USMLE OFFICIAL NBME 20 - Questions & Answers - Explanations & Discussions ?

[MegaKleos]

So let's continue the trend of this forum and discuss the doubts of the test. I intend on taking this as soon as it is out. Please post below if you wish to discuss and let's get together and solve our doubts.

DISCLAIMER: As has been said in the forum previously, posting COPYRIGHTED content of the NBME is a CRIME. Please do not do so. The intention of this thread is NOT to promote that but rather to discuss in a way that does not break the law. According to copyright act of united states, under DMCA, there is a special provision for "FAIR USE". Which means that people are able to discuss, critic and have an academic conversation as long as it is within reason and of course verbatim questions are unacceptable. To the admins of the forum, please dont delete this, i dont intend on posting anything against the law and hence please dont delete this thread.

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[crathnam]

During a procedure, the thoracic duct is damaged in the post. mediastinum. This is most likely to impair normal lymphatic return of which structure? Heart, left breast, left upper extremity, right kidney, right lung. Answer is right kidney but wouldn't left upper extremity and breast also be correct answers?
I was looking at this too. I think it's because the apical lymph nodes even on the left side may not all drain into the thoracic duct. From radiopedia: " Apical (terminal) lymph nodes drains into: subclavian trunk (may drain into jugulosubclavian venous trunk, subclavian vein, jugular lymphatic trunk, right lymphatic duct (left into thoracic duct), inferior deep cervical nodes)". Also the parts of the left breast can drain parasternally to the right breast. No option for the kidney to go anywhere but to the para-aortic --> cisterna chyli --> thoracic duct.

After some digging around, I believe the answer has to do with Virchow's node (left supraclavicular lymph node involvement). See here: Supraclavicular lymph nodes - Wikipedia

Apparently Virchow's node acts as a sentinel lymph node to detect intra-abdominal malignancies (e.g. ovarian/testicular, gastric [classic example], renal) since these organs cannot be easily visualized since they are intra-abdominal. Also, Virchow's node occurs where the thoracic duct drains into the left brachiocephalic vein so it has been implicated that the thoracic duct has something to do with Virchow's node. Thus, of the choices, the only intra-abdominal structure is the kidney

 

[M&Mgroot]

Hello, I need your help in this question= NBME 20

The frequency of an autosomal recessive disease in a population is 1/1600. A deletion has been identified that accounts for 80% of the mutations at this locus. Twenty percent of the mutations result from point mutations. The frequency of deletion carriers in the population is closest to which ?
the answer is 1/25

 

[DrOxyBella]

Someone can explain this question: the 56 years old man that is brought to the emergency department after 30 minutes of chest pain...What is the dx? Pulmonary hypertension?, and I can't understand why the interstitial oncotic pressure is decrease?in the correct answer.

He is late 50s chest pain Dx left sided heart failure due to a MI. FA state that L-sided heart failure will cause inc. capillary hydrostatic and increase interstitial pressure pushing transudative fluid into the interstitium dilating protein content

Hello everyone, i just took and reviewed the answers to NBME 20. I have a few questions that I am still not sure about. Any help will be appreciated, thank you in advance.

section 3, question 25: the question stem describes a pt with chest pain for the past hour. The pt has a history of HTN and type 2 diabetes. The pts vitals are pulse:120, RR:24, BP:98/60. The pt has JVD and crackles are heard in the lungs. The question asks what ECG changes will you see in this pt?

• The correct answer is ST segment elevation.
• Another answer choice is QT interval shortening. Can someone explain to me why this pts QT interval is not shortened. My understanding of the QT interval is that it is inversely related to HR. this pt is tachycardic thus will have a short QT interval.

Section 3 question 6: the question stem describes a pt which a hemoglobin concentration of 18.5 and then shows a peripheral blood smear.

• What is in that blood smear which points to COPD?

Section 4 question 15: a 17YO girl with right sides weakness, slurred speech, elevated pyruvate and lactate and has a NADH dehydrogenase deficiency.

• The question shows a pedigree and asks what is the mode of inheritance? The answer is mitochondrial.
• My question is, why are mothers not passing on the disease to all their children. One mother passed on the disease to 2 of her 3 children while another mother passed it on to 1 of her 2 children.

Section 4 question 20: a 36YO pt with decreased urinary output for 3 days was diagnosed with bilateral hydronephrosis. The pts BP is 150/96, pulse is 112, Na: 138, K: 5.9, HCO3: 22, creatinine: 5

• Bilateral nephrostomy tubes were placed
• The question asks which will happen to the pts urine output and urine K?
• I understand that his urine output will increase. What I don’t understand is why is urine K will increase also. If the nephron is secreting K then it must be reabsorbing Na which will worsen the HTN

Isn't QT interval shortening has increase of v. fib leading to sudden death in younger males not MI which is what the symptoms showing in this patient.

