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Comment of the Week

After the cuff is tied, the cells and tissue distal to the cuff will continue consuming ATP (ATP->ADP), but no fresh blood will be delivered to “clear” what will be an accumulating amount of ADP and other metabolites. ADP (=Adenosine) is itself a proxy of consumption and drives vasodilation of arteries! (Evolution is smart!) Increasing ADP/Adenosine in a “local environment” is a signal to the body that a lot of consumption is occurring there; thus, arteries and arterioles naturally dilate to increase blood flow rates and “sweep away” metabolic byproducts.

          —drdoom, nbme24/Block 3/Question#2

Lol of the Week

Which of the following reasons is why this question is bull?

1) Using the word "cyclic" instead of tricyclic for clarity

2) Knowing all of epidemiology of all drugs

3) having to reason out that anticholinergic effects are probably the worst over alpha1 or H1 effects to no certainty.

4) The crippling depression of studying for days-to-weeks on end to probably do average on the test.

          —seagull, nbme22/Block 2/Question#36

Help your fellow humans! (see more)

blueberrymuffinbabey asks:
I got this one wrong, but based on the ITT perspective others mentioned, maybe the "in their primary analysis" part of the question is a tip off. They'd start with including them in the original groups and then do additional analysis to try and tease out the impact? IDK help answer!
diabetes asks:
how is adrenal medulla has ACH nicotinic receptor which are ligand-gated Na/k channeles ? muscarinic ACH receptors are G-protein-coupled receptors. help answer!
diabetes asks:
can somebody explain how energy production by glycolysis increased, since aerobic glycolysis produce 32 net ATP,compare to 2 net ATP through anaerobic glycolysis ? help answer!
diabetes  i think the stem should be "energy production by an anaerobic glycolysis "
blueberrymuffinbabey  yeah that's the bit that tripped me up too. i get that there would be increased glycolysis in general to compensate for lack of TCA function but...the fact that it says "energy production by glycolysis" is kind of misleading/confusing.
medninja asks:
This question sounded like botulism, anybody knows why is tetanus? help answer!
hello36654 asks:
so why is "cessation of fast axonal transport" wrong? Don't myelinated axons, by definition, have fast conductance? So demyelinated axons would have "cessation of fast axonal transport", which is the answer A, right? help answer!
diabetes  i think it slows down ,no cessation .
hello36654 asks:
I understand why it's lung now, but I picked thyroid gland because often times thyroid tumors press on the parathyroid sitting above, which causes the parathyroids to secrete more Ca...can someone comment if they've read this too? help answer!
paulkarr  I personally have not read that, but I wouldn't be surprised by that fact. I think with these NBME problems though, if you can get the answer within one "step" that should be your choice. Here you can just go Squamous Cell Carcinoma with a direct action on serum calcium levels (via PTHrP). Thyroid requires a few more steps, (assuming your statement is true) so in the eyes of NBME, it ain't gonna be the right choice. Always follow the "KISS" logic!
yobo13 asks:
Can someone explain why it can't be Crohn's since that would also cause a non AGMA? help answer!
elf16 asks:
How is this different from the question on NBME 21 in which a 68-year old man also had psychogenic ED? But the answer was normal libido and nocturnal erections. help answer!
cat5280 asks:
Could someone please explain why you were able to eliminate the spinocerebellar tracts? help answer!
ergogenic22  Spinocerebellar is only responsible for Proprioception (unconscious). This patient also has reduced vibration sensation, which the dorsal column tracts are responsible for.
krewfoo99 asks:
Why would decreased movement through the cerebreal aquaduct be wrong? With all the build of blood in the CSF tract without absorption, wouldnt movement also be decreased through the aqueduct? help answer!
