welcome redditors!to snoo-finity ... and beyond!
Welcome to mnemonia's page.
Contributor score: 6
School:


Comments ...




Subcomments ...

submitted by magrufnis(0),

I’m confused about this one. Weakness of extension and pronation of the right forearm, with a decreased triceps muscle stretch reflex. The answer was C7 nerve root, but how are you able to localize to C7 and not C6 or C8? I figured that extension is radial, C5-T1, and pronation is median, also C5-T1. Triceps reflex is C7-C8 (FA2019 says C6-C7). How would you narrow down to just C7 damage?

txallymcbeal  My FA2018 has “C7” bolded, meaning it is the main nerve root. But I also got this one wrong so I can’t be much help besides that. +  
mnemonia  Honestly just a guess but I have this vague understanding that intrinsic hand muscles are C8-T1 so we might’ve expected more hand motor findings as well with a C8 lesion. +1  
theecohummer  I narrowed it down to C7 using the fact that the C7 myotome is elbow extension. I also learned that the C7 nerve root was the main contributor to the triceps DTR so I just went with that. +  
mchu21  They also mentioned that the person had weakness pronating the right forearm which is performed by the biceps. Biceps is innervated by the musculocutaneous nerve which is C5-C7 and that's what helped me pick C7 > C8. +  
mcl  Sorry, I thought the biceps was a supinator of the forearm? +1  
henoch280  yes.. its the supinator not pronator +  


submitted by pipter(4),

Does anyone have any specific idea on the mechanism of the p53 mutation question regarding the TATA box (the one with the single amino acid conversion and the different hydrogen bonding)?

I chose the decreased binding of RNA polymerase on the TATA sequence of genes that inhibit cell division based solely on the fact that p53 is a tumor suppressor (aka mutated p53->less inhibition of division->multiple divisions).

joha961  From a random paper I found, “Arguably p53’s most important function is to act as a transcription factor that directly regulates perhaps several hundred of the cell’s RNA polymerase II (RNAP II)-transcribed genes.” So normally it increases RNA pol binding; a mutation would decrease it. +  
estsosa  The TATA box is part of the promoter region site where RNA polymerase II and other transcription factors bind to DNA. A defect would therefore decrease binding of RNA polymerase. +4  
mnemonia  Also you can reason it out (I got this wrong because you have to be really meticulous) since we know that loss of p53 = cancer. Cancer = want more cell division = don’t want inhibitory gene = less transcription of said gene. +  


what is happening in this stem? unable to occlude the radial artery ? Can someone please explain?

lilamk  I chose atherosclerosis because they said “radial artery is non-pulsatile but remains palpable even as the cuff is inflated”--> my reasoning was that normally you can’t feel the artery anymore once you overflate the cuff bc this occludes blood flow and arteries are squishy (compliant); BUT if you had atherosclerosis, which is literally a hardening, you would not be able to compress the artery, and neither would you expect the normal radial (outward) expansion of an artery during systole. (that is, the pulses!) +4  
mnemonia  I think athero is just a subtype of arteriosclerosis. Also my thought process was (like Lila) if something were to not be palpable then it would have to collapse and athero prevents this from happening. +3  
yb_26  FA 2019, page 299: types of Arteriosclerosis: arteriolosclerosis and Mockenberg sclerosis. then on page 300: Atherosclerosis - form of arteriosclerosis caused by buildup of cholesterol plaques. +  


submitted by hungrybox(254),

Following a stroke, this patient had weakness of her left face and body, so the stroke must have affected the right side of her brain. B was the only choice on the right side of her brain.

Still confused? Read on...

The voluntary motor fibers (corticospinal tract) descend from the primary motor cortex, cross (decussate) at the medullary pyramids, and then synapse at the anterior motor horn of the spinal level.

Because of decussation at the medullary pyramids, you should make a note of where any stroke occurs. Is it above the medullary pyramids? Then it will affect the side opposite the stroke (contralateral). Is it below the medullary pyramids? Then it will affect the same side as the stroke (ipsilateral).

