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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Anyone mind answering these two for me?

34.
A previously healthy 55-year-old woman comes to the physician because of the gradual onset of fever, fatigue, and pain in her muscles and joints during the past 3 weeks; she has had a 3.6-kg (8-lb) weight loss during this period. She does not smoke cigarettes, drink alcohol, or use illicit drugs. She takes no medications. Her temperature is 38.2°C (100.8°F), pulse is 90/min, and blood pressure is 140/95 mm Hg. Examination of the trunk and extremities shows areas of raised, reticular, cyanotic discoloration consistent with livedo reticularis. There is left footdrop. Laboratory studies show:

Erythrocyte sedimentation rate 110 mm/h
Urine
Blood 2+
Protein 2+
RBC casts present

Serum test results are positive for perinuclear antineutrophil cytoplasmic antibodies. Which of the following is the most likely diagnosis?

A Allergic interstitial nephritis
B Antiphospholipid antibody syndrome
C IgA nephropathy
D Occult neoplasm
E Vasculitis


36.
A 50-year-old man comes to the physician for a follow-up examination. He has been receiving nortriptyline twice daily for major depressive disorder. The dosage of his medication was doubled from once to twice daily 2 months ago because the initial dosage was ineffective. At this visit, the patient tells the physician that his symptoms have not improved. Mental status examination shows a flat affect. Laboratory studies show a plasma nortriptyline concentration 30% of the lower end of the normal range. Nortriptyline is eliminated mainly by hepatic metabolism catalyzed by the cytochrome P450 2D6 (CYP2D6). Which of the following best explains the patient's lack of clinical response?

A Induction of CYP2D6 by nortriptyline
B Inheritance of an amplified CYP2D6 locus
C Inheritance of two inactive CYP2D6 alleles
D Inhibition of CYP2D6 by nortriptyline
E Pharmacodynamic tolerance

 
Anyone mind answering these two for me?

34.
A previously healthy 55-year-old woman comes to the physician because of the gradual onset of fever, fatigue, and pain in her muscles and joints during the past 3 weeks; she has had a 3.6-kg (8-lb) weight loss during this period. She does not smoke cigarettes, drink alcohol, or use illicit drugs. She takes no medications. Her temperature is 38.2°C (100.8°F), pulse is 90/min, and blood pressure is 140/95 mm Hg. Examination of the trunk and extremities shows areas of raised, reticular, cyanotic discoloration consistent with livedo reticularis. There is left footdrop. Laboratory studies show:

Erythrocyte sedimentation rate 110 mm/h
Urine
Blood 2+
Protein 2+
RBC casts present

Serum test results are positive for perinuclear antineutrophil cytoplasmic antibodies. Which of the following is the most likely diagnosis?

A Allergic interstitial nephritis
B Antiphospholipid antibody syndrome
C IgA nephropathy
D Occult neoplasm
E Vasculitis


36.
A 50-year-old man comes to the physician for a follow-up examination. He has been receiving nortriptyline twice daily for major depressive disorder. The dosage of his medication was doubled from once to twice daily 2 months ago because the initial dosage was ineffective. At this visit, the patient tells the physician that his symptoms have not improved. Mental status examination shows a flat affect. Laboratory studies show a plasma nortriptyline concentration 30% of the lower end of the normal range. Nortriptyline is eliminated mainly by hepatic metabolism catalyzed by the cytochrome P450 2D6 (CYP2D6). Which of the following best explains the patient's lack of clinical response?

A Induction of CYP2D6 by nortriptyline
B Inheritance of an amplified CYP2D6 locus
C Inheritance of two inactive CYP2D6 alleles
D Inhibition of CYP2D6 by nortriptyline
E Pharmacodynamic tolerance



First one is Churgg-Strauss syndrome. It has a peripheral neuropathy that manifests as foot/wrist drop, and is one of the p-ANCA vasculitides. It's in FA.

