NBME 11 question

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.

Master Deep

Full Member
15+ Year Member
Joined
May 16, 2008
Messages
154
Reaction score
1
Can anyone whos done NBME 11 explain how to figure out the serum protein electrophoresis question. 12 yr old boy admitted to hospital because of lethary, hip pain and fever. hes been admitted many times becaues of pneumonia. And then it gives the diff kinds of serum protein electrophoresis.
Thanks!

Members don't see this ad.
 
Some questions that weren't answered:

what type of collagen is defective in EDS?

what cellular changes do you see in Type 1 DM vs Type 2?

and what biochemical pathway is tetrahydroptersomething involved in?!

thanks in advance!

(edited for vagueness)
 
Last edited:
Some questions that weren't answered:

3 y/o boy w/ easy bruising, scarring, hyper flexible joints:
-aberrant production of elastin
-abnl synth of extracellular glycoprotein (wrong)
-defect in synth of fibrillar collagen

this is ehler's danlos, so is it fibrillar collagen?

T3 collagen is fibrillar collagen

6 y/o girl presenting w/ DKA basically, type 1 Dm. bx of pancreas shows:
-cellular nec and lymphocytes
-decrease in mass and amyloid deposition (wrong)
-marked atrophy and fibrosis

cellular necrosis and lymphocytes; T1 DM is basically autoimmune, so that's the only one that fits.

increased serum phe, decreased brain conc of serotonin, dopamine; defect in:
biotin
glutamate (wrong)
NADH
tetrahydropterin
b12

thanks in advance!

tetrahydropterin -> defect in tryptophan and tyrosine metabolism.
 
This is probably a really dumb question, but do T cells ever play a role in the vaccine response? I got the Polio vaccine question wrong (Sabin/Salk), where it basically asked what the common feature of the 2 vaccines are, and options had to do with:
- activated CD8 cytotoxic T lymhocyte effectors
- CD8 memory T lymphocytes
- neutralizing antibodies

Is it ever the case that CD8 T cells participate in developing immunity and memory? (Partly, I was just thinking viruses=T cells, bacteria=B cells that led me to the wrong answer)
 
Members don't see this ad :)
The 45y F with 2mo history of fatigue, bone pain, weight loss... 4mo history of renal insufficiency... presenting with pallor and 2+ pitting edema. Lab confirms anemia and declining renal function. Bone x-ray shows widened osteoid seams and subperiosteal erosions.

First Q: is this renal osteodystrophy (kidney failure -> mineral imbalance -> bone issues) and therefore...
- Calcitriol - low
- Calcium - low
- Phosphate - high (because of renal dysfunction)
- PTH - high
??

Second Q: this is more likely renal osteodystrophy rather than multiple myeloma just because "widened osteoid seams" is suggestive of osteomalacia, not the "punched out lesions"? and the anemia is simply due to decreased erythropoietin?
 
What's everyone's opinion on NBME 11? Hard or easy? Is it still relevant to current Step 1 subject trends and score prediction?

I ask because I scored a 245 today after taking it. I scored around a 215 a month ago when I took my school's CBSE, but have since studied every subject except endocrine, repro and neuro. I assumed my score would go up, but I was quite shocked to see a 30 point jump when I have still yet to study those 3 very large subjects and hammer the fine details.
 
-- type 2 DM pt w/ chronic kidney failure, taking glipizide; Cr clearance is 20% of normal; lvls of Ca, PO4, PTH?

I thought (-) Ca, (-) PO4 ('cuz of hypovitamin D), (+) PTH... but this is wrong; is it (-) Ca, (+) PO4, (+) PTH ?

lower Ca, higher PO4 and high PTH. Increased PO4 because of the renal failure. PTH acts on the kidneys to decrease PO4 via increasing PO4 secretion. So without the kidneys and without Ca2+ to bind it up PO4 increases in the serum.
 
Question on Malaria that doesn't seem to be answered:

18 y/o boy develops a fever after returning to Wisconsin from a trip to India, took no prophylaxis. Got Malaria (P.vivax), takes Chloroquine, symptoms clear up but they return in 6 months. Why?

A) Activation of Exoerythrocytic forms - Dormant forms in the Liver? (What I think it is now)
B) Dual infection w/ P.falciparum
C) Poor compliance with Antimicrobial therapy (wrong)
D) Reinfection
E) Resistance to Chloroquine
 
Question on Malaria that doesn't seem to be answered:

18 y/o boy develops a fever after returning to Wisconsin from a trip to India, took no prophylaxis. Got Malaria (P.vivax), takes Chloroquine, symptoms clear up but they return in 6 months. Why?

A) Activation of Exoerythrocytic forms - Dormant forms in the Liver? (What I think it is now)
B) Dual infection w/ P.falciparum
C) Poor compliance with Antimicrobial therapy (wrong)
D) Reinfection
E) Resistance to Chloroquine
It's A for the reason stated
 
  • Like
Reactions: 1 user
Top