hungrybox  Woops, E is also on the right side (also remember that imaging is looking up at someone, feet first). But a cerebellar stroke would have caused ataxia. +  
mnemonia  Very nice!! +  
usmleuser007  What gets me is that they mention that Left 2/3 of face is affected. This should indicate a non cortical innervation as most of the cranial nuclei are bilaterally innervated from the left and right hemisphere. If left 2/3 of the face is affected then it should also mean that the lesion is after CN5 nuclei. +1  
yotsubato  @hungrybox Thats not the cerebellum thats the occipital lobe. You would see leftsided homonymous hemianopsia in that lesion +1  
mrsmac  To my mind, it is simpler to consider the question first in terms of blood supply distribution. Left sided hemiparesis and weakness of lower 2/3 of face are both indicative of a MCA rupture/stroke (First Aid 2018 pg. 498). Furthermore, since the injury has affected motor function we would be considering the descending tract i.e. lateral corticospinal which courses through the ipsilateral posterior limb of the internal capsule then decussates in the caudal medulla. +1  
mrsmac  You're considering the wrong CN here. CN5 motor function involves muscles of mastication and lower 2/3 of tongue. The nerve in question in this case is CN7/VII Facial n. CNVII UMN injury affects the contralateral side, whereas LMN injury affects ipsilateral (First Aid 2018 pg. 516). i.e. before and after the nucleus in pons respectively. I hope this helps. +1  
nala_ula  Spastic means UMN lesion, since they also don't specify if there is arm or leg weakness, I didn't assume it was MCA stroke. I went with the reasoning that for there to be spastic hemiparesis, there must be damaged to the UMNs and therefore the internal capsule is where these tracts are. +  
champagnesupernova3  Omg this whole discussion is confusing. Internal capsule contains ALL corticospinal and corticobulbar fibers = contralateral hemiparesis and UMN facial lesion +1  


submitted by hungrybox(254),

Long answer ahead, but bear with me.

HINT: v looks kind of like y, whereas k looks more like x.

y-intercept = 1/Vmax

  • Vmax is the upper limit on how fast a reaction is catalyzed by enzymes.

x-intercept = 1/Km

  • Km is a ranking of how good an enzyme is at binding its substrate. An enzyme with a ranking of 1 is better at binding its substrate than an enzyme with a ranking of 5. (Lower Km = better enzyme)

Note that Vmax, as a measure of performance, can be altered through many things. Meanwhile, Km is a set characteristic of the enzyme, and cannot be altered.

In this example, the enzyme performance (Vmax) is increased by increasing the vitamin cofactor so that it reaches a "normal" activity. However, the enzyme is still inherently shitty due to a congenital defect, so the Km stays the same.

mnemonia  Awesome. +  
ht3  wait line B shows the vmax doesn't change and that the km is getting larger (enzyme is still shitty so larger km) so -1/km would be a smaller number and would approach 0 +1  
lamhtu  You say Km cannot be altered and its staying the same, but the answer of the graph demonstrates a higher Km value. Needing "higher concentrations" of the B6 for enzyme activity is another way of saying Km is higher since more is required for 1/2 vmax activity +2  
sbryant6  Yeah this explanation is wrong. +  


submitted by oznefu(7),

What are the words that point to Carcinoma rather than Fibrocystic or Fibroadenoma or Fat Necrosis (not an answer)?

Those can have masses and calcifications right? Is it only the irregular margins?

mnemonia  Fibrocystic changes doesn’t technically encompass sclerosing adenosis, which is the one where you would get calcifications. Cysts and fibrosis don’t usually present with calcifications. Fat necrosis I’m sure they would give history of trauma in the stem. +  
mnemonia  Calcifications = fat necrosis, sclerosing adenosis, and DCIS/IDC. Microcalcifications specifically I would venture to say is a buzzword ductal carcinoma specifically. Either way, of these 3, only cancer is an answer choice. +  


submitted by oznefu(7),

What are the words that point to Carcinoma rather than Fibrocystic or Fibroadenoma or Fat Necrosis (not an answer)?

Those can have masses and calcifications right? Is it only the irregular margins?

mnemonia  Fibrocystic changes doesn’t technically encompass sclerosing adenosis, which is the one where you would get calcifications. Cysts and fibrosis don’t usually present with calcifications. Fat necrosis I’m sure they would give history of trauma in the stem. +  
mnemonia  Calcifications = fat necrosis, sclerosing adenosis, and DCIS/IDC. Microcalcifications specifically I would venture to say is a buzzword ductal carcinoma specifically. Either way, of these 3, only cancer is an answer choice. +  


Why is the answer decreased blood volume as opposed to decreased plasma sodium concentration?

tea-cats-biscuits  I think it might just be what NBME feels “decreased plasma sodium concentration” means, since through the mechanism that BV is lowered in bedrest, you would definitely have a decreased plasma sodium concentration compared to not-bedrest. However you won’t be presenting with any pathologic signs of hyponatremia because the Na+ would still be maintained in normal limits. Low blood volume is the cause of one of the main pathologic states associated w/bedrest -- cardiac deconditioning and postural hypotension once out of bedrest. Seems like poor wording though. +2  
mnemonia  Remember that changes in sodium concentration over a long period time need to be due to a water dysregulation problem (like SIADH, polydipsia, HF, etc.). Here we just have physiologically increased effective circulating volume, and the body will compensate by diuresing, and since Na+ (and K+) are regulated ions, their plasma levels will not fluctuate. +2