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Welcome to littletreetrunk’s page.
Contributor score: 17


Comments ...

 +3  (nbme22#42)
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I nthki het eensaric in alsapm einrn tiatyicv whti SNDIAs sha to do ihwt tniihioibn of nfeterfe rtayer nloadtii yb adpsitlnsnaorg PG)E(,2 isecn 'shtta hawt sDSINA od yb bniiithgin COX. isTh cederesda elrna olodb olfw esald ot SARA ovaitctina ot sencvoer ewtra adn malytlitue iernn srnisce.ea

htballer55  Afferent artery dilation* +5
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. +1




Subcomments ...

submitted by sympathetikey(1253),
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oure:Sc pyw:/ow/ekishndpkgM.t/entlii/eiiira.

iylmn"e psdese eth sntmassoriin fo lieleacrct pmueilss alelcd aintco oitspnealt gnalo lmentydeia oasxn yb unngsiatli the nxoa and neigrdcu alxano emremnba icecaptnaac"

littletreetrunk  I think this makes total sense, but how does it not ALSO stop fast axonal transport? +3  
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." +3  
yotsubato  axonal transport is mediated by kinesin and dynein. Microtubule toxins like vincristine block these +3  
drdoom  @littletreetrunk "axonal transport" is movement of bulk goods via microtubules (which run from soma to terminus); ions, on the other hand, move in an "electrical wave" that we call an action potential! no axonal (microtubular) transport required! in other words, de-myelination will have no effect on the transport of bulk goods; but it will really mess up how fast "electrical waves" traverse the neuron! +  


submitted by sympathetikey(1253),
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Mad at symelf for nnagichg ym .raenws

uaFlty olicg emda em odwern if ihnttig oryu ahed udwlo uscead icesrande ICP ,so klie a cuisngh ercl,u uyo olwdu etg rdcsaniee gusVa rnvee vtiiycat nad beamy ardycadibar + ostonpei.nhy tBu I ugsse the ASRA mtsyes dulow ahve oteanccdruet ttah and saudce ovncrtacintosios vero 24 hs,uor so ocHyvpemilo shock si tedlifeniy the etsb o.iecch

alwAsy olshdu go iwht teh oobisvu arewns ):

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. +13  
uslme123  The Cushing reflex leads to bradycardia! +4  
purdude  Wait I'm confused. I thought hypovolemic shock leads to an increased SVR? +2  
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. +3  
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 +2  


submitted by sympathetikey(1253),
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Mad ta slmfye for anigcnhg ym .nwsear

Fyaltu oglic emda em doenwr fi ntgtiih your heda uoldw daucse nredecisa IPC os, iekl a inugsch rlu,ec yuo lwdou gte ineasdrce Vuags erven tavityic and aemyb aadrridbyac + ho.psninetoy Btu I suesg hte ASAR sestym dlowu hvea cedacntrtuoe that nad deuasc tnvoicsrcaotsino vroe 24 r,souh os eloHimvpcoy okhcs si lyidniefte teh etbs .ciceoh

Aayswl dlshou go ihtw the ibouvos sarnwe :)

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. +13  
uslme123  The Cushing reflex leads to bradycardia! +4  
purdude  Wait I'm confused. I thought hypovolemic shock leads to an increased SVR? +2  
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. +3  
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 +2  


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rciAdogcn to ,AF het senlaelrpon glamtnei sacniotn het ialt fo het nceraspa nad the piecnsl eyrrat &apm; nvie

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. +11  
andersen  FA 2019 page 355 / / +