DIP Episode 54 - Comprehensive USMLE Step 1 Renal Review (Session 3 of 3)

So welcome to this review. This is the final part of our renal review and again we'll try to go really, really quickly today so that we can get through all this material. So the first slide at 26-year-old female presents to the idiotic chief complaint of right flung pain. The patient has a history of IV drug use, CMP so that's a comprehensive metabolic panel is notable for creatinine of six. That's not great at all. A pelvic exam reveals a fungidine mass at the level of the ectoservic so you probably won't know this since you haven't done repro. ultrasound is consistent with right-sided hydrogen afrosis. ultrasound is consistent with right-sided hydrogen afrosis right so what kind of cancer does this person have if you just have to predict? Is a cervical cancer? So the big thing you want to take away from this slide is that the most common cause of death in patients with cervical cancer is actually hydro like renal failure from involvement of the like the irritors by the malignancy okay. So cervical cancer, most common cause of death is like hydrogen afrosis leading to renal failure because cervical cancer like directly extends to the irritors okay. Now what's the most common cause of hydrogen afrosis detected on a fetal ultrasound? So if you see a fetus like you do an ultrasound of the fetus and you see hydrogen afrosis what are you thinking about? posterior what? Very good posterior urethrobalms okay.

posterior urethrobalms and this we kind of alluded to this yesterday but what is the likely location of an obstruction from like field recolonization? the UPJ right so the junction between the irritors and the renal pelvis, the ureteral pelvic junction okay and if you see a hydrogen afrosis in like a two-year-old male has recurring UT Is what does it have? V1. V1 okay. So vesico ureteral reflux. What in your to think about posterior urethrobalms okay. Well when the kid is born think about vesico ureteral reflux and if you see a 65-year-old male with hydrogen afrosis what are you thinking of?

BPH right, B9 prosthetic hyperpleasure okay and what's the likely cause of hydrogen afrosis in a 45-year-old male presenting what acute onset severe flank pain so flank pain and they know your analysis your cropped on a red blood cells sodding onset kidney stones very good that's nephrolethyases very good remember kidney stones can sort of include the urinary tract right and urine can build up behind it and I mean as you're basically trying to contract on those rocks it hurts a lot I mean like kidney stones like if you see patients that have kidney stones it really hurts really bad okay now likely cause of hydrogen afrosis in a 65-year-old male with a history of prostate cancer treated with external beam radiation so if a patient has got in relation to the pelvis is there something that would happen that may potentially cause like poor drainage of urine this is just an assumption I need to know I've got to run over retroperitoneal fibrosis okay so remember your urethra is a retroperitoneal right so if you get like radiation to the pelvic cavity one relatively common complication of surgery is to have like fibrosis of your urethra and that can sort of cause problems with a drain urine okay so that can cause a hydrogen afrosis and then really if a patient has a kidney urinary obstruction the way you treat that is you just look at the thyracicion okay just insert a catheter and that drains the urine does this make sense any questions on this like okay now a 6.46 inch male is accompanied to the e.d.

by his wife and maternal uncle 30 minutes after he began to complain of a weird sensation in his right eye. Phonoscopic exam is notable for an upward dislocation of the lens in his right eye and floating debris in the posterior chamber of the same eye there are no deficits in the left eye vital signs are notable for a blood pressure of 160 over 95 s1 and s2 are normal with no murmurs robs of gallops your analysis reveals 10 red cells per high power field with a large number of red blood cell casts the patient's uncle is wearing hearing aids and has been on dialysis for the past nine months the most likely theology of this of the patient's shift complaint is what? give you a minute to think about this be okay D okay any other answers? okay maybe we're for a D C D okay E okay so we're between C and D so the answer is actually D right so this question illustrates classic mbm testing strategy right in fact I wrote this question with that in mind okay so basically I know many of you diagnosed this person with morphine syndrome it's not morphine syndrome okay because morphine does morphine cause like any kind of nephritic syndrome? No does morphine cause troubles with hearing?

No right but upward syndrome causes troubles with seeing which this patient has troubles with hearing which I mean this patient can kind of see right is uncle is wearing hearing aids has been on dialysis right so it's a genetic condition right so this is actually upward syndrome remember the triad of can see can pee and can't hear high C okay so you can see visual problems you can pee nephritic syndrome you can hear high C hearing problems okay and the path of physiology involves problems with type 4 collagen so B is wrong because B goes with what syndrome? Good pastures very good okay so again the answer is not C because even if this has many of the morphine's presentations morphine does not cause an aphritic syndrome and morphine does not cause hearing problems okay does that make sense? So be careful on your mbm if something is not there okay don't pick that answer basically you will be making assumptions to defend B as I mean to defend C as the right answer so you sort of want to watch out for that on exams does that make sense?

This is just a testic in strategy question but again I have virtual answer so upward syndrome x-linked okay it's a type 4 collagen defect buzzword you want to remember for your exam is that this can cause C like this arises from COL45 mutations okay like type 4 collagen okay the alpha 5 chain okay this shows up very commonly on the exams this specific mutation name so sort of keep that at the back of your mind okay and you have type 4 collagen in like the different organs that are affected like the eyes the ears and the kidneys that's why you have that cluster of symptoms okay and if you do a renal biopsy like the electron-wide crosscopy will show like a basket we have appearance of the glomerular bismen membrane are we all good on this? Good now next question says an asarca and 4-plus proteinuria in a 14-year old with a 9-week history of a 10-pound weight loss fevers night sweats and hepatospleno megaly a biopsy of one of these lymph nodes seven weeks ago revealed by nucleotid CD19 and 20 positive cells so what's your diagnosis? Okay so what's your diagnosis? 14-year-old with generalized anasarca that's like a boss phrase for like ridiculous a D-my everywhere this is minimal chain disease right and what kind of a cancer is does this patient have? Sorry?

Hodgkin's lymphoma because they have biocletate CD19 and 20 positive cells right those are your redstone bird cells okay so remember hematologic malignancies have an association with with minimal change disease in fact I promise you it is very very high yield to know the conditions that are associated with your different nephrodite syndrome right so it's like if they tell you that a patient has nephrodite syndrome on behalf of HIV what what do they have? Collapsing FSGS what if a patient has like colon cancer and they have an ephrodite syndrome? Remember not the frappathy remember it's actually those solid cancers okay what if a patient has one kidney? FSGS very good FSGS what if a patient uses like IV drugs? Like heroin for example also FSGS very good what if a patient is obese? Also FSGS very good I promise you those things are high yield to know so this patient has minimal chain disease okay and the pathophysiology basically involves destruction of the photosite food process right so the bus for you looking for on test is like a photosite food process if basement but what are the kinds of cells that mediate that damage? Are they B cells or T cells?

T cells very good right so like T cells and cytokines in fact they believe that the redstone bird cells in Hodgkin's disease release cytokines that attract the immune system to those photosite food processes and cause their destruction okay so it's very high yield to know that now minimal chain disease is obviously an erratic syndrome would you find anything on light microscopy? No right so on light microscopy there is minimal change that's why it's called minimal change disease okay would you see anything on electron microscopy? photosite food process if basement very good how about immunofluorescence? nothing good okay and this classically shows up in what age group? Kids very good if I use the most common cause, high yield, most common cause of nephrodite syndrome in kids and how do you treat this? Steroids very good and basically every nephrodite nephrodite syndrome should respond to steroids well not all the time okay and again it's associated with hematologic malignancies right so like leukemias lymphomas stuff like that and if a patient has an nephrodite syndrome what would know your analysis indicates what kinds of casts are found in the urine? What kinds of casts? Fimicast very good with a multis cross appearance remember yesterday we said that if you see like multis crosses in red blood cells what's the bug?

Babesia very good Babesia microdic, good okay and the thing is you probably heard of this term in your reno block light point nephrodite syndrome the reason there is that because you basically destroy the photoside foot processes you you filter a lot of lipids into the urine okay but the proximal convoluted you will actually has the ability to reabsorb those lipids so if you look at the PCT cells under the microscope you see a lot of like lipid inclusions okay that's why it's known as a lipoid nephrosis okay any questions on this slide? Good so next one what's the most common cause of nephrodite syndrome in hispanic and African-Americans? FSGS good and what mediates the damage in FSGS what kind of cell? T cells very good T cells okay T cells also mediates the damage in FSGS and what would you see on light microscopy is it negative? No so what would you see just go with the name of the disease FSGS what would you see? You'll see glomerulus chlorosis right and will it be less than or greater than 50% of glomerular than effective? Less than 50% okay and would it be the entire glomerulus that's affected? No just a small section very good that's why it's known as focal segmental glomerulus chlorosis okay and what would you see on electron microscopy just think back to me more changes is what do you see?

Photoside foot process effacement and immune fluorescence is usually negative but sometimes you may see like IGGC3 or that is almost never tested so I won't worry about that and what is the one immunodeficiency syndrome that has an association with this? HIV very good okay and what's the specific type of FSGS that's associated with HIV? Collapsing right so just think of a building collapsing does like a terrible outcome everyone in the building would die okay so collapsing FSGS is like the worst kind of FSGS okay and then the other disease associations right like Bino Bis okay being an IV drug user okay having one kidney those are like high-high value associations with FSGS and how do you treat FSGS? steroids very good so don't get that kind of stuff wrong on you exam right pretty more the same thing for everyone right so steroids and compared with minimal change disease does this really or usually proceed to end-stay-fernal disease? Usually right there's greater than a 50% chance and if you have FSGS you're gonna get end-stay-fernal disease okay but minimal chain disease almost everyone recovers okay responds really well to steroids FSGS barely if ever response to steroids does that make sense?

okay now RT As RT As RT As so let's talk about the RT As and their associations and then we're going to like some quick mechanisms okay the truth is the mechanism is behind RT As you really don't need to understand them for any exam you just kind of need to be able to recognize the RTA you're dealing with so basically if you get a metabolic acidosis question you should always just make it a discipline always calculate the anion gap okay always calculate the anion gap if you calculate the anion gap and it's normal then that basically narrows down your answers for you treat the diarrhea or an RTA for the most part okay so if a patient has an RTA and they have picked T waves what kind of RTA we describe in a type 4 very good remember a type 4 RTA is associated with low levels of what? of our doster are very good right so type 4 RTA is associated with high power of the steronic states so if you have low levels of our doster if you think about your principal cell right that in a channel no longer works so you never create like the negative charge in the on the urine side of the principal cell that draws out potassium so you retain potassium so type 4 RTA is at the hyper keyemic RT As okay now RTA in a patient with skin hyperpigmentation hypotension and a history of hashimotos do you know the disease this person has yeah you haven't done endocrine yet so this is Adesins disease but basically Adesins disease you destroy the entire adrenal gland right so what kind of RTA will this be?

you'll be type 4 because if you destroy the adrenal gland you're not making any out of the steronic in the first place okay now RTA in a patient with a history of show grids what's the RTA that has a very strong in fact this is probably the most commonly tested association for that RTA is it type 2 or type 1?

