA because you're literally, you're essentially having a pharmacologic induction of a type 4 RTA, right? Or if, for example, a person has a sense disease, the adrenal glands are being shot, especially the cortex, right? Remember, artisans disease is a destruction of the adrenal cortex, not the adrenal medulla. That's a classic mystic people make. Remember, the adrenal cortex is derived from from misoder, if I'm not mistaken, the adrenal medulla is derived from neurocressels. They have two totally different embryologic origins, right? So, like, autoantibodies against the cortex are not necessarily going to torture potassium's medulla, just something to keep in mind, right?

So, if a person's adrenal cortex is gone, well, sadly, they're not going to be able to produce our dosterone. So, they're going to get a type 4 RTA as a result of that. Another classic one is in Waterhouse Friedrichs syndrome, right? Remember, a person has been in gochokominin giitis, and as they have them in gochokominin giitis, right? That thing unfortunately in some cases can spread to the adrenal glands. Well, if you hit so the adrenal glands, especially the cortex, you're going to have a hemorrhagic infraction of the adrenal glands, right? That can cause a primary adrenal insufficiency. That can cause a type 4 RTA. Another classic one is a person that has congenital adrenal hyperplegia, especially the most common cause, 21 hydroxylase deficiency. If you have 21 hydroxylase deficiency, right? Think about it, you're not going to be able to make cortisol, right? You're also not going to be able to make our dosterone, right? So, if you're not able to make our dosterone, that's going to cause a type 4 RTA, right? That's going to cause a type 4 RTA. That's, again, that's very high yield. That's very high yield to keep at the back of your mind, for example, right? So people that have congenital adrenal hyperplegia, they have a normal lana-yonga metabolic acidosis because they have a type 4 RTA, right? Because they have a type 4 RTA.

So, one very nice, unusual question your friends at the end of the mecan throwing there is, which of the congenital adrenal hyperplegia is associated with low levels of our dosterone, or the person does not have type 4 RTA. Without hoping, those circumstances, you're thinking of 11 hydroxylase deficiency, right? So, remember, an 11-bit hydroxylase deficiency, you're not able to make cortisol, you're not able to make our dosterone, but because of the enzyme defect, you have a buildup of this compound called 11-deoxy corticosterone, which pretty much works like our dosterone, right? So, it has a mineral corticoid-like effect, right? So, it's going to be like you have high levels of our dosterone, but your actual dosterone levels are low, right? You can maybe almost think of it as a pseudo-hyper- our dosterone, if you may, although I don't think that's a term that's used in the literature, right? So, we're talking about RT As, right? So, we say that RT As, if you're not using present potassium, it's high, right? It's going to be a type 4 RTA, the end. Now, if you're not using that present potassium, it's low, then all you need to look at is the urine pH. If the urine pH is more than 5.5, right? So, remember, we're talking about urine pH.

If the urine pH is more than 5.5, that's going to be a type 1 RTA, that's going to be a distal RTA, because remember, normally, your alpha-intercaledate cells, they are very helpful in acidifying your urine, you know, to try to keep your urine pH below 5.5. So, if whatever bizarre reason, a person has a type 1 RTA and the alpha-intercaledate cells don't work, remember, if they don't work, that means that proton pump on the epicose surface, the urine surface is not working. You're not going to be able to dump protons into the urine, and if you can put protons in your urine, your urine is going to be very basic. It's going to be more than 5.5, right? So, if the urine pH is more than 5.5, think about a type 1 RTA. If the urine pH is less than 5.5, think about a type 2 RTA, okay? So, those are the ways your T's are part of those RT As, right? So, again, back to this urine pH business, we've talked about how in a type 1 RTA, the urine pH will be more than 5.5, when in a type 2 RTA, the urine pH will be less than 5.5. Remember, another thing, I guess, this is not urine pH, but it's a closely related concept, is vaginal pH, right? Especially, with those vaginal infections, right? If you're comparing tricklemonas to Candida, to Gardenerino vaginalis with bacterial vaginalis, remember, in bacterial vaginalis and in tricklemonas vaginalis, right? The vaginal pH in those people, right?