Dude in second one just has a genetic difference, and metabolizes the drug faster. You would see that as well if he were on a P450 inducer, but he isn't, and it doesn't make much sense for a drug to induce its own metabolism mechanism (A).
 
First one is Churgg-Strauss syndrome. It has a peripheral neuropathy that manifests as foot/wrist drop, and is one of the p-ANCA vasculitides. It's in FA.

Dude in second one just has a genetic difference, and metabolizes the drug faster. You would see that as well if he were on a P450 inducer, but he isn't, and it doesn't make much sense for a drug to induce its own metabolism mechanism (A).


Thanks, I got caught up in the second one thinking it might be like Carbamazepine which does actually induce it's own metabolism.
 
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Hey guys,

Kinda really bummed bc I'm not improving much.
Do you think you could help me with these questions?

45 yo guys got shot in his abdomen. 70/40 bp. there's a ct scan shown. laparotomy shows that abdominal cavity is filled with blood. What was damaged?
1. descending colon.
2. left adrenal
3. left kidney.
4. spleen
5. tail of pancreas

65 y.o had abdominal mass. mass had lots of blood vessels. Further analysis shows increased VEGF in the tumor. What stimulated the VEGF?
Decreased endostain
Decreased PCO2
Decreased PO2
Decreased thrombostatin
Increased endostatin
Increased PCO2
Increased PO2
Increased thrombostatin

30 y.o woman has scars on her antecubital fossae and she's in a methadone program. chest xray shows small nodules in perihilar lung fields. What would the biopsy show? Foreign particles surrounded by what?

Granulation tissue ( NOT RIGHT)
Granulomatous inflammation ( i guess this?)
Hemosiderin laden macs
Neutrophils
Proliferated capillaries

30 y.o woman with calcium oxalate renal calculi. 24 hr urine reveals increased [ca]. the physician recommends pharmacotherapy with a drug that decreased urinary calcium concentration. what it the mechanism of action of this drug?

( I though it would be a Loop-no?)

decrease 1,25 dihydroxycholecalciferol synthesis
decrease H+ secretion in distal tubule
decrease Mg reabsorption in TAL
increase Ca reabsorption in distal tubule
icnrease bicarb secretion in proximal tubule
increase phosphate reabsorption in proximal tubule
inhibit parathyroid hormone secretion

lady with a baby with minimal fetal movement. no congenital anomoly family hx. ultrasound shows decreased amniotic fluid and normal sized fetal kidneys but the fetal bladder and ureters bilaterally are markedly distended. fetus is male. what is the abormaluty?
penile hypospadias
placental insuff.
PCKD
posterior urehtral valve
prostatic nodular hyperplasia


What's the difference in the 2 programs ( one with 2200 ppl, one with 1900 ppl) with a success rate difference is statistically significant ( P<.01) ?
Difference due to chance
Distinguished btwn stasitical sig. and practical importance
p value too small
samples size too small.

54 y.o woman with 5 cm coin lesion in right upper lobe of lung. proliferation of irregularly shaped glands with hyperchromatic and pleomorphic nuclei invading the pulmonary parenchyma and lymphovascular spaces.

Adenocarcinoma
Carcinoid tumor
Hamartom
Small cell carcinoma
Squamos cell carcinoma

70 y.o with painless jaundice.dark urine with white stool for 7 days. CT shows poorly defined soft tissue density in head of pancrease. What is cause of jaundice?
Cholelithiasis
common bile duct obstruction
liver met.
pancreatic duct obstruction ( not this one :( )
porta hepatitis met.

young girl with burn on finger. it formed a blister. when the blister resolves, epithelium forms at the base. what is involved in re-epitherliazation of blister?

basal layer keratinocytes
dermal dendritic cells
epitherlial langerhans
fibroblasts
macs.

25 y.o. pilot is 3 days w/o good. "Adipocytes play an important role in maintainign homeostasis in this woman b/c which of the following effects."?

glucagon activates glycerol utilization as a source of carbon for gluconeogensis by adipocytes?
glucagon activated glycogen mobilization to form free glucose.
glucagon activates hormone sesntive lipase
insulin activates free acid synth.
insulin activates hepatic lipoprotein lipase.

what in the world do adipocytes have to do with glucagon? i thought glucagon only effectd the liver?