it's actually type 1 is a type 1 so the distal RTA has an association with a show grids disease okay now RTA in a patient with a history of fancony syndrome that's a type 2 right that's a proximal RTA basically fancony syndrome is a global defect at the proximal concluded to be a way you cannot essentially reabsorb anything okay please do not confuse fancony syndrome with fancony anemia fancony anemia is an actual like a problem where you have issues repairing DNA so it causes all these mutations that can basically cause like a bone marrow failure and usually kids with fancony anemia they have problems with their thumbs they don't have like no thumbs or like hypoplastic thumbs stuff like that okay so fancony syndrome is a PCT problem fancony anemia is a completely different problem okay and what's this disease I'm referring to where like oh you look at the urine and you see stones that look like benzene rings very good system error right so it's a cola-transporter defect okay so you have trouble reabsorbing basic amino acids okay contrast that with a heart-nob disease where you have yeah sorry yeah yeah that's right contract a heart-nob disease where you have trouble absorbing what kinds of amino acids neutral very good okay so and multiple myeloma again also causes a type 2 RTA proximal RTA so basically here's the algorithm that if you know this all your RTA problems will go away literally the thing you need to do is I guess I'll make it with this marker but basically the thing you do is look at the potassium in the question is the patient hyperchalineic or hypochalineic if the patient is hyperchalineic what kind of RTA are you dealing with the type 4 good if the patient is hypochalineic what are the the the two options that are remaining a type 2 and a type 1 right and then the next thing you look at is the urinary pH if the urinary pH is greater than 5.5 what's the

kind of RTA type 1 very good so urinary pH greater than 5.5 urinary pH less than 5.5 literally if you know this algorithm that's literally all you need to know about RT As for the most part okay well let's go into some quick pathophysiology here right so let's talk about probably the easier one to understand the type 4 RTA the type 4 RTA is associated with low levels of what about Dosterone low levels of our Dosterone okay the thing is if you remember from our discussion yesterday our Dosterone we said in accent three regions of the nephron what are those three regions the Dosterone low levels you will okay good where else sorry sorry the collecting doctor I saw like the principal cell and then there is another cell at the collecting dog that it also acts very good the offer intercalated cell okay so at the DCT right remember that our Dosterone increases the activity of that sodium chloride same order right at the principal cell our Dosterone increases the activity of the inech channel right and then at the alpha intercalated cell our Dosterone increases the activity of a proton pump that literally extrudes hydrogen ions into the into the into the urine right so if you have low levels of our Dosterone this pump doesn't work as well so you retain protons so that can potentially cause a metabolic acidosis okay the thing is I promise you there is a lot more stuff than I'm leading you into here but if you're interested in that just let me know at the end I'll be more than happy to give you well within reason I but more than happy to talk you through those artis well that's what I'm going to say about that one and the reason your hyperacletic is that if our Dosterone is not doing its job of activity in this inech channel will you be creating negative charges here no right if you're not creating negative charges here you will not be able to draw potassium ions okay so you r

etain potassium so you get a hyperkalemia so that's why this is the hyperkalemic RTA now let's go to the type one RTA the Distal RTA so the problem in a Distal RTA is that you have issues at the level of the alpha intercalated cell okay usually you can have problems with the proton pump but another thing you also have issues with what's the other like anti-porer that is found at this region of the nephron so the hydrogen potassium anti-porer right very good so the hydrogen potassium anti-porer so the thing is this anti-porer if it does not work if it's not bringing out hydrogen ions will you be reabsorbing potassium at the level of the alpha intercalated cell no so if you're not getting rid of your protons you get an acidosis because you're retaining acid right but if you're not reabsorbing these potassiums right you'll be wasting more potassium in the urine so what happens to your blood potassium levels it should go down very good so this is why this is a kind of hyperkalemic RTA does that make sense again I promise you there is a lot more stuff here than I'm mentioning but all that if this thing I'm probably not very important for your future right but I just want to give you some context to use to understand this and then the last RTA is the type 2 RTA the proximal RTA that problem is at the level of the PCT right and basically that can arise if you cannot reabsorbed bicarb right so let's say you're taking a sedansolomide for example right or you have like a fancone syndrome where like you're basically dumping bicarb in the urine if you keep dumping bicarb in your urine what happens to your acid-based stannas you get a metabolic alcolysis or acidosis a metabolic acidosis very good you get a metabolic acidosis and the reason you get a hypochylemia has to do with something involving the generation of ammonia okay well that is the kind of worms I do not want to open r

ight now if you're interested in it you can ask me at the end okay so but the big thing is for those to look at the urine page because the thing is for a type 1 RTA your offer intercalated cell really is not functioning well and that offer intercalated cell is what helps you acidify your urine so if it's not working well you don't acidify your urine so your impugnems are being greater than 5.5 okay you have a very basic urine does this kind of make sense but again this is probably what you should do on your exam right but just for your own personal fulfillment you can also try to sort of understand these things I've mentioned okay good so okay I've talked about Fankone syndrome so that's the thing that causes what kind of RTA type type 2 okay and really is there a weird 30-s inhibitor that would actually cause Fankone syndrome expired tetracycline these are going to do bizarre things you want to remember it's fire tetracycline can actually cause Fankone syndrome how no one knows but it has that association okay so next question right so I've sort of talked about many of these already what embatter syndrome where's the defect what part of the nephron?

the thickest end in the name of the loop of Heleneer right and that's like taking what kind of diuretic a loop okay how about gyroments DCT and that's like taking a thiazide okay and how would you differentiate between batters and gyroments based on your blood calcium levels? gyroments has high blood calcium right so you have hyper calcium and gyroments and hypo calcium in batters right and how are those two diseases inherited? very good or is it more recessive okay now what's the path that we haven't talked about little so how does little work what's the path of this? overactive inak right so what part of the nephron is that? the collecting duct right the principal cell you just have overactive inak so let me ask you this question if you have overactive inak okay what happens to your blood volume and your blood pressure? it will go up right and if your blood volume and blood pressure go up what happens to the activity of your reigning and your tensin out of the sterent system? it goes down so if a patient has little syndrome will be trove their reigning? how about and your tensin 1 and 2? how about out of the sterent? it'll be low as well right because again everything is being turned off right you'll basically dial down your reigning and your tensin out of the sterent system because you have a low blood volume so that means you also have a low blood pressure does that make sense? okay but if a patient has badders or get old man's syndrome right?

will be true of their blood volume and blood pressure it'll be low why is it low? very good right because they're basically like wasting electrolytes and watering their urine right so what happens to the activity of those people's reigning and your tensin out of the sterent system? it goes up right so their levels of reigning and your tensin 1 and your tensin 2 and out of the sterent all go up very good does that make sense? and how is the inheritance of little different from badders and giddlements? or the zomodominant very good or the zomodominant okay or the zomodominant okay so badders versus giddlements is the calcium that helps you and real quick oh I love this question I love this question okay so if a patient has badders syndrome okay what kind of acid base and mummally would they have? so if you have badders syndrome will you be volume up or volume down? volume down okay so if you're volume down what happens to your reigning and your tensin system? it goes up okay the reigning and your tensin system goes up right now we know that our industrial one of the things it does is to promote the activity of this proton pump and we also know that and your tensin 2 right makes you like dump more protons in the urine at the PCT with that sodium hydrogen anticoler we talked about yesterday what kind of acid base and normally will accompany badders syndrome?

metabolic alkalosis okay so let me ask you a quick question will we trouble your urinary chloride if you have badders syndrome will it be high or low? okay it will be high why? very good because you're blocking the transporter that helps you reabsorb chloride does that make sense? okay but let's assume one of these like oh god a lose weight I want to lose weight as quickly as possible right so you're like no right you just vomit all the time right if you vomit then you're losing all your stomach acid do you get a metabolic acid dose or metabolic alkalosis? get a metabolic alkalosis okay so if a patient has that metabolic alkalosis I mean sorry alkalosis from vomiting what happens to be a volume status? I be volume up or down down so what happens to the activity of the reigning and your tensin out of the industrial system? it goes up okay so we'll be trouble urinary chloride for those people it'll be low why is the urinary chloride low in vomiting as a cause of metabolic alkalosis?

very good right because you're vomiting in a lot of acid right so your hypochloramic for starters that's one and then the second thing is our dose turn is doing its job so as your reabsorb in a ton of sodium to conserve volume you also reabsorb a ton of chloride okay so your urinary chloride will be low the reason your urinary chloride is high in badders and getlements is because the chloride transporters it themselves are like physically like defective so you just waste that chloride in the urine does that make sense? any questions on that and I've talked about how you can differentiate between these things based on our dose turn levels okay so if a patient overdoses on salicylates what are the what are the two classic acid base anomalies they get? and a metabolic acid dose is why do they get the respiratory alkalosis?

because it stimulates the respiratory centers in the medulla right so if you increase your respiratory rate to get a respiratory alkalosis right and the metabolic acid dose is we just get it because salicylates are literally acids right acetylacetic acid and when we talked about when we talked about the electron transport chain we talked about how like aspirin is an non-copline agent right so if you are non-copline agent you basically kill the electron transport chain right so your body begins to depend more on glycolysis as a source of energy okay and if all you're depending on is glycolysis and you want to keep that case or other high 3, 4, 5, behind your knee step going okay you will keep making a ton of lactic acid right so that lactic acid doses can also cause a high anion gap metabolic acid doses okay and how do you treat salicylate like overdose what do you give sodium sodium bicarb sodium bicarb okay so that you can basically trap the salicylic acid in the urine and pee it out okay and if a patient odyssey on heroin what kind of electrolyte and normally I mean acid based and normally would you expect respiratory acid doses right because what do opioids like heroin do to your respiratory rate decrease if you're high more ventilate what happens to your PCO2 goes up because you're not blowing it out very good so you can get a respiratory acid doses with that now if a patient has a PE a pulmonary embolus so let's assume you feel shot of breath what are you doing you feel shot of breath try to catch my breath right you're trying to breathe you're trying to breathe you're trying to breathe so you're hyperventilating so what kind of acid based anomaly will be found in a PE respiratory alkalosis okay what is a patient going through an asthma exacerbation you're like what kind of acid based anomaly are you looking for respiratory alkalosis in fact a classic question on

step one is if for example a patient has an asthma exacerbation I know you check your PCO2 and it's like four right it's like 50 what is the next step in the management of who's behind what do you need to do next sorry you need to secure the airway very good the next thing you need to do is you need to into be those patients fronto because the thing is if you have an asthma exacerbation the lower response is to hyperventilates so you get a respiratory alkalosis so if the PCO2 is beginning to normalize or beginning to rise into like acidotic mold the patients are beginning to get tired they cannot breathe out that's your 20 more so you need to into be those patients like ESAP okay does that make sense that's a very classic step one question okay now if a patient is so that's the ominous sign if a patient is vomited what kinds of acid based anomalies do they get metabolic alkalosis good okay what is a patient has cons syndrome it's an alkalosis what kind of alkalosis is in respiratory metabolic metabolic very good because what's the pathophys of cons syndrome what's the tumor making our doctor very good to make it a ton of our doctorate proton bomb just basically think about it this way if you're in and you're tensing out the external system is wrapped up you have a metabolic alkalosis simple as that and there are many reasons right one proton bomb working too hard you don't pretend in the urine right there is actually carbonic amydrates in this cell so as you don't be flage proton you don't out you reabsorb one by car okay and they remember and you're tensing to at the level of the principle proximal congluelectribule that sodium hydrogen entry powder okay you dump hydrogen in the in the urine you reabsorb sodium well as you're dumping that hydrogen in the urine you also reabsorb in one by car okay so those things cause an alkalosis very good now if you're taking a lo

op and a thiazide or a thiazide diuretic what happens metabolic alkalosis why very good right because those drugs make you volume down so you rev up your ringing and your tensing out of the sterine system does that make sense okay now what if a patient is taking acidosolomide and acidosis right because how does acidosolomide work where does it inhibit carbonic amydrates if you inhibit it carbonic amydrates what happens to so you're basically waste by carb in the urine so you get a metabolic acidosis now let's be a little more specific what kind of metabolic acidosis normal and ion gap metabolic acidosis let's be a little more specific what kind of RT is that a type 2 RTA okay because remember as the zolomide works at the level of the proximal tubule right okay but do you get a high pouquilinha or a high perquilinha with acidosolomide high pouquilinha right high pouquilinha because again as a diuretic it makes you volume down okay so that reabsorb your ringing and your tensing out of the sterine system so you get a metabolic acidosis okay basically my go to these I'm going to touch on you so much with these electrolyte disorders that if someone like rouses you from sleep and asks you a question you only one thing you just say that's my go yes quick question so we have a zolomide in my type 2 RTA which we see and acidotic urine pH how does that work?

