NBME Answers : alienfever's page

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submitted by happysingh(57), visit this page

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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 ?

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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 FA 19 p510 +3

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

submitted by happysingh(57), visit this page

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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

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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 FA 19 p510 +3

alienfever If anyone chose F, communication hydrocephalus is caused by decreased absorption and not increased production. FA 19 p510. +3

submitted by xxabi(293), visit this page

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Stent thrombosis vs re-stenosis. Stent thrombosis is an acute occlusion of a coronary artery stent, which often results in acute coronary syndrome. Can be prevented by dual antiplatelet therapy or drug-eluting stents. Re-stenosis is the gradual narrowing of the stent lumen due to neointimal proliferation, resulting in anginal symptoms.

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sunshinesweetheart so just to clarify - it's the "symptom-free for 3 months" that rules out thrombosis? +9

hpsbwz It's moreso that at rest there's no changes, but during exercise there is. Like the pathophys of stable angina. +8

suckitnbme I think it's more because of the 2-month history of PROGRESSIVE angina sx with exertion. This points to a chronic process rather than an acute event. +

alienfever Drug-eluting stents prevent re-stenosis (rather than thrombosis) by releasing sirolimus which by blocking cell proliferation. +3

submitted by sugaplum(487), visit this page

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phenylpropanolamine is an alpha agonist that stimulates urethral smooth muscle contraction. - from uptodate, however, it also says it is not recommended treatment anymore

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ugalaxy α1 stimulation (via α1 agonist) constricts the bladder sphincter thereby, preventing sudden bouts of micturition during coughing/sneezing (abdominal stress). +10

sammyj98 I thought that B3 stimulation stopped urination +9

adong @sammyj98 B3 would facilitate bladder relaxation +

hvancampen @sammyj98- were you thinking of oxybutynin? (thats what I thought of!) According to FA, its used for urge incontinence not stress. +2

drzed Nah he/she's talking about Beta-3 receptors which are Gs coupled. Gs increases cAMP thus it would cause smooth muscle relaxation -> bladder relaxation! +1

donttrustmyanswers From Mayo: "There are no approved medications to specifically treat stress incontinence in the United States. The antidepressant duloxetine (Cymbalta) is used for the treatment of stress incontinence in Europe, however." +1

nreid4 @hvancampen oxybutynin is an M3 muscarinic antagonist, not B3. +

alienfever I thought about B3 agonist as well and got this wrong. I think maybe B3 agonist can be used for bladder (URGENCY incontinence) where the main issue is detrusor over reactivity. In STRESS incontinence however the problem has nothing to do with detrusor, so we use α1 agonist to constrict the sphincter. +2

fatboyslim (FA 2020 242) Mirabegron is a B3 agonist. B3 stimulation causes detrusor muscle relaxation, hence it is used for URGE incontinence, not STRESS incontinence. I think the drug they are referring to is Ephedrine? Also, remember "O"xybutynin (muscarinic antagonist) is for "O"veractive bladder (urge incontinence) +1

handsome what is the educational objective of this question? what is the author trying to ask and want us to learn/know? +

bcher @handsome I would add another line to the table on FA2020 p237: alpha agonists; +alpha-1 receptor which causes bladder sphincter muscle contraction; treats stress urinary incontinence with sphincteric incontinence +

l0ud_minority I thought that females didn't have the internal urethral sphincter only external thus a more appropriate drug for stress urinary incontinence would be something that affects the nicotinic receptors????? Am I missing something??? If this was a male then yes alpha 1 receptors are located on the internal urethral sphincter and stimulation of them would help with symptoms in question. +