44 y.o woman with new symptoms of numbess over the right thenar eminence. percussion of the area btwn the flexor carpi radialis and palmaris longus tendons at the distal palmar wrist crease produces a painful shock-lick sensation radiating into the affect area of palm. what nerve was injured in surgery?
dorsal sensory branch of ulnar
lateral cutanous nerve of forearm
palamar cutaneous branch of median
recurrent motor brnach of median ( WHY NOT THIS ONE? :( )
sensory branch of radial nerve.


i know it's super long but it's only 1 week till my test and I can't believe I got these wrong and don't know the right answer. :(
 
Hey guys,

Kinda really bummed bc I'm not improving much.
Do you think you could help me with these questions?

45 yo guys got shot in his abdomen. 70/40 bp. there's a ct scan shown. laparotomy shows that abdominal cavity is filled with blood. What was damaged?
1. descending colon.
2. left adrenal
3. left kidney.
4. spleen (you can see the bullet in the spleen)
5. tail of pancreas

65 y.o had abdominal mass. mass had lots of blood vessels. Further analysis shows increased VEGF in the tumor. What stimulated the VEGF?
Decreased endostain
Decreased PCO2
Decreased PO2 (HIF regulates VEGF)
Decreased thrombostatin
Increased endostatin
Increased PCO2
Increased PO2
Increased thrombostatin

30 y.o woman has scars on her antecubital fossae and she's in a methadone program. chest xray shows small nodules in perihilar lung fields. What would the biopsy show? Foreign particles surrounded by what?

Granulation tissue ( NOT RIGHT)
Granulomatous inflammation
Hemosiderin laden macs
Neutrophils
Proliferated capillaries

30 y.o woman with calcium oxalate renal calculi. 24 hr urine reveals increased [ca]. the physician recommends pharmacotherapy with a drug that decreased urinary calcium concentration. what it the mechanism of action of this drug?

( I though it would be a Loop-no?)

decrease 1,25 dihydroxycholecalciferol synthesis
decrease H+ secretion in distal tubule
decrease Mg reabsorption in TAL
increase Ca reabsorption in distal tubule (HCTZ)
icnrease bicarb secretion in proximal tubule
increase phosphate reabsorption in proximal tubule
inhibit parathyroid hormone secretion

lady with a baby with minimal fetal movement. no congenital anomoly family hx. ultrasound shows decreased amniotic fluid and normal sized fetal kidneys but the fetal bladder and ureters bilaterally are markedly distended. fetus is male. what is the abormaluty?
penile hypospadias
placental insuff.
PCKD
posterior urehtral valve
prostatic nodular hyperplasia


What's the difference in the 2 programs ( one with 2200 ppl, one with 1900 ppl) with a success rate difference is statistically significant ( P<.01) ?
Difference due to chance (p < 0.05 so it's not chance)
Distinguished btwn stasitical sig. and practical importance
p value too small (this would be better)
samples size too small. (the N is huge)

54 y.o woman with 5 cm coin lesion in right upper lobe of lung. proliferation of irregularly shaped glands with hyperchromatic and pleomorphic nuclei invading the pulmonary parenchyma and lymphovascular spaces.

Adenocarcinoma (pretty sure this was the answer, can someone else confirm?)
Carcinoid tumor
Hamartom
Small cell carcinoma
Squamos cell carcinoma

70 y.o with painless jaundice.dark urine with white stool for 7 days. CT shows poorly defined soft tissue density in head of pancrease. What is cause of jaundice?
Cholelithiasis
common bile duct obstruction (the tumor is squeezing it shut, may also present with courvoisier sign)
liver met.
pancreatic duct obstruction ( not this one :( )
porta hepatitis met.

young girl with burn on finger. it formed a blister. when the blister resolves, epithelium forms at the base. what is involved in re-epitherliazation of blister?

basal layer keratinocytes
(epithelial stem cells)
dermal dendritic cells
epitherlial langerhans
fibroblasts
macs.

