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| Step I Discuss strategies and issues for the USMLE and COMLEX Step 1. | RSS: |
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#1 |
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Senior Member
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A. Neither cortex nor medulla will be at risk due to collateral flows B. Cortex C. Medulla D. Both cortex and medulla will be equally at risk E. Initially the cortex, but subsequently the medulla will be most at risk Now I understand the prox Tub located in the cortex and is the most metabolically active, but wouldn't the Slow Flow characteristics of the Medulla mean that you're not delivering very much oxygen therefore making it more susceptible to Ischemia? That's what my understanding was from Dr. Dunn's physio.... but Gunnertraining has the answer as Cortex |
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#2 | |
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#3 | |
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PGEEE2 mediates FEEEVER
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#4 |
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PGEEE2 mediates FEEEVER
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In addition, think back to zones 1-3 of the hepatic acinus. Remember zone 3 having the least oxygenation? You injure the liver and it's that zone 3 area around the central vein that gets knocked off first. Zone 1 is all nice and happy being around the portal triad and getting all the good stuff. It can deal with a little less blood flow more easily than zone 3, who is already starving as it is.
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#5 |
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2K Member
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Hmmm...I'd like to know the answer to this as well. I just figured that the medulla of the kidney did not need as much blood supply/oxygen, thus it wouldn't be affected as much. A 50% drop in the medulla would mean that relative to the amount of blood it normally receives it would be like it only receiving 5% of normal total renal perfusion. On the other hand a 50% drop in the cortex would be the equivalent of going from 90% of normal renal blood flow to 45%, which is a much greater relative drop. Therefore, ischemia in the kidney is going to affect that portion the most. Perhaps this would make more sense with some made up values (because I don't know actual renal blood flow values and I sure as hell am not going to look them up right now). If the kidney normally receives 100 ml/min with 90 mL/min going to the cortex and 10 ml/min going to the cortex a drop of 50% would mean 45 ml/min to the cortex and 5 ml/min to the medulla. The drop off is much greater in the cortex is much greater, thus it would be more affected. That was just my interpretation of the GT explanation, but I'm not sure if that is completely correct. If the medulla of the kidney is in fact operating on the brink of hypoxia normally, then I imagine any drop would be bad (although from an evolutionary perspective that doesn't seem like a very smart way to evolve).
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#6 | |
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PGEEE2 mediates FEEEVER
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I see what you're saying about relative drops (using both % and mL/min). In addition, that PCT area is reabsorbing 67% of all things filtered, so that single area in the cortex is what is using the most O2. Still, that medulla is almost ischemic as is, so probably doesn't take much. |
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#7 | |
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Here is how I understand things according to the papers below. Albeit, there may be a different mechanism. The cortex is over-perfused. So, in low blood flow conditions, the mitochondria in the TAL are unable to obtain adequate nutrition to create ATP and power the active pumps for sodium. As a result, there is increased salt delivery to the macula densa. The macula densa fires its signal and the afferent arteriole is clamped. This further decreases blood flow. Now, we already know that the medulla operates on less blood flow than the cortex. The blood flow distribution keeps the medulla in near anoxic conditions, which is great because the medulla can handle the conditions. The end result of all this is a medulla that can deal with a little blood loss because it's been doing so for as long as it can remember, but the cortex is gasping because it's lived an privileged life and is now in poverty. http://qjmed.oxfordjournals.org/cont...4/807.full.pdf http://circres.ahajournals.org/conte...1/167.full.pdf |
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2K Member
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#9 | |
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I've found quite a few discrepancies between kaplan and gunner now... and I can't remember which version I have stored into my brain the kaplan or GT version haha, guess I should stick with kaplan and FA versus going with what gunner says. |
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#10 | |
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Senior Member
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That said, I'm inclined to believe GT on this one. Why else would you get diffuse cortical necrosis (which selectively affects the cortex and spares the medulla) in catastrophic hypotensive situations like abruptio placentae? Also someone above linked some journal articles (can't look at them on my iPad) in support of cortex being hit first. I've found mistakes in Kaplan, FA, and GT - you really can't trust anyone completely
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#11 |
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1K Member
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I can see the logic to both sides, but I think the cortex would be worse off (esp. PCT and thick ascending LOH) given all of the active transporters in those regions.
I also recall something from Goljan audio saying those are the two most susceptible parts of the kidney to ischemia, given their high energy demands.. I haven't looked into the linked articles.. i'm too damn lazy
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#12 |
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Senior Member
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I think kaplan is wrong on this, but it's weird because he makes a point of explaining it.
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#13 | |
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Senior Member
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Guess everyone has their own way of interpreting things including the people/sources we learn from. |
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#14 |
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Junior Member
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Goljan metions in his Audio (Fluid and Hemodynamics chapter) that in a drop in blood pressure the Medulla is affected first
He also gives a clinical correlate of how a patient with sickle cell trait can get kidney disease because the oxygen tension in the medulla is low enough to induce sickling in the peritubular capillaries causing Microinfarctions , microscopic hematuria , and can lead to ATN but the above explanations for cortex as the answer also seem reasonable so what answer chocie do we go for in the main exam? |
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#15 | |
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Senior Member
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If it shows up on my exam, I'm going with cortex I think
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#16 | |
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PGEEE2 mediates FEEEVER
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