yes that's a great question so the thing is in a type 2 RTA right you will think that because you're dumping by carb in the urine you'll see like an alkalotic urine pH right but that's not the case because the thing is all that by carb is somehow before you even get to the distone effron reabsorbed the primary thing that controls your urine's pH are those proton pumps at the level of the operator collided cell okay because by carb classically they tell you oh by carb is reabsorbed and the PCT that is true that is where by carb is primarily reabsorbed but by carb is reabsorbed by many other spots in the nephron okay does that make sense? yeah good so what if you're taking spirano lactone what kind of acid based on normally would you have a metabolic acid dose is metabolic acid dose is how does that how does final lactone work? it's an outdoor urine receptor blocker right so if you're basically an anti-out dust urine agent this proton pump will not work so you're routine protons so you get a metabolic acid dose is with that does that make sense? okay good now how do you compensate for metabolic acid based disorders? you change your respiratory rate very good okay and how do you compensate for respiratory acid based disorders? very good right so either claim more by carb or with small by carb right depend on your kidneys okay so let's talk about the anion gap equation okay the anion gap so what's the equation for the serum anion gap?

okay so sodium minus chloride plus by carb right and this is usually like an annoying concept for people to understand but really let's think of it this way the thing is the normal body for this is between it and 12 okay that's a normal anion gap because the truth is in the body you try to almost maintain a perfect balance between the cations in the blood and the anions in the blood okay sodium is like the big guy cations in the blood these guys are anions but they don't match up to the total amount of sodium because the thing is there's some other anions in the blood if you added up those other anions theoretically to this and this that should equal the amount of sodium so the ideal gap should be like zero there should be like no difference but this is classically 8 to 12 because we do not measure these other anions okay so the thing is if a patient has a metabolic acidosis what's the component of these three things that helps us buffer that acidosis? by carb okay by carb so think about it if you buffer the metabolic acidosis you have with by carb okay what will happen to this part of this equation does he go down or go up?

he goes down right if he goes down the only thing that can keep this equation constant is if this the fraction of this goes up so let's assume as you're losing by carb as by carb is buffering the acidosis chloride ions are replacing that by carb in the circulation okay that will cause a normal anion gap because it's like as this is going down this is going up to compensate but if you have a metabolic acidosis and all your consuming is by carb but the anion you're bringing back to replace the bicarb that's going is like a lactate anion right then that gap will increase that's what causes a high anion gap metabolic acidosis for example if a patient is in decay right and they have like beta hydroxybutyric acid do you see butyric acid in this equation? no well this by carb will buffer the butyric acid but because the anion coming into play is not like chloride for example okay this gap will begin to widen more and more because you have the pleating the side of fins does that make sense? any questions on like the reasoning behind this equation okay now what are the causes of a high anion gap metabolic acidosis rule them out? methanol? uremia? decay? diabetic acidosis so what pulse okay? properly in glycol of per-hour the height what else? isoniasid? iron? lactic acidosis that's probably the most common causes? ethylene glycol right so stop drinking antifreeze at home what else?

salicylics like aspirin very good okay now what are the common causes of a non anion gap metabolic acidosis? hyperalimentation I've actually seen that tested once what else? adhesives disease diarrhea very good what else? RT As very good or in multivilacidosis the ones that are most commonly tested are diarrhea and RT As what hyperalimentation I've seen that tested okay so we definitely definitely definitely want to keep that in mind okay and adhesives disease as well right because it causes a high-poil dose to rune state so it causes a type 4 RTA does that make sense? there's like a hard-ass mnemonic for what causes a magma but those are really tested but hyperalimentation adhesives disease RT As and diarrhea so like remember the word hard okay hard hyperalimentation is the H adhesives disease is the A RTA is the R and these diarrhea okay good now what is winter's formula? so what is the actual formula? times plus very good plus or minus two okay I will sneak this equation into one of the problems that's coming up shortly okay now let's assume a patient let's assume we have two patients right so one patient is vomiting and the other patient has con syndrome and again you see like oh the virus is getting so much time on this slide is a high old slide right so we just need to get it down right there's no substitute for understanding this stuff so if a patient is vomiting what kind of acybase are normally what they have?

but a body calcullosis okay and rope wake if a patient is vomiting will they be volume up or volume down they'll be volume down does that make sense? okay so they'll be volume down okay and what will happen to the activity of these people's raining and jutez in our doctrine system? it goes up very good to they have increased that activity of the Iranian and jutez in our doctrine systems okay so for these people who will be trove their urinary chloride will it be higher low? are you sure? what do you think?

it'll be low very good again stick to your convictions okay that is one of the most common causes of people doing poorly on mdmi exams the the first thing that comes to their mind is correct and they're like wait but if you go this way and that's what's known as overthinking overthinking is the thief of mdmi grades okay usually the person that comes to your mind is correct so the urinary chloride is down so they have they have a low urinary chloride okay let's go to concentra walking of acid based anomaly a company's concentra but the molecule alkalosis okay at these people volume up or volume down volume up very good because the area absorbing a ton of sodium at the principal cell okay so they're absorbing a ton of water because in concentra we are making a ton of our dust here it's a hyper our dust urine state you're not going to read that okay good so these people are volume up okay what happens to the activity of the rain and dirt and our dust urine system in these people is dialed down because the volume up very good so they have decreased the activity of the rain and dirt and our dust urine system and this is where the fun starts what is true of the urinary chloride in concentra it's so it's high at some point but initially it could actually be low okay so did you guys talk about something known as the our dust urine escape fantastic very good so let's talk about it now so the thing is let's assume a patient like develops concentra like this evening okay ton of our dust urine absorbing a ton of sodium in the in the principal cell chloride goes alongside so the urinary chloride is initially low okay but the thing is I know one of my instructors always says this right would you keep absorbing sodium water sodium water sodium water and then like pop no you I mean you don't see human beings up it so this is kind of just okay so I will not find a way okay so you don'

t pump right so think about this if your blood volume is just expanded expanded expanded expanded from concentra what will happen to the size of your H-trained ventricle they will expand if they expand if there's something they begin to release into the circulation and PNBMT very good now what do amp and PNT do to your blood volume because diurestics right because they dilate the afran material and constrict the effran material if you do those two things what happens to your GFR it increases very good so your diurestics but what do amp and BMP do to the synthesis of bringing the decrease the synthesis of bringing right so it's like you have an unopposed diurestics so if you're then we see ions like sodium and everything in the urine or happen to urinary chloride you'll go up very good so initially you'll have a low urinary chloride but by reason of the outduster and escape the urinary chloride will ultimately go up because you don't want to keep your absorbing water and just explode right that's obviously not what happens does that make sense so one more annoying concept I want to talk about is the responsiveness of these two kinds of metabolic alkalosis to a saline infusion you guys talk about like a saline responsive versus a saline resistant alkalosis chloride sorry it's the same business chloride responsive chloride resistant okay so let's talk about it so to discuss that we need to basically talk about the beta intercalidity itself so beta intercalidity okay so let's see this is the urine side and this is the blood side what do we have on the epical surface of a beta intercalidity itself very good we have a chloride by carb exchange and you can go in both directions okay so we can reabsorbed fluid right and dump out by car okay we can reabsorbed fluid and dump out by car okay so the thing is patients that are vomiting right so they are volume down okay they have

a lot of they have a metabolic alkalosis right and if you have a metabolic alkalosis the ideal thing you should be doing right is to dump by carb in your urine do we agree with that but let me ask you a quick question if a patient is vomiting will they actually be able to dump by carb in your urine no why because they have no chloride that's one and another thing is they are volume down so the urine and your tensileodosterone system is like in charge and if you are in and your tensileodosterone system is in charge and your tensile too be doing its job of maintaining that contraction alkalosis does that make sense so let's assume you gave these people chloride like normal ceiling like sodium chloride or you gave them like potassium chloride right by giving them like fluid that contains ions the first thing you do is you expand the intravascular volume if you expand your intravascular volume what happens to the activity of the urine and your tensileodosterone system it does that so you're sort of fixing some of the things creating the alkalosis you're dialing down the reading system but another thing you do is that by infusing this when these chloride ions are filtered at the net front do you see that you're supplying chloride ions for this transporter that can then help you get rid of that by carb and propriety so will these people's alkalosis respond to the administration of chloride it will very good so vomiting is associated with a chloride responsive basically it's chloride responsive okay or they can call it like ceiling infusion responsive does that make sense okay but if a patient has concentric right they already volume up they're in an entertaining system is already dialed down right so really those giving fluid or like chloride to these people do anything it doesn't this is a chloride on a responsive metabolic alkalosis chloride on a responsive metabolic alka

losis arising the setting of volume expansion chloride responsive metabolic alkalosis arising the setting of volume depletion does that make sense this chloride business chloride responsive chloride not responsive is very high you to understand for step one any questions on this slide or these two things I discussed are we all good okay and real quick con syndrome you're making a ton of outdostery how do we treat con syndrome pharmacologically it's very good we can give something that blocks the outdostery receptors right and remember that in con syndrome you have an increased plasma or doster to reigning ratio okay your plasma or doster to reigning ratio is high right because your secretion of all about doster and your volume up you dial down your reigning system so your doster your your reigning goes down so this ratio is high okay alternatively you can also do surgery any questions on this slide are we all good yes yeah let me ask you a quick question it's perinolactone pleurinone perinolactone has side effects if pleurinone has fewer side effects is there is a white doctor who still keeps prescribing perinolactone exactly it's perinolactone is a lot cheaper than a pleurinone yeah a pleurinone is very expensive very expensive I have never seen anyone using a pleurinone ever yeah everyone I know uses perinolactone super expensive yeah oh the decrease in urinary chloride so the thing is it's not like the moment you develop con syndrome you're really not doing your doster and system are sponsored instantly no right initially you I mean your body also notes is a weird there's a lot of our doster around our dozer will be doing is drop for like a few hours two days right which is like we're absorbing like sodium at the level of the principle cell and chloride alongside so initially your urinary chloride will be down okay it's worth saying that's before a vast and the ele

ctrons are safe exactly does that make sense okay good so the urinary ion gap basically it's you've sort of seen this slide for urinary ion gap please don't mix this up with the serum and ion gap okay this is sodium plus potassium minus chloride okay basically in the urine the number of car ions usually equals the number of anion so this is usually zero okay but let's assume a patient has like a metabolic acidosis okay a billion has a metabolic acidosis what kind of ion would you try to get rid of in the urine you want to get rid of H plus right well you cannot pee out of electricity right in the words of some of our famous instructors so that hydrogen ion is complex with ammonia all right to form a monium but again you cannot pee out of electricity so what do you need to do to a monium sorry you need to complex it with chloride very good so if you have a metabolic acidosis and you're complexing a lot of those hydrogen ions with ammonia and then the ammonium with chloride all happen to the chloride in your urine you'll go you'll go up very good because there is a lot of chloride with ammonium chloride right so if your chloride goes up in the urine all happen to this urinary ion gap it'll become negative very good so if for example the patient has diarrhea as the cause of the metabolic acidosis because like you're losing things from here that not from your stomach right if you're vomiting you're losing acid if you're diarrhea that's the word you get a metabolic acidosis right those people they will try to get rid of hydrogen ions in the urine as ammonium chloride so they'll be more chloride in the urine okay so the urine and ion gap will be negative okay so if you see an RTE basically an example of two things I mean sorry if you see a no-monet and ion gap in the metabolic acidosis on your test take of two things either an RTA or diarrhea okay and then the next thing yo

