Cram The Pance - S1E1 Renal cram session!

Episode Date: December 24, 2020

All you need to know for your PANCE, EOR and exams for renal in 20 minutes!►Paypal Donation Link: https://bit.ly/3dxmTql--- Support this podcast: https://anchor.fm/scott--shapiro/supportBecome a supporter of this podcast: https://www.spreaker.com/podcast/cram-the-pance--5520744/support.

Okay, so the first system that we're going to be going to be the renal system. I'm going to try to make this short and sweet. That's how all my podcasts are going to be. I'm only going to be the high-yield stuff and I'm going to give you little tips and tricks to remember this stuff along the way. So let's get started. Nephritic system. I'm sorry, nephritic syndrome. So that's going to be things you can see with your eye.

Nephritic has an eye versus nephrodic, which has an O. So when you see nephritic, think of eye, things I can see with my eye. Hematuria. You can see that with your eye. hypertension, you can see when you're pumping up the blood pressure cup that the patient has high blood pressure. You can see those things with your eye. Now, when we go into nephrodics syndrome, nephrodic has an O in it. So when do you think of two things. O looks like a big fat belly and O, also words that have O in them. So protein urea Oval fat bodies is something you'll see in the urinalysis, also known as Maltese

Cross has an O in it, frothy urine has an O, hypoalbumiaemia has an O. And edema, in England or the British way to say it is oedema. So that has an O in it as well. And that's all things that you'll see in the Phrodic syndrome. And then when you think of nephrodic, think of O as a big fat belly. And that's going to lead you to think about the edema, the Oedema, the big fat belly, the oval fat bodies. And it's also going to make you think of hyperlipidemia, which also is seen as nephrodite. So O big fat belly makes you think of those things. And then when we're talking about different diseases in nephrodite syndrome, the first thing that I want to go over as minimal change disease. So when I think of minimal change disease, I see the first

word in there, mini in minimal. Mini makes me think of many adults, children, and that makes you think that minimal change disease is most common in children. So many, many adults, children. And then I also want you to think about the patho behind minimal change disease. And that's a loss of negative charge of the basement membrane, which promotes the protein urea. So you have a loss of a negative charge. So when I think of minimal change disease, I change the name. And instead of thinking of minimal change disease, I think of minimal charge disease, which makes me think of the loss of negative charge in the basement membrane. All right.

So the next nephronic syndrome that you need to know is focal segmental glomerulosclerosis or FSG. So there's three things that you need to know for this as far as causes and clinical manifestations. And that's going to be HIV, heroin, and hypertension. This is what always comes up on exams for FSG. So the two big secondary causes of FSG are viral infections, in particular HIV and drugs, in particular heroin. And then also severe hypertension may be present in up to 20% of patients with this condition. So these three are really important because, like I said, they always come up on exam questions.

So again, FSG, you need to know HIV, heroin, and hypertension. You need to know that for focal segmental glomerulisclorosis, aka FSG. The way that you remember that is by remembering the letters of focal segmental glomerulaclaclacloresis FSG stand for fornication, shooting up, and giant blood pressure. So fornication helps you remember HIV, as obviously fornication can lead to HIV. The S stands for shooting up. That's going to help you remember heroin as another major secondary cause. And then finally, the G stands for giant blood pressure, which helps you remember the severe

hypertension present in up to 20% of patients with this condition. Then moving on to some glomerial nephritis or nephritic syndrome causes. So IGA nephropathy. It's the most common cause of acuclomeronean nephritis. I break that down into letters and it gives me two ways to remember it. IGA infects guys always because it's most often in young males. So IGA nephropathy. IGA infects guys always.

Another way, IGA infects gastric and alveoli. So that's because it occurs after an upper respiratory infection or GI infection. So I think of IGA infects gastric and alveoli. makes me remember upper respiratory infection and GI infection. All right. Next one is post-streptoccal or post-infectious glomerion nephritis. So post-streptoccal or post-infectious is most often caused by group A strep. Those letters are G-A-S, gas.

