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 +2  (nbme24#1)

According to Goljan: "B12 (cobalamin) has cobalt in it. Circulating form of folate is methyltetrahydrofolate. Purpose of cobalamin (B12) is to take the methyl group off of methyltetrahydrofolate. Then it’s called tetrahydrofolate. If you don’t get the methyl group off of folate, you will not make DNA. So, if you are B12 def, you can’t get the methyl group off and cannot make DNA. If you are def in folate, you can’t make DNA."


 +0  (nbme24#13)

There are questions about splinting on Pastest and UW. UW q id 11885 shows another scenario. Good images on the explanation though. Nulliparous, nonobese 39 y/o pelvic pressure & constipation and does splinting to defecate, bla bla bla. Exam: irregularly enlarged uterus. Dx was posterior subserosal uterine leiomyoma and rectocele was on the options... Splinting is NOT just for rectocele.


 +1  (nbme24#43)

This also refers to chronic inflammation & granuloma formation.


 +0  (nbme24#34)

I think they are referring to Kulchitsky cells = pulmonary neuroendocrine cells (PNEC). According to Wikipedia: Specialized airway epithelial cells that occur as solitary cells or as clusters called neuroepithelial bodies (NEB) in the lung. They are located in the nasal respiratory epithelium, laryngeal mucosa and throughout the entire respiratory tract from the trachea to the terminal airways. They can be the source of several types of lung cancer- most notably, small cell carcinoma of the lung, and bronchial carcinoid tumor.


 +1  (nbme24#3)

This was on a previous NBME. How I got it? Intercostal (posterior) is how you get to the vertebral bodies; the other vessels are anterior.


 +1  (nbme23#7)

Hmmm. Well my mind has blown off because what hit my mind was dehydration since he was in the desert. As soon as my mind started to wander about all of the other options that could make sense... I just clicked and moved!

charcot_bouchard  Smart boi




Subcomments ...

submitted by neonem(278),

This patient has pulmonary fibrosis, which causes a restrictive (not obstructive)-type disease. Since there was no occupational exposure, I'm assuming this is idiopathic pulmonary fibrosis. This causes thickened alveolar membranes, limiting gas diffusion. Therefore, eventually O2 won't be able to diffuse quickly enough into the blood across the alveolar-arterial membrane, resulting in a larger A-a difference. (I think there's normally a small A-a gradient, from 2-14 mm Hg, but when this gets too big, you get hypoxic)

yex  UW q id 7648 +1  


submitted by dbg(32),

WTF is "weakness of plantar dorsiflexion" ????? it's like saying "extension flexion" This is not the only obvious technical mistake in the new NBMEs ...

karthvee  loool +2  
yex  Funny Board!! Yeahhhhh +  


yex  There is a Q on UWorld about rotator cuff tendinitis #380186 w/ a similar presentation... I kind of remembered about that, but honestly I do not know how I got it right. +  
yex  Correction: Q id is # 1732 +  


submitted by lsmarshall(215),

Urea Cycle Disorders > Isolated severe hyperammonemia (> 1000; i.e., no other severe metabolic disturbances

Ornithine transcarbamylase deficiency > (most common urea cycle dis.) orotic acidemia/aciduria, hyperammonemia

Organic Acidemias > Hyperammonemia, anion-gap acidosis, ketosis (from hypoglycemia)

Medium-chain acyl-CoA dehydrogenase deficiency > Hyperammonemia, hypoketotic hypoglycemia (seen in β-oxidation disorders, EXCEPT adrenoleukodystrophy)

Liver dysfunction > Hyperammonemia, LFTs messed up, older pt.

