9/ We have established that heparin can cause hyperkalemia via decreased aldosterone production.
But we're still left with the question, how does heparin mediate this effect?
10/ Aldosterone production from the adrenal gland's zona glomerulosa is stimulated primarily by angiotensin II (in addition to ACTH), as part of the Renin-Angiotensin-Aldosterone system.
18/ Heparin seems to have potential diuretic effects through its ability to inhibit aldosterone production.
But the arrival of more effective and safe diuretics in the 1960s (eg furosemide) likely explains why additional studies of this potential drug effect never occurred.
19/SUMMARY
🍌 Heparin can cause hyperkalemia by ⬇️ aldosterone production
🍌 This occurs b/c heparin ⬇️ adrenal angiotensin II receptor expression, and possibly inhibition of intracellular signaling
🍌 Heparin may also have indirect diuretic effects as a result of ⬇️ aldosterone
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2️⃣ I ❤️ the way he zooms in on individual stories and then zooms out. One chapter he’s in a ramshackle hut in rural Haiti, the next he’s building Haiti’s first neurology residency or meditating on the sociocultural basis for global health inequities
3️⃣ Through the stories he tells he actually manages to teach a decent bit of neurology (whether intentional or not)
1/🧵
Why does Wenckebach AV nodal block (aka Mobitz type 1) present with progressive prolongation of the PR interval and eventually a non-conducted P wave?
3/ The pattern Wenckebach observed corresponds exactly w/ the progressive PR prolongation, followed by a non-conducted P wave, that characterizes what we call “Wenckebach” heart block.
💥 Amazingly, he observed this BEFORE the AV node was discovered.
3/ This question had major implications for the nascent field of anesthesiology.
Some practitioners began to use curare alone during surgery, without sedation, believing that curare adequately sedated patients in addition to paralyzing them.