defalty98 asks:
Why are we complicating things? Change in the bases will destroy the palindromic sequence required for any restriction endonuclease to work. Methylation is the only option that makes sense. help answer!
jigyasa asks:
Why have you taken 180 as patient years? Isn't patient years calculated as no of patients multiplied by the number of years they suffer? help answer!
titanesxvi asks:
why not decrease CA activity in the proximal tubule? this also could lead to metabolic acidosis. help answer!
ergogenic22  carbonic anhydrase inhibitors can cause Type 2 RTA but it is not the cause here (cystinosis)
krewfoo99 asks:
Why would perforins be the wrong answer? Wouldnt accumulation of toxic proteins cause the cell to undergo apoptosis ? help answer!
ergogenic22  Bortezomib does not directly activate perforin. It directly inhibits the proteasome which → enables CD8+ T cells to initiate apoptosis → via perforin release (in essence a downstream effect).
krewfoo99 asks:
In what situations will HbH be formed (3 alpha chain deletions)? help answer!
ergogenic22  one parent has 2 deletions on the same gene, the other parent has 1 deletion, and the offspring receives all three. In this question, both parents have alpha 1 deletion
ergogenic22  actually its possible that they both have 2 gene deletions, but regardless, a-thalassemia trait is more likely
ergogenic22  and someone above said Asian people are cis-2 deletion so the offspring will not receive two deletion from one parent
ergogenic22  ↑↑ I made a mistake by confusing trans and cis cis has deletions on the same chromosome and can pass two deletions to off spring, therefore a chance of allowing HbH
krewfoo99 asks:
Can someone explain what the picture is supposed to show? Is it supposed to be segmented neutrophils? help answer!
titanesxvi  yes do to B12 deficiency
krewfoo99 asks:
Wouldnt the HCOM murmur be best heard in the aortic area? help answer!
krewfoo99  Correction: Shouldnt it be heard best in the left upper sternal border?
krewfoo99 asks:
Anyone know why heart sounds would be distant in COPD exacerbation? help answer!
yng  Patient is usually obese (blue bloater) --> diaphragm movement is limited --> can't take deep breaths, and in extreme cases, the chest size increased and causing distant heart sound.
krewfoo99 asks:
Anyone know why heart sounds would be distant in COPD exacerbation? help answer!
marat  Cause lungs are overextended
marat  overexpanded
krewfoo99 asks:
In boards and beyond, It is said that third degree heart block is due to block in the HIS Purkinjee system. So why would ablation of AV node cause this disease? Wouldnt destruction of part of left ventricle be a better answer ? help answer!
amirmullick3 asks:
Is this Guillain barre though? I felt it was Acute inflammatory demyelinating polyradiculopathy, discussed on page 512 FA 2019. There is no relation to C jejuni here nor does the patient have any other relations to infection such as eating something or etc. help answer!
wishmewell  Acute inflammatory demyelinating polyradiculopathy is a subtype of GBS.
niboonsh asks:
external carotid branch supplies the superior parathyroid glands as well........? help answer!
yng  Yes the superior part supplied by superior thyroid gland which is a branch of external carotid branch.
divya asks:
Can anyone discuss what's responsible for inhibiting the processes given as other options? help answer!
divya asks:
Why is there rhinorrhea in opioid withdrawal? And also, if stimulants like cocaine cause nasal vasoconstriction, shouldn't opioid withdrawal do the same? help answer!

Recent comments (see more)

... divya made a comment on nbme23/block4/q#45 (A 32-year-old man has a diastolic blood pressure...)
 +0  upvote downvote
submitted by divya(2)

i don't think you need to think all that much. look at all the options and think of what happens when they increase. A, B, C, D and F all can cause interstitial edema. But increasing precapillary resistance definitely doesn't.