lsmarshall  Summary of metabolic issues relating to hyperammonemia +3  
seagull  i'm leaning towards Ornithine transcarbamylase deficiency. +2  
notadoctor  Not sure why this isn't considered a mitochondrial disorder since the issue is Ornithine transcarbamylase deficiency in the mitochondria? +1  
charcot_bouchard  if it was mitochondrial disorder no one would escape +1  
wowo  figure in OTC deficiency, they might have to explicitly mention the orotic aciduria AND typically presents earlier, around 24-48hrs of life after they've fed (at least per BB) + also per BB, propionic acidemia and MM acidemia have an onset of weeks to months and lead to build up of organic acids --> acidemia in addition to hyperammonemia (not sure why, but several aa enter the TCA cycle via propionyl CoA --> methylmalonyl CoA --> succinyl CoA, but now this is defunct d/t enzyme deficiencies...?). Anywho, propionic acidemia described on FA2019 p85, but doesn't list hyperammonemia +1  
artist90  i think it cannot be Ornithine transcarbamylase deficiency bc it is XR disease. this pt has a healthy 2yr old brother which rules out X-linked recessive disease correct me if i m wrong +  
artist90  it is 100% Propionic acidemia Uworld Q-id: 1340. it is an exact copy question of uworld. i got it wrong bc i forgot these are organic acids. But i am still confused on 2 things 1-how does acidosis cause Hypoglycemia and Ketosis. 2-why is Ammonia elevated in these pts bc urea cycle will be fine? +  
yb_26  1) hyperammonemia is seen in all urea cycle disorders except arginase deficiency 2) organic acids directly inhibit urea cycle => hyperammonemia (from UWorld) +  
yex  According to UW, there is another question # 1341. This one refers to methylmalonic acidemia (ORGANIC ACIDEMIA). HYPOGLYCEMIA results from overall increased metabolic rate leading to increased glucose utilization and direct toxic (-) of gluconeogenesis by organic acids. The presence of hypoglycemia leads to increased free fatty acid metabolism that produces KETONES, resulting in a further anion gap met acidocis. Finally, organic acids also directly (-) the urea cycle, leading to HYPERAMMONEMIA. +5  


submitted by doodimoodi(12),

Did no one notice that the Odds ratio on the top left is wrong? Am I missing something? If you calculate it, it's 6 just like the top right one....

mjmejora  thats actually really funny +  
yex  Because I said so, applies here... :-/ +  
doodimoodi  Cant believe we pay $60 for this crap +6  


submitted by catch-22(21),

I woud do a retrospective cohort here. I don't think this question is correct and provides too little information to get the correct answer. "Time efficient" is the operant word here but they simply didn't consider that retrospective cohort would be a better design here as long as the variables are coded.

sherry  I agree. I was hesitating between the two choices. I still think cohort study is better regarding the "risk". I hope this kind of questions wont pop out on the real thing. +1  
soph  I think key here was they were measuring risk though +  
yex  I also chose cohort, since it is comparing a given exposure. +  


Skin provides insulation and prevents heat loss. This patient's body will compensate for increased rate of heat loss by increasing metabolic rate.

davidw  This is directly from Goljan I) Hypovolemic shock may occur due to loss of plasma from the burn surface (refer to Chapter 5). • Loss of protein from the plasma loss may result in generalized pitting edema. II) Infection of the wound site and sepsis may occur. (a) Sepsis due to Pseudomonas aeruginosa is the most common cause of infection in burn patients. (b) Other pathogens include methicillin-resistant S. aureus and Candida species. (3) Curling ulcers may occur in the proximal duodenum (refer to Chapter 18). (4) Hypermetabolic syndrome may occur if >40% of the body surface is burned. +4  
yex  Can someone explain why is it not increased ECF? +  
charcot_bouchard  i picked same. Increased ECF but cant remember why. Can you explain WHY it is increased ECF? what was ur reasoning +1  
isotopes  Burns would lead to a decrease in ECF because the protection from fluid loss is absent; it can lead to shock. :) +  
tinydoc  My reasoning behind picking ↑ ECV was that your losing fluid but not electrolytes with the burn ⇒ the ecv would have increased osmolarity, so the fluid from the ICV would be pushed the the ECV. It made sense to me at the time. I guess technically its wrong because the loss of fluids and the gain of fluids would amount to pretty much the same thing. But the insulation and heat loss thing makes sense I guess. +  
yex  Increased ECF, bc I was thinking about the edema formation.... :-/ +  
atbangura  I picked increased ECF because burns increase the capillary permeability coefficient, but now that I am going over it I realized that increasing the permeability would only transfer plasma volume to the interstitial volume, which are both a part of the ECF so therefore ECF would not change. SMH +1  


