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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

Recent comments (see more)

... cmoralara made a comment on nbme18/block3/q#40 (47 yo woman with irregular, raised, multicolored dark lesion)
 +0  upvote downvote
submitted by cmoralara(0)

The subcutaneous tissue is highly vascularized and has larger blood vessels than the dermis, leading to a higher risk of metastasis and worse prognosis (TNM staging system)

... ivypoison made a comment on nbme22/block2/q#6 (A 52-year-old man is brought to the emergency...)
 +0  upvote downvote
submitted by ivypoison(0)

Oxygen can compete CO to bind Hb but i think not all CO-Hb can be removed. Notice " ALL" the C0-binding RBC so go with CO-Hb RBC die. though i spent a lot of time for this question too

... newrose made a comment on nbme24/block3/q#2 (A 28-year-old man has a blood pressure cuff placed...)
 +0  upvote downvote
submitted by newrose(0)

Can someone clarify why Prostacyclin was wrong? I knew the CHALK thing but for some reason had trouble ruling out prostacyclin since it's a vasodilator

... stepwarrior made a comment on nbme20/block4/q#10 (A 65-year-old woman who has a 25-year history of...)
 +0  upvote downvote
submitted by stepwarrior(0)

Wouldn't chronic alcoholism also reduce available NAD and thus inhibit pyruvate decarboxylation by PDH?

... stepwarrior made a comment on nbme20/block4/q#34 (A 20-year-old man is brought to the physician by his...)
 +0  upvote downvote
submitted by stepwarrior(0)

You're just going to diss the son like that right in front of him?

... stepwarrior made a comment on nbme20/block4/q#16 (An investigator wishes to determine the...)
 +0  upvote downvote
submitted by stepwarrior(0)

all fine and dandy except bicarbonate isn't constant with flow rate

... stepwarrior made a comment on nbme20/block1/q#41 (A 45-year-old man has fever, chills, dysuria, and a...)
 +0  upvote downvote
submitted by stepwarrior(0)

They love picking these cases right on the border. Just barely outside of that sexually active age range

... stepwarrior made a comment on nbme20/block1/q#24 (A 50-year-old man comes to the physician because of...)
 +0  upvote downvote
submitted by stepwarrior(0)

this is clearly another one of those trap questions for overthinkers

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Help your fellow humans! (see more)