u want to do is a urine and ion gap if you're not ion gap use negative think about diarrhea as the cause of the RTA the thing sorry as the cause of the non-anion gap metabolic acidosis okay well if you see a positive urine and ion gap think about diarrhea as sorry think about an RTA as the cause of the magma okay so again negative are negative urine and ion gap equals diarrhea remember a negative sounds like negative guttive okay negative guttive right so negative guttive so that helps you remember my diarrhea negative urine and ion gap okay and then a positive urine and ion gap tells you that it's an RTA that is the cause of the magma okay the thing is not all RTA is cause of positive urine and ion gap but that is a okay approach in addition to take away for any exam you take in the future okay so if you go into a renal like nephrology after internal medicine a residency okay so basically explain all of this okay next question a patient presents with a chief complaint of cough and high fevers for the past two days physical exam is notable for anasaka with a urinalysis revealing four plus proteinuria what is the mechanism behind this patient's increased infection risk so if any of us nephrodix syndrome why do they get recurrent infections because they are losing immunoglobulins in the urine does that make sense okay now if what's the defining feature of nephrodix syndrome how many grams of proteinuria greater than 3.5 grams in what time frame 24 hours very good okay now if a patient has a demon in nephrodix syndrome why do they have why do they have that demon what's the pressure that's decreasing your blood on quality pressures remember your stomach or stomach so if you have blood you mean your blood because you have peanut oil you're quite a pressure in the blood holes now okay so you cannot retain the water with your muscle history okay so that's why they get a dem

on okay and is there a kind of pluralization that's found in nephrodix syndrome is it a transodillative fusion or an acudelab fusion it's a transudillative fusion the thing is many people say oh define it so hard to remember what causes what kind of effusion versus the other here is the principle you just need to remember anything that increases hydrostatic pressures in the body or decreases on quality pressures in the body causes a transudillative effusion for example if you have CHF right that will raise the hydrostatic pressures in your pulmonary veins if you get a plural fusion with that that's a transudillative fusion okay if you have nephrodix syndrome your peanut protein in your urine that lowers your protein in the bloodstream so you get low on quality pressures transudillative fusion if you have cirrhosis what's the primary organ that makes protein in the body the liver good liver is gone by by protein by by on quality pressure you get a transudillative fusion does that make sense and then uniquely you want to remember that a PE causes both a transudillative and an exudillative fusion okay a PE causes both a transudillative and an exudillative effusion okay and don't forget your light scratch here they test that all the time on the eczimilis okay now I'm sure you'll learn that in poor okay now what if a patient so this vision has nephrodix syndrome he has complained of acute onset shortness of breath and you do like an ABG and you see hypoxia so starting on set shortness of breath and we showed them with an ephrodix syndrome what do they have they have a PE what's the mechanism behind that very good you're losing antitron being three in the urine right thankfully you've all done him out right so antitron being three inhibits what two coagulation factors factor ten and factor two very good the inhibits factor ten and factor two so if you have a deficiency of a

ntitron being three factor ten and two run well okay and they can cause thrombosis okay so you can get a PE with that okay now this one is something you may not know but it's ridiculously high yield for step one and step two actually and step three as well if a patient with nephrodix syndrome has like starting on send severe flank pain what kind of thrombosis are you thinking about it's a renal vein thrombosis it's a renal vein thrombosis okay again because they are hyperfaculable they can have thrombosis of multiple vessels in the body but one big one you want to remember is the renal vein okay renal vein thrombosis has a very strong association with nephrodix syndrome and what kind of nephrodix syndrome has the strongest association with renal vein thrombosis think about the one that's associated with this now think about the solid cancerous membranose nephropathy very good membranose nephropathy is the nephrodix syndrome that most commonly causes renal vein thrombosis so if you notice in this slide I just said two other high yield iterations for your US70s in the foreseeable future there are three high yield venous thrombosis you want to know about I've talked about the first one renal vein thrombosis in the setting of nephrodix syndrome classically membranose nephropathy the second one is thrombosis of the splinning vein, splinning vein thrombosis that classically arises in the setting of acute hypertitis okay like if you see like starting on set like severe metamorphosis in addition that have hypertitis like within the last few days think about thrombosis of the skinny vein okay and then the third one you've read about in hemorrh is associated with missions that have like polycytemia there or taking OC Ds for prolonged period of time right that's balkyri syndrome right that's thrombosis of what vein the hepatic vein okay a hepatic vein thrombosis I know sorry so a

hepatic vein thrombosis is what you'll find in a balkyri syndrome right that classically arises in patients with polycytemia mirror or patients that have pussy because those are basically the two people that get it on MDM's because other people get it in the real world of course on an MDM is those are the only two that get that disorder okay now we say that you find what kinds of cast in the phytix syndrome phytica is good okay now what's the most common cause of nephrodix syndrome in Caucasians membranous nephropathy okay how about African-Americans Hispanics FSGS kids minimal change disease okay now if you get this last question wrong just go on and cry after this session go on cry after you examine just keep crying forever okay now nephrodix syndrome in a patient with a renal biopsyrivilian positive upper green birefringian steining okay what is that that's a mellow doses you will see this question at least 30 times before you graduate from med school okay in different countries there are many cancers that have associations with that Congo and what are the two kinds of amyloidosis there's like one kind and the other ill and a which one is primary ill right that's the one associated with multiple myeloma right and then you have a amyloidosis you learn more about that in your rheumatology block now what's the most common cause of chronic kidney disease in the US diabetes was the second most common cause hypertension okay the most common cause actually is diabetes because like 30% of cases hypertension I think causes like 25% okay so I remember it becomes before H and the alphabet okay so diabetes is more common than hypertension okay is we remember that okay now if a patient has diabetic kidney disease what would you classically find if you do like my crusty the chemo steel well seen nodules right the KW nodules right the looking on my crust okay and what does diabe

tes do to your ifrin arterial it was like that buzz word so there is like highly noticeable there's like a buzz word equal to it causes like an arterial oscarosis but there's something else in the lung non something very good non enzymatic glycosylation okay of your ifrin arterial so what would that do to your to the pressures within your glomerulus it increases it right and that can cause intra glomerular hypertension okay and if you remember from a ring of multi call it like hyperfiltration injury that can ultimately basically destroy the bimmeras okay so is there a particular drug we could give or drug classical give to slow down the damage to the kidneys heavidors how do those help what do they do to the ifrin arterial be dilated ifrin arterial right so what happens to your GFR if you study them and eat them better you'll go you'll go down right very good you'll go down okay but that would reduce the intra glomerular pressures and that would decrease the risk of the progression of hyperfiltration does that make sense okay again does the thing i'll just encourage you for the future like i know it really to be honest with you it sucks to like be like patiently learn all these mechanisms but more than exams in the future this will just make you a much better doctor right that's what separates you from the algorithms that you have to read up on up to this and all that stuff like actually understanding why things work you'll just make you a more well rounded clinician if you may may not see many of these things but i promise you when you go into residency and when you're on the words you'll see where this understanding can sort of like separate you from people that are just like oh i memorized this factoid and i moved on with my life okay and you also see some step one questions where memorizing factoids will not save you it's understanding that will save you under tho

se circumstances okay um so that's all i'll see with this now 33-year-old male presents with a three-week history of red urine he has also been complaining of pain in his fingers and toes whenever he steps out in cold weather your analysis is notable for red blood cell casts his blood pressure is 170 over 100 orino biopsy is obtained with electron microscopy revealing large deposits completely covered by the glomerular basement membrane for the workup of this patient will most likely reveal which of the following additional findings this question is kind of hard there's just one concept i want you to realize here i figured most people will not get this one correct so sorry in advance so think of something where you find dense deposits somewhere i'm describing those dense deposits and there's a weird antibody you make that keeps something going for prolonged periods of time see three nephritic factor okay so see three nephritic factor is an auto antibody but that auto antibody what does it stabilize see three convertates see three convertates is super stable what happens to your levels of see three you go down okay and that is the only thing that is generally down in this disorder what's the disorder i'm referring to in this question mpg n type type two very good okay so this is type two mpg n type two mpg n because if you notice i put the competing answer here is probably e okay but the right answer is actually a okay so the thing is n type two mpg n you have see three nephritic factor it's an antibody that stabilizes see three convertates so you constitutedly bring down your see three three levels are like super alone okay versus type one mpg n where all with all the inflammation and the anti-gen antibody complexes blah blah blah you ultimately have like decreased levels of like c1 c2 and c3 okay so if only c3 is low and you see these other clusters of symptoms like

they can have like renolds phenomenon and all that stuff think about type two mpg n it's also known as a dense deposit disease okay so that's why i give you those the thing is your friends at the mbne right there are certain things that the new everyone has memorized right so if you begin to run out of ways to make questions difficult to begin to like try to be a little more like innovative with your question right so like i'm giving you the classic one you will hear about some homobodies you probably heard about them already right the very rarely put some homobodies on the exams right they usually put like the replacement term laminated calcifications if you see laminated calcifications they expect you know that it's a summer buddy right or like you see what i did you have something like dense deposits i sort of like give you this like verbal description of like weirdness okay so just sort of keep those things at the back of your mind so the thing is if you're reading like a format for example and he describes a certain finding sort of keep that description in mind because maybe that description that shows up as the answer choice on an exam okay so like one mpg and i've talked about the difference and these diseases are very heavy and see okay so let's do some triggers the answers are here i won't show you okay so read urine and sub epithelial humps what's that post-traptococcal glomeradine fritis and that's what kind of hypersensitivity reaction type three very good good posture syndrome is what kind of hypersensitivity type two very good now read urine and sub endothelial tram tracks mpg and type one good now put aside food process of basement in a child with lymphoma many more change disease good now put aside food process of basement in a heroin user fsgs now anasarca and a sub epithelial spike and doom membranostephropathy very good membranostephropathy now read

urine basket weave appearance on electron microscopy and deafness outboard syndrome very good outboard syndrome okay now read urine intra membranost dense deposits on electron microscopy mpg and type two very good now mesangel deposits plus palpable pepper below the buttocks ij and frapathy very good but what else what's like this a systemic disease they have with the ij and frapathy hsp very good what does hsp stand for oh so he knock you guys have murdered the me he knock shangline pepper okay basically if you see poppable pepper below the buttocks in a kid just stop reading the question it's nothing else it's never anything else it's just hsp okay simple as that is the systemic manifestation of a ij and okay now acelula highland deposits plus four plus proteineria plus a hemoglobin is once you have nine percent that's diabetic nephropathy and what do i what am i referring to by the acelula highland deposits good those are the chemo steel well-send modules fantastic okay now he mortises he maturion and a sadu knows the formatee that's wegners right what's the other name for wegners very good use in a fele granulomatosis or polyngitis and is that positive for cnk or pnk cnk okay and what what a cnk represent antibody is against what against protein is three very good also okay now he mortises and he matria with no sinusitis that's good posture syndrome very good and how do you treat good pastures and and like cyclophosphamone very good okay now cvc notable for ten percent use in a fele plus you read urine plus asthma that's church troughs very good church troughs here is how you recognize church troughs when you're tested the vision will have asthma you have elevated eocino fields and you have an ephrotic syndrome if you see that try it that is church troughs right and church troughs i believe their name is like um eocino phylic right so eocino phylic granulomatosis

with polyngitis versus wegners that is just granulomatosis with polyngitis if you put eocino phylic in front of that that becomes troughs syndrome does that make sense okay now apple grain bi-refringence with congruared staining are you sure you better be okay now linear i gg deposits on immune fluorescence that's good pastures very good what do you make the auto antibodies against i for collagen the alpha three change good those are your answers and remember you have linear immune fluorescence versus granulomatosis i showed us schematic of that yesterday any questions on this good so as an aside chrysenti glomerulon of fright is right so again it's really kind of hard for people to remember like which one is which but the thing is i sort of remember them in a gradation and it makes a lot of good sense right so i remember that it's like you have linear staining on one end of the spectrum and no staining on the other end of the spectrum and then in the middle you have granulistin and if you notice type one so that looks like the second letter linear okay so type one RPGN has a linear staining so type one RPGN has to be what syndrome good pastures very good type two is the granulistin right so like post-reptococcal glomerulon of fright is will fall under the purview of type two RPGN okay those are the ones that are associated with immune complex deposits and then type three are like the anca people right so like webinars chakstrals um microscopic polyngitis okay and did you guys talk about the huge proliferative glomerulon of fright is just remember that's a social lupus okay that's a no lupus okay and again remember the type two RPG Ns right the basically has to be like three hypersensitivity reaction and to get antibody deposits what type one is a type two hypersensitivity reaction okay so type two's a type three's type one's a type two's just add one extra number and

