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 +4  (nbme22#42)

I think the increase in plasma renin activity with NSAIDs has to do with inhibition of efferent artery dilation by prostaglandins (PGE2), since that's what NSAIDs do by inhibiting COX. This decreased renal blood flow leads to RAAS activation to conserve water and ultimately renin increases.

htballer55  Afferent artery dilation*
link981  There is decreased afferent renal artery dilation (less blood flow) leads to increased renin release from the juxtaglomerular cells (located near the afferent artery) to try to increase blood flow. I got it wrong but after reviewing saw my idiotic mistake.




Subcomments ...

submitted by sympathetikey(313),

Source: https://en.wikipedia.org/wiki/Myelin

"myelin speeds the transmission of electrical impulses called action potentials along myelinated axons by insulating the axon and reducing axonal membrane capacitance"

littletreetrunk  I think this makes total sense, but how does it not ALSO stop fast axonal transport? +2  
laminin  axonal transport is transport of organelles bidirectionally along the axon in the cytoplasm since myelin is on the outside of the axon demyelination doesn't affect this process. source: https://en.wikipedia.org/wiki/Axonal_transport "Axonal transport, also called axoplasmic transport or axoplasmic flow, is a cellular process responsible for movement of mitochondria, lipids, synaptic vesicles, proteins, and other cell parts to and from a neuron's cell body, through the cytoplasm of its axon." +1  
yotsubato  axonal transport is mediated by kinesin and dynein. Microtubule toxins like vincristine block these +2  


submitted by sympathetikey(313),

Mad at myself for changing my answer.

Faulty logic made me wonder if hitting your head would caused increased ICP so, like a cushing ulcer, you would get increased Vagus nerve activity and maybe bradycardia + hypotension. But I guess the RAAS system would have counteracted that and caused vasoconstriction over 24 hours, so Hypovolemic shock is definitely the best choice.

Always should go with the obvious answer :)

seagull  I had the idea that this was a neurogenic shock and increasing intracranial pressure could affect the vagus too. I think the question really wants us to go that direction. +1  
uslme123  The Cushing reflex leads to bradycardia! +1  
purdude  Wait I'm confused. I thought hypovolemic shock leads to an increased SVR? +1  
littletreetrunk  apparently, there's a thing called sympathetic escape that can happen after a while (i.e. he's been out for 24 hours): Accumulation of tissue metabolic vasodilator substances impairs sympathetic-mediated vasoconstriction, which leads to loss of vascular tone, progressive hypotension and organ hypoperfusion. +  
littletreetrunk  also also if he hit his head he could have loss of sympathetic outflow from a hypoxic medulla which could lead to vasodilation, which further reduces arterial pressure, but this was a hard one for me lol. I also put increased ICP wah. +  
catch-22  Any lack of sympathetic outflow/increased vagal outflow should reduce HR, not increase it. Further, you would expect brainstem signs if there was hypoxia to the brainstem. For example, if you had damage to the solitary nucleus, you wouldn't be able to regulate your HR in response to reduced BP. Since this patient has reduced BP and increased HR, this indicates that the primary disturbance is likely the reduced BP. He's also been in a desert for 24+ hours so. +1  
charcot_bouchard  In a patient who develops hypotension following high-energy trauma, neurogenic shock is a diagnosis of exclusion that is made after hypovolemic and obstructive cardiogenic shock have been ruled out! Plus Absent Bradycardia rules it out +  


submitted by sympathetikey(313),

Mad at myself for changing my answer.

Faulty logic made me wonder if hitting your head would caused increased ICP so, like a cushing ulcer, you would get increased Vagus nerve activity and maybe bradycardia + hypotension. But I guess the RAAS system would have counteracted that and caused vasoconstriction over 24 hours, so Hypovolemic shock is definitely the best choice.

Always should go with the obvious answer :)

seagull  I had the idea that this was a neurogenic shock and increasing intracranial pressure could affect the vagus too. I think the question really wants us to go that direction. +1  
uslme123  The Cushing reflex leads to bradycardia! +1  
purdude  Wait I'm confused. I thought hypovolemic shock leads to an increased SVR? +1  
littletreetrunk  apparently, there's a thing called sympathetic escape that can happen after a while (i.e. he's been out for 24 hours): Accumulation of tissue metabolic vasodilator substances impairs sympathetic-mediated vasoconstriction, which leads to loss of vascular tone, progressive hypotension and organ hypoperfusion. +  
littletreetrunk  also also if he hit his head he could have loss of sympathetic outflow from a hypoxic medulla which could lead to vasodilation, which further reduces arterial pressure, but this was a hard one for me lol. I also put increased ICP wah. +  
catch-22  Any lack of sympathetic outflow/increased vagal outflow should reduce HR, not increase it. Further, you would expect brainstem signs if there was hypoxia to the brainstem. For example, if you had damage to the solitary nucleus, you wouldn't be able to regulate your HR in response to reduced BP. Since this patient has reduced BP and increased HR, this indicates that the primary disturbance is likely the reduced BP. He's also been in a desert for 24+ hours so. +1  
charcot_bouchard  In a patient who develops hypotension following high-energy trauma, neurogenic shock is a diagnosis of exclusion that is made after hypovolemic and obstructive cardiogenic shock have been ruled out! Plus Absent Bradycardia rules it out +  


According to FA, the splenorenal ligament contains the tail of the pancreas and the splenic artery & vein

littletreetrunk  The pancreas is supplied by the pancreatic branches of the splenic artery. The head is additionally supplied by the superior and inferior pancreaticoduodenal arteries which are branches of the gastroduodenal (from coeliac trunk) and superior mesenteric arteries, respectively. +5  
andersen  FA 2019 page 355 / / +