NBME 11 question

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Master Deep

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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!

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why do mitochondria encode their own tRNA?
a- cannot important proteins or RNA
b - produce large amts of reactive O2species
c - use a non stndard genetic code
d - unusually high mitochondrial pH denatures nuclear encoded tRNA
e - unusually low mitoc. pH hydrolyzes nyclear encoded tRNA...

i thought it was e.. but its not.. and i really have no idea.. is it a?
 
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oh jeez.. thanks. haha. i need to read better.

A good thing to look for is the location of the injury. If the Median n is lesioned past/at the wrist, you only have sensory loss. So in Carpel Tunnel for example, patients won't have Ape Hand or Hand of Benediction, because the Median n and the Recurrent branch are sparred. Honestly, from what I hear the brachial plexus questions aren't as in depth on the real exam. You pretty much have to be able to ID the nerves on an image, and know the main branches.
 
i cant figure this one out...
cough suppresant drug X is copared to codeine with the following results.
characteristic codeine drug X
cough suppresion ++++ +++
analgesia +++ minimal
constipation +++ minimal
abuse potential ++ +

drug x most closely resembles:

a = chlorpheniramine
b - dextromethorphan
c - guaifenesin
d - meperidine
e - phenylephrine

c is an expectorant, not cough suppressor.. the only cough suppresor on the list is b but i thought that has decent abuse potential...?


i think that it is b

it is the only cough supressant of the drugs listed (if not someone please let me know which other ones are), and they're acknowledging its abuse potential by giving it a + instead of a 'minimal', which is probably about right for that sweet sweet sizzurp
 
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why do mitochondria encode their own tRNA?
a- cannot important proteins or RNA
b - produce large amounts of reactive oxygen species
c - use a non stndard genetic code
d - unusually high mitochondrial pH denatures nuclear encoded tRNA
e - unusually low mitoc. pH hydrolyzes nyclear encoded tRNA...

i thought it was e.. but its not.. and i really have no idea.. is it a?

They have there own tRNA, with different genetic codons and a different genetic code.
 
They have there own tRNA, with different genetic codons and a different genetic code.
thanks!!

another ones...
on review of data, statisticlaly fewer death among drug X subjects in subgroup of nontransmural MI than in placebo group. a retrospective assessment of database for drug X supported the obserbation. most approrpiate next step.?

a - cross sectional populationstudy of Drug X vs placebo after nontrasnmural MI
b - prospective randomized controlled study of drug x vs placebo after non transmural MI
c - tx of all pts with drug X after MI
d - tx of only pts with nontransmural MI with drug X
e - tx of only pts with transmural MI with drug X

i eliminated C and E.. and thought D bc the retrospective assessment supported the conclusion.. but thats wrong.. so it is b?
 
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thanks!!

another ones...
randomized cohor study of drug X for MI found there was no decrese in mortlaity conpared to placebo , but on review of data, statisticlaly fewer death among drug X subjects in subgroup of nontransmural MI than in placebo group. a retrospective assessment of database for drug X supported the obserbation. which of the following is the most approrpiate next step.

a - cross sectional populationstudy of Drug X vs placebo after nontrasnmural MI
b - prospective randomized controlled study of drug x vs placebo after non transmural MI
c - tx of all pts with drug X after MI
d - tx of only pts with nontransmural MI with drug X
e - tx of only pts with transmural MI with drug X

i eliminated C and E.. and thought D bc the retrospective assessment supported the conclusion.. but thats wrong.. so it is b?[/QUOTE]
you guys are awesome. thanks for the help!

18 yr old brought to ER in rural illinois bc of fever, confusion, right arm weakness for 8 hours. sx began with tingling and numbness 2 days ago. temperature si 40C. nothing on physical exam. lumbur puncrture showed
glucose 58
protein 50
leuukocyte 28/mm3
lymphocytes 93%
erythrocyte count 3/mm3

mri of brain shows nothing. oriented to person but not to place or time. during next 4 days, confusion progresses and he develops hypersalivation and respiratory failure. continutes to deteriorate despite intubation. dies 4 days later. which of the following animals is the most likely source of this pts infection?
a - bat
b - cat
c-cow
d- dog
e - sheep..


it sorta sounded like rabies but that was fast! so i thought too fast for rabies and picked sheep.... *shrug* that ws wrong..
 