you're good to go okay the type one RPG Ns are type two HS Rs the type two RPG Ns are type three HS Rs does that make sense okay good now in comparing minimal change disease to membranous nephropathy which one is associated with hematologic malignancies sorry my nemoaching disease okay now which is that so is that solid malignancies membranous nephropathy now solid onset flankin and profound hematuria in addition to the histral membranous nephropathy I give you three iterations of that concept very good renauve intranbosis fantastic now what's the classic electron microscopy finding in membranous nephropathy the spike in dome is it sub epithelial or sub endothelial sub epithelial okay sub epithelial spike in dome if i'm not mistaken there is only one thing that is sub endothelial that you need to remember for your exam right why am i hallucinating yeah type one MPGN is sub endothelial oh that's also sub endothelial okay because pretty much every other thing is sub epithelial because that's how I've always remembered it is like the major because they almost never test DPGN but it actually it is quite I think that but it is quite commonly on step one maybe not necessarily here but on step one but pretty much every other thing is sub epithelial okay that sort of helps me remember remember it quite easily okay now would you find granola deposits or linear deposits on immune fluorescence for membranous nephropathy granular very good and we know that membranous nephropathy is the pathophysian walls like forming an antigen antibody complex right so what's the antigen in that antigen antibody complex in membranous nephropathy fantastic wow that's impressive you guys did you guys talk about antibodies against the phospholibase H2 receptor it is ridiculously high yield to know this for the future okay they love to test this nasty bugger okay so just keep it at the back of your min

d the antigen is the phospholibase H2 receptor okay um and again don't forget is that it will have been H2 okay so periobralladema hematuria plus resolved in petygo you're gonna get a headache after this series of questions I just keep twisting your brain but all these things are high up so periobralladema hematuria resolved in petygo that began three weeks ago what is this psg in right so this is phosphatococcal glomerulonephritis okay now how do we differentiate psg in from ig in nephropathy sorry time course okay so what's the time course so ig in nephropathy is like during the episode of the operaspertory infection right so it's called like a sin-farring gytic nephropathy right versus psg in that is how many weeks after two to six weeks right so basically people usually say two to six days versus two to six weeks two to six days is ig in nephropathy two to six weeks is psg in okay um and you find the pauses like in the misangium for ig in nephropathy okay um and what would you see on electron microscopy in psg in sub epithelial humps very good sub epithelial humps okay and real quick what kinds of findings would be present on immunofluorosensuality linear deposits or granular deposits granular fantastic okay now what are the other one what are the antibodies that associate out psg and there's two high old ones anti-structuralizing all good and what else anti-dene is be very good so anti-structuralizing all and anti-dene is be so you knew this next question was coming which one is more specific for a strep skin infection is the anti-dene is be okay so anti-dene is be antibodies are more specific for strep skin infection as the inciting agent in psg in okay now does taking anti-biotics reduce the incidence of post-tructococcal glomerulina fritis no I will encourage you to sort of like walk with me here this is super important you get this on your usb is and psg atte

nd because you all the piece rotation at some point in the future love to paint students on these things so if you take anti-biotics that does not decrease the incidence of post-tructuralizing the glomerulina fritis okay now if you take anti-biotics does that do anything to the risk of you developing rheumatic fever yes what does it do to that risk it decreases the very good okay now let's assume you have a strep upper respiratory infection can you get rheumatic fever from that if you have a strep upper respiratory infection and get a money fever from that you can very good okay if you have a strep skin infection like in the thieco can you get rheumatic fever from that no you cannot okay so strep upper respiratory infection can give you rheumatic fever a strep skin infection can not give you rheumatic fever okay let me touch you a little bit more if you have a strep upper respiratory infection can you get post-infectious glomerulina fritis you can very good now if you have a strep skin infection can you get post-tructural glomerulina fritis you can very good that's why I talked about the anti-DN As B antibodies okay yeah I remember when I was pin band attending with the series of questions I was like you've got to be kidding me and literally it was my first day of the rotation was like come on make it stop and it was very persistent it was just patient it was just yeah when I got home that night I knew the kind of reading I had to do okay so just quick summary the fridic syndrome what medias the damage is it t cells or neutrophils nephritic it's neutrophils it's neutrophils that mediate the damage in nephritic syndromes okay and what's the amount of proteinuria that differentiates nephritic from nephritic less than three and a half grams in 24 hours for nephritic and greater than three half grams in 24 hours for nephritic fantastic very good okay and what's the kind of

cast that goes with nephritic syndrome a fatty cast nephritic ribloxel cast good okay and if you see periobinola dima I mean I know you can find it in both but which syndrome is more specific for periobinola dima nephritic syndrome very good okay and which one tends to have hypertension as a carry-on nephritic very good nephritic the instructor here says that nephritic syndrome is hot okay because it's hypertension there's a lot of information okay okay now we've basically talked about everything on this slide but I'll just say it again steadily rising creatinine plus microscopic hematuria plus a hemoglobin of eight in a patient that takes a daily daily medication for disabling right knee osteoarthritis what is this sorry no so if you're taking a mat for disabling osteoarthritis you're taking an inset like all day every day we talked about this yesterday very good this is renal population of crosses renal population of crosses and I talked about three things yesterday that could present as renal population of crosses what is the inset's criterion was the second one sickle cell disease was the third one sorry diabetes and on those three we just mentioned which is the most common cause sickle cell okay okay let me see okay let's make up on the money so if you remember the cause of renal population of crosses that's where sickle cell is an unknown disease exactly like your insets and then the disease for diabetes I can't quite remember if I use that can also cause rpn sorry obstructive like urofathy okay okay oh yeah yeah that I'm actually ready yeah so so say you're in something new today so sickle cell disease and all g6 acute pylon arthritis diabetes that's the most common cause of renal population of crosses and then obstructive urofathy okay okay good so if a patient has a temperature of 103 you have a tronco rash behalf of eocinophiloria seven days after studying

an oral medication focus part of my side is what is this acute interstitial arthritis good okay yeah okay that's a great question so in this first part of this did I say anything about your synafils in the blood ourin no again on mbm is if information is not there don't create that information to make an answer sound good to you okay that is a classic thing that happens to people on mbm is if information is not there it's not there right the way I think about it so I don't sound racist if for example the question like puts my picture what it don't say that I'm my journey in the picture and not my gerium don't bring you that extra piece of information to make a question sound good to you okay that is one classic thing to just kill people on mbm is an answer sounds good so they just make up the own information I'm putting into the question it's not there it's not the answer does that make sense if I wanted you to think that like I wanted here I put your synafils good on that okay and I will try to trip you guys up with some more questions like this in the future since I know that's your all weakness I will torture you with this in the future okay this one actually has no answer so but this is a good thinking series of questions okay so much the combination of effects to the most likely drop okay so let's begin the craze levels of 100 tens in 2 and out of 2 room increased levels of really and 100 tens in 1 hyperchirinia type 4 RT and this is a teradogin that's an ace inhibitor very good because ace inhibitors right the inhibit the conversion of 100 tens in 1 to 100 tens in 2 so they're basically lower your blood pressure and all that stuff but everything proximal to 100 tens in 1 will run like rain in like a and your 10 in 1 okay but you're 10 in 2 and your out of 2 will go down and because this causes a high poll out of 2 room seat you get a type 4 RT and please do not

prescribe these inhibitors to moms you can basically like explode the fetal kidneys and there'll be some nice lawyer that will come after your license in the future okay so back to this the craze levels of 100 tens in 1 and your 10 in 1 out of 2 room increased levels of raining hyperchirinia type 4 RT a also teradogin what is this?

Heliskirin very good a less teradogin I don't really know how to pronounce it right but let's see so a less teradogin a less teradogin so this is a direct reading inhibitor right so if you inhibit the activity of raining right you're 100 tens in 1 and your 10 in 2 out of 2 and everything will be all know right now this they always confuse me so I specifically looked it up will be true of your levels of angiotensinogen if you took a direct reading inhibitor you'll be high very good because your body will want to rev up your rain and your 10 in our doster and system but basically raining doesn't work okay so your 100 tens in 1 gene levels actually go up does that make sense okay now what happens to your levels of raining all right I give you the answer it actually goes up so the thing is you think that by inhibiting a rename yeah you have like low levels of raining that's actually not the case the thing that happens is you make the raining first and then a less teradogin then inhibits the raining okay so your raining levels actually high with a less caring does that make sense okay and because these drugs are basically blunt in the activities of angiotensin to an outdoster what kind of potassium balance would you have with these drugs like ACE inhibitors while a scary hyperkalemia okay now would you get a metabolic acidosis or metabolic alkalosis acidosis very good because if you have no of course I erased it if you have no outdosterion that proton pump at the alpha intercalated cell doesn't work should become hyper no you get you retain proton so you get a metabolic acidosis does that make sense okay good now so don't this one this one okay so increased angiotensin 1 and you're tensing to an rain decrease outdosterion hyperkalemia typhoidal teradogin no decrease outdosterion what's like the close cause enough ACE inhibitors ARB is very good angiotensin 2 receptor block

ers right so if you block the angiotensin 2 receptor angiotensin 2 is around is just like important basically right so everything is possible to angiotensin 2 be high angiotensin 2 and 1 rain will all be high but remember angiotensin 2 goes to what region of the adrenal cortex so na glomerulosa to make you see create outdosterion very good so there angiotensin 2 receptors in the zonal glomerulosa of the adrenal cortex okay so if you like angiot if you basically block those angiotensin 2 receptors and it's actually super high for step one remember that the angiotensin 2 receptors are known as type 1 receptors angiotensin 2 type 1 I have seen that there's a many times okay you'll not be able to make outdosterion okay next one increased angiotensin 1 angiotensin 2 raining and outdoster these rocks cause hyperchylenia the pathogens that they can cause a type 4 RTA that's preinolactone very good how does preinolactone work it's an outdosterion receptor and antagonist very good so if you block outdosterion receptors your outdosterion will be high everything proximal to outdosterion will be high does that make sense so this was just look hard but you're not just figure out where the block is and then everything proximal to the block will be high everything this those will the block will be low good okay now how do you treat lithium induced nephrogenic diabetes insipidus try amterine or amylorite right they are innec channel blockers okay now switch to this drug in a patient with a dry cough taking in a l al enala prea you switch to an ERB right so like low sartan can the sartan tell me sartan while sartan you switch to an ERB why do e-s inhibitors cause a dry cough build up of pretty kinding very good because angiotensin convertin enzyme helps you break down pretty kind okay now lip swelling and respiratory difficulty in a patient that was recently started on a drug for hype

rtension he's died died of hypoxic respiratory failure after a similar episode what's your diagnosis very good this is hereditranjodema and let's talk about the mechanism real quick so the thing is hereditranjodema what do you have a deficiency of any stumb there so we cover it okay so you have a deficiency of the C1 esterase inhibitor like literally the name of the enzyme is C1 esterase inhibitor the thing is if you have a deficiency of this enzyme there is some deeper stuff I can discuss here but let me give you the cliff snows version okay see what esterase inhibitor one of the things it does is to convert pretty kinding to inactive so let's call it ibriety kinding okay but it so happens that angiotensin convertin enzyme can also help us make this conversion right so if a patient has a deficiency of C1 esterase inhibitor really not that one pathway that helps them break down pretty kinding do you see a problem with giving those people like an ACE inhibitor yeah you'll knock out the second pathway so there's I mean there are other pathways to break down pretty kinding but these are the two majors they'll have very high levels of really kinding and that can like increase vasculopremibility and cause all this inflammation and they can get a hereditranjodema so ACE inhibitors and actually AR Bs are contraindicated in those patients the risk of hereditian like getting like like an attack is lower with an ARB but you just also don't give AR Bs to those patients as well does that make sense okay now um so the drug class is ACE inhibitors other contraindications to ACE inhibitors if you're pregnant um if you have bilateral renal artery stenosis should you get an ACE inhibitor no why so think about it this way if you have stenosis of your renal artery what's trouble your GFR it's low because there's not enough blood coming to the afrin material right so if you then added an A

