@AnKing-Maintainers recommend cloze change
nid:1581191946613 also specifies “Liver failure → ↑ NO → splanchnic vasodilation → ↓ SVR” in the context of hepatorenal syndrome (but still the emphasis is on insufficient NO metabolism)
Sketchy mostly takes their info from UpTpDate, endothelin is from UTD.
“ In support of these processes, preclinical and clinical studies suggest that increased NO and endothelin-1 (ET-1) levels may play a role in pulmonary vasodilatation [28,35-45]”
@AnKing-Maintainers another suggestion for this change was made today. I say reject both. Just because it’s not mentioned on AMBOSS doesn’t mean it should be removed.
I just scanned the UTD section, and from my understanding
- ED-1 causes vasodilation by increasing NO levels
- I am not quite sure if ED-1 is increased because of “decreased metabolism” as the card suggests (UTD: In an experimental rat model of HPS (common bile duct ligation), proliferating cholangiocytes produce and secrete ET-1 that binds to an upregulated endothelin beta receptor (ETB) in the pulmonary vasculature, resulting in intrapulmonary vascular dilatations (IPVDs) by increasing the production of NO"
Overall, support the change and remove ED-1 only from the text “keep it in sketchy section” since it’s a LY thing to know
I like the idea of removing from text or at minimum the cloze
If removing from text completely what about moving it to extra field instead of just sketchy section?
Agree, or if people want to keep it, I think it would be good to include an explanation of how it uses the ETB receptors for vasodilation rather than the ETA for vasoconstriction (because otherwise people will check AMBOSS/FA and assume this card is wrong because it only claims endothelin-1 as a vasoconstrictor)