I want to say rabies. Depends on where he got bit. If he got bit on the triangle of death he is f'd. Bat would be the most common source.

Plus it isn't meningitis so the cow (listeria) can be ruled out.
Cat gives the bartonella so that should cause more than lymph issues.
 
4 yr old with pain in r ear and red, opaque bulging tympanic membrane ---> strep pneumoniae?

50yr old woman with night sweats and feeling of intense hear on trunk and face. pelvix exam: atrophic vaginal mucosa and pap smear w\shows increase in parabasal epithelial cells with no dysplasia. due to decreased production of? ---> is it steroid hormones by ovarian follicles?
(hmm must be.. i just now read the RR chp on female repro disorders)
 
4 yr old with pain in r ear and red, opaque bulging tympanic membrane ---> strep pneumoniae?

50yr old woman with night sweats and feeling of intense hear on trunk and face. pelvix exam: atrophic vaginal mucosa and pap smear w\shows increase in parabasal epithelial cells with no dysplasia. due to decreased production of? ---> is it steroid hormones by ovarian follicles?
(hmm must be.. i just now read the RR chp on female repro disorders)

otitis media is most commonly caused by strep pneumo

menopause
 
For recurrent Neisseria infection I put complement deficiency - I didn't get that one in my "wrong" answers so I'm assuming it was right. Even if African American you can't simply assume sickle cell without other symptoms (recurrent acute attacks of pain in bone due to infarctions, frontal bossing, etc).


can anyone explain why he has recurrent neisseria infections? i know recurrent neiserria think C5-C9, MAC, deficiency and petechia +prupura = complement def... is it just that their is no choice to MAC def?
 
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drug X added to muscle bath containing vascular smooth muscle precontracted to 5g of tension. effects of drug x and others on the force of muscle contraction are shown:
force before X force after X
drug vehicle 5.0 4.9
norepi 15.1 6.8
isoproterenol 0.5 0.6
phenylephrine 13.0 5.5
and they ask which of the following drugs is most likely to produce effects similar to those of drug X?
a- albuterol
b- atropine
c-methoxamine
d-prazosin
e- propranolol

so its not like norepi ad phenyephrine which are alpha agonists mostly... so that eliminates methoxamine..... but then im not sure where to go? it seems most like isoproterenol which is a beta agonist.. so is the answer albuterol?
 
also cleft lip is due to failure of fusion of maxillary and nasal prominences? if so.. can someone tell me what the frontonasal prominence is? is it just a precursor that then leads to medial and lateral nasal prominences? thanks!
 
the question about drug X with spare receptors in asbence and presence of 2 diff concentrations of Drug Y which alone has no effect and they show an image of drug x alone with its curve and with a small amt of drug Y which just shifts the curve to the right and 10x more drug Y shifts the curve down.. does that make drug Y a noncompetitibe antagonist? i wsa confused bc the first effect with a small amt of drug Y which shifts it to the right makes it seem like a competitive antagonist. but shfiting it down is a hallmark of noncompetitibe antagonists and thats what is important?
i sometimes feel like i overthink the questions and then think them into weird places and get them wrong
 
the question about drug X with spare receptors in asbence and presence of 2 diff concentrations of Drug Y which alone has no effect and they show an image of drug x alone with its curve and with a small amt of drug Y which just shifts the curve to the right and 10x more drug Y shifts the curve down.. does that make drug Y a noncompetitibe antagonist? i wsa confused bc the first effect with a small amt of drug Y which shifts it to the right makes it seem like a competitive antagonist. but shfiting it down is a hallmark of noncompetitibe antagonists and thats what is important?
i sometimes feel like i overthink the questions and then think them into weird places and get them wrong

i got this one wrong too

The answer is that it is a noncompetitive antagonist in the setting of excess receptor. Since there is excess receptor, the non-competitive antagonist knocking out receptors actually has no effect on the efficacy(vmax), but does decrease the chance of the drug binding the receptor--> decreasing potency. At higher doses it brings the amount of receptor down past excess levels and begins to effect efficacy (vmax).
 
