NBME Answers : potentialdoctor1's page

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+15 visit this page (nbme24#14)

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p-value refers to the probability of making a type I error (probability of having a false positive). When the 95% confidence interval does not include the null value (1 for ratio, 0 for difference), 0 < p < 0.05 (between 0% and 5% chance of having a false positive). However, when the 95% confidence interval includes the null value, 0.05 < p < 1.0 (between 5% and 100% chance of having a false positive).

Think of it as follows ---> If the 95% confidence interval includes the null value, then you have somewhere between 5% and 100% chance of being wrong if you conclude it is right. Conversely, if the 95% confidence interval does not include the null value, then you have between 0% and 5% chance of being wrong if you conclude that is is right

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drippinranch Excellent explanation! +3

+7 visit this page (nbme23#38)

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Informed consent should be obtained by a provider who has sufficient knowledge to give an accurate description of the intervention, the risk and benefits, alternative treatments and to answer all of the patient's questions

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stinkysulfaeggs Hate this question though... the first thing you would have to do in this situation is refuse to do what the resident asks you to do. Then you could accompany them.... +14

peqmd If not for the additional "refuse to sign consent". I think the answer would have been extremely straightforward. +2

dyckim4 I was taught that that the person who is operating should get the consent that's why I got this wrong.. +4

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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 tea-cats-biscuits(273), visit this page

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Partial agonists have weak agonist activity on their own (thus in this case it causes HR to increase, b-adrenergic effect) but when an actual agonist is present (aka when you are exercising, you are producing NE and E that have full b-agonist effects), partial agonist actually have a mild antagonist effect (thus the heart rate decreases).

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potentialdoctor1 Might be relevant to add that there are two beta-blockers that are actually partial beta-agonists (exert their blocking effects due to lesser effect when compared with endogenous catecholamines) ----> Pindolol and acebutolol +10

thelupuswolf Key to note as madojo said that a partial agonist will compete with the full agonist in the presence of the full agonist, preventing the full agonist's maximum effect +