25 y.o. pilot is 3 days w/o good. "Adipocytes play an important role in maintainign homeostasis in this woman b/c which of the following effects."?

glucagon activates glycerol utilization as a source of carbon for gluconeogensis by adipocytes?
glucagon activated glycogen mobilization to form free glucose.
glucagon activates hormone sesntive lipase
insulin activates free acid synth.
insulin activates hepatic lipoprotein lipase.

what in the world do adipocytes have to do with glucagon? i thought glucagon only effectd the liver?


44 y.o woman with new symptoms of numbess over the right thenar eminence. percussion of the area btwn the flexor carpi radialis and palmaris longus tendons at the distal palmar wrist crease produces a painful shock-lick sensation radiating into the affect area of palm. what nerve was injured in surgery?
dorsal sensory branch of ulnar
lateral cutanous nerve of forearm
palamar cutaneous branch of median (it's a sensory deficit)
recurrent motor brnach of median ( WHY NOT THIS ONE? :( )
sensory branch of radial nerve.


i know it's super long but it's only 1 week till my test and I can't believe I got these wrong and don't know the right answer. :(

Pretty sure these are all correct.
 
Pretty sure these are all correct.


Thank you SO much! I appreciate it.

I can't believe I got some of these wrong. I feel so F*cking stupid sometimes to get stupid stuff wrong! :(
It's like why the hell am I studying so much and then marking dumb stuff on the test.
 
Thank you SO much! I appreciate it.

I can't believe I got some of these wrong. I feel so F*cking stupid sometimes to get stupid stuff wrong! :(
It's like why the hell am I studying so much and then marking dumb stuff on the test.


We all do it. You know the question with the two bell curves that was asking about where the cut off for the test should be? I didn't realize they were bell curves and couldn't figure out why the curves doubles back on themselves. If you can find a stupider mistake than that I will be impressed.
 
Uh, yeah, I made that one too.
I just feel like I can't trust myself now because I wasn't tired or hungry when I was taking it and I was focused. And I thought I was doing sooooo well.

Anyway, thanks again for your help! Good luck to you!
 
Hey guys, how about this one:

A 59 year old man comes to the physician because of a 3-day history of yellow-tinted eyes and intermittent regurgitation of small amounts of blood. He has had progressive fatigue and increased abdominal girth during the past month. Physical exam shows scleral icterus, pale conjunctivae, and a protuberant abdomen. An abdominal fluid wave is palpated. Laboratory studies show:

Hb: 9.8 g/dL
Hct: 29%
MCHC: 28%
MCV: 70

Serum:
Alk phos: 210
AST: 20
ALT: 10

A biopsy specimen from the liver is shown in the photograph, and it wants to know what you'd be most likely to see on upper GI endoscopy:

Esophageal varices
Hemorrhagic gastritis
Hiatial hernia
Mallory-Weiss laceration
Schatzki ring



The photo looks like centrilobular fibrosis, but wtf is with the elevated Alk Phos with normal AST / ALT levels?
 
Hey guys, how about this one:

A 59 year old man comes to the physician because of a 3-day history of yellow-tinted eyes and intermittent regurgitation of small amounts of blood. He has had progressive fatigue and increased abdominal girth during the past month. Physical exam shows scleral icterus, pale conjunctivae, and a protuberant abdomen. An abdominal fluid wave is palpated. Laboratory studies show:

Hb: 9.8 g/dL
Hct: 29%
MCHC: 28%
MCV: 70

Serum:
Alk phos: 210
AST: 20
ALT: 10

A biopsy specimen from the liver is shown in the photograph, and it wants to know what you'd be most likely to see on upper GI endoscopy:

Esophageal varices
Hemorrhagic gastritis
Hiatial hernia
Mallory-Weiss laceration
Schatzki ring



The photo looks like centrilobular fibrosis, but wtf is with the elevated Alk Phos with normal AST / ALT levels?