drug X added to muscle bath containing vascular smooth muscle precontracted to 5g of tension. effects of drug x and others on the force of muscle contraction are shown:
force before X force after X
drug vehicle 5.0 4.9
norepi 15.1 6.8
isoproterenol 0.5 0.6
phenylephrine 13.0 5.5
and they ask which of the following drugs is most likely to produce effects similar to those of drug X?
a- albuterol
b- atropine
c-methoxamine
d-prazosin
e- propranolol

so its not like norepi ad phenyephrine which are alpha agonists mostly... so that eliminates methoxamine..... but then im not sure where to go? it seems most like isoproterenol which is a beta agonist.. so is the answer albuterol?

prazosin

basically the vehicle control is telling you that the drug has no effect on smooth muscle by itself (which in an in vitro experiment would be the case for prazosin becasue there is no endogenous signaling going on so inhibitors will have no effect by themselves)

Then it shows you that it inhibits the effects of NE (alpha and beta1), phenylephrine (only alpha), but doesnt' effect isoproteronol (beta only), this tells you that the drug is selective for alpha antagonism-->prazosin


I do not know what methoxamine is
 
prazosin

basically the vehicle control is telling you that the drug has no effect on smooth muscle by itself (which in an in vitro experiment would be the case for prazosin becasue there is no endogenous signaling going on so inhibitors will have no effect by themselves)

Then it shows you that it inhibits the effects of NE (alpha and beta1), phenylephrine (only alpha), but doesnt' effect isoproteronol (beta only), this tells you that the drug is selective for alpha antagonism-->prazosin


I do not know what methoxamine is
methxamine is an alpha 1 agonist...
thanks! that makes sense.. def need to process it for a moment.. never encountered a question like that before..
 
does anyone know the asnwer tothe question were they show the 1 yr old with the 2 day hx of diaper rash, 6 day hx of temperature, swelling of hands and feet. face and lips are red and conjuctivae appear injected. bilateral cervical lymphadenopathy ad S3 gallop with no murmur. edema and erythema on hands and feet.

a- acute arteritis with aneurysms in coronary arteries
b - epidermal hyerplasia with epidermal microabscesses and parakeratosis
c- granulomas with caseous necrosis and cervical LN's
d - granulomatous arteritis in cervical and temporal arteries
e - paracortical lymphoid hyerplasia with eosinophilic intranucelar inclusions in perihilar LN's

i can tell you its not e..
 
i just want to say thank you guys for your help!!! i dont have any other questions from NBME 11 apart from the ones posted.. i really appreciate it and would love to be of as much help as i can be
 
does anyone know the asnwer tothe question were they show the 1 yr old with the 2 day hx of diaper rash, 6 day hx of temperature, swelling of hands and feet. face and lips are red and conjuctivae appear injected. bilateral cervical lymphadenopathy ad S3 gallop with no murmur. edema and erythema on hands and feet.

a- acute arteritis with aneurysms in coronary arteries
b - epidermal hyerplasia with epidermal microabscesses and parakeratosis
c- granulomas with caseous necrosis and cervical LN's
d - granulomatous arteritis in cervical and temporal arteries
e - paracortical lymphoid hyerplasia with eosinophilic intranucelar inclusions in perihilar LN's

i can tell you its not e..


kawasaki's. glad to help out and definitely thankful for those that answered my questions as well.
 
does anyone know the asnwer tothe question were they show the 1 yr old with the 2 day hx of diaper rash, 6 day hx of temperature, swelling of hands and feet. face and lips are red and conjuctivae appear injected. bilateral cervical lymphadenopathy ad S3 gallop with no murmur. edema and erythema on hands and feet.

a- acute arteritis with aneurysms in coronary arteries
b - epidermal hyerplasia with epidermal microabscesses and parakeratosis
c- granulomas with caseous necrosis and cervical LN's
d - granulomatous arteritis in cervical and temporal arteries
e - paracortical lymphoid hyerplasia with eosinophilic intranucelar inclusions in perihilar LN's

i can tell you its not e..

