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Welcome to happysingh’s page.
Contributor score: 35


Comments ...

 +4  (nbme24#10)

http://www.lumen.luc.edu/lumen/MedEd/Radio/curriculum/Surgery/aneurysm2.htm

hope this helps everyone, even the ones that just "like" everything


 +12  (nbme24#17)

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 ?

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 +6
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 +
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. +5
alienfever  FA 19 p510 +1
alienfever  If anyone chose F, communication hydrocephalus is caused by decreased absorption and not increased production. FA 19 p510. +

 +0  (nbme22#32)

Wallerian Degeneration : axonal degeneration distal to site of transection + proximal axonal retraction

Axotomy (axonal tran-section) of peripheral nerves results in, Schwann cells : a. breaking down myelin into small fragments and englufs it b. recruiting macrophages to dispose of axonal debri c. producing growth factors to promote regeneration of axons


 +2  (nbme22#43)

https://www.youtube.com/watch?v=Zlozkdj6wjU

Posterior cord Lesions are called: Radial Plus Palsy.

Cuz Posterior cord has BOTH Radial Nerve & Axillary nerve & cuz they are the 2 terminal branches that come off the posterior cord, so Sx include: triceps & wrist weakness, limitations finger extension indicate injury to radial nerve is located above innervation of triceps Injury of radial nerve occurs in axilla / above weakness of wrist, finger extension Axillary N. injury : weakness of abduction (paralysis of deltoid muscle), sensory shoulder loss. Axillary nerve also innervate teres minor muscle.

Hope this helps


 +1  (nbme22#28)

Hemochromatosis (Auto Recessive HFE Gene on Ch.6) Labs :

↑↑ Serum Iron & Ferritin & Transferrin saturation

↓TIBC


 +2  (nbme22#3)

Injection = ONLY IgG
Vs Oral = IgG & IgA

Cholera is transmitted via GI (oral) route , so you'd need the IgA protection, since it's mostly IgA that protects from GIT pathogens


 +0  (nbme22#1)

i kinda of feel "odd" asking this question : but the patient had an MI 6 months ago, so why would it be unlikely that he was told to "restrict salt, restrict fluids (water) " ??

Guess what i'm asking is : what makes choice E such an unlikely choice (JVD, bi-basilar crackles, peripheral edema) ?

& @meningitis : his bp is 135/82 mmHg ... why is that "HIGH" ??





Subcomments ...

submitted by keycompany(268),
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gemIa owssh secrCnet Sgni, a moomnc nngifid in nAbaildom toAirc yneumssAr ude to lurma hbsmtrou us.onoiclc

happysingh  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 +12  
sabistonsurgery  @happysingh - Thank you. You are correct indeed. +  
suckitnbme  Adding on, this patient is a >65 yo Male with a 120 pack year smoking history. Both are significant risk factors for AAA. +  


submitted by whoissaad(65),
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Aeryrt fo uustdc eeersnfd si a rhbacn of nerfioi svcalie y.raetr So hyw is B gnwr?o

happysingh  the question is asking about "adequate arterial supply" +  
azibird  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. +  


submitted by usmleuser007(326),
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happysingh  i've never heard of " 6. Small Blue Cells" cancer / tumor / carcinoma .... +1  
niboonsh  might want to look at fa pg 665 +  


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sbryant6  I'm going to go take a big bicarbonate poop now. +20  
happysingh  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) +1  
lola915  I thought diarrhea causes Non anion gap metabolic acidosis @happysingh +1  
texasdude4  easy way to remember : "Bicarb out the Butt" +