Did anyone else go down the: she's hypotensive so maybe she'll get waterhouse friderichsen syndrome because nothing else is making sense to me at this point??? route -

Turns out, severe malaria can cause cardiovascular collapse and hypotension.

shriya goyal  yes I answered it like that +1  
redvelvet  me too :( +  
abigail  me three :( +  
yex  Me four :-/ +  
link981  Slowly raising my hand as well +  
tinydoc  Sammmme +  
bullshitusmle  same here!!!:@ +  


Skin provides insulation and prevents heat loss. This patient's body will compensate for increased rate of heat loss by increasing metabolic rate.

davidw  This is directly from Goljan I) Hypovolemic shock may occur due to loss of plasma from the burn surface (refer to Chapter 5). • Loss of protein from the plasma loss may result in generalized pitting edema. II) Infection of the wound site and sepsis may occur. (a) Sepsis due to Pseudomonas aeruginosa is the most common cause of infection in burn patients. (b) Other pathogens include methicillin-resistant S. aureus and Candida species. (3) Curling ulcers may occur in the proximal duodenum (refer to Chapter 18). (4) Hypermetabolic syndrome may occur if >40% of the body surface is burned. +4  
yex  Can someone explain why is it not increased ECF? +  
charcot_bouchard  i picked same. Increased ECF but cant remember why. Can you explain WHY it is increased ECF? what was ur reasoning +1  
isotopes  Burns would lead to a decrease in ECF because the protection from fluid loss is absent; it can lead to shock. :) +  
tinydoc  My reasoning behind picking ↑ ECV was that your losing fluid but not electrolytes with the burn ⇒ the ecv would have increased osmolarity, so the fluid from the ICV would be pushed the the ECV. It made sense to me at the time. I guess technically its wrong because the loss of fluids and the gain of fluids would amount to pretty much the same thing. But the insulation and heat loss thing makes sense I guess. +  
yex  Increased ECF, bc I was thinking about the edema formation.... :-/ +  
atbangura  I picked increased ECF because burns increase the capillary permeability coefficient, but now that I am going over it I realized that increasing the permeability would only transfer plasma volume to the interstitial volume, which are both a part of the ECF so therefore ECF would not change. SMH +1  


yex  There is a Q on UWorld about rotator cuff tendinitis #380186 w/ a similar presentation... I kind of remembered about that, but honestly I do not know how I got it right. +  
yex  Correction: Q id is # 1732 +  


submitted by yotsubato(306),

Was it just me, or did "age at onset in years" appear RIGHT above the number of patients, rather than the mean. Which confused me for a good 3 minutes.

fulminant_life  Definitely was the same for me. I was so confused for like 5 mins +5  
d_holles  dude i almost didn't get the question bc of this ... i thought the age of onset was the actual age of onset (36) +3  
mellowpenguins  Are you serious. NBME strikes again with shitty formatting. +  
yex  OMG!! Now I just realized that. Super confused and also thought onset of age was 36. :-/ +1  
monkey  what is 36 supposed to be? +  
thomasburton  Think the number of people in that group +1  
paulkarr  Yup...was looking at it for a good 3 min before just doing the "fuck it..it's gotta be 99" +  


submitted by usmleuser007(136),
1. Aortic Diastolic Pressure 1. High TPR = high DP 2. High HR = high DP 3. High SV = high DP 2. Aortic Systolic Pressure 1. High Contractility = high SP 2. High SV = high SP 3. Low Compliance = high SP
yex  https://cvphysiology.com/Microcirculation/M012 This helps somehow, the first part about capillary pressure. +  
usmlelol  that's the exp part:: The average capillary hydrostatic pressure is determined by arterial and venous pressures (PA and PV), and by the ratio of post-to-precapillary resistances (RV/RA). An increase in either arterial or venous pressure will increase capillary pressure; however, a given change in PA is only about one-fifth as effective in changing PC as the same absolute change in PV. Because venous resistance is relatively low, changes in PV are readily transmitted back to the capillary, and conversely, because arterial resistance is relatively high, changes in PA are poorly transmitted downstream to the capillary. +  


submitted by mousie(88),

Can someone please explain this to me? I don't understand why starting the other drug would not count as exclusion criteria?