Yah, it's A. With questions like this, I think it's good practice to try to know what the other choices are describing so you can be familiar with them in case you see a different question stem but the same his to description.

A- Kawasaki's B- Verrucae/HPV C - TB D- Temporal Arteritis....

But do you guys know what E is describing? Is it CMV, EBV or HSV?
 
Yah, it's A. With questions like this, I think it's good practice to try to know what the other choices are describing so you can be familiar with them in case you see a different question stem but the same his to description.

A- Kawasaki's B- Verrucae/HPV C - TB D- Temporal Arteritis....

But do you guys know what E is describing? Is it CMV, EBV or HSV?
i think e is CMV maybe?
 
Yah, it's A. With questions like this, I think it's good practice to try to know what the other choices are describing so you can be familiar with them in case you see a different question stem but the same his to description.

A- Kawasaki's B- Verrucae/HPV C - TB D- Temporal Arteritis....

But do you guys know what E is describing? Is it CMV, EBV or HSV?


good call, but I think that B is psoriasis, hpv would have 'koilocytic atypia' or perinuclear halos or something like that

not sure about e, of the herpesviruses it is definitely CMV, hsv is in neurons and ebv is in b cells (would be in cortex not paracortex)
 
good call, but I think that B is psoriasis, hpv would have 'koilocytic atypia' or perinuclear halos or something like that

not sure about e, of the herpesviruses it is definitely CMV, hsv is in neurons and ebv is in b cells (would be in cortex not paracortex)

Oops, you are definitely correct about it being Psoriasis. I read it kind of quickly and for some reason must have thought it said koilocytosis, not parakeratosis. :confused:
 
can anyone explain why he has recurrent neisseria infections? i know recurrent neiserria think C5-C9, MAC, deficiency and petechia +prupura = complement def... is it just that their is no choice to MAC def?


wow i am totally losing it.. i was thinking about coagulation factors.. jeez.. i dont know why. feel like an idiot.. all this studying i guess is gettting to me...
 
wow i am totally losing it.. i was thinking about coagulation factors.. jeez.. i dont know why. feel like an idiot.. all this studying i guess is gettting to me...

Sounds like you need to step away from the books and take a half day off or maybe even full day off. Sometimes it's more productive to do so, and your brain and body will thank you for it later by functioning better. I know it's hard because no matter what we always feel behind, but it truly helps to do so sometimes.
 
I have a question if someone can answer please:

Q. Someone who has major depression is given Nortripytiline and has sub therapeutic levels and the drug is hepatically metabolized by the P450 system.

Ans choices:

a) Induction of CYP2D6 of nortripytiline
b) Inheritance of an inactive CYP2D6 locus
C) Inhibition of CYP2D5 of nortripyline
D) Inheritance of 2 inactive CYP2D6 alleles
e) Pharmacodynamic Tolerance

answer A is NOT correct because I chose that - anybody else?

Thank you everyone for this thread!
 
id love to take a half day off but i am 10 days away from step 1!! :( but i def get more loopy in the evenings. i get to the library at 7am.. and after like 4pm im a little disjointed.
 
I have a question if someone can answer please:

Q. Someone who has major depression is given Nortripytiline and has sub therapeutic levels and the drug is hepatically metabolized by the P450 system.

Ans choices:

a) Induction of CYP2D6 of nortripytiline
b) Inheritance of an inactive CYP2D6 locus
C) Inhibition of CYP2D5 of nortripyline
D) Inheritance of 2 inactive CYP2D6 alleles
e) Pharmacodynamic Tolerance

answer A is NOT correct because I chose that - anybody else?