He's got really bad liver failure, so most likely high portal pressure leading to Esophageal varice.
 
I was also confused by the normal AST/ALT... As for the alk phos; that is normally elevated with hepatic obstructive disease (right?)
 
I was also confused by the normal AST/ALT... As for the alk phos; that is normally elevated with hepatic obstructive disease (right?)


I'm pretty sure if you have cirrhosis following a chronic condition then your ALT and AST wont be elevated. The elevation is only while the damage is actually being done. Please correct me if I'm wrong.
 
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I'm pretty sure if you have cirrhosis following a chronic condition then your ALT and AST wont be elevated. The elevation is only while the damage is actually being done. Please correct me if I'm wrong.

Indeed, biliary obstruction only elevates GGT and alk phos. This patient absolutely did not have biliary obstruction, though, as the correct answer was esophageal varices
 
Question was about the guy who had TB. he tells the physician to not report the disease b.c he might get deported. after emphatizing, what would you do?

i know that TB is a reportable disease but would it be:
-report it to health department and assure patient no other individuals will be notified
-report case to the health department to make sure work site contacts are identified and evaluated

well im guessing its the 2nd one, but was confused b/w the 2 while taking the exam!
 
Ya, its the 2nd one, you can't assure the patient that noone else will be notified. Also, it is the physician's duty to prevent harm to others if possible, so it is important to test the close contacts.
I was stuck on that one for a little bit also.
 
Ya, its the 2nd one, you can't assure the patient that noone else will be notified. Also, it is the physician's duty to prevent harm to others if possible, so it is important to test the close contacts.
I was stuck on that one for a little bit also.

Thanks for the help!
 
nope, the others didn't really fit..serotonin syndrome is right. right off pg. 455 of FA.

yea I mean I got the question right bc nothing else was remotely correct but Selegeline is a MAO-B inhibitor not MAO-A so it is specific for NE metabolism not Seretonin.

edit: ...right?
 
Last edited:
Hey guys, I've got a few questions that I don't understand:

Man w/SOB, fever, and cough. Temp is 101 F and resp 18/min. Cold hemagglutinin test is positive. Interstitial markings are present on the X-ray. What is the infectious agent susceptible to?

A. Amox
B. Azithro
C. Ceftriaxone
D. Gentamicin
E. Piperacillin

(And what is the bug?! I know the cold hemagglutinin test is important, but I don't know what that tells you specifically)


500 workers w/bladder cancer and 200 w/o bladder cancer are selected for a study. Hx obtained of aniline dye exposure. Of the 500 w/bladder cancer, 250 have exposure to aniline dye. Of the 200 w/o bladder cancer, 50 have exposure. What's the odds ratio for exposure variable?

A. 1/3
B. 1/2
C. 1
D. 1.5
E. 2 (not it)
F. 3

I thought 250/500 = .5 and 50/200 = .25 .5/.25 = 2

...Yeah I don't know biostats :(


Last one:
Woman has panic disorder with agoraphobia. Drug prescribed that activates benzo binding site on the GABA receptor. What drug is it?

A. Alprazolam
B. Buspirone
C. Flumazenil
D. Hydroxyzine
E. Ramelteon

Thought it was alprazolam. But changed my mind to buspirone based on the symptoms.

EDIT: I lied.... Two more. Sorry

What effect do trinucleotide repeats cause on transcription of the FMR1 mRNA?
A. Alteration of mRNA splicing
B. Decreased transcription (guessing this is it)
C. Enhancement of mRNA degradation.
D. Incorporation of CGG repeats in mRNA
E. Increased binding of RNA Polymerase

10 y.o. w/mental ******ation and pigment anomalies. Underwent surgery at 3 y.o. to correct syndactyly. Has streaky hyperpigmentation. Chromosome shows 46,XY in 15 cells and 69, XXY in 5 cells. Explanation of karotype findings?
A. Deletion
B. Duplication (not it)
C. Inversion
D. Mosaicism
E. Ring chromosome
F. Translocation
 
Hey guys, I've got a few questions that I don't understand:

Man w/SOB, fever, and cough. Temp is 101 F and resp 18/min. Cold hemagglutinin test is positive. Interstitial markings are present on the X-ray. What is the infectious agent susceptible to?

