to snoo-finity ... and beyond!
Welcome to shaydawn88's page.
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Why can it not be arterial hypertension?
I think Arterial HTN is referring to Pulmonary Artery HTN which would be present in LT HF in the long run with RT HF and edema. Pulm HTN would cause a backflow, and doesn't really answer the question "explain the patients Dyspnea". At least, that's how I saw it. Hope this helped.
the question has 2 murmurs, so does she have aortic stenosis too?
i guess it is not relevant since it asked for what is causing her SOB
I guess pulmonary HTN would happen in response to increased pressure after the edema happens, and would cause backflow (to the RV) over pulmonary edema.
I would also like to know if anyone can answer this question - I saw it as a Sattar "one day, one week, one month" kind of question. Its probably very simple but I still don't get it
I posted a new comment explaining: basement membrane integrity is the strongest determinant of full fx recovery following pulmonary insult :)
You have to think about it this way: the basement membrane is the “scaffolding” on which [restorative] healing occurs. So, yes, stem cells (type II pneumocytes) would be involved in that healing process but they couldn’t restore the *normal* architecture (“no abnormalities”) without the ‘skeleton’ of the basement membrane telling them where to go, in what direction to grow, which way is “up”, etc. If the basement membrane is destroyed, you can still get healing, but it won’t be organized healing -- it’ll be *disorganized* healing, which does not appear as normal tissue. (Disorganized healing is better than no healing, but without a BM, the regenerating cells don’t have any “direction” and therefore can’t restore the normal architecture.)
Yes, this a great summary to the post by @bubbles and the article he posted! Another way to think of the question is not, what causes repair, but what causes irreversible injury/fibrosis. That article explained an experiment that showed TGF-beta was necessary to initiate fibrosis, but if BM was intact and TGF-beta was removed, the fibrosis didn't persist, i.e. intact BM is protective against TGF-beta. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645241/