When I think of gas, I think of something that gives you gas, which is drinking coke. And that makes me remember that group A strep and post-streptoccal glomeranopritus, you have Coca-Cola colored urine. So you drink Coke, it gives you gas. You have Coca-Cola colored urine, not flavored. And then it also makes me think of the letters GAS again. And that makes me think of generally adolescent son, which makes for me remember that this is normally seen in a 2 to 14-year-old boy. Good Pastor disease, that's going to be anti-GBM antibodies that are seen in this.

And then Good Pastor disease, I break down the G and the P and Good Paster. And that makes me think of G&P standing for glomerary lenephritis and P standing for pulmonary, which you see hemoptosis in this disease. So good pasture disease, G&P, think about glomerary thanephytes and pulmonary or hemopstice, which are seen in this disease. And then also remember that there's anti-GBM antibodies against type 4 collagen of the glomerary low basement membrane seen in this. So moving on to pre-renel acute kidney injury.

What I want you to remember is pre-renal is going to be mainly caused from hypovalemia. The patient is volume depleted, decreased renal profusion. The kidneys completely fine. The patient is just volume depleted. So think of GI losses, you know, whether or another thing is, too, they may have overdosed on nseds or ACE inhibitors, which is going to cause either an aferent or an efferent dilation or vasoconstriction. The way I remember which causes which ncest.

versus ACE inhibitors, Ns, I take the S and the A and Ns, and I think of shrinking aferent, and that makes me remember that Ns are aferent arterial vasoconstriction, so Ns SA, shrinking aferent, and then ACE inhibitors has an E in it, which Ns doesn't. So I take that E, and that makes me remember, eferent expansion, which is ACE inhibitors calls eferent arterial dilation. So eferrin expansion, I remember from that E. Next thing to remember with pre-renel, the big thing here is that the BUN-Creatin ratio is going to be over 20 to 1. That's really big. Remember that. That'll definitely come up in your exam. So BUN-Createning over 20 to 1. The urine's going to be concentrated. The treatment's very straightforward. It's basically volume

repletion. This patient is hypovalemic, so you want to give them IV fluids, and they should rapidly recover. Post-renel azotemia is very straightforward. There's not much to know with it. Post-renal is most likely caused from an obstruction, whether it's BPH, it's a tumor, it's a kidney stone. There's something obstructing past the kidneys that's not allowing the urine to flow through. So all you're going to do to diagnose it, you're going to do an ultrasound, find that obstruction. And treatment is basically just removing that obstruction, whether it's a urinary stent, removing a stone, catheter placement, you're just removing that obstruction. So that's really easy and straightforward.

Pre-renal and post-renel, both easy and straightforward. Intrrenal or intrinsic renal failure gets a little bit more involved. There's a couple of different causes. The first one is acute interstitial nephritis. What I want you to remember with acute interstitial nephritis is that this is almost always caused from drugs. 70% of the time it's caused from a drug. And one of the most common drugs is inseds. Other causes, other medications, penicillin, sofa, but insides is the main one.

So what I want you to remember with acute interstitial nephritis, AIN, acute interstitial nephritis, AIN stands for always involving inseds. That'll help you remember that inseds are one of the most common causes. Patients can present with fever, eocinophilia, rash. Diagnosis, one of the main things you want to remember is that you're going to see white blood cell casts in the urinalysis. That's big, that's huge. Remember it, the way you remember it. Again, AIN, remember now always involving neutrophils.

that leaves you, you know, brings your mind back to remembering. This is white blood cell, white blood cell casts, always involving neutrophils and always involving insides when you think about acute interstitial nephritis. You won't forget that. And treatment just remove the offending agent. Very straightforward. Next one with intrinsic renal failure is going to be acute tubular necrosis. It's the most common type of acute intrinsic kidney injury, about 50% of the causes.

