-
CycleTrack and SDN are teaming up to make medical school admissions more transparent and accessible! Read the announcement to learn how we’re supporting the future of CycleTrack’s free application-tracking tools .
Step II Siadh
Started by zenna
Get help with your application
Use all the free resources available to you from SDN: articles, guides, expert advising, forums discussions, and school research.
Escape phenomenon allows renal tubules to 'escape' from the sodium retention effect of aldosterone. As a result, natriuresis (as well diuresis) occurs. This phenomenon is due to: (1) intrinsic adaptation ability of renal tubules due to change in renal hemodynamics and (2) increased ANP levels, which stimulates natri- and diuresis as a result of systemic hemodynamics.
Edema is usually not seen due to this effect in primary aldosteronism.
As for the secondary hyperaldosteronism, you have to think about the etiology. What causes renin to increase in secondary aldosteronism? It may be due to a renin-producing tumor, a decrease in renal blood flow (like renal artery stenosis) or decrease in renal perfusion pressure. CHF, cirrhosis and nephrotic syndrome causes a decrease in effective arterial pressure (through different mechanisms), which is manifested as decreased renal perfusion pressure in kidneys. Therefore RAAS is activated. These diseases also cause edema as well (e.g. NS: loss of albumin in urine). Therefore, it may be more accurate to say that secondary aldosteronism is co-present with edema, rather than being the causative mechanism of edema.
Goljan step2ck tapes explain this quite well. I would have to listen to them again to be able to explain it to you.