Usually, it's going to be more than 4.5, but if it's 4.5 or less, you're probably thinking more along the lines of Candida, in terms of the vaginal pH, right? And then, remember that whenever you have a urine pH that is very low, a urine pH that is very acidic, you can actually increase your risk for certain kinds of stones, right? You can increase your risk for like uric acid stones, you can increase your risk of cysteine stones, right? So, CYSTIN, right? Because those are acidic environments promote precipitation of those kinds of stones, right? Whenever you have an overall abundance of hydrogen ions, that's going to promote the presence of like a uric acid stone and cysteine stone, because those are acid-based stones in a sense, right? So, remember, like bigots, right? So, if an acidic-like stones is an acidic environment, they'll be like, oh yeah, time to enjoy, right? Time to have things given, right? So, just something to keep in mind. But if your urine pH is very high, right? And usually, you'll make this like crazy high, like seven or something ridiculous, right? Remember that there are certain things you may want to keep in mind there, right? One is it increases the presence risk for like, true white stones. Remember, those things are also called magnesium, sorry, ammonium magnesium phosphate stones, right? And also calcium phosphate stones, those are also promoted in the presence of a basic, basic urine, right?

And remember that your friends at the MBMD love to test this basic urine with nephrodithiasis as well. Remember if you notice that the presence of a kidney stone, whether urine pH is really high, then you want to be thinking about bugs that are ureth positive, right? Bugs that have the ability to split ureth, right? So, for example, like proteus merabilis, that's a classic one, they love to test with those staccone calculi. Remember, one buzzword on MBMD sounds for proteus merabilis is the fact that it has swarming motility, right? It has swarming motility. And they don't forget staphsaprophidicus. Remember staphsaprophidicus is the second most common cause of utias. Remember the number one is ecoli, right? About 85% of utias are caused by ecoli. But staphsaprophidicus is ureth positive, right? It causes about 10 to 15% of utias, especially in sexually active young females. And then don't forget as well, ureth plasma urelidicum. Again, that's another ureth positive bug. It can absolutely cause a very high urine pH, right? So, you know, those things you want to keep at the back of your mind for, for exams, right? When you keep at the back of your mind for exams. Now, another classic thing when your analysis, I guess since I've kind of hit on the pH pretty hard, is just looking for blood in a person's urine, right? Looking for blood in a person's urine. Again, if a person's urine analysis is showing like a ton of blood, right? Let's see, three-plus blood or four-plus blood.

If you do a urine microscopy, you're supposed to find a commensurate number of red blood cells, right? So, like, you know, red blood cells in the tens per high-power field. So, unless you're seeing like four-plus blood in your urine, right? On your analysis, you should be seeing like 30, 40, 50 red blood cells per high-power field. But if you notice that you only seen zero to two red blood cells per high-power field, on your microscopy in the presence of three or four-plus blood on your analysis, then you know that that person has ruptomyolysis, right? The person has ruptomyolysis. Remember, I think ruptomyolysis as the opiuminocyteologic dissociation of the urine. Remember, opiuminocyteologic dissociation is a classically described concept in a person that has Guillain-Berry syndrome. Guillain-Berry syndrome, right? Because, okay, let's maybe look at normal CSF, normal CSF. If you notice that it's an increase in protein, there's usually an increase in white blood cells to go along with it, right? But if you notice that, wow, the protein is very high in the CSF. But I see very few white blood cells, like zero to two white blood cells per high-power field. There is no agreement between the amount of protein and between the number of white blood cells. That's why it's called opiumin, opiumin protein, cytologic cytosel, dissociation, right? So that's how you tease those two apart, right?

