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Comments ...

 +0  (nbme23#28)

But doesn't subacute combined degeneration lead to impairment in DCML, spinocerebellar and corticospinal tract? I get the ataxic gait - DCML/spinocerebellar. But the sensation to pinprick, wouldn't that be the spinothalamic tract? That is not usually affected in subacute combined degeneration.


 +1  (nbme20#41)

so how would the graph look for protein x expresses all of the epitopes expressed by protein y, but protein y does not express all of the epitopes expressed by protein x?

drw  then some anti-X cannot relocate to Y even Y is added at whatever high dose. at this condition, the line can never touch the axis-Y. on the contrary, if Y express all epitopes on the X, but X does not express all epitopes on the Y, that means some Y epitopes are not seen on X. at this condition, I don't know what will be the line looked like.

 +4  (nbme21#24)

so for this one you have to look at the diastolic blood pressure and that's the values you're supposed to read. not the numbers in the columns. Like group X's mode is 70 because it has that value 32 times. group y's mode is 80 because it appears 20 times. for median, you would have to write the diastolic number 50-120 how ever many times it appears and then find the middle. tricky question.

sahusema  Wow. I hate this. I only looked at the number of participants and completely ignored the Diastolic BP readings




Subcomments ...

submitted by seagull(352),

What a terrible picture. They they covered up part of it with lines. WTF

sympathetikey  Agreed. +  
catch-22  Start at the pontomedullary junction and count from superior to inferiorly (or medially to laterally): VI, VII, VIII, IX. +  
yotsubato  I looked at the left side (cause the nerves arent frazzled up). Saw 7 and 8 come out together nicely. Then picked the right sided version of 8 +  
lolmedlol  why is it not H or I on the right side; the stem says he has hearing loss on the right side, so the lesion should be ipsilateral no? +  
catch-22  You're looking at the ventral aspect of the brainstem. +2  
catch-22  ^Also, you know it's the ventral aspect because you can see the medullary pyramids. +  
amarousis  think of the belly of the pons as a pregnant lady. so you're looking at the front of her +1  


In psychogenic polydipsia, serum sodium is low, and after water deprivation test, urine osmolality is increased. Urine osmolality does not increase with vasopressin injection

In nephrogenic diabetes insipidus, serum sodium is high and there is no change/mild increase in urine osmolality after water deprivation

yotsubato  This patient does not undergo a water deprivation test +3  
niboonsh  Compulsive water drinking or psychogenic polydipsia is now increasingly seen in psychiatric populations. Effects of increased water intake can lead to hyponatremia causing symptoms of nausea, vomiting, seizures, delirium and can even be life threatening if not recognized and managed early. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5579464/ +2  
missi19998  Just wondering why it in not resistance to ADH action of vasopressin +  
amarousis  because he would be hypernatremic with no ADH. can't resorb any water +1  
minhphuongpnt07  low osm/urine, low os/plasma => psychogenic polydipsia +  


according to uworld hypersensitivity pneumonitis is due to dust and that was also an option....

amarousis  so it's definitely dust but the specific type of dust was the most important in this question. the fact that they mentioned the birds is important. the dusty books would cause it but the bird dust is more important -.- +  
charcot_bouchard  Hypersensitivity Pneumonitis - Organic dust (like moldy hay) Pneumocniosis - Inorganic dust none help here though because both will present with same restrictive lung disease picture. i think since dust in library arent neither organic or inorganic and also u dont see many librarians with lung disease but bird ownership is specifically mentioned as cause of HP disease. +  


submitted by strugglebus(63),

Propanolol is a non-selective Beta blocker. So your HR will decrease (B1), which will cause a compensatory increase in TPR.

home_run_ball  ^ Above is partially right: Propranolol is non-selective Beta blocker: Beta1 stimulation causes inc HR, therefore blocking it will dec HR and dec Cardiac output Beta 2 stimulation causes vasodilation, therefore blocking it will CAUSE UNOPPOSED alpha1 activation --> therefore increasing total peripheral resistance. +7  
amarousis  so why tf do we give beta blockers for hypertension -.- +2  
dr_jan_itor  I would also add that the patient was previously on an a2 inhibitor (clonidine), which he ran out of. So he is rebounding on that with upregulated a1 receptor activity. Adding labetalol would cause a greater degree of unopposed alpha, increasing tpr +  


submitted by moo(0),

if the lungs were clear to auscultation and the kid even said he doesn't want to be on the team anymore why couldn't it be malingering?

amarousis  malingering would be a conscious faking of symptoms to avoid being on the team. he wouldn't have the mid-systolic click and he would probably complain of his symptoms all the time and not just limited to during exertion. +  
temmy  malingering is also doing it for some external gain. which was not indicated in the stem +  
garibay92  Also, patients with asthma are usually asymptomatic at the time of physical exam unless they are examined precisely during the attack. +