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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
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
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.
If anyone chose F, communication hydrocephalus is caused by decreased absorption and not increased production. FA 19 p510.
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.
crescent sign is a finding on radiographs that is associated with avascular necrosis, NOT aneurysms !!!
what you're seeing is Calcification of wall of the aortic aneurysm
@happysingh - Thank you. You are correct indeed.
Adding on, this patient is a >65 yo Male with a 120 pack year smoking history. Both are significant risk factors for AAA.
the question is asking about "adequate arterial supply"
The artery of the ductus deferens is USUALLY a branch of the SUPERIOR vesical artery, although it can branch from the inferior vesical artery in some individuals.
A of ductus deferens would be the direct supply, vesical artery would be indirectly (via a of ductus def)
i've never heard of " 6. Small Blue Cells" cancer / tumor / carcinoma ....
might want to look at fa pg 665
I'm going to go take a big bicarbonate poop now.
i would suggest that you look into it a bit more. Why ?
Had an nbme question (which confused the shit out of me) cuz, Bluemic Pt. who was abusing Laxatives (had the up & down arrows) and this is what it gave :
Laxative Abuse — Metabolic Alkalosis :
↓K+ ↑Cl- ↑pH ↓HCO3-
so one of the points of distinction IS the increase in Cl- with laxative abuse (vs. vomiting, which was a knee-jerk reaction when i hear bulimia)
I thought diarrhea causes Non anion gap metabolic acidosis @happysingh
easy way to remember : "Bicarb out the Butt"