So, whenever you look at the presence of urine, and you're noticing that, wow, I see three-plus blood, I see four-plus blood on your analysis, right? But then I'm seeing only like zero to two red blood cells per high-power field. That person has wrapped up my analysis, right? From muscle breakdown of some sort, right? But again, if you're seeing pure red blood cells in the presence of urine, you know, that tells the person has hemoglobin oria. The person may have like kidney injury, right? They can have nephrolithiasis. Classically, people that have nephrolithiasis, they have red blood cells in their urine. On MBME exams, people that have nephrol... I mean, sorry, no, nephrol... Nephrolic syndrome. They have red blood cells, right? But those red blood cells are described more as being dysmorphic, right? So, like red blood cell castes, they can call them dysmorphic erythrocytes on MBME exams. Or if you see pure blood again, that can also be a telltale sign, especially in a present that has most wheat or a big long-term smoker. They're probably thinking of the person having renal cell carcinoma, right? Or bladder cancer, right? Renial cell carcinoma bladder cancer, those things tend to cause, like, just straight-up red blood cells in a presence of urine, right? And also, if a person has a womb strumor, right? A womb strumor can also cause hematuria, right? Womps strumor can cause hematuria. I remember in a child, right? That had an upper respiratory infection recently.

Red blood cells, again, you know, like two to six days ago, you're thinking about an IgN Fropathy. Or if it's two to six weeks ago, you're thinking about along the lines of a post-infecture. So, what is also called post-reptococcal? The very little one is right. So, those are all things you want to keep at the back of your mind on one exam, right? Just things you want to keep at the back of your mind on exams. And then, glucose, right? If you detect the external glucose in a presence of urine, that's usually because the plasma glucose is pretty high, especially if it's more than one edmg per deciliter. If your plasma glucose is more than one edmg per deciliter, you're actually going to start seeing glucose in the presence of urine, right? But again, it's not the only that a person has diabetes that makes them have glucose in their urine, right? If a person has like fancone syndrome, remember, fancone syndrome is a proximal tubular problem, right? So, that will obviously cause a type 2 RT as well. But in addition to that, you can also have glucose uria as a result of that, right? You can also have glucose uria as a result of that. And whenever you have a ton of glucose in your urine, that's going to increase your risk of candidate infections. That's going to increase your risk of neck fascia of the perineum, right? That's the thing that's called phony's cancric, right?

I mean, like they can very easily give you an SGLT-2 inhibitor question with this, whether a person has like this, and this is going to be in a diabetic, like usually people that have neck fascia, namely, in exams, almost as a rule, have a pac medical history of diabetes, right? So, you check the persons, you check the persons, because SGLT-2 inhibitors, right? What did they do? So, drugs like cancels, flosing, the pagli flosing, and pagli flosing, they inhibit the SGLT-2 receptor, right? They inhibit that SGLT-2 receptor in the proximal tubule, right? So, that you don't remember SGLT-2 means sodium glucose links transporter to, right? So, you don't reabsorb glucose in the urine, for the proximal tubule. So, if you don't reabsorb that glucose, right? It's going to shorten your urine, going to increase your risk of UT Is, especially candidate, right? And you may also wonder, why do pregnant women get UT Is? Well, pregnant women get UT Is for many reasons, right? The main primary reason on NBM is, they have high levels of progestin, right? And progestin is a smooth muscle relaxant. So, it will cause dilution, it will cause relaxation of the urators, right? So, they will have urinary stasis, and that's going to increase the risk of having UT Is, right? Because whenever you have stasis of anything, Bugs can build up in that thing, right? Bacteria can build up in that thing.