A. Amox
B. Azithro
C. Ceftriaxone
D. Gentamicin
E. Piperacillin

(And what is the bug?! I know the cold hemagglutinin test is important, but I don't know what that tells you specifically) I'm guessing mycoplasma.


500 workers w/bladder cancer and 200 w/o bladder cancer are selected for a study. Hx obtained of aniline dye exposure. Of the 500 w/bladder cancer, 250 have exposure to aniline dye. Of the 200 w/o bladder cancer, 50 have exposure. What's the odds ratio for exposure variable?

A. 1/3
B. 1/2
C. 1
D. 1.5
E. 2 (not it)
F. 3

I thought 250/500 = .5 and 50/200 = .25 .5/.25 = 2 OR= AD/BC so 250x150/250x50=3

...Yeah I don't know biostats :(


Last one:
Woman has panic disorder with agoraphobia. Drug prescribed that activates benzo binding site on the GABA receptor. What drug is it?

A. Alprazolam
B. Buspirone
C. Flumazenil
D. Hydroxyzine
E. Ramelteon

Thought it was alprazolam. But changed my mind to buspirone based on the symptoms.


Think those are right anyhow.
 
Hey guys, I've got a few questions that I don't understand:

10 y.o. w/mental ******ation and pigment anomalies. Underwent surgery at 3 y.o. to correct syndactyly. Has streaky hyperpigmentation. Chromosome shows 46,XY in 15 cells and 69, XXY in 5 cells. Explanation of karotype findings?
A. Deletion
B. Duplication (not it)
C. Inversion
D. Mosaicism
E. Ring chromosome
F. Translocation

D- Mosaicism. Can present with differing chromosome numbers , etc.
 
EDIT: I lied.... Two more. Sorry

What effect do trinucleotide repeats cause on transcription of the FMR1 mRNA?
A. Alteration of mRNA splicing
B. Decreased transcription (guessing this is it)
C. Enhancement of mRNA degradation.
D. Incorporation of CGG repeats in mRNA
E. Increased binding of RNA Polymerase

yep. Its a trinucelotide repeat in the untranslated region that affects its transcription
 
During eval for renal lithiasis, a 46-year old man undergoes a series of imaging studies. (... blah blah blah, findings point towards hyperparathyroidism). A parathyroidectomy is recommended, and during the operation, two parathyroid grlands are found posterior to the thyroid gland on the left side, but only one, which appears to be the inferior, is present on the right. Because of the similarity of its developmental origin, which of the following additional organs should be explored to find the remaining parathyroid?

A) Palatine tonsil
B) Parotid gland
C) Sublingual gland
D) Submandibular gland
E) Thymus


I want to say the thymus, but they said the superior parathyroid is missing, not the inferior (which originates with the thymus). What's the deal???
 
During eval for renal lithiasis, a 46-year old man undergoes a series of imaging studies. (... blah blah blah, findings point towards hyperparathyroidism). A parathyroidectomy is recommended, and during the operation, two parathyroid grlands are found posterior to the thyroid gland on the left side, but only one, which appears to be the inferior, is present on the right. Because of the similarity of its developmental origin, which of the following additional organs should be explored to find the remaining parathyroid?

A) Palatine tonsil
B) Parotid gland
C) Sublingual gland
D) Submandibular gland
E) Thymus


I want to say the thymus, but they said the superior parathyroid is missing, not the inferior (which originates with the thymus). What's the deal???

They said which "appears" to be the inferior. Nothing else on the list originates from the 3rd or 4th pouch so there is no other good answer.
 
They said which "appears" to be the inferior. Nothing else on the list originates from the 3rd or 4th pouch so there is no other good answer.