Thank you everyone for this thread!
You're leaving out the pivotal points and making this impossible for us to answer: he was on the max dose for like 2 months and had blood levels <30% of lower end of normal. The max dose wouldn't be the max dose if induction of a P450 enzyme made it ineffective or there was significant tolerance (in the normal population). He's obviously got an inherited defect which is increasing the clearance.

Answer B should read: inheritance of 1 *amplified* locus and is the correct answer. (It is a gain of function mutation and thus would exhibit an autosomal dominant inheritance pattern.)

(You could imagine a variation on this question in which some drug's active metabolite does not reach therapeutic levels due to two inactivated alleles.)
 
You're leaving out the pivotal points and making this impossible for us to answer: he was on the max dose for like 2 months and had blood levels <30% of lower end of normal. The max dose wouldn't be the max dose if induction of a P450 enzyme made it ineffective or there was significant tolerance (in the normal population). He's obviously got an inherited defect which is increasing the clearance.

Answer B should read: inheritance of 1 *amplified* locus and is the correct answer. (It is a gain of function mutation and thus would exhibit an autosomal dominant inheritance pattern.)

(You could imagine a variation on this question in which some drug's active metabolite does not reach therapeutic levels due to two inactivated alleles.)
i knew the answer choices sounded weird...
shouldnt D read inheritance of 2 amplified alleles?
 
You're leaving out the pivotal points and making this impossible for us to answer: he was on the max dose for like 2 months and had blood levels <30% of lower end of normal. The max dose wouldn't be the max dose if induction of a P450 enzyme made it ineffective or there was significant tolerance (in the normal population). He's obviously got an inherited defect which is increasing the clearance.

Answer B should read: inheritance of 1 *amplified* locus and is the correct answer. (It is a gain of function mutation and thus would exhibit an autosomal dominant inheritance pattern.)

I apologize for the inaccuracy. Thank you for your reply.
 
I apologize for the inaccuracy. Thank you for your reply.
No way, don't be sorry. I'm just trying to help, my bad if it sounded snappy.

You need to know literally NOTHING about P450 or TCAs to answer this Q. I was trying to draw your attention to the only relevant parts (e.g., the parts you left out :)). Whenever you're totally unsure about a question, I suggest re-reading the stem and writing down the salient points. There are lots and lots of "reasoning" problems on NBMEs that can totally throw you off if you hone in on details such as the number of the P450 enzyme.
 
There are lots and lots of "reasoning" problems on NBMEs that can totally throw you off if you hone in on details such as the number of the P450 enzyme.

You are right. I really appreciate the advise. I do get bogged down by details and nerves...thank you.
 
B) For Multiple Myeloma pts with accompanying renal deficiency, would you have increased renal phosphorus? If so, would that increase your PTH to increase secretion (or is it decreased due to hypercalcemia)?


Thank you!

Renal deficiency means no 1a hydroxylase activity (so decreased Vit D, and increased PTH trying to activate Vitamin D) and no phosphate elimination (@ the PCT via Na/PO4- exchange if you recall)

So the PRIMARY defects are INCREASED PHOSPHATE and DECREASED VITAMIN D

The secondary defects are decreased calcium (due to decreased Vitamin D) and increased PTH (to try to offset the decreased calcium and Vit D)

A 4 yo girl with a burn on her finger brought to the ER has a fluid filled blister, what causes the INITIAL re-epithialization in healing?

A) Basal layer keratinocytes
b) dermal dendritic cells
C) fibroblasts
D) epithelial Langerhans cells
E) macrophages

The answer is A. I am not very eloquent, but just think of what choice A is describing and the layers of the epidermis.
 
Can someone please help em with this question?

A 3 week old newborn has a mobile mass in the epigastrium to the right of the midline. (I am thinking it is a pyloric atresia). If the condition has a lower threshold of liability in males than in females, which of the following relatives is at highest risk?