But under class decreasing, why people that have, that have pregnant get UT Is, is people that have pregnant, they tend to have a higher incidence of glucose urea, right? Why? The thing is, if you remember from step one, you probably remember learning about like transport maximums of the glucose transporters in the kidneys in the proximal tubule. The thing is, those transport maximums, they actually go down when a person becomes pregnant, right? So, let's say maybe what maybe, again, I'm just making up numbers here, right? Let's see what is one eb milligrams per deciliter as a threshold for it to start seeing glucose in the urine in a normal person. It's not like 140 milligrams per deciliter in a person that is pregnant, right? So, people that are pregnant tend to have a ton of glucose in the urine, right? That's why they have a higher risk of UT Is. That's why it's very important as a pregnant person to basically not have diabetes, if you can avoid it, right? So, I really tell people that are pregnant, you know, watch your weight, exercise all those things. It just makes your pregnancy go a whole lot smoother, right? And it also makes your delivery go a whole lot smoother. Again, remember, though, those podcasts is, I'm going to put this disclaimer, those podcasts is not from medical advice, right? It's not from medical advice, primarily for example, exam purposes, right? So, please don't necessarily follow or reject any advice in this podcast.

Just FYI, I feel like I need to throw in that legal legal disclaimer, right? So, those are all things you find with glucose, your own immune exams, right? And then, if you find ketones in a person's urine, right? If I think it goes in a person's urine, well, remember the ketones that you can detect in the urine are acetone. You can detect acetone in a person's urine. You can detect acetylacidic acid in a person's urine. You absolutely cannot detect beta hydroxybutyrate in a person's urine. That's very important to know. That's very high urtuno. Right? So, what are some things that can cause ketones in a person's urine? The obvious decay, right? The obvious decay, right? Decay can cause a ketosis, right? So, you can see ketonoreal, right? But also, don't forget if a person has starved, right? I mean, if you're, if you've starved, then you're going to be using ketone bodies as your source of energy. So, those ketone bodies, again, acetylacidone and acetylacidic acid, those will show up in your urine, right? If a person has been vomited and vomited and vomited and vomited, right? If you're vomited, right? That means you are not usually people that are vomited for, you know, for a lengthy period of time. They are not able to get any food into them, right? They're not able to keep any thinned out. So, because they're not able to keep any thinned out, well, their body will be like, okay, well, you're not eating. Let's go ahead and start making ketone bodies for energy, right?

So, those people can have a ketoneuria. And again, also if you're pregnant, right? Pregnancy can all is also one of those natural, relatively natural causes of some ketoneuria, right? And then, lucoside esterides. Remember if lucoside esterides is positive, that tell you remember lucosides esterides, right? So, esterides, that means it's an enzyme that is found in lucosides, right? Not a, not a big huge surprise there, right? So, the thing is, it just tells you that, oh, there's white blood cells in your urine, right? So, that can be from a UTI, right? That's probably like the classic, classic, classic thin one, MBM exams, right? And one thing I just want to mention, if you notice that a person's lucoside esterides is positive, well, you're not seeing any bugs, you're not seeing any bacteria. That's a tell-tale sign on MBM is that the person likely has chlamydia, infection, just something to keep at the back of your mind. And then nitrites, right? Remember nitrites, if it's positive in your urine, it pretty much suggests that the person, you know, very likely has some kind of UTI, because remember, bacteria, they convert my traits to nitrites. So, if your urine is nitrite positive, that tells you that the person likely has a UTI. And, what having a negative nitrite, though, there's no rule out of UTI, right? I'll just see that right now. The thing is, this nitrite test in the urine is, is very specific for UTI, but it's not sensitive, right?

So, if you have nitrite negative urine, and the person has like the right symptoms, you should still treat them for UTI. That's a very classic MBM scenario that they love to, that they love to go after, right? Now, let's maybe go over some other quick hits, and then maybe we'll go ahead and wrap up here. So, what if you find scrimos cells in a person's urine, right? What does that tell you? Well, that just tells you that you've is a contaminated urine specimen, right? So, you should, you know, do a better job on obtaining the person's urine next time, right? And then, if you see highly incast, in a person's urine, well, what does that tell you? Usually, your name BM exams, it means the person's urine is concentrated, right? And usually they will give you corroborating information like a fair, again, an elevated urine specific gravity, which is, you know, more than 1.012, right? And then, don't forget, if you find these granular casts, right? Sometimes, they may call them pigmented granular casts, sometimes they may call them moody brown casts, right? These are classically associated, right? With acute tubular necrosis on MBM exams. Remember, acute tubular necrosis on MBM is, they don't always have to call it acute tubular necrosis, they can call it intra-renal ikia, right? It's literally the same thing, right? Just something will keep in mind on exams. And then, don't forget your ribloxel cast, right? You're going to find that with like an efferidic syndrome, right?