CE inhibitor on top of that what do ACE inhibitors do to your effrin material did they leave them so what would that do to your GFR even more it would decrease it even more and that can throw you into like like legiferinophia okay so in bilateral renal artery stenosis ACE inhibitors and AR Bs are contraindicated does that make sense okay now slows down kidney damage in diabetic kidney disease ACE inhibitors and AR Bs good now hyperkelimia gynecomastia and decreased libido spirano lactone what's the mechanism behind the gynecomastia decrease libido adrenergic adrenergic adrenergic right so adrenergic receptor blockade from spironolactyl okay so how can you fix that problem give a pleridone give a pleridone okay now what's the most powerful diuretic loops good how do you reduce the hyperkelimia ulcerative the use of your someone what kind of diuretic you want to give a potassium or a case bearing diuretic what are the two classes of case bearing diuretics how does your receptor antagonist very good and in a channel blocker right so like triumptory nanomilurin okay good so what will be trouble the renal filtration giving the following parameters okay so what's the formula for the filtration fraction very good so gfr over rpf okay so filtration fraction is gfr over rpf so let's take this one by one if you take it on and say what happens to the synthesis of first the glandins goes down if the first the glandin synthesis goes down what happens to your aphrenatural constriction or dilation constriction what happens your renal plasma flow goes down what happens to your gfr goes down so if this is going down this will go up if this is going down this will go down so is there any net change no good no change okay now let's assume a patient has multiple myeloma what happens to the amount of protein in their cereals it goes up okay so what happens to the uncodic pressure in the glo

merular capillaries it goes up what does an increase in uncodic pressure inside the glomerular capillaries due to gfr it decreases it because you're holding on to more fluid right so your gfr goes down does anything happen to your renal plasma flow no so overall what happens to your filtration fraction with multiple myeloma goes down fantastic okay now let's assume a patient has any kind of volume depletion excuse me if your volume depleted what happens to your gfr it goes it goes down what happens to the flow of plasma through your kidneys it goes down as well so what happens to your filtration fraction it actually does not stay the same okay so here's why if your volume down is there some weird thing that sort of comes on board brass okay what does that you're tensing too do to your efferent arterial at what it constricts it so between your gfr and your rpf which one goes down even more your rpf right because you're like literally clamping down on the efferent arterial so if this is going down more than this what happens to your filtration fraction it actually goes up right that's primary and unentencing to effect so your filtration fraction actually goes on in the setting of volume depletion okay now let's assume you have a kidney stone that is obstructing the erytero vesico junction so the junction between the eryters and the bladder what happens to the iconic pressure in woman space if you have an obstructive uropathy sorry yeah you're right what happens to the hydrostatic pressure you're ready in my mind the hydrostatic pressure in woman space goes up very good so you have an increase hydrostatic pressure in woman space what does that do to the gfr it decreases the gfr right because if you are pushing back against the glomerular capillaries they stop draining stuff good does anything happen to the renal plasma flow no good so what happens to your filtration frac

tion it goes down do you think they love to test this stuff on step one yeah I know the good answer will be no but unfortunately they do okay they test this all the time does this make sense any questions okay now estimating gfr so what's the best substance well what's the most commonly used substance where estimating gfr creatinine very good does it overall under estimating gfr over estimate why because in addition to binfield trade also secret some creatinine good now how do you estimate your renal plasma flow pah right paramino hiporec acid okay and the thing is pah is fully filtered and it's also secreted in super super large amounts basically every paramino hiporec acid that makes its way to the net front makes its way to the urine what is it all pah that makes its way to the urine no so those pah over or under estimate your renal plasma flow it under estimate your renal plasma flow okay okay for renal clearance that formula is your concentration times low rate of flow is raised by the by plasma concentration yes so for pH if everything is x created out of plasma yes the plasma concentration never reaches zero because 100% of your cardiac output does not go to the kidneys the only organ that receives a 100% of cardiac output is what the lungs very good the lungs so yeah you're basically the plasma concentration of anything your body can never get to zero even though you probably be probably be dead at that point right yeah yeah yeah your plasma concentration never ever attained zero even if in a dead person if you measure the electrolyte there'll be something in your blood okay yeah does that's the answer a question yeah okay good so yeah it cannot be infinity right will not be human beings if that was the case okay now what are the two high-yield auto regulatory mechanisms to sort of maintain GFR there are two mechanisms you must have talked about to blue glue v

erila feedback and the myogenic mechanism right I have slides coming up on that so just keep that for now okay now is there a particular drug that in World War II they actually test this on step one maybe they're not is it's a drug where if you gave it with like an anti-bodies like penicillin it actually reduce the number of doses of penicillin that you have to give that's with a P useful doubt as well pro probenesid very good it's probenesid probenesid so the way probenesid works is that it inhibits something known as the organic anion transporter in the nephron the organic anion transporter has two rules one is that it helps with reabsorbing uric acid if you inhibit it what happens to your absorption of uric acid it goes down because this is the transporter that we absorb you reabsorbs uric acid so if you inhibit this you develop uric acid so uric acid goes in your urine so it decreases in the blood that's how it's used for doubt but the other thing is that this organic anion transporter helps you get rid of like penicillins in the urine it helps you secret penicillins into the urine so if you inhibit this what happens to the secretion of penicillins and sephalus porins into the urine it goes down so what happens to the levels of those things in the blood it'll go up very good okay and we said crabbing clearance over as it meets a GFR because some of it is secreted and what happens to your GFR would age it decreases right decreases with age and why is that come on endomnie or downer let's give some physiology behind it so that we feel better what happens to your BUN with age normally you should not change much right but really why does your GFR go down with age urinal function declines with age right but it does not decline to the point where you go to like 20% of your GFR right there are certain things that can speed that process along like going to McDonald's pret

ty regularly taking a ton of soda right those can sort of spread those processes along okay now to calculate clearance the formula you just need to remember is like is this the one I learned I was like a picture is like you view over a P like they shoot someone like looking up at the sun and the person was P but it's a very like striking I know it's a very striking memory tool like very pretty I'm like looking up at the sun I'm like just you know this really I was like oh yeah you'll be like sun key and so that's an easy way to remember that okay so you can estimate like GFR by calculating the clearance of inulin you can estimate the renaul plasma flow by calculating the clearance of pH okay so you view over P and that will help you I'm sure you will never forget that ever again for the rest of your life okay so what happens to your GFR in cirrhosis it decreases why because you lose on cardiac pressure in the glomerulus remember your liver makes protein no liver no protein no protein no on cardiac pressure GFR goes down okay how about an patient that has an euphrodite central goes down because the appeal now protein okay how about an acute urethral obstruction goes down what's the pressure that increases in in bone space very good in bone space and we've talked about the factors that affect GFR basically my goal with this review was not to like make it a stock if you're like oh what are the things that affect this I just want to give you scenarios so that you can think about the concepts because that's the way step one will approach many of the questions okay so real quick what's the best measure of GFR in your land does creatinine overall underestimate GFR over underestimate I mean over sorry overestimate because you secret some creatinine how do you calculate clearance your view over P very good and what does the clearance of inulin approximate GFR okay now what's t

he relationship between the clearance of creatinine and the GFR is it the same slightly higher or slightly lower slightly higher yes you had a question yeah so it's about cirrhosis causing increases in GFR so if you're not making protein you're on high pressure is decreasing no that should not increase GFR wait oh wait if you're not making protein so the oncotic pressure in your glomerular capillary is going down so that actually increases GFR that is absolutely correct yeah that is true right yeah yeah yeah sorry sorry so in the phytix syndrome your GFR also goes on sorry about that I can think about it in the wrong direction so in the phytix syndrome you lack protein in in cirrhosis you also lack protein right so if you lack protein in your blood yeah you cannot keep fluid in your vascular tree so your GFR actually goes on yeah I think I was thinking more about plural effusions they're like oh if you have a decrease in oncotic pressure you will not be able to keep fluid in your blood in the like long capillaries so you have an extra position of fluid so you get a trans-unitive effusion yeah that is correct thank you for thank you for calling me out on that that's actually a good thing I'm glad he made its way to the recording so whoever is listening to this recording in the future cirrhosis and the phytix syndrome resists your GFR okay scratch away what I said like a couple of minutes ago got it I hope so okay back to this so if you slip through the section of the recording you miss out on this factor I know kind of terrible okay so what is the relationship between the clearance of inline and the GFR are they the same higher lower the same very good how about the clearance of pH on the GFR they're not the same right which which is higher pH clearance right because you filter pH but you also secret pretty much all of it okay so the pH clearance is a lot higher than t

he clearance of creatinine okay so it's like let's assume your bar is the GFR in your linus here pH is here creatinine is here does that make sense so you secret some creatinine you secret pretty much all your pH okay so your GFR inline is a perfect measure creatinine is not so perfect pH is you should not use pH to measure GFR she is not to measure your renal plasma flow does that make sense okay now if a patient has S I A D H S I A D H what will be trove the plasma or similarity it will be low because the area of the internal water right what will be trove the urinous molarity it will be high very good okay so if you're retaining a lot of water what can you say about your free water clearance bless you in S I A D H you have a negative free water clearance okay because you're retaining more water than you should and real quick is there a particular kind of lung cancer that is associated with S I A D H H there's a perneoplastic phenomena small cell lung cancer very good what are the other perneoplastic phenomena that account a uh go along with a small cell lung cancer question syndrome from making a C T H and what else think of think about neuro Lambert good Lambert eating myestemic syndrome so remember from your neuro block you make auto antibodies against the pre-symptych voltage heated calcium channel does that make sense fantastic okay now if a patient has diabetes in sypedus won't be trove the serimus molarity it'll be high why because you're you don't have any H and border right so you're wasting a lot of water on your urine so what will be trove your urinous molarity it'll be low so we'll be trove your free water clearance it'll be positive very good because you're wasting more water than you should good okay we've started to talk about this already right but let's just walk through them in like two minutes so at the proximal tubule what the diuretics that work

there chrabonic and hydrates inhibitor is like acetylzolo one right so inhibitor chrabonic and hydrates right so those consumable acidosis are colosis acidosis because the hypochylinear hypochylinear hypochylinear right because they are diuretics they make you volume down so that rest of your russ system so get a hypochylinear okay now if we go to the thick ascended limb of the lupus heli does that apply to the manitone?

um yeah manitone will cause a hypochylinear and a metabolic alkalosis because it just makes you volume down it doesn't make you waste my crabby the ureth like acetylzolo mine does it just makes you volume down so that already is okay russ system is that a vasidosis for manitone yes does that make sense? good okay now at the thick ascended limb of the lupus heli right we have that NGCC transporter okay what's the drug that inhibits that sodium potassium tucloride transporter? look diuretics very good okay and um at the distal convoluted tubule we have the sodium chloride symporder what's the drug that inhibits that? the phyasides and then is there a particular hormone that increases the activity of that sodium chloride symporder? of the sodium chloride symporder? our dosterone very good okay now what's the other hormone that acts at that level of the nephat? pth right it makes you insert more of those calcium channels on the ureth side, the typical side of the dCT cell so that you can reabsorb more calcium okay and where else those pt's act in the nephat? very good on the sodium phosphate symporder right it causes endocytosis of that symporder okay good um now we go to the principal cell right so the principal cell has an inachannel and a rompichannel right so what increases the activity of that inachannel? our nostril very good okay and are there drugs that block those inachannels? like?

like triantrine and amylo right okay and we said that our dosterone increases the activity of the inachannel okay um let's see what's the other hormone that acts at the level of the principal cell? adh very good so adh acts on what kinds of receptors are the principal cell? vasopressin v2 and vasopressin v2 receptors works through what signaling cascade is it gs gq or gif? gs very good the increase the activity of adh helix cyclase do you think you need to know that for step one? yeah good okay and then we go to the alpha intercalated cell on the apical side the urine side we have the proton pump okay and then we have that hydrogen potassium antiporter what's the hormone that acts at the level of the alpha intercalated cell? our nostril increases the activity of that proton pump right? does that make sense? okay good and how does pth help us um increase the synthesis of active vitamin D? what's that enzyme in the kidney that it activates? one of my drugs is very good okay and then how is the kidney effect to your red blood cells? the iphone very good right? your peritobloc apeliers make iphone so that you can activate your red blood cell precursors okay good so this is the part I'm sure you've been waiting for okay so do not panic you'll be an expert at the hyponychromies after this discussion this will probably take us like 10 minutes to be honest okay so how do we do this?

