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Contributor score: 39

Comments ...

 +1  (nbme22#14)

Got this wrong, but when looking this up, I saw that SCID is associated with a lack of adenosine deaminase --> accumulation of adenosine, which is lympho-toxic.

 -1  (nbme22#7)

But he doesn't feel healthy...he's been coughing for 6 months, with blood for a week. If I were him, I'd think something was really wrong with me, and that I was certainly NOT healthy...By telling him it must be hard, yeah, it's compassionate, but you're not answering his question at all. He asked you, "How can this be happening to me?"

 +14  (nbme20#23)

The way I approached the question was to consider what happens 1. When you grow from a baby to a child, and 2. when you grow from a teenager to an older adult. Whatever remained true between both of them was the right answer.

Right answer: The resting BP of a newborn is 65/40 (google), while that of a 1-month old is 95/60. The average adult is higher, with the American Heart Association citing (absurdly, IMO) that "normal" is <120/<80. Nevertheless, the trend is that BP increases as we age, whether we are newborns or old people.

Wrong answers: Development of coronary atherosclerosis: Perhaps due to the American diet it can be argued that the development of atherosclerosis is almost inevitable as you become an older adult. Certainly not true as a baby --> child.

Development of mitral stenosis: Similar reasoning as coronary atherosclerosis; you MAY develop it as an adult (not nearly as common as a buildup of atherosclerotic plaques), but sure, let's say that it can happen. Not true as a baby --> child.

Increased basal heart rate: The opposite is actually true. The basal heart rate of a newborn can easily exceed 150, and that's considered normal. As we age, this heart rate goes down.

Increased cardiac muscle mass: This one was the hardest to work through. It is true that as we age from a baby --> child our heart grows in size. But if we tweak our assumption from before with the American diet, and instead put our patient on a more moderate diet, realistically his heart shouldn't increase in size too much, at least to the point of cardiomegaly.

Increased compliance of arteries: As we become older adults, the compliance of arteries decreases and stiffness increases (careful not to confuse arteries with lungs, which actually do increase in compliance as we age!)

rockodude  basically the American diet is... SAD;) +1

 +2  (nbme20#39)

Reason why it's not E: While it's true that mycoplasma pneumoniae uses sterols for its cell membrane, it's the lack of a target for amoxicillin (peptidoglycan) that renders it ineffective. Classic test technique where they include a right answer but isn't the correct answer

 +0  (nbme20#6)

For those curious why it's not D, the way I reasoned it out was that 1. they were referring to opioids, so 2. withdrawal would be

Diarrhea (opposite of constipation that they feel) + nausea Mydriasis (opposite of the miosis) Piloerection Seizures are rare, and they're more associated with alcohol (and also benzos) You may get mild hypertension

misterdoctor69  The choice said "Narcotic pain medication" not withdrawal to the narcotic pain meds. Adverse effects of narcotics would be constipation, miosis, and respiratory depression. +

 +4  (nbme20#21)

Why the other answer choices aren't correct

A - Not an anaphylactic reaction mainly due to chronicity (consumption of soy, which has glycoproteins that people may have allergies towards)

B - Not asthma (characterized by more acute episodes of bronchoconstriction, wheezing)

D - Anemia (B6, B9, B12), or maybe a pulmonary embolism due to B9 or B12 deficiency --> elevated homocysteine levels --> thrombosis --> DVT?

E - Pulmonary anthrax; The time course would be much more acute, and would also present with symptoms of flu-like symptoms. Rapid death too

 +4  (nbme20#47)

A = Maybe the superficial dorsal vein

B = Areolar tissue

C = Urethra (surrounded by corpus spongiosum)

D = Corpus cavernosum (correct answer)

Sildenafil increases blood flow to the penis by dilating the corpus cavernosum (increased NO via inhibition of PDE5 --> cGMP --> smooth muscle relaxation). It doesn't actually affect the blood vessels supplying the corpus cavernosum, I believe

mangotango  This pathway causes relaxation of vascular smooth muscle so it causes vasodilation and increased blood flow to the corpus cavernosum, causing an erection. +