 

[DrOxyBella]

I haven't yet.


The question asks what the most likely predisposing factor in developing the ureteral lesion is. The answer is cigarette smoking. The attached histo slide also goes with the kidney picture if that helps.

Is there a link between smoking and PKD? I can't seem to remember. If so, I think you're right!

i feel like whenever they put smoking as a option then its most likely the answer. But i kinda see the link of high risk of heavy bleeding after MVA.

 

[teatime4449]

Hello, I need your help in this question= NBME 20

The frequency of an autosomal recessive disease in a population is 1/1600. A deletion has been identified that accounts for 80% of the mutations at this locus. Twenty percent of the mutations result from point mutations. The frequency of deletion carriers in the population is closest to which ?
the answer is 1/25

Part 1: I used the equation: (freq. autosomal recessive)^2 +2(AR)(AD)+ (freq. autosomal dominant)=1
To get the freq. of a single allele: Square root of (1/1600) =.025, then
Part 2: (.8+.2)=1 which is provided. You are looking at the heterozygote frequency (2pq)
so again p(^2) +2pq + q(^2) =1 ... plug it in... so you will be doing the square root of .8 and .2 which is about .9 and .4 then you must do (.9*.4*2) and get about .8

So now you take the answer from part 1 and 2 and
(.025 x .8 x .2) = .004 =1/25

Please someone tell me if this is wrong.. but this was my thought process..

 

[teatime4449]

A 77 yr old has difficulty fastening buttons, weakness in intrinsic muscles of hands, loss of sensation in little fingers. What is the cause?

A. Chronic lunate subluxation w/ Median N compression.
B. Compression of radial N. in spiral groove.
C. Compression of ulnar N. in carpal tunnel
D. C7-T1 foraminal stenosis.

Why D? And what did you do to rule out the others?

 

[popopopop]

A 77 yr old has difficulty fastening buttons, weakness in intrinsic muscles of hands, loss of sensation in little fingers. What is the cause?

A. Chronic lunate subluxation w/ Median N compression.
B. Compression of radial N. in spiral groove.
C. Compression of ulnar N. in carpal tunnel
D. C7-T1 foraminal stenosis.

Why D? And what did you do to rule out the others?

Little finger = ulnar nerve. D is the root of the ulnar nerve, which is a branch of the medial cord. C isn't right because the carpal tunnel contains the median nerve.

 

[M&Mgroot]

Part 1: I used the equation: (freq. autosomal recessive)^2 +2(AR)(AD)+ (freq. autosomal dominant)=1
To get the freq. of a single allele: Square root of (1/1600) =.025, then
Part 2: (.8+.2)=1 which is provided. You are looking at the heterozygote frequency (2pq)
so again p(^2) +2pq + q(^2) =1 ... plug it in... so you will be doing the square root of .8 and .2 which is about .9 and .4 then you must do (.9*.4*2) and get about .8

So now you take the answer from part 1 and 2 and
(.025 x .8 x .2) = .004 =1/25

Please someone tell me if this is wrong.. but this was my thought process..

 

[M&Mgroot]

thank you

 

[teatime4449]

30 yr old man w/ 3 month hx of jaw and left arm pain. Increased thirst, increased urination. Peptic ulcer 2 months ago. Elevated calcium, elevated PTH. X-ray w/ normal humerus. What is the best mechanism for explaining the impaired homeostasis in this patient?

A. Decreased Ca+2 reabsorption by renal tubules.
B. Decreased expression of PTH hormone receptors on osteoblasts
C. Decreased hydroxylation of Vit D. by renal tubule epithelial cells.
D. Increased calcitonin secretion by thyroid.
E. Increased motility of monocytes in bone marrow.
F. Increased osteoclast maturation and activity.

Why F? Is this primary hyperparathyroidism? Osteitis fibrosa cystica? And why is a decrease/defected in hydroxylase in kidney to get active Vit D not correct? Not sure where I am not connecting something! Thank you!

 

[YoungDoc25]

30 yr old man w/ 3 month hx of jaw and left arm pain. Increased thirst, increased urination. Peptic ulcer 2 months ago. Elevated calcium, elevated PTH. X-ray w/ normal humerus. What is the best mechanism for explaining the impaired homeostasis in this patient?

A. Decreased Ca+2 reabsorption by renal tubules.
B. Decreased expression of PTH hormone receptors on osteoblasts
C. Decreased hydroxylation of Vit D. by renal tubule epithelial cells.
D. Increased calcitonin secretion by thyroid.
E. Increased motility of monocytes in bone marrow.
F. Increased osteoclast maturation and activity.