Brother, if newborn is F
Brother, if baby is M
Sister is newborn is F
Sister if newborn is male
Fraternal male twin, if newborn is male.

I chose B, but I am thinking that is must be A???? Am I right??
 
Can someone please help em with this question?

A 3 week old newborn has a mobile mass in the epigastrium to the right of the midline. (I am thinking it is a pyloric atresia). If the condition has a lower threshold of liability in males than in females, which of the following relatives is at highest risk?

Brother, if newborn is F
Brother, if baby is M
Sister is newborn is F
Sister if newborn is male
Fraternal male twin, if newborn is male.

I chose B, but I am thinking that is must be A???? Am I right??

I think I put A for this one and got it right. What the question is saying is that pyloric stenosis is more common in boys, so which person would be at the highest risk. If the baby is a girl, then her brother would have a higher risk than her. it is an odd question though and I think the wording of the answers might have gotten it thrown out/into the nbme pile because in reality her living brother would have either already had it or not developed it but..:shrug:
 
I think I put A for this one and got it right. What the question is saying is that pyloric stenosis is more common in boys, so which person would be at the highest risk. If the baby is a girl, then her brother would have a higher risk than her. it is an odd question though and I think the wording of the answers might have gotten it thrown out/into the nbme pile because in reality her living brother would have either already had it or not developed it but..:shrug:

Yeah that was a crap question. I just picked C because I literally had no clue what to put for it.
 
Can someone please help em with this question?

A 3 week old newborn has a mobile mass in the epigastrium to the right of the midline. (I am thinking it is a pyloric atresia). If the condition has a lower threshold of liability in males than in females, which of the following relatives is at highest risk?

Brother, if newborn is F
Brother, if baby is M
Sister is newborn is F
Sister if newborn is male
Fraternal male twin, if newborn is male.

I chose B, but I am thinking that is must be A???? Am I right??

I believe it's A because pyloric stenosis has a higher incidence in 1st born males.
 
I believe it's A because pyloric stenosis has a higher incidence in 1st born males.
Yes, the defect has an easier time being expressed in males. Thus for it to be expressed in a female = very "strong genetics" for CPS, and subsequent male children will have a higher likelihood than if it had first been diagnosed in a male child.
 
that question was so horribly worded. thanks for the answer tho guys! i got it wrong bc i chose C and thought that the correct answer needed to be B upon review but A makes sense now tha ti understand what the hell they were asking really.
 
What about block 2 Q29
26 y/o male- fever/cough/chest pain/malaise 2 weeks. Went to central Cali. Has eosinophillia. Culture of sputum shows mold(shows a pic of culture)
A israelli
coccidio
histoplasma
legionelle
TB
nocardia
staph
strep
i wanted coccidio but the sputum didnt match....
 
What about block 2 Q29
26 y/o male- fever/cough/chest pain/malaise 2 weeks. Went to central Cali. Has eosinophillia. Culture of sputum shows mold(shows a pic of culture)
A israelli
coccidio
histoplasma
legionelle
TB
nocardia
staph
strep
i wanted coccidio but the sputum didnt match....


It is cocciodiodes

The question stem said "in culture" which would mean the mold form.

The mold form of Cocciodiodes is "box car like hyphae"
 
What about block 2 Q29
26 y/o male- fever/cough/chest pain/malaise 2 weeks. Went to central Cali. Has eosinophillia. Culture of sputum shows mold(shows a pic of culture)
A israelli
coccidio
histoplasma
legionelle
TB
nocardia
staph
strep
i wanted coccidio but the sputum didnt match....

Everytime i see california and pulmonary mycoses, i think coccidio. I have yet to be ****ed by that. (knock on wood)
 
Also, California is *always* a hint for Coccidio

yep Earthquakes send the spores flying into the air.


The only slightly tricky one is Histoplasmosis and Blastomyces.

Their geographic regions slightly overlap

but the rest of the clues should give it away.
 
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