 +0  (nbme20#41)

The crux of the question is asking, if the patient feels decreased pain (which is driven by opioid molecules; that's why opioids are administered as painkillers), then how do you stop the inhibition? An opioid antagonist (naloxone is the only one that is an antagonist)

neovanilla  wrong answers: b-endorphin - an endorphin and ACTH hormone (similar to ACTH, POMC) that can bind to the µ-opioid receptor Enkephalin - a neurotransmitter involved in the indirect basal ganglia pathway (along with GABA); it can also bind to delta-opioid receptors Morphine - an opioid agonist (used for pain relief) Oxycodone - Another opioid agonist (~same potency as morphine) +4
kevin  enkephalin, endorphin, dynorphin are the bodies endogenous opioids +1

Subcomments ...

submitted by lfcdave182(31),

Pg 366 FA 2020.

  • Below pectinate line: External hemorrhoids: Painful if thrombosed: Inferior Rectal Vein.
neovanilla  Note: pg 365 FA 2020 states: anorectal varices: portal <--> systemic: superior rectal <--> middle and inferior rectal. Not sure if that's correct, but definitely the info cited in pg 366 is correct +1  
cheesetouch  FA 2018 p360 +  

submitted by nicsar(1),

a)abduction: supraspinatus-deltoid-triceps-serratus anterior

b)adduction: subscapularis-pectoralis major-lattisimus dorsi- teres major

c)extension=horizontal abduction; post. deltoid, infraspinatus, teres minor

d)internal rotation: subscapularis

for isolated work out, d is better.


thotcandy  teres major also internally rotates? It's attached to the medial lip of the humerus +3  
neovanilla  teres minor externally rotates (+ad-duction) +  

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thepacksurvives  Yeah, this was my issue. I got it wrong because of this-- still don't understand the logic bc you can get chlamydia multiple times +5  
hungrybox  FUCK you're right. Damn I didn't even think about that. That's fucking dumb. I guess this is why nobody gets perfect scores on this exam lol. Once you get smart enough, the errors in the questions start tripping you up. Lucky for me I'm lightyears behind that stage lmao +9  
usmile1  to make it even more poorly written, it says they are doing a screening program for FIRST YEAR women college students. So one year later, are they following this same group of students, or would they be screening the incoming first years? +5  
dashou19  I think the same at first, but after a second read, the question stem said "additional" 200 students, which means the first 500 students don't count. +  
santal  @hungrybox You are me. +2  
neovanilla  @usmile1 I was thinking the exact same thing... +1  
happyhib_  I agree this is a trash question; I was like well if this is done yearly for new freshman the following year would be of the new class (but the word additional made me go against this). Also you could assume that they were treated and no longer have the disease... I dont like it honestly but know for incidence they want you to not include those with disease so i just went with dogma questions on incidence to get to 10% +  

submitted by dentist(53),

So do you ignore the distraction about his mother and consider which of the organisms can lead to nodule formation on the vocal cord?

neovanilla  yep _(ツ)_/¯ +1  

submitted by drw(3),
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dulxy071  A stronger factor though is diet and other habits. no matter who it is, if you eat more high sodium food you're going to need a treatment which targets ridding the body of sodium more than anything else and so on so forth. This is something that the world medicine needs to understand better +3  
neovanilla  Maybe, but this is NBME, and while diet can play a role in different pharmacological responses, what they might be emphasizing here is that no one drug affects all people the same way. There's an incredible bias in medicine towards white males because older drug clinical studies only recruited these patients. It was only once the drug was in the market that doctors and patients realized that certain drugs didn't work as well for them. That's just a fact, and is what NBME is testing us on +7  