Or a person having like some kind of gliburary linoid arthritis, right? And then, if you see lucoside casts, right? Again, that's usually indicative of like pylonofritis on MBM exams. If you find your synophils in the presence urine, right? Don't forget acute intestitial arthritis, right? Don't forget acute intestitial arthritis. That's something you may see. You may see on an MBM exam, right? And then, don't forget, right? Again, the shapes of your urine crystals, right? And when a person has like a nephrolithiasis, right? So if a person has a cough, calcium oxalite stone, remember, this can be people that have Crohn's disease, because when people have Crohn's, their terminal helium is torched, when torched, the terminal helium, that's going to cause the increased absorption of oxalite, right? That's going to predispose the presence of forming oxalite stones, or you know, pressing drinks, a ton of antifreeze, right? Usually like an alcoholic ethylene glycopoisonin, right? Think about calcium oxalite stones. Remember, those things are envelope shaped, right? Very important. Those things are envelope shaped. Sometimes if they want to mess with your head, they will tell you that it's dumbbell shaped, right? So calcium oxalite crystals on MBM exams say that envelope shaped or dumbbell shaped. Just remember the term ED, like emergency departmental, I guess you can think of your retell dysfunction, the E for envelope, the D for dumbbell, right?

And you keep that, you keep that straight, right? And then remember, if a pressing has like calcium phosphate stones on MBM exams, right? Like those stones, they tend to be like almost like star shaped, right? This is not something for any many resources, but it look like prisms in a sense, they're like needle shaped or like star shaped. Think about calcium phosphate stones in those circumstances. And remember, calcium phosphate stones, people that have a distal RT, especially like the type 1 RT, they tend to have a very high incidence of calcium phosphate stones. Again, that's an association. You want to keep at the back of your mind on MBM exams, right? And then remember, if a pressing has like a uric acid stone, right? A pressing has a uric acid stone. Again, those tend to be a rhomboid shaped, right? Remember, you can give uric acid stones in a pressing that has like tumor lysis syndrome, right? So for example, let's say, I've been treated for chemotherapy, right? For some cancer, for some sort. Right? And then, you know, killing a ton of, especially these mitologic malignancies, a ton of cells are dying, well, they're going to release all those purines. So since they're going to be converted by xanthin oxidis into uric acid, right? That's why those people tend to give them like alopeurinol of a buxostat, right? Xanthin oxidis inhibitors. So they don't get a crystalline nephropathy. And the thing can also do is to just hydrate them a ton, right?

But also, you can also give a uric acid and a log. Remember, drugs like raspberries, or piglotticis, those are uric acid blocks, they convert uric acid to a lantone. They convert uric acid to a lantone, right? That lantone is soluble in urine. Uric acid is not, right? That's how you're going to get in the, get in the crystalline nephropathy in the first place, right? So those uric acid stones, they tend to be a rhomboid, rhomboid shaped, or an embium exams, right? And they remember, strovid stones, right? Those looks look like coffins, right? They have like these coffin-led shapes to them, right? Again, the presence urine is alkaline because they have like some ure-responsive bog that's causing problems like proteosmerabilus, ure-plus-my-uere-ledicum, right? Staffs are profidicus. You can remember them with a, with a nomonic POS, you know, like POS, like PUS. So, you know, proteosmerabilus is the P, ure-plus-my-uere-ledicum is the u, and then Staffs are profidicus is the yes, right? And then cysteine stones, right? Cysteine stones, cysteine stones. Remember, if people have like a colac, C-O-L-A transporter defect in the proximal tubule, they'll make a ton of cysteine stones. Remember, those are shaped like benzene rings, right? So, those are hexagonal, right? Those are hexagonal. Again, there's just high urtuno, high urtuno for purposes of your semi-liquinsams. And then, please don't forget, if you have more than 30 milligrams of urine in 24 hours, right?