I think I's come to this side of the room let's talk about the hyponychromies so you can see what I'm writing on the board okay you all see everything here with this okay good because I get right there so that the recording and training captures okay so there are three kinds of hyponychromies right three kinds of hyponychromies so first things first what's the equation for serum or similarity?

two times sodium plus plus bn over 2.8 plus plus those glucose over 18 very good okay and we know that a blood glucose level is usually like 90 right 90 mix per deciliter your period is usually like minus course so no one really cares about this stuff so the biggest contributor to this is your sodium okay so under like rational circumstances if a patient's sodium is low what should happen to the serum or similarity it should be low as well that's the regular thing that should happen do we all agree with that okay so if your hyponychromic the normal thing to happen should be that you should be you should be hypos smaller if you make hypos smaller okay you can call this a hypotonic hyponychromia any questions so far okay but let's assume for some reason the patient is in DKA or something known as HHS you learn about this in December okay your blood glucose levels can be as high as like 900 for example if your blood glucose is 900 can you see that in like with another blood glucose you are dividing 90 by 18 that's a 5 but if your blood glucose is 900 the dividing 900 by 18 that's a 50 what would that do to your serum or similarity you'll increase it very good so there's such a kind of hyper if I can only more space for this bad boy so hyper or smaller hyponychromias or also call them hypotonic hyponychromias they can arise in patients that have DKA or HHS or a patient that takes like a non-reabsorbable sugar like man at all okay these things can all cause a hypotonic hyponychromia okay hyper or smaller again because if your blood glucose level is super high then this becomes an important part of this entire equation yes oh HHS you learn about in December it's like hyper or smaller hypokitonic non-sumpting yeah it's something that happens in time to diabetes it has like four or five different names the endocrinology people cannot agree on like one name but it's like a thi

n I promise I promise okay so how does this cause hyponychromia right so if a patient the easiest we don't understand hyponychromia is a sodium of the water right so if you have DKA your sodium is fixed right but because you have such high levels of glucose in your serum what does that do to the water in your muscular tree it goes up right because all that sugar that's hanging out in your blood draws in water okay so because you're diluting a fixed amount of sodium right you get a hyponychromia but because of this equation that we talked about right your serimos polarity is actually high do we all agree with this okay so now let's assume you run an eligible hospital right you don't want to spend any money right so you're using like the worst lab equipment in the work so let me give you an example here so let's assume this is a person's block okay let's assume this is like the solid component and this is the liquid so liquid component solid component okay the right thing to happen is that you should measure your sodium in this liquid component okay but if you have like a terrible like lab machine that measures sodium what measures it in this entire volume right you can see that oh your sodium is the same but the volume that you're measuring that sodium in is higher than normal so what would that do to your sodium balance all right so let's assume a patient has multiple my lower right where the abnormal proteins in the form of immunoglobulins to the acere you can see that you're bumping up this volume measure even more so if you keep the volume in the form of the sodium you can see that the volume is even more terrible right so let's assume a patient has multiple my lower right where the abnormal proteins in the form of immunoglobulins to the acere you can see that you're bumping up this volume measure even more so if you keep bumping up this volume measure more happen

to your your sodium concentration you'll go down okay this is what is known as a pseudo hyponytremium sometimes it's known as an isoosmola or an isotonic hyponytremium does that make sense any questions on these two okay good so now let's talk about the scary one okay so again let's just boil it down to this one equation right so sodium over water okay so let's sort of like assume three scenarios right so let's assume you're losing if let me ask you this question how do we divide these three hyponytremias the hypotonic hyponytremias how do we divide those things up by volume right so you can be you volimic right you can be hypolimic and you can be hypervolimic right so let's just go by the volumes if you're hypervolimic what has to be true of the denominator and this equation must be higher must be go up or go down oh very good so it goes up right so let's assume this is also going up because generally think about it right if you're bringing more volume into the body usually you're bringing more salt alongside right so but if you're bringing salt and water into the body but sorry into the body which has to be coming in in larger quantity for you to be hyponytremic the water very good so you can begin sodium and water we're getting more water than sodium okay that is the pathophysiology behind the hypervolimic hyponytremia right so you may see like divide how does that work so let's assume a patient has congestive heart failure right if a patient has congestive heart failure what happens to the profusion of the afferent arterios it goes down okay so what happens to the activity of the raining and juteins in our dust urine system goes up so your levels of our dust urine go up do we agree with that and your levels of ADHD go up as well do we agree with that okay so if your level of our dust urine goes up and your level of ADHD goes up let me ask you a quick question what

does our dust urine do to the absorption of sodium it increases it what does our dust urine do to the reabsorption of water it increases it okay does ADHD do anything to the reabsorption of sodium now does ADHD do anything to the reabsorption of water yes go so can you see two things making your absorbed water one thing making your reabsorbed sodium so this will be a cause of a hypervolimic hypotonic hyponitrinia I know does that make sense okay well let me ask you a quick question since you're rearing out your tensin out dust urine system is like working super hard will be trove your urinary sodium for like this cause of our hyponitrinia you'll be low you'll be less than I think 10 that's the number I think the usual less than 10 but let me ask you another question there's another thing that can also actually cause our whips shouldn't do that there's another thing that can cause hypervolimic hyponitrinia let's see if patient has renal failure remember renal failure makes your routine volume right so you can be hypervolimic in that sense well let me ask you a quick question would your rearing and your tensin out dust urine system be working properly if you have no kidneys no so we'll be trove your urinary sodium under the circumstances you'll be high you'll be like greater than 20 I think some people use 40 use whatever value you got in class those are your hypervolimic hyponitrinia your hypervolimic hypotonic hyponitrinia good you're gonna agree with that good okay so dealt with this one problem so that is fixed so now let's talk about the hypervolimic one right so again let's go back to this equation sodium over water okay so if your hypervolimic what's happening to your water is it going down or going up going down but again let's look at this rationally if you're losing volume in the body it usually means that volume is chasing your sodium right so as you're losi

ng sodium you're losing volume okay but if you're losing sodium and losing volume which has to be lost in greater quantity sodium very good so you can lose sodium you can lose water or you lose more sodium than water does that make sense so let's give an example right the classic one that's tested on exams is vomiting right vomiting right so if you vomit you're losing a lot of electrolyte rich fluid right so that can make you hyponitrinic well let me ask you a question in the setting of vomiting right so again you're losing more sodium than water right because vomit is not like you vomit like buckets and buckets and buckets of stuff right but if you're vomiting you're losing electrolyte rich fluid what happens to the activity of your running and your tensing out of the strain system because if that's the same goes of all the trouble your urinary sodium you'll be low because our doctrine is doing its job of keeping that sodium very good so urinary sodium will be less than 10 it's like milli equivalence per liter if you may okay now let's assume let's talk about another thing that causes hyponvolimic hypotonic hyponitrinic let's assume one of you wants to lose with high force right so you start taking diuretics like loops right if you take loop diuretics right you're losing a lot of salt we are losing water alongside but you're losing a ton of salt with that so let's assume you're taking a diuretic what will be true of your urinary sodium if you're taking a diuretic it'll be high very good so that's how you can differentiate between these two causes of hyponvolimic hypotonic hyponitrinia does that make sense okay so fix this problem now the last one is the uvolimic hyponitrinia if your uvolimic what happens to that water content in your denominator it doesn't change so this is where you're gonna hate me it actually does change but I promise I'll explain why that causes

uvolimia right so let's see you have sodium over water and it's only this that changes let me ask you a question if you give a patient like free water does that really expand the volume much why not because it just goes into the cell right because if you think about it right if you give a patient free water what happens do you guys remember like the 60 40 20 row where is most of your water tied up in the body intercellulatively very good so if you give a patient free water you're like oh great I'm expanding the aboscow tree no you're not like 75% of that food you're giving them is going straight to cells so yeah does that increase your volume status a little yes it does but it doesn't increase it by an appreciable amount does that make sense relative to what you gave so well think about it if you're just giving fluid that would at least in some way shape of form dilute your sodium because you're just getting free water right so there are two things commonly on exams that cause a uvolimic hypotonic hyponitrinia one is SIBH and then the other is psychogenic polydipsia although if you also go like a beer binge or whatever it's called like they call it the beer putomania that also puts you in that in that but let's discuss how you differentiate these on exams let's look at the serimosmolarity and the urinospolarity will be trove your serimosmolarity if you have SIBH you'll be low why because your area is warming too much water so this will be low will be trove your urinospolarity you'll be high because your urin is very concentrated because your area is not going to turn off water okay now if you have psychogenic polydips you're like drinking a ton of water what happens to your serimosmolarity it goes down right because you're diluting your serum by just let's say you drink like 12 gallons of free water every day right now we lower your serimosmolarity what would that do

to your urinospolarity it will be low as well why because you're trying to get rid of that fluid right so your urinospolarity will be low as well in fact if they want that to really like scre your heads on these exams will be trove your levels of ADHD and SIBH it'll be high good you have high ADHD will be trove your levels of ADHD in a psychogenic polydipsia you'll be low because you don't want to re-absorb any water you want to waste it does this make sense any questions on the hyponic trimmius good okay good treatment generally not very relevant for step one more relevant for step two well basically for the urinvolimics your restrict fluid okay for the hypervolimic your restrict fluid as well for the hypervolimic you'll give normal saline so restrict fluid for your volimic and hypervolimic give normal saline for hypervolimic treat the underlying disease for the other kinds okay that's it that's like the high level thing you need to lose like more stuff there but we don't have time for that it's not necessary for step one okay now what is the 60 40 20 year old okay 60% of if your body weight is water good how about the 40 interesting like 40% of that's like like 40% of your total body weight okay and then what does it stand for extra center like 20% of your total body weight okay so when I keep going because we're short on time potassium calcium and magnesium metabolism we've sort of talked about calcium already okay we've talked about potassium we talked about the achievements of hypercalemia right and what does hypercalemia do on an EKG?

talk these T-waves what does hypercalemia do on an EKG? Flots T-waves what other wave can show up?