Is that a frequent feature of USMLE questions? Because I find that to be incredibly poor question writing.
 
Is that a frequent feature of USMLE questions? Because I find that to be incredibly poor question writing.

Considering you didn't need that info to get the question right I would say it's just an extra little hint that they added to help out. I just thought about DiGeorge syndrome when I got the question and it made it fairly simple.
 
yea I mean I got the question right bc nothing else was remotely correct but Selegeline is a MAO-B inhibitor not MAO-A so it is specific for NE metabolism not Seretonin.

edit: ...right?
YES. I hated this question. I only picked selegiline because it was the only one even close to being right.

I guess just think of MAO-B being relatively specific for dopamine. No drug is perfect so it would still inc. serotonin
 
Considering you didn't need that info to get the question right I would say it's just an extra little hint that they added to help out. I just thought about DiGeorge syndrome when I got the question and it made it fairly simple.

It's only "fairly simple" if you underthink the question. Knowing "thymus and parathyroids are related" is a fairly limited degree of knowledge and understanding. If the question wasn't poorly written (and was actually trying to say that the missing parathyroid gland was the superior one), you'd have gotten it wrong by not recognizing that the superior parathyroids co-originate in the same pouch as the ultimobranchial body, which becomes the medullary parenchyma of the thyroid.
 
It's only "fairly simple" if you underthink the question. Knowing "thymus and parathyroids are related" is a fairly limited degree of knowledge and understanding. If the question wasn't poorly written (and was actually trying to say that the missing parathyroid gland was the superior one), you'd have gotten it wrong by not recognizing that the superior parathyroids co-originate in the same pouch as the ultimobranchial body, which becomes the medullary parenchyma of the thyroid.

Even if you know every detail, the only answer is still thymus. The parathyroid glands come from pouches 3 and 4 and the thymus comes from 3. Show me one other item on the list that makes any sense. They made it pretty obvious when they said "appears." You can say that it was a poorly worded question until your blue in the face, but really it was just a slightly tricky question and it got you. I don't think it's unreasonable for the Step 1 to be a little tricky. If they give you a patient, say the CT appears to show pneumonia, and it ends up being bronchioalveolar cancer are you going to say that was poorly worded too?
 
Even if you know every detail, the only answer is still thymus. The parathyroid glands come from pouches 3 and 4 and the thymus comes from 3. Show me one other item on the list that makes any sense. They made it pretty obvious when they said "appears." You can say that it was a poorly worded question until your blue in the face, but really it was just a slightly tricky question and it got you. I don't think it's unreasonable for the Step 1 to be a little tricky. If they give you a patient, say the CT appears to show pneumonia, and it ends up being bronchioalveolar cancer are you going to say that was poorly worded too?

I'm sorry if my post was worded confusingly. On that specific question (with those available answers), the only possibility was indeed the thymus. However, relying on loose keyword associations to reach the answer wouldn't necessarily fly on other, similar questions
 
I'm sorry if my post was worded confusingly. On that specific question (with those available answers), the only possibility was indeed the thymus. However, relying on loose keyword associations to reach the answer wouldn't necessarily fly on other, similar questions

I agree, but I also think they put enough effort into writing questions that if they had any derivatives from the 4th pouch as answer choices then they would not have included the tricky wording.
 
Hey everyone!!! I wanted to get some opinions on this question, I am pretty sure I have answered it correctly but the extended version of the NBME 11 is marking it incorrect and none of the other answer choices make sense to me.

30. A 60 year old man develops pain, erythema, and swelling of the right great toe. Serum Uric Acid concentrations are three times normal. Which of the following findings is most common in patients with this condition?

A. Absence of Aminotransferase
B. Absence of Glucose 6-Phosphatase
C. Absence of Glutathione Peroxidase
D. Absence of HGPRT
E. No specific enzyme or renal defect

I answered D!!!

My logic was that primary gout arises from inborn errors of metabolism involving purine metabolism such as Lesch-Nyhan Syndrome = Def of HGPRT!!!