When you do like the spot urine tubule, you mean creatinine, you know, ratio, especially in diabetics. If you have more than 30 milligrams of urine in 24 hours, sometimes they make only 30 milligrams per 24 hours of 30 milligrams per gram, right? That's the threshold for microabominory in a diabetic, right? And then, if you multiply that number by 10 and take it to 300, then you'll hit the lower limit of lower limited threshold for macroabominory, right? So, again, I'll say that again, if you have more than 30 milligrams per gram of urine in 24 hours or 30, so they may call it 30 milligrams per gram or 30 milligrams to 24 hours. And the obvious thing to creatinine ratio, the spot, you know, take the urine and do the album to creatinine ratio, diabetics, that's microabominory. So, 30 other way to 300 is microabominory. 301 or higher is macroabominory. So, 301 or higher milligrams per gram, obvious thing to creatinine ratio, milligrams per 24 hours. Album into creatinine ratio tells you that the person like he has, the person like he has a microabominory, right? And then, don't forget that on MBME exams, right? 1, 2 and 3 plus per tenoria is nephritic range per tenoria. In general, on MBME exams, if they want you to think of nephritic range per tenoria, again, this rule doesn't always work, but it's a pretty consistent pattern like that works like maybe like 90% of the time.

For you to see a person has nephritic syndrome on an MBME exam by looking at the per tenoria of the urine, it has to be 4 plus or higher, right? 4 plus or higher, right? So, that's very important and high yield to know. So, let me go ahead and pause this. Go ahead and stop here. I think I've pretty much covered all the things I want to heat up with with urinose molality. So, if you're, so you know, I'd offer a tutor in for many exams. Step one, step two, CK, step three preclinical med school exams, third year shelf exams, and if you're a medicine resident, a tutor for the medicine boards and the medicine in training exam. So, if you need to read for any of those things, feel free to reach out to me through the website. Just shoot me an email and I'll be happy to point you in the right direction. I mean, I've worked with tons of people that have, you know, never passed the practice test, failed a USML exam, have very poor knowledge basis. And again, I've had a very, an extremely good track record with these people. I mean, I've had tons of people that, you know, going through the match now and I've done really well on the real exam after, you know, having like non-passing scores on practice exams, right? And many of these people have worked with them for just a short period of time. Obviously, if I work with you longer, it's better.

But I've had many of my students have 30 pointing permits, 40 pointing permits, 50 pointing permits, 60 pointing permits from the tutoring that I gave them. I gave them for these USML exams. So, you know, I have a great track record as a tutor and I've tutored for many, many years. And you know, I've thankfully also won a national tutor of the year award. That was actually when I was in undergrad. And again, you know, I've tutored for a long time. So, if you need to read for any of these exams, I'll be more than happy to help. So, just ship me an email through the website. And then I also do a lot of application advising, especially as air ass seasons come upon us. I don't know of advising and consulting in those areas. And then please subscribe to the website. Again, divineinterventionpodcast.com. If you subscribe, whenever I make a new podcast, you get a notification. And then also for people that, you know, use Apple Podcast or Google Podcast or Spotify, I do actually have the podcast on there, right? So, again, feel free to do subscribe if you can. Any feedback, any, be the help or support, definitely is appreciated. And then the You Tube channel, you know, divine intervention, USMD podcast and videos. Subscribe. That's where you see whenever I post a video, I put it on there. So, again, if you want to get those things, subscribe to these different resources. And then I'm going to talk about a quick life lesson for today.