submitted by johnthurtjr(142),
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neovanilla  Don't force it out, you gotta relax and it'll come out naturally ;) +  
mysteriousmantyping  Why couldn't the answer be Inferior rectal nerve since that controls the external anal sphincter? +1  
draykid  @mysteriousmantyping I think this question is looking at complications of T2DM, more specifically diabetic autonomic neuropathy. Patient more than likely has diabetic gastroparesis which may explain his constipation and abdominal distension. +1  
cuthbertallg0od  Pudendal nerve controls external anal sphincter (per FA), and gastroparesis wouldn't have anything to do w pelvic splanchnics but instead vagus nerve... Don't know why pudendal nerve couldn't be right if he was just clogged up from not being able to relax his sphincter anymore ---- is parasympathetic just more likely to be the issue statistically or something? +1  
cuthbertallg0od  Or would losing pudendal nerve result in incontinence... Its never been clear to me if activation/inactivation opens/closes sphincters... +1  
cuthbertallg0od  Just realized that says perineal... whoops +2  
vivijujubebe  External sphincter is innervated by pudendal nerve, more often damaged during labor. DM patients have autonomic neuropathy with parasympathetic/sympathetic nerves more likely damaged +  

submitted by mbourne(78),

I think that if they had something like "statin therapy" as an answer choice, we would have an argument for that as it would decrease mortality by helping prevent ANOTHER heart attack. However, I think that anti-depressant therapy will do a LOT to prevent suicide, while omega-3 fatty acids (healthy as they are) wouldn't do AS MUCH to prevent a heart attack.

The question is basically asking, "You can only prescribe one of these to keep this dude alive as long as possible. Which one will have the best chance at accomplishing that?"

Therefore, the answer should be anti-depressant therapy.

bharatpillai  why antidepressant therapy though? there are not enough features given to suggest MDD. He's 56 years old, not an elderly single male so not at the highest "classical" population at risk of suicide? the question is so ambiguous... Given MI, wouldn't chronic alcoholic intake predispose him to dilated cardiomyopathy? +  
neovanilla  I don't believe it's that he has MDD by the clinical definition. It's more that his QoL has probably changed drastically since the MI and MIs are strongly associated with decreased outlook on life, especially considering how common it is to get a second MI soon after the first. I don't know the stats on suicide post-MI, but helping the patient's depression to make him more pro-active to help himself prevent another MI would be better than "a diet high in omega 3 FAs" (at least, this was my justification, as mbourne was saying) +  
drzed  First sentence of the stem: he has a 6-week history (e.g. >2 weeks) of depression (1), difficulty sleeping (2), fatigue (3), decreased appetite (4), and poor memory/concentration (5) For a diagnosis of MDD, you need a 2 week history of 5 of the SIGECAPS symptoms which he meets (he is only missing suicidal ideation and interest in activities). Thus he meets the diagnostic criteria for a major depressive episode, which means that treatment is indicated with an SSRI. +1  

submitted by pg32(151),

Can anyone explain why the lipase concentration is so high if there is an issue with LPL in hyperchylomicronemia?

garima  due to pancreatitis +5  
neovanilla  ELI5? +  
suckitnbme  @neovanilla Type 1-hyperchylomicronemia has increased risk of pancreatitis +  
makingstrides  I don't understand why this isn't hypertriglyceridemia because this also causes acute pancreatitis. Maybe because overproduction of VLDL isn't an answer? +  

submitted by neovanilla(39),

The crux of the question is asking, if the patient feels decreased pain (which is driven by opioid molecules; that's why opioids are administered as painkillers), then how do you stop the inhibition? An opioid antagonist (naloxone is the only one that is an antagonist)

neovanilla  wrong answers: b-endorphin - an endorphin and ACTH hormone (similar to ACTH, POMC) that can bind to the µ-opioid receptor Enkephalin - a neurotransmitter involved in the indirect basal ganglia pathway (along with GABA); it can also bind to delta-opioid receptors Morphine - an opioid agonist (used for pain relief) Oxycodone - Another opioid agonist (~same potency as morphine) +4  
kevin  enkephalin, endorphin, dynorphin are the bodies endogenous opioids +1  

submitted by ye2019(3),
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adong  honestly think this was a typo. hot trash +2  
neovanilla  Assuming it was not a typo, how would the costophrenic angles be tender in this condition? ...From crying...? +1