U waves and we're going to do your QT interval can prolong it's very good now real quick for calcium excuse me what does calcium if you have hypercalemia what does that do to your QT interval it shortens it what does hypercalemia do to your QT interval it prolongs it remember any motorbike electrolyte anomaly that has high point in the knee prolongs your QT interval there's maintenance behind that we run that in cardio so hypermagneseemia right will also prolong your QT interval right and real quick what's like the telltale sign of magnesium toxicity your deep tendon reflexes go down very good your deep tendon reflexes go down okay um yeah so I'm gonna keep going so these are the fluid compartments of the body I'll let you go over that on your own I'll let you go over the other regulatory mechanisms on your own I explained them okay so next question 55-year-old female presents with the worst headache of her life physical exam is notable for bilateral, palpable, flank masses what's your diagnosis ADPKD so what does this person have that's causing the worst headache subarachnoid hemorrhage right because they can get aneurysms in the circle of willis okay now how is this inherited in an orosomal dominant fashion good don't get that wrong right okay um and there are two potential mutations you could get right so what are the rotations PKD1 and PKD2 what's the chromosome that has the mutation in PKD1 16 how about PKD2 4 very good okay and between PKD1 and PKD2 which one gives you enough failure early what okay PKD1 is number one so it gives you a renal failure early PKD2 you can have renal failure like in your 80s okay now if a patient has has ADPKD excuse me and they have a murmur with a mid systolic click that's microbial prolapse that's just an association with ADPKD so you just want to keep that in mind you learn about that in cardio okay and then the severe headache i

s a subarachnoid hemorrhage you get a CT scan without contrast right so that you can see the bleeding in the brain okay now why would patients with ADPKD get any stage liver disease because of cysts in the liver very good okay now what's the most common cause of death in patients with ADPKD there is something they want you to think on step one but that's not a thing you're supposed to think about yeah it's not the aneurysms it's actually heart disease that kills these people that is the most common cause of death in ADPKDY no one else but the thing is in general if your kidneys are not functioning well your heart will feel at some point you'll get basically like I think I read this study that said that vision with kidney disease have like a 40 40 increase risk of M Is okay so heart disease the most common cause of death what's the second most common cause of death actually infection okay why the one really knows and then the third most common cause of death of the rupture of the very very aneurysms okay so what you think will kill them is not really not the most common it's actually heart disease okay and you'll treat this you can give like an ACE inhibitor to sort of like protect the kidneys but you know ultimately going to renal failure now a newborn that dies within the first 12 hours of life from hypoxic respiratory failure and then they tell you that you pop it by lateral masses in the lower abdomen what does the kid have very good or does someone recessive polycystic kidney disease okay and how is this inherited or does someone recessive fashion yeah don't get those kinds of questions wrong on tests okay good and the mutation is in what gene is it PKD1 it's PKHD1 okay PKHD1 and it's in chromosome 6 I've actually seen this tested before see chromosome 6 okay and if your kidneys are not working will you be making enough urine as a fetus now so what will be from the

amount of amniotic fluid it'll be low very good that's known as oligo hydramneus okay so is there a bad thing that could happen if you have oligo hydramneus and powder sequins very good right so like pulmonary problems twisted face scale limbs extremities issues right well yeah the thing that kills them is the pulmonary problems okay because basically as a kid the way your lungs develop is whatever you basically pee and swallow your pee as a kid you pee swallow your pee as a kid that pee expands your lungs okay so you swallow the pee at some point in the past I know everyone feels gross now okay good enough that people skin okay but air PKD the prognosis is horrible most of these kids die pretty quickly okay can you guys give me like just 10 more minutes and we'll be done the thing is we won't be able to get to the end of the slide set but the other slides have keys these ones have keys but your high-yield concepts I want to discuss okay what's the most common malignant renal tumor RCC good where do RC Cs arise from and yeah actually they're answers for this one so they arise from the PCT okay now what are the two genital urinary cancers as they were smoking so RCC and TCC right transitional cell cancer of the bladder okay now how would what's the classic triad of renal cell carcinoma although it shows up in like 10% of people here material flank pain and a palpable flank mass very good okay now how can you differentiate between a left-sided renal cell carcinoma and a right-sided renal cell carcinoma based on a varicoseal right so go back to anatomy right on the left side of the body where does the left like conato vein draining to the renal vein so if you have renal cell carcinoma on the left side of the body and it involves the left conato vein B testicle ovarian vein who you are that can cause something known as a varicoseal you learn about varicoseal in ripper a c

lassic realization like a bug of worms sensation so if I be the testicles it sort of feels like a bug of worms okay and it kind of grips right maybe I'm discouraging people from going into erology okay so what if you have a right-sided right-sided RCC right the right-sided conato veins be drained directly into the IEC they do not drain into the renal vein on the right okay so a right-sided renal cell carcinoma may not necessarily cause a varicoseal does that make sense okay now how does bladder cancer spread does this spread hematogenously by direct extension okay how about renal cell carcinoma hematogenous okay now if a patient has renal cell carcinoma they have hypercocemia will it be like a lidic problem or a plastic problem we'll learn about this in ripper as well well you probably talk about it in on it's lidic because this thing can produce PT HRP, peroxide who won't release that type real quick since you're finished point what's the lung cancer that makes for a thyroid who won't release that type squamous cell very good squamous cell squamous cell good okay now how do you treat renal cell carcinoma does this respond to most forms of chemotherapy no what do you give you're giving to looking too all those lukin it's a nasty drug it's like giving like a nuclear bomb to a presence kidneys all those lukin it's an IL2 analog it spurses up your T cells and they come and destroy the cancer okay but the cancer almost always comes back terrible cancer okay now what's the genetic syndrome as such that renal cell carcinoma there's this weird genetic syndrome that does renal cell car like bilateral RCC and also like hemandial blastoma VHL very good when hipolinda when lipo when hipolinda okay now where do renal cell carcinomas make the size three terms of lymph nodes or retroperitoneol lymph nodes fantastic good now hematocryd of 57% in the patient with renal cell carcinoma

was being produced hipol very good pernioplastic phenomenon and what's the most common kind of renal cell carcinoma clear cell fantastic okay so those are your answers okay I will let you let me see is Daniel the thing here really want to talk about okay so oh this is perfect so here's what is going to happen I am going to discuss question 44 because there's no key and question 45 because there's no key as well every other thing has a key okay there are any questions on any of this stuff email me I'm going to pause these slides on the website okay so let's do 44 so coliciflank pain and hematuria in a patient with a history of Crohn's disease I know you haven't done GI it but you're a particular kind of kidney stone that is founding Crohn's disease pretty commonly oxalate why what does Crohn's disease torch in your GI tract the terminal helium the terminal helium okay the terminal helium so here's what happens your terminal helium is where you were to absorb bile salts okay your terminal helium is gone bye bye absorption of bile salts bile salts will bind up calcium ions okay basically bile salts basically make calcium sheet on oxalates okay so calcium marines the bile salts oxalates are then angry right and then they migrate through your terminal helium go to your kidneys and then cause badness okay and how do those oxalates stones look what's the shape envelope very good your envelope shaped are crystals okay now this question shows a very commonly on step one and people almost always get it wrong in a patient that has like calcium nephrolithiasis what is usually trove their blood calcium normal what is usually trove their urinary calcium hi so they have like an idiopathic hypercalciuria but they actually have normal calcium the classically tests this in the context of like arrows they'll show you like oh blood calcium they put like flat line up down and then test d

ifferent permutations okay now what's the kidney stone that does not show up on x3 ureth acid right it's radio nu-sim well you see it on a cat scan basically for a patient has a kidney stones I'm gonna send them for a cat scan it's pretty standard okay yeah assisting me also not sure but sometimes it actually does show up on image yeah okay now um well a uric acid stone be more likely to precipitate on their low pH conditions or high pH conditions in the nephrol low pH okay precipitates on their acidic conditions but it dissolves on their basic conditions okay now what kind of kidney stone be found in a patient with a high anion gap metabolic acidosis that is uptunded from some stuff it picked up at the dealership calcium oxalates what did he drink from the dealership ethylene glycol very good anti-freeze okay now patient taking 5,000 milligrams of vitamin C because he believes he will make him live to the age of 150 what kind of kidney stones can you get with that oxalate very good you can get hyproxyluria and get oxalate stones with that okay now what's the diuretic that is good for preventing or treating calcium nephrolithyases thiazides because they cause hypochalcemia and hypochalcyuria okay now how do you treat cystinuria with the diuretic I talked about this yesterday how can you solubleize those cystine stones acid azolomide very good because you'll make the urine basic and dissolve those stones okay now what's the kind of stone you'll find in the patient with urine culture revealing a bug with swarming motility on eager that's proteosmirabel is very good so that's a strobeite stone okay that's an ammonium magnesium phosphate stone good okay those you have to call your ology there's no drug you're given they need to take take it out themselves okay now severe flank pain and rising creatine in a patient being treated with chemo for lymphoma this is tumor lysis

syndrome so what kind of kidney stones may they have uric acid stones and how could you have prevented this I'll appear in all of your books or stats you can give vigorous hydration what else could you give no you don't want to give prevent it come on you don't want to be preventive it's a terrible idea that we're safe this because that would basically like make you not reabsorb some of those uric acid not a good idea for this person you want to give life for us burikis or pitlotykis right those uricis and alums remember from the biochemistry said that those converts uric acid to alantoin okay now recurrence uti is in a patient with a history of congenital lymphodema and let me give you a hint the lymphodemias around here recurrence uti is congenital lymphodema and let's assume this patient is 4 foot tall she'll never have mences and she has tanner stage 1 breasts it's a genetic problem it involves the excrimusum that's tanner syndrome very good okay and why do they get recurrence uti is what's like that kidney pathology is common in tanner syndrome or should keep me right so the infeuripus of the kidney stiff use and the occipital uti is very good infeurimacentary counter okay and I don't expect you to know this just yet but patient with tanner syndrome they can tend to get by cost periodic valves okay your cardio will be a sweet block for you that's we learned so many awesome things there okay so by cost periodic valves and they'll also get a quartetion of the yoder okay quartetion of the yoder okay now 25-week fetal ultrasound revealing dilation of the bladder and bilateral hydrolyphrosis what is that if there is an anterior there is a posterior withdrawal valve very good okay now will this cost pulling hydramials for legal hydramials posterior withdrawal valves or legal hydramials because you're not draining urine right so you get oligo hydramials so that's can ca

use like a potter sequence kind of disease okay and is there a particular brain condition that you learned about last semester that can cause polyhydramials that's for the A the swallowing center by by and encephaly very good so you don't have a swelling center so you don't swamp like swallowing your urine basically so you have polyhydramials very good okay and what's the most common location of an obstructive kidney stone is it the UPJ or the UVJ it's the UVJ okay is the uiterrophysical junction so it's the junction between the uriders and the bladder and here's one basically the size of the pipe gets smaller as the approach to blood okay so because the pipe is just smaller by the bladder that's your stone most likely launched does that make sense okay good then most common location of failed recolonization leading to sorry about that leading to hydramnal process and a fetus the UPJ the uiterrophobic junction so it's the junction between the renal pelvis and the uriders okay and where does the collecting system come from what's the embryologic structure the uriteric body and where the other parts of the kidney come from the better an effort blast them okay so any questions over anything we have discussed today how do you feel about renal better good so we're gonna end here and I wish all the best in the future

Minimal Change Disease (MCD) and primary membranous nephropathy.

Type 4 RTA.

Methanol, Uremia, Diabetic Ketoacidosis (DKA), and Ethylene Glycol (EG).

The ureterovesical junction (UVJ).

Goodpasture Syndrome (Anti-GBM disease).

Membranous Nephropathy.

Hypertension, hypokalemia, and metabolic alkalosis.

A negative urine anion gap (UAG < 0).

Post-Streptococcal Glomerulonephritis (PSGN) or Lupus Nephritis.

Subepithelial "spike in dome" deposits.

ACE inhibitors and AR Bs (Angiotensin-Converting Enzyme Inhibitors/Angiotensin Receptor Blockers).

Hyperkalemia; associated with low aldosterone.

Syndrome of Inappropriate Antidiuretic Hormone (SIADH).

Diabetes Mellitus and Hypertension.

A negative urine anion gap (UAG < 0).

Post-Streptococcal Glomerulonephritis (PSGN) or Lupus Nephritis.

Subepithelial "spike in dome" deposits.

ACE inhibitors and AR Bs (Angiotensin-Converting Enzyme Inhibitors/Angiotensin Receptor Blockers).

Hyperkalemia; associated with low aldosterone.

Syndrome of Inappropriate Antidiuretic Hormone (SIADH).

Diabetes Mellitus and Hypertension.