My life lesson for today is living a high-end life, right? Living a high-end life. So, what do I mean by living a high-end life? Well, the thing is, I will encourage you to maybe do this exercise where you'll take like your last three days and ask yourself, what did I do during the day? Like literally, what did I do during the day, right? Many people, they don't realize that they waste their lives doing things that don't contribute any thin positives, like anything positive to their future, right? Like, what percent of your day is invested in low-yield activities, what percent of your day is invested in high-yield activities? Again, I'm not saying that, I'm not using this to see, what divine says I should never rest. No, that's ridiculous. In fact, to be honest with you, sometimes I take my own personal deeds, right? Because again, rest is good for present mental health, just so you don't fall apart, right? So, whenever you have a deal of work, let it be a deal of work, right? So, use your deeds for high-yield activities, because you see many people, they go about their days and they spend three hours on social media, two hours watching TV, three hours chatting with people, blah, blah, blah, blah, blah. And then they notice that all of a sudden, man, like the day I was going, what did I accomplish with my day, right? And if we check their whole days, they probably spent like two hours doing anything that was not worth it, right?

Anything that will actually contribute substance to their lives. So, I'll encourage you to kind of be mindful of that. I mean, this plays out with many medical students, right? They indicated periods. And then, let's say this indicated period is nine weeks long. And then by weeks six, they start panicking. And then they want you to wonder, I thought you studied for six weeks, what happened? Well, the thing that happened is, those six weeks, they kept changing their study plans, kept changing their study resources, they never said to them one thing. So, they keep changing, changing, changing, changing, changing, changing. Again, the thing I encourage people is, it's not every time that life is supposed to be fun and games. There are sometimes areas just supposed to do the boring hard work, stick with one thing and just go all the way, right? Even the Bible says that he that end just to the end is the one that will be saved, right? So, the thing is, sometimes you just need to pick one resource and stick with it. Even if it doesn't seem like he's working out, keep using it. At some point, things will start clicking for you, especially if it's like a well-selected resource at the beginning, right? That's why when you're doing these long term things, make one good plan from the beginning, that you know that, oh, okay, most people have used this plan and succeeded with it and again, those have to be something or shatter. You don't have to use like 10 different things, right?

So, pick one thing and just stick with it and then you see consistent, don't keep changing, changing, changing, changing, or you see a friend that is using this new onkey deck that you've never heard of before, that's all pressing used and go to 270. Again, the fact that the person used a deck and go to 270, those in here are going to use it, they can get a 270. There are also people forever, one person that uses a deck and gets a 270, there's probably like 10 people that use that same deck and get like a mediocre score, something like in the 210s or 220s or whatever. Again, I'm not necessarily calling those mediocre scores, right? Again, everything in life is all relative, right? Or you see like residents, you see residents and you're like, man, sign out is at three, you see these residents at 2230, they are still banging out nodes, banging out nodes, banging out nodes. What are you doing with your D? Let me tell you this, it doesn't matter how busy you are, in general as a resident, I will say like almost like 95% of the time, you can get your work done in an extremely timely fashion. Well, you see many people, they spend two hours of the AD, chatting, chatting, chatting, chatting, chatting with all the other residents, things that are not profitable, right? You see them, they go around, they do this, they do that, just dragging their feet, right? No sense of urgency.

Remember, there's a part of the Bible that says that we should redeem the time because the days are evil, right? And because you see people, they just think that they are dead like this, oh, that the day is going to wait for them. Let me tell you this, when time is gone, you are not getting it back, right? So leave your life as a higher life, and one great way to leave your life as a higher life is to have a plan for your D, have a plan for your D, plan out your rest times, plan out your goof off times, but also plan out your D, when you plan out your D, very highly unlikely to waste your D on fluff, right? So I can, I know this thing is very basic, but it's extremely important. Many people, especially in health care, they waste their lives because you see people, they have four or five patients that they are taking care of, and you see them around 2 p.m. In the afternoon, they are still struggling to write notes, they are still struggling to keep in others, they are still struggling to call in consults. No, it's not supposed to be. In fact, there are some people that I almost do like an intern school for, where I coach them on how to do it as interns. And one of the things I go through with these people is just how to be efficient. You see people, they are meeting a patient, they're taking them three hours to do an admission.