... blueberrymuffinbabey made a comment on nbme23/block2/q#3 (A prospective study is done to assess the relative...)
 +0  upvote downvote
submitted by blueberrymuffinbabey(0)

I got this one wrong, but based on the ITT perspective others mentioned, maybe the "in their primary analysis" part of the question is a tip off. They'd start with including them in the original groups and then do additional analysis to try and tease out the impact? IDK

... drdoom made a comment on nbme24/block3/q#46 (A 15-year-old girl with cystic fibrosis has a...)
 +0  upvote downvote
submitted by drdoom(232)

The CFTR protein is a transmembrane protein. Like all proteins, its translation begins in the cytosol; that said, CFTR contains an N-terminus “signal sequence”, which means as it is being translated, it (and the ribosome making it!) will be transported to the Endoplasmic Reticulum.^footnote!

As it gets translated, its hydrophobic motifs will emerge, which embeds the CFTR protein within the phospholipid bilayer of the ER itself! That means the protein will never again be found “in the cytosol” because it gets threaded through the bilayer (which is, in fact, how all transmembrane proteins become transmembrane proteins at the cell surface -- they have to be made into transmembrane proteins in the ER first!).

So, yes, ultimately, these misfolded proteins will be directed toward a proteasome for degradation/recycling, but that will happen as a little vesicle (or “liposome”); the misfolded protein, in this case, is not water-soluble (since, by definition, it has hydrophobic motifs which get “threaded through” a bilayer to create the transmembrane pattern), which means you won’t find it in the cytosol.

\ footnote! \ The hitching of active* ribosomes to the Endoplasmic Reticulum is why we call that area of ER “rough Endoplasmic Reticulum (rER)”; on electron microscopy, that section was bespeckled with little dots; later, we (humans) discovered that these dots were ribosomes!

\ * \ By “active ribosomes”, I just mean ribosomes in the process of converting mRNA to protein! (What we call “translation” ;)

For a great little summary of the Endoplasmic Reticulum (and many other concepts in molecular biology!), see this from Alberts’ Molecular Biology of the Cell:

... diabetes made a comment on nbme23/block3/q#49 (Genetic analyses of cells obtained on amniocentesis...)
 +0  upvote downvote
submitted by diabetes(3)

how is adrenal medulla has ACH nicotinic receptor which are ligand-gated Na/k channeles ? muscarinic ACH receptors are G-protein-coupled receptors.

... wishmewell made a comment on nbme18/block1/q#46 (65 yo man, generalized tonic-clonic seizures)
 +1  upvote downvote
submitted by wishmewell(1)

I think they are talking about Glioblastoma multiforme because it "crosses over to the left hemisphere" this is the only CNS tumor that does that and it is Grade IV meaning high grade. Glioblastoma multiforme is a type of Astrocytoma thats why its GFAP + page 510 FA 2018

... wishmewell made a comment on nbme18/block1/q#11 (67 yo man, fine resting tremor in both hands)
 +0  upvote downvote
submitted by wishmewell(1)

I was confused between Alpha- Synuclein and Tau. This patient has parkinsons diseases and thus we would see Alpha synuclein.

Tau is seen in patients with Picks disease, aka Frontotemporla dementia AND alzheimers disease. page 504. FA 2018

... wishmewell made a comment on nbme18/block1/q#33 (35 yo woman with pain and swelling of breasts, pelvic discomfort)
 +0  upvote downvote
submitted by wishmewell(1)

In my opinion this is kinda rude as an intial action. if the person continues to go back to the topic, I would say having a chaperone would help.... idk why Interrupting the patient with a more neurtal topic isnt the answer

wishmewell  NVM! i read the question again. The patient has visited already 4 times with cheif complains regarding sexual organs in a short period of time. According to FA page 262 (2018) at this point a chaperone should be added, if this doesnt help then the patient needs to be forwarded to another physician.
... wishmewell made a comment on nbme18/block1/q#28 (Cholera toxin is a catalyst that results in the inhibition of GTPase activity of G-stimulator protein)
 +0  upvote downvote
submitted by wishmewell(1)

Cholera roxin overactivates adenylate cyclase ( increases cAMP) by permanently activating Gs and thus icnreases Cl- secretion in the gut and H20 efflux Page 132 FA 2018