newrose asks:
Can someone clarify why Prostacyclin was wrong? I knew the CHALK thing but for some reason had trouble ruling out prostacyclin since it's a vasodilator help answer!
stepwarrior asks:
Wouldn't chronic alcoholism also reduce available NAD and thus inhibit pyruvate decarboxylation by PDH? help answer!
stepwarrior asks:
You're just going to diss the son like that right in front of him? help answer!
kllrsouth asks:
Couldn't the answer also be IL-2? Why can't you use cyclosporine in this patient with RA? help answer!
misterdoctor69 asks:
Anyone else got thrown off by their use of HNPCC rather than Lynch syndrome? help answer!
misterdoctor69 asks:
How come melanocytes:basal keratinocytes don't also have a desmosomal connection (in addition to their E-cadherin link)? help answer!
vivijujubebe  melanocyte is not part of the epidermal structure. they're at the epidermal-dermal junction and they produce melanin which is transported to the epidermal
skip_lesions asks:
Can't histamine also cause swelling or is it just not involved in the pathology of gout? help answer!
zevvyt  yes. Histamine causes vasodilation and increased vessel permeability. But it's not involved in Gout. Gout is more about Neutrophils and Macrophages activating eachother and not really about Mast cells.
b1ackcoffee asks:
Any good material for this and lymph node drainage in general? Is this common knowledge or low yield stuff? help answer!
mdmofongo  I got this question right thanks to the 100 high yield concepts of anatomy pdf, learn the lymph node drainage from there and you will be all right.
b1ackcoffee asks:
confused why this is not autonomic dysfunction or hyponatremia due to sweating and why is this orthostatic hypotension? help answer!
mdmofongo  This one is tricky and come downs to choosing the “best” option. I can see why you were confused. However do note that in an autonomic dysfunction you will never present tachycardia as this patient does. I guess the key here is seeing how her BP normalizes once she is laying down? Sorry, this one is a kinda unusual presentation of Orthostatic hypo.
mamed  Not sure if this is correct thinking but how I got this right was: 1. She is hypovolemic 2. Likely retaining salt so water follows (ADH or just renal dynamics in general). This is how I ruled our hypokalemia and hyponatremia 3. If she is hyponatremic b/c sweating then why wouldn't she also be hypokalemic? so both have to wrong because both can't be right 4. Volume depletion ==> orthostatic hypotension
b1ackcoffee asks:
I am wondering which parasite is this actually? -- help answer!
mdmofongo  The clinical presentation sounds like a GI parasite, which are transmitted via fecal-oral route, so ingestion of soil would be the most sensible answer. All the other routes are of parasites with more severe or systemic infection.
b1ackcoffee  @mdmofongo I know this. But which parasite is this?
drblu92  The parasite is most likely Trichuris trichiura (human whipworm). Trichuriasis is often asymptomatic and adult forms can reach 2 cm in length (visible with naked eye). A lot more common in tropical areas but there have been cases in the southeastern US (ex: Kentucky). All other GI worms would present with either a fever or a cough. Treat with mebendazole or albendazole.
amy asks:
HHV8 belongs to Herpesviridae family. Is it true that all members of this family have multinucleate cell with intranuclear inclusion body? HSV and VZV(cowry type A inclusion), EBV and CMV(owl-eye internuclear inclusion) certainly have them. Did anyone pick E for this reason? help answer!
peridot asks:
While I understand why it's hyperplastic arteriosclerosis and how it classically occurs with HTN, I was wondering why it couldn't be berry aneurysm? Is it because the question is asking which is "most likely", making C the better answer? Thank you. help answer!
mannan  Berry Aneurysm is not CAUSED by HTN. It's caused by weakening of the arterial wall (at bifurcations). Hypertensive disease exacerbates them and causes the clinical picture of SAH (worst headache of life) when they rupture. Hope that helps -- Reference: FA CNS pathology, aneurysms.
skip_lesions asks:
Why would there be hyperkalemia if total body potassium is decreased in DKA? help answer!
drdoom  super high blood glucose; super high glucose spillage into urine; lots of peeing = volume depleted (“osmotic diuresis”)
alphatnf  because insulin normally stimulates Na/K ATPase, which sequesters K inside cell. lack of insulin means that there will be more K outside of the cell causing hyperkalemia. however, you are still total body K depleted due to osmotic diuresis. so the hyperkalemia is mainly due to a shift of K from the intracellular (where the vast majority of your K is inside your body is) to the extracellular space.
alphatnf  *where the vast majority of your K is inside your body
pharmtomed asks:
Could anyone help me on why this couldn't be C (facial portion of the homonculus in the primary motor cortex)? It explicitly mentions motor issues with the face - not just speech. I understand why it would be Broca's - that's what I put originally. But the last sentence mentioning motor disruption caused me to change my answer. Thanks. help answer!
jaeyphf  I didn't even think about the motor part during the question, but it might be related to the homonculus (FA 2020 pg 502). Motor and sensory areas of the lower face generally fall towards the lower half of the brain. Answers B/C/D would probably show some hand or arm involvement.
123ojm asks:
Specifically didn't choose coronavirus due to the evidence that COVID-19 is spread fecal-orally. How does it get through the GI tract if it's inactivated by pH < 6? Can someone explain why my thinking is wrong? help answer!
hello  ...COVID-19 is transmitted via respiratory droplets.
123ojm  Right but some research has come out saying it's also spread fecal-orally. So I'm wondering what I'm missing in this question.
trump2020 asks:
How do we know the inferior aspect of the tube doesnt rupture, releasing fluid down in between the layers of the broad ligament? help answer!
melchior  What is special about the Pouch of Douglas is that it is the lowest point of the peritoneal cavity, so even if blood gets in between the layers of the broad ligament (which I agree with you, it looks like it should), I bet it somehow makes its way down to the Pouch of Douglas due to gravity.
joanmadd asks:
I know that small cell carcinoma wasn't an option in this question, but would there be any possible way to distinguish small cell from squamous cell on this specific gross pathology? help answer!
irgunner asks:
I was thinking signal sequence on the N-terminal end that would direct the protein into the RER to be then implanted into the plasma membrane. I guess transmembrane region is the better more specific answer? help answer!
drdoom  A bilayer has hydrophobic tails (polar head + nonpolar tails). If the N-terminus could be embedded in there, it would also have to be hydrophobic; but if an N-terminus were hydrophobic, it wouldn't dissolve well in the cytosol (=mostly water). In fact, an N-terminus probably wouldn't dissolve at all. If it were hydrophobic, it would aggregate with other, nearby N-terminuses (or other hydrophobic motifs). But if that happened, shuttle proteins couldn't recognize N-terminuses in the first place (they wouldn't be sterically accessible), nor deliver them to the rER.
arkanaftus asks:
Is it appropriate to ask a question about the structure which is absent on the picture? It was super confusing! How can you say it was not a defect of the tissue cut? help answer!
drdoom  why did this get downvoted?
therealslimshady asks:
Given the diagnosis of AAA, why did he have syncope? I was first thinking it was from rupture, but his blood pressure is not hypotensive, so how could he get syncope from that. Or maybe the AAA was compressing the inferior vena cava, causing syncope? help answer!
mdmikek89 asks:
Spindle cells....sarcoma or carcinoma Kaposi *Sarcoma*... Why y'all make this shit so complicated? help answer!
drdoom  This explanation only begs the question. (It's a tautology.)
haozhier asks:
Why is it not hypoglycemia?? Hypoglycemia can also lead to seizure help answer!
cuthbertallg0od  Same thoughts here, and I think hypoglycemia occurs earlier in kids/infants than in adults (like 8 hours?) -- maybe just more likely to be hyponatremia since Na+ lost in the diarrhea...
waterloo asks:
If you think about it this way, his free T4 is normal and his TSH is normal. Would any other option allow this to happen? A step further would be, why is his free serum T4 okay but his T3 and T4 dec. His total T4 must be decreased then, which one of those can cause that while keeping free T4 normal. help answer!
haozhier asks:
From FA, succinylcholine can be reversed during phase 2 by cholinesterase inhibitor. Can someone explain if succinylcholine is metabolized by cholinesterase, how can we use cholinesterase inhibitors to reverse it? help answer!

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