Again, I'm not saying that a person cannot be slow starting out, but the thing is after a while, you need to take responsibility and be better, be better at your job, right? And many times, if you check those three hours, those people don't have any streamlined process, they use for any of these things, right? Just to admit a new patient, they spend three hours. No, it's not supposed to be so. Like really, if a person is doing a good job, you should be able to, from when you get called on an admission, to when you've written your note, seen the patient and everything, that process should take you no more than an hour, if you know what you're doing, right? So these things are just things that if you practice, prepare plan for, you don't put yourself in these sticky situations. So again, I encourage you as a sign of today, leave a high-yield life, leave a high-yield life, it will be to your benefit, right? Leave a high-yield life as a resident, leave a high-yield life as a med student, leave a high-yield life as a parent, what are you focusing on? Like literally, what are you focusing on? You see some people, they spend so much time at work, they abandon their family, right? They are like absent parents to their kids. Guys, gals is not supposed to be so, right? If you'd have certain priorities in life, like for me, what are my priorities in life? My priorities in life are, my relationship with God, that's one.

But other priorities I have, my family, my family comes second for me, is very important, right? For using my talents and gifts to glorify God, right? Like I know I love to teach, right? So like, I spend most of my life on those three things, right? You know, the other things that I mess around with here and there, but those things ultimately are not for my benefit, right? So like at the end of the day, like you need to make sure that you are spending your life, like you see some people, they say like, or wherever, that's why I don't, this mentality of, wow, see wherever the wind takes me, I do not believe in any of that, right? Or wherever the wind takes me, or wherever the day goes, let's see how to dig, oh no, no, no, no, don't have that mentality of, oh, let's see how to dig, oh no, detamin how your dig goes, take charge of your D, right? So again, let's be wise, let's be wise as people, let's not be foolish, because the thing is, foolish people are the people that they come to the end of their lives, and they're like, wow, what did I achieve with my life? No, you can achieve something with your life if you take control of your life, right? If you take control of your life. So again, it's very, it's very important. So thank you for listening to this podcast. Let me get off my soapbox now, but I'll see you in the next podcast. God bless you. Thank you.

1.012. Below this, the urine is diluted; above it, it is concentrated.

Small cell lung cancer (paraneoplastic), SSRI use, or CNS processes like meningitis.

Hyperkalemia (high potassium). This is due to impaired K+ excretion in the collecting duct.

High urine dipstick blood (3-4+) but very few red blood cells (<5/HPF) on microscopy.

Struvite stones; associated with urease-producing organisms like Proteus merabilis.

The presence of white blood cells (pyuria), indicating inflammation/infection.

Dysmorphic erythrocytes.

Type 4 RTA (low aldosterone effect).

11-beta hydroxylase deficiency.

Envelope or dumbbell shaped (E/D).

Cylindrical casts (or leukocyte casts if infection is present).

Proteus merabilis (P), Ureaplasma urealyticum (U), and Staphylococcus saprophyticus (S).

>30 mg/g or 30 mg/24 hours.

Increased risk of UT Is and potential for ketoacidosis (if diabetic).

Type 4 RTA (low aldosterone effect).

11-beta hydroxylase deficiency.

Envelope or dumbbell shaped (E/D).

Cylindrical casts (or leukocyte casts if infection is present).

Proteus merabilis (P), Ureaplasma urealyticum (U), and Staphylococcus saprophyticus (S).

>30 mg/g or 30 mg/24 hours.

Increased risk of UT Is and potential for ketoacidosis (if diabetic).