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It would affect the dorsal column tract and the spinothalamic tract. It wont affect the spinocerebellar tract (Thus Rombergs sign in B12 deficiency will be positive)
All three of the tracts are affected in Friedrichs Ataxia
Sorry. Just checked on FA. It will also affect the spinocerebellar tract
Sensation to pinprick is DCML
UWORLD ID:65 "many patients develop neurologic manifestations due to: axonal degeneration of the peripheral nerves, leading to numbness, paresthesia, and depressed motor reflexes." So, I think the sensation to pinprick was describing the paresthesia!
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.
I think that the line's downward slope would be steeper, since Y has more sites that the antibody would bind to.
Wow. I hate this. I only looked at the number of participants and completely ignored the Diastolic BP readings
Everyone commented how to get the mode right. But there is an easier way to realize that the median in Y is higher without all the calculations. If you see, the last Diastolic BP in group X is 110 (as there are ZERO people with 120). While group Y has 8 people with 120 DBP. This automatically shifts the median to the higher side.
I got this wrong though at first I didn't pay attention to the "0" number at group X for 120 DBP
I think there's another easy way to find the median without writing out every value. There are 100 total people in each group, so that means the median (if the DBPs are written in ascending order, which they are) is the 50th person.
Group X: 8 + 12 + 30 = 50, so median is 70
Group Y: 2 + 8 + 10 + 20 +10 = 50, so median is 90
I did it the way @brasel explained. The way @ma_rad did it could give the incorrect answer in some cases (e.g. Group X had 0 ppl with 120 BP but a ton of ppl for 110 BP etc. + Group Y had 10 ppl with 120 BP but basically none with 110 BP etc.). In this question that way worked but it's not always guaranteed since median doesn't sway with outliers, but mean does. // FA 2019 pg. 261
Start at the pontomedullary junction and count from superior to inferiorly (or medially to laterally): VI, VII, VIII, IX.
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
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?
You're looking at the ventral aspect of the brainstem.
^Also, you know it's the ventral aspect because you can see the medullary pyramids.
think of the belly of the pons as a pregnant lady. so you're looking at the front of her
which letter is CN IX in this diagram?
there is no VI nerve. That's the thing. The VI nerve should be in the angle between the pons and the medulla. Parallel to the pyramid. It goes V then VII and then VIII. I make the same mistake and I thought it was the picture but there is no VI par in the photo. They know We count from superior to inferior.
Don't G and H lowkey look like VII and VIII? I chose H b/c of that
G and H are CN VII and VIII on the left side, while this guy has right sided hearing loss. CN VI is not labeled in this photo, but is the smaller nerve that arises medial to CN VII and us cut most of the way up the pons.
Mother Fuckers took this with a disposal camera then deep fried it. What is this grainy ass picture
There's over a million pics of the brainstem on the internet and of course, the NBME picked the worst quality, most blurry one for this Q.
This patient does not undergo a water deprivation test
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.
Just wondering why it in not resistance to ADH action of vasopressin
because he would be hypernatremic with no ADH. can't resorb any water
low osm/urine, low os/plasma => psychogenic polydipsia
In this question the pt had a normal urine osm (80) a low urine osm would be <50mosmol/kg.
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 -.-
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.
^ 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.
so why tf do we give beta blockers for hypertension -.-
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
@amarousis They are used for hypertension because the hypotensive effect of the reduced CO is greater than that of the effect of the increase of TPR. Cheers.
@dr_jan_itor Adding labetalol would not cause unopposed α1 because labetalol and carvedilol are α1 blockers in addition to being nonspecific β blockers (great name btw, I love scrubs haha)
Beta 1 blockade in the kidney (JG cells) would also decrease renin release, which would also help with HTN. FA2019 pg 245
@dr_jan_itor clonidine is an a2 agonist not an a2 inhibitor
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.
malingering is also doing it for some external gain. which was not indicated in the stem
Also, patients with asthma are usually asymptomatic at the time of physical exam unless they are examined precisely during the attack.