It can be caused from a couple different things, ischemia. So it can actually be caused from a prenaturally. pre-renal azotemia, so from the lack of blood flow, so ischemia. And then it can also be caused from nephrotoxic agents. Contrast dye and amyglicicides are your biggest ones that can cause this. So remember that. That's going to be big. There's also endogenous causes like tumor lysis syndrome, myoglobinuria.

I wouldn't spend too much time remembering those. Q2 glaryngosis, remember that it can be caused from pre-renal. And again, it can be caused from iodinated contrast dye or aminooglycosides. are the ones you should remember. One of the big things here when you're diagnosing it, when you're looking at the urinalysis, you're going to see granular or muddy brown cast. This is from the epithelial lining, breaking off and breaking down into the urine. So remember, this is big on acute tubular necrosis, muddy brown cast or granular casts in the urinalysis. How do you remember that? Acute tubular necrosis, I think tubular like a tube. And then I think of

mud. I don't know if you've ever seen these people doing mudding, like they're on like an inner tube and they're doing like going through the mud those two always come back to I I always remember that so I just think of a cut tubular necrosis and I think of muddy brown cast treatment remove offending agent and IV fluids is going to be first line so going moving on one another thing that I want you to remember too with the cut tubular necrosis the bune to creatin ratio is going to be in the range of 10 to 15 to 1 compared to pre renal which is always going to be over 20 to 1 so that's something big a couple things to review for urinalysis findings. This is a review what we talked about earlier, but certain things

you'll see in the urinal analysis is going to point to certain diagnoses. So remember if you see red blood cell casts, you should be thinking of acute clomaryl nephritis or vasculitis. If you see white blood cell casts, again, remember AIN, acute interstitial nephritis, always involving neutrophils. So think about acute interstitial nephritis when you see white blood cell cast, fatty cast oval fat bodies. Remember nephrodic syndrome like we talked about. And then waxy casts, you're going to see an end-stage renal disease. Moving on here to horseshoe kidney. That's going to be the fusion of one pole of each kidney, usually at the lower pole. Not a lot of high-yield stuff here can be associated with other urologic abnormalities. Turner syndrome is actually

something that you can see in this. And the way I remember that is the horseshoe kidney at the bottom makes kind of like a U-turn connecting the two. And that makes me think of Turner syndrome. So a little U-turn of the kidneys when they connect Turner syndrome. There's a risk of pylonephritis. horseshoe kidney that's due to the stagnant urine. And most patients are asymptomatic. The diagnosis can be a CT urography. That's your best initial test. And then treatment. Most patients don't require any treatment unless they have a UTI or a stone and then you just treat that as that comes along. Polysistic kidney disease is the next thing. Remember, this is an autosomal dominant disorder. You're going to have cyst in the kidneys, obviously. But if it's not in it, if you don't have a

cyst in the kidney, one of the most common other places you may see as, cyst is going to be the liver. That's the most common other organ. Patients are going to present with abdominal and flank pain. Some extra renal manifestations that's really important. You should remember this. This is a polycystic kidney disease. A patient can have cerebral berry aneurysms, mitral valve prolapse. These are two things that I feel like is really high yield that you should remember. The way I remember this, you're just going to have to paint a picture in your head here, but I remember a parrot named Polly, which makes me think of polycystic kidney disease. I think of a parrot sitting on top of your head named Polly that keeps on like hitting your head with its beak

and that that hitting of your head causes a very aneurysm. And then I think that parrots named Polly are the most violent pet, MVP because they're hitting your head. They're the most violent pet. That makes me think of MVP, which makes me think of much of valve prolapse. Hopefully that helps you. It always helped me. It's a weird way to remember it, but that's the best type of ways to remember.

