Time wasn't a big issue for me in general, had around 40 min left to go through the 20 or so questions I had marked but I could see how you could get behind because almost all of the stems are long. Worth going through the 10 pages of peoples posts here as well because I did have 2-3 similar/same questions as others. Don't even begin to waste your time on that stuff. Lange was better than pretest for simulating questions but would recommend doing both if possible (I think pretest got me 1 or 2 I would not have gotten and almost all their stems are short so it doesn't take long to do all 500).īiggest thing I can stress-absolutely none of that stupid stuff like erik erickson crap so skip those chapters in whatever sources you do end up using. Uworld was great for simulating the real shelf as well but overall too easy and not enough questions. Those questions seemed very similar to the real thing. Overall, I thought nmbe 1 was the best thing to prepare and would have done nbme 2 given more time. I also did nbme 1 the weekend before which helped boost my confidence (93). After that I just finished lange, did all of uworld psych qs the weekend before my shelf and then the week of I went through my notes and did random pretest questions. Starting my 2nd, I went through all of FA psych and took notes on anything I didn't feel comfortable with which seemed to help a lot. The 1st two weeks I mainly just did random questions from pre-test and lange (probably 200 total). My rotation was 4 weeks but the hours were nice so I felt like I had plenty of time to study compared to other shelves. I used lange q&a, uworld, pretest and FA psych. One caveat to this may be patients who have developed an interstitial nephritis (secondary to calcium deposition in the medulla ) from prolonged hypercalcaemia.Took this shelf last Friday and got my results back today. Thankfully, the polyuria and concentrating defects associated with hypercalcaemia tend to regress with correction of the calcium levels. Activation of these, in the setting of increased distal calcium delivery, down-regulates AQP2 expression, again resulting in an inability to concentrate the urine.įinally, there may be hypercalcaemia-induced PGE2 production in the thick ascending limb, which can further inhibit sodium chloride reabsorption. This in turn inhibits potassium recycling and thereby shuts off the NKCC2 cotransporter, leading to decreased reabsorption of sodium, potassium and chloride in this segment.įollowing on from this, the medullary concentration gradient is diminished, leading to an inablility to concentrate urine and subsequent polyuria.ĬaSR are also found on the luminal surface of cells in the inner medullary collecting duct. Binding of calcium, with subsequent receptor activation, appears to induce a downstream message to close off the luminal K channel. I wanted to share what I have learned in relation to the mechanisms of this phenomenon.Ĭalcium-sensing receptors (CaSR) are found on the basolateral membrane of the cells of the thick ascending limb of the loop of Henle. So Leo’s post got me thinking about the pathophysiology of hypercalcaemia-induced polyuria.
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