seagull  This has to do with Intention-to-treat analysis. Essentially, when participants are non-adherent but the data shouldn't be lost. They just undergo another statistical model to account for their changes. Here is a nice video https://www.youtube.com/watch?v=Kps3VzbykFQ&t=7s +7  
dr.xx  Where does the question mention "intention-to-treat"? +  
notadoctor  They seem to be pretty obsessed with "intention-to-treat" it's been asked in one way or another in all the new NBMEs that I've done. (Haven't done 24 as yet) +4  
wutuwantbruv  They don't, intention-to-treat is just the best way to go about it @dr.xx +  
smc213  Great for ITT: https://www.youtube.com/watch?v=Kps3VzbykFQ +  
yex  I agree with @notadoctor !! +  
ergogenic22  i think if it were per protocol, both groups would be excluded, the ones that were inconsistent, the ones that dropped out, and the ones that switched. But answer choices only allow ITT or exclusion of one group. +  


submitted by whossayin(8),

the question was very poorly worded in my opinion, anybody else agree?

niboonsh  yea it was a dumbass question, whoever is writing these questions is undoubtedly a crazy genius but homeboy (or homegirl...homeperson?) needs a few grammar lessons. +1  
yex  I agree. We know that it is a teratogen, but how does that question directs you to think about teratogenic effects instead of something physiologic? +2  
dr_jan_itor  The questions in the NBMEs by default are reject questions. So highly selective to be awful questsions. I am recieving regular heads up that the stems on the real thing lately are like 10-12 lines long. So these questions are not anywhere near like the test. NBME has f'd us good for this particular round of practice forms. +  


submitted by jotajota94(10),

Use the Hardy-Weinberg equation

  1. Take the square root of 1/1600, and that will give you the frequency of the recessive allele = 1/40.
  2. Calculate the frequency of the dominant allele with p+q=1, which is p= 0.975.
  3. They are telling you to calculate the frequency of the disease carriers, which is with the equation 2pq.
  4. They want only the disease carriers in which deletion is present. To calculate this, use the q value (1/40) and multiply by 80% in this should give you 0.02.
  5. Finally, calculate for 2Pq 2 (0.975)(0.02)= 0.04 = 1/25.
yex  Nice! ...and we are supposed to read the stem and do all this in a minute or so? :-/ +3  
charcot_bouchard  Allele frequency 1/40. so carrier freq 1/20. 80% of 1/20 is 1/25 (80/100 x 1/20) +5  
dickass  Ah feck, 2pq got me +  


Can somebody please explain why the pKa has to be 6 instead of 10?

masonkingcobra  Since an ionized form is charged (by definition), it will not easily cross a nonpolar lipid membrane. Thus, it is important to recognize the potential of the drug to ionize in order to predict its solubility and the degree to which it can be reabsorbed. The degree of ionization is determined by the drug’s pKa and the pH of its environment. Weak acids and bases are 50% ionized and 50% unionized when the surrounding pH equals the drug’s pKa. At 2 pH units above or below the pKa of the drug, nearly 100% of the drug is ionized or unionized. +3  
masonkingcobra  Basically weak acids are best excreted in alkaline urine, but weak bases are excreted more readily in acid urine. +  
masonkingcobra  In summary, because this is a weak acid at pKa 6, making the urine alkaline will result it its ionization and excretion. Ionized cant move through lipid membranes so can't get reabsorbed and is pissed out. +2  
yex  Following on masonkingcobra explanation: A pKa 4-9 can be either weak acid or base. Weak acid pKa 4-7; strong acid pKa 1-3 Weak base pKa 7-9; strong base pKa above 9 Differents pHs: stomach: 1-2 duodenum: 3-5 early jejunum: 5-7 late jejunum: 7-9 ileum: >9 urine: 4.5-8 Weak acids (pKa) gets absorbed in acidic (pH) environments and cleared in basic. Weak bases gets absorbed in basic environments and cleared in acidic. THIS DOES NOT APPLY TO STRONG BASES OR ACIDS!!!! The best explanation for this is a Biochem lecture from Pass Program and it is available on YouTube, its long but it is for sure worth it!! Look for 19 Biochemistry 1 from Pass Program on YouTube. +1