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 +0  (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 catch-22(14),

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. +1  
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.... :-/ +  


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 +  


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. +1  
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.... :-/ +  


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. +  


submitted by yotsubato(207),

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 +2  
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. 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. +  


submitted by mousie(74),

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 +5  
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) +2  
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 !! +  


submitted by whossayin(2),

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. +  
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? +1  
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? :-/ +1  
charcot_bouchard  Allele frequency 1/40. so carrier freq 1/20. 80% of 1/20 is 1/25 (80/100 x 1/20) +2  


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. +1  
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. +1  
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