Patient may present with hypertension. They may have a palpable flank mass. diagnosis straightforward renal ultrasound your treatment is going to be increasing fluid intake aces or arbs nothing really specific or high yield there chronic kidney disease there's not much for you to know here i wouldn't i wouldn't waste your time remembering the stages the only stage i would remember is less than 15 gfr is end stage renal disease and this is where you need to um start using dialysis for treatment so less than 15 stage five dialysis for chronic kidney disease Another thing to know is to remember, the most common cause of chronic kidney disease is going to be diabetes.

That's big. As far as diagnosis, your best predictor for chronic kidney disease is going to be proteinuria. And you can test this in a patient either doing a 24-hour urine collection or a spot urine albumin. You can also see waxy cast in the urinalysis. And as far as treatment, it's just basically making sure that the patient is controlling their blood pressure, controlling the hypertension. ACEs and ARBs are a big medication used here. If they're diabetic, you want to keep their A1C less than seven. And then, of course, at stage 5, GFR less than 15, you're going to have them do dialysis.

Moving on to Wilms tumor, also known as a nephroblastoma. It's most commonly seen in children in the first five years of life. The way I remember the presenting symptoms or the patient's presentation for Wilms is I take Wilms tumor, W-I-L-M-S, W-S-W stands for Wilms tumor, I stands for, iris malformation. These patients have an absence of the iris sometimes, also known as anoridia. So W-I, L is going to stand in for locked in position. That's because the tumor is actually locked into one side of the abdomen. It doesn't cross the midline. And this helps differentiate it from a neuroblastoma, which you can see on the adrenals, which can cross the midline. M stands for mental retardation, which is seen in patients

with this. And then finally, S stands for sexual malformations like hypospatias, Cryptokidism can be seen. So W. I.L.MS, Wilms, tumor, I, iris malformation, L, locked in position, M, mental retardation, and S sexual malformation. Patient may have a palpable abdominal mass. It's one of the most common findings, eematuria and constipation. Diagnosis is, again, like a lot of the other things in renal, it's going to be an ultrasound, and treatment is going to be a total nephrectomy. With chemo has about an 80 to 90% cure rate, so most people do pretty well with this. Rinal cell carcinoma, only a few things I think you should know for this. It's the most common tumor in the kidney, 95%, and the most common type is going to be a clear cell.

The patient's going to have a triad of hematuria, flanker abdominal pain, and a palpable abdominal mass. Those are the only things I think you should really know. Two more things, actually, that are important. The patient may have a left-sided varicoceal with renal cell carcinoma. That's because the tumor can actually block the left testicular vein. And then finally, they may actually have hypercalcemia, which is important. And that's because the tumor secretion in a renal cell carcinoma can actually secrete parathyroid hormone-related protein, which is going to mimic primary hyperparathyroid and increase your calcium.

Diagnosis for this is going to be a CAT scan. Treatment's going to be a radical nephrectomy. A couple other things I think you should know. The acid-based disorders, I'm not going to go over in detail. the one thing I think you should remember this to memorize it is remember Rome and that stands for that's ROME and that stands for respiratory opposite and metabolic exact and that basically means if your pH is going up and your PCO2 is going up, respiratory opposite that means it's not going to be a respiratory condition but metabolic exact meaning metabolic the the bicarb and the pH go in the same direction. respiratory would be if the pH and the PCO2 go in opposite directions. That's an easy way to remember

that respiratory opposite or metabolic exact. Again, that's something you should probably read about. I don't want to go into it in a podcast. I don't think that's a good way to remember it. So I'll move on to a couple more things that I think are high yield. I'm not going to go into hypomagnesemia or hypermagnesemia. I don't think those are high yield, but I do think hypercalemia and hypokalemia are important. So I'll go over those. So hypercalemia is going to get potassium over five. The way you can remember the causes is going to be with the mnemonic cares. C stands for cellular lysis. That's things that damage the cell. That can be anything from burns, rhabdo, tumor lysis syndrome, anything that's going to pop open that cell and spill

out all the potassium into the extracellular space. A stands for decreased aldosterone. So hypoidosteroneism, adrenal insufficiency. R stands for renal failure, which is one of the biggest causes, and that's the one you should really know. E stands for excessive potassium intake. You're only going to see this in patients who are on dialysis or an end-stage renal disease. The normal person could eat five, ten bananas, and their kidneys are going to get rid of it just fine. These are only going to be patients who are on dialysis that may have excessive potassium intake. And then finally, D is another important one that stands for drugs, ACEs and ARBs, potassium sparing diuretics like spiroin, lactone.