I checked Goljan and FA and thats what they all say... I still figured well maybe its a trick question and I am missing something and tried to see if any of the other answers could be correct but they either have nothing to do with gout or such as E the total opposite of what is actually occuring...

ANY OPINIONS???
 
Hey everyone!!! I wanted to get some opinions on this question, I am pretty sure I have answered it correctly but the extended version of the NBME 11 is marking it incorrect and none of the other answer choices make sense to me.

30. A 60 year old man develops pain, erythema, and swelling of the right great toe. Serum Uric Acid concentrations are three times normal. Which of the following findings is most common in patients with this condition?

A. Absence of Aminotransferase
B. Absence of Glucose 6-Phosphatase
C. Absence of Glutathione Peroxidase
D. Absence of HGPRT
E. No specific enzyme or renal defect

I answered D!!!

My logic was that primary gout arises from inborn errors of metabolism involving purine metabolism such as Lesch-Nyhan Syndrome = Def of HGPRT!!!

I checked Goljan and FA and thats what they all say... I still figured well maybe its a trick question and I am missing something and tried to see if any of the other answers could be correct but they either have nothing to do with gout or such as E the total opposite of what is actually occuring...

ANY OPINIONS???

Answer is E, no specific enzyme defect (got it right so sure about it). Gout is pretty common and can occur in other disease states due to overproduction of uric acid or underexcretion. Enzyme defects in general are very rare. Plus this is a 60 y/o person, an enzyme defect would likely present at an earlier age.
 
Thanks!!! I Def didn't think about the age thing... And I figured E was wrong because it said no renal defects and since there is underexcretion... Oh Well, I guess I still need to polish up on that... But Thank you for all the replies... Def helps to see other perspectives...
 
25 year old man, HIV +, progressive apathy and dysarthria for 3 mo. Homonymous Hemianopsia, and MRI with multiple enhancing lesions in cerebral cortex. Diagnosis?

A. Colloid Cyst
B. Craniopharyngioma
C. Ependymoma
D. Ganglioneuroma
E. Lymphoma
F. Medulloblastoma
G. Meningioma
H. Retinoblastoma
I. Schwannoma
 
25 year old man, HIV +, progressive apathy and dysarthria for 3 mo. Homonymous Hemianopsia, and MRI with multiple enhancing lesions in cerebral cortex. Diagnosis?

A. Colloid Cyst
B. Craniopharyngioma
C. Ependymoma
D. Ganglioneuroma
E. Lymphoma
F. Medulloblastoma
G. Meningioma
H. Retinoblastoma
I. Schwannoma

I'd say Primary CNS Lymphoma (E). Only one on that list I can relate to HIV and multiple enhancing lesions.
 
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Great!!! Thanks!!! I still haven't reviewed Neuro, and I wanted to go with Lymphoma for some reason, but I have still not mastered the art of following my gut!!!
 
They said which "appears" to be the inferior. Nothing else on the list originates from the 3rd or 4th pouch so there is no other good answer.

haha i know... i fumbled with this question forever too until i decided that i was just too tired and probably had very little reading comprehension left and thought: ahh just go with thymus and move on!! im glad im not the only one :p
 
quick question for the nbme masters out there....

carbonic anhydrase knockout in RBCs ONLY. Compared to norm. would --> an increase in venous concentration of ?

-Calcium 2+
- Chloride -
- HCO3 -
- K+
-Mg 2+
-Na +
 
quick question for the nbme masters out there....

carbonic anhydrase knockout in RBCs ONLY. Compared to norm. would --> an increase in venous concentration of ?

-Calcium 2+
- Chloride -
- HCO3 -
- K+
-Mg 2+
-Na +

I'm relatively sure I already answered this question in this thread. Anyway, the answer is Cl. RBCs have a HCO3/Cl exchanger. In venous blood there is CO2 that enters the RBC and CA makes it into HCO3 which is then pumped out while Cl is pumped in. In the lungs the process reverses to get rid of the CO2.
 
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