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potentialdoctor1
Exactly. To add to this, communicating hydrocephalus can be subdivided as follows:
Normal-pressure hydrocephalus: Chronic/gradual decrease in CSF reabsorption at arachnoid granulations, usually due to calcification due to aging. CSF accumulates slowly, so ventricles are able to widen without causing an important increase in intracranial pressure. Symptoms occur due to compression of periventricular white matter tracts ---> Wacky, wobbly, wet
High-pressure hydrocephalus: Acute decrease in CSF reabsorption at arachnoid granulations, usually due to inflammatory state in the subarachnoid space (eg, meningitis, sub-arachnoid hemorrhage). CSF accumulates suddenly, causing an acute-onset increase in intracranial pressure
+9
sunshinesweetheart
not to take away from your perfect explanations, but if it were a woman with neck stiffness and fever (rather than circle of willis rupture) that could lead to increased CSF production, right? I think that's the only case where CSF production would increase. Also I think decr absorption in arachnoid granulations in that situation as well so it'd be a shit question
+1
peqmd
If anyone like me also got "decreased absorption in choroid plexus", as their wrong answer it's because the choroid plexus doesn't "absorb" it produces.
+18
alienfever
If anyone chose F, communication hydrocephalus is caused by decreased absorption and not increased production. FA 19 p510.
+3
an_improved_me
So she has a leaking aneurysm for how long.. gets it repaired, and then within 2 days has an inflammatory response that leads to decreased CSF absorption at arachnoid granulation... Is it the bleeding associated with the aneurysm causing it? The surgery? I'm inclined to say the latter, given that it happens coincidently after the surgery, and not for however long it was leaking beforehand. Thats what tripping me up.
+1
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keycompany
Also take into account this patient had surgery that requires penetration into the subarachnoid space (hence through the arachnoid mater). This can lead to scarring of the arachnoid granulations and subsequent communicating hydrocephalus.
+17
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zbird
So this patient has a leaking berry aneurysm which undergone to surgery and repaired but in two days she developed widening of the SA space which could be explained by increased CSF production but a decreased in absorption, which is due to blockage of the arachinoid granulations by the leaked red and white cells therefore there is a decreased movement of the CSF via the arachinoid villi
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madamestep
I was thrown off for a second because I'd never heard of them called "villi" rather than "granulations". But if NBME loves anything it's using obscure language
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ergogenic22
this would cause a non-communicating hydrocephalus with enlarging of the lateral and 3rd ventricles but normal 4th ventricle and subarachnoid space
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submitted by โhappysingh(57)
so, the Key words that no one is mentioning : communicating hydrocephalus
the pathophys goes like this :
an inflammatory setting (i.e., subarachnoid hemorrhage) yield fibrosis / scarring of the arachnoid granulations => impaired CSF drainage
the key points / concepts they are trying to test here : 1. do you know what communicating hydrocephalus (without them telling you those words) 2. do you know what's the pathophysiology (of communicating hydrocephalus) is ?