That's another important one. So if you're going to remember, only two of these, I would say to remember, for renal failure and D for drugs, ACEs, potassium sparing diuretics like sparenylactone. Patients are going to have muscle weakness, flacid paralysis. They may have arrhythmias and that's the most important thing because that's the most dangerous. You may have abdominal distension and diarrhea. Your EKG is going to have tall peak T waves. You'll never forget that.

I don't think I ever will. That's one of the, if I forget everything else about EKG, I'll never forget that hypercolemia has tall peak T waves. Remember those tall peak T waves can eventually lead to QR. interval shortening and eventually a widened QRS. As far as treatment, the way you're going to remember your treatment is going to be C, big K drop. So that's C, the letter C, B, I, G, K, and D. So C, big, K drop, thinking of your dropping your potassium. That's how you remember the pneumonic. So C stands for calcium gluconate. That's going to stabilize your cardiac potential or increase your threshold of the cardiac potential. That's going to prevent some of these arrhythmia. So C, calcium,

Glucinate B is going to stand for beta 2 agonists like albuterol, which is also going to push the potassium into the cells and bicarb as well. Bicarb isn't used very much anymore. Insulin is the next big one. That leads us into the next one for G, which is glucose or dextrose that you're going to be using with the insulin. K stands for KXolate, often, also not often used because it takes so long to actually work. And D stands for dialysis, which would be like refractory patients. So C, big K drop, C, C, calcium, gluconate, B,

bicarb or beta 2 agonis, I, insulin, G, glucose, or dextrose, K, k-exolate, and D-dialysis for refractory. Finally, last thing I want to go over that I think is important, hypokalemia. There's a few different causes of hypokalemia. The only ones I think you should remember is urinary or GI loss. So either diarrhea, vomiting, diuretics, things that push potassium into the cells, basically things that you treated hyperculemia with. So that's going to be like insulin, beta, two agonists can obviously cause hypokulose. And then finally, the last important one, I think, is hypomagnosemia because low magnesium opens magnesium-dependent potassium channels and it basically spills potassium into the urine,

which would cause hypokulemia. And that's an important one to remember because if you treat a patient with hypokalemia and you're giving them potassium and their potassium's not coming up, they may also have a concurrent hypomagnesemia and they're not going to get any better until you treat the low magnesium. So that's important to remember for treatment in real life and on the boards. Patient is going to have severe muscle weakness. This is going to be more pronounced than hyperculemia. They're going to have decreased deep tender reflexes, palpitations, arrhythmias.

On the EKG, the big thing here, remember U waves. U waves. That's going to be after your T wave. You're going to see another small hump. And if you see that, you should think that this patient may have potassium depletion. Treatment, oral potassium is going to be your mainstay. You're only going to give IV potassium in severe. cases. So guys, that was a quick review of renal. I hope this is helpful for you. I know it's

nice and fast, but I know I wanted something like this in PA school just to give me a quick 15, 20 minutes to review everything. And that's how these podcasts are going to be. It's just going to be quick, straight to the point, some good ways to remember this stuff. You know, if you want to longer drawn out more in detail, I also have a YouTube channel, which is under the same name, cram the pants. You want to check that out. And then I also have an Instagram page as well, cram the pants where I have some mnemonics and pictures and things to help you remember. I hope that was helpful. Let me know in the comments if you guys felt like this was something beneficial to you and I'm going to be releasing more very soon.