Why F? Is this primary hyperparathyroidism? Osteitis fibrosa cystica? And why is a decrease/defected in hydroxylase in kidney to get active Vit D not correct? Not sure where I am not connecting something! Thank you!

Ya I went with primary hyperparathyroid and chose F. Didn’t like C because increased PTH should increase that process instead of decrease. If he had hypocalcemia with elevated PTH, I would think C would be correct and they would be describing pseudohypoparathyroidism.

 

[JooceMan137]

Hi everyone! I have (quite a few) questions from NBME 20 that I can't seem to figure out. If anyone is able to help, I'd really appreciate it!

16 yo student with uncontrollable sleepiness. Why is the answer direct transition from wakefulness to REM? Is it because they have narcolepsy?

Did you ever figure this out? When I look back at the answer while reviewing, I don't know why I thought the guy didn't have nacrolepsy. I think when they said "He can be easily awakened" made me think it's something else.

 

[JooceMan137]

Question 18. on the second block on the 4-year old boy with the bloody diarrhea.

I chose E. coli because I know EMB agar is used to isolate EHEC, but it turned out to be shigella.

I'm assuming that: There was no mention of undercooked beef, and the "Several children in the day care" was indicative of some sort of fecal-oral transmission going on?

I looked on amboss and they mention that shigella is highly contagious (low dose needed), as well as it has an incubation period of 0-2 days (vs. 2-10 days for EHEC) as well as the duration of shigella is 2-7 days or so. Given that the boy had his symptoms over the past 3 days, it kind of makes sense.

Any input?

 

[YoungDoc25]

Question 18. on the second block on the 4-year old boy with the bloody diarrhea.

I chose E. coli because I know EMB agar is used to isolate EHEC, but it turned out to be shigella.

I'm assuming that: There was no mention of undercooked beef, and the "Several children in the day care" was indicative of some sort of fecal-oral transmission going on?

I looked on amboss and they mention that shigella is highly contagious (low dose needed), as well as it has an incubation period of 0-2 days (vs. 2-10 days for EHEC) as well as the duration of shigella is 2-7 days or so. Given that the boy had his symptoms over the past 3 days, it kind of makes sense.

Any input?

I had the same exact thought process and was super frustrated by this question. If I remember right though, they explicitly say it was an invasive pathogen. If that’s right, EHEC isn’t invasive and shigella is, and that was supposed to be the giveaway I think.

 

[JooceMan137]

I had the same exact thought process and was super frustrated by this question. If I remember right though, they explicitly say it was an invasive pathogen. If that’s right, EHEC isn’t invasive and shigella is, and that was supposed to be the giveaway I think.

The thing is, EHEC is also mentioned to have fecal-oral transmission. I'm assuming that shigella is just more likely to transmit via that method because of the low dose.

 

[AnatomyGrey12]

A 77 yr old has difficulty fastening buttons, weakness in intrinsic muscles of hands, loss of sensation in little fingers. What is the cause?

A. Chronic lunate subluxation w/ Median N compression.
B. Compression of radial N. in spiral groove.
C. Compression of ulnar N. in carpal tunnel
D. C7-T1 foraminal stenosis.

Why D? And what did you do to rule out the others?

Little finger = ulnar nerve. D is the root of the ulnar nerve, which is a branch of the medial cord. C isn't right because the carpal tunnel contains the median nerve.

Also that the issue was bilateral and in all the other answers it would be pretty unlikely to have those problems bilaterally.

Question 18. on the second block on the 4-year old boy with the bloody diarrhea.

I chose E. coli because I know EMB agar is used to isolate EHEC, but it turned out to be shigella.

I'm assuming that: There was no mention of undercooked beef, and the "Several children in the day care" was indicative of some sort of fecal-oral transmission going on?

I looked on amboss and they mention that shigella is highly contagious (low dose needed), as well as it has an incubation period of 0-2 days (vs. 2-10 days for EHEC) as well as the duration of shigella is 2-7 days or so. Given that the boy had his symptoms over the past 3 days, it kind of makes sense.

Any input?

Shigella is inflammatory and the kid had mucous and WBCs in his stool as well. E-Coli doesn't have inflammatory diarrhea. I too picked E-Coli but going back through it there really wasn't anything in the stem that screamed e-coli outside of a kid with bloody diarrhea.

 

[popopopop]

^Enteroinvasive E Coli has inflammatory diarrhea. I put ecoli too, but the stem didn't mention a green sheen in the algar.

*edit: Just read from UW that EMB would stain lactose fermenters black. This makes e coli even less likely.

 

[Azaelea]

Did you ever figure this out? When I look back at the answer while reviewing, I don't know why I thought the guy didn't have nacrolepsy. I think when they said "He can be easily awakened" made me think it's something else.

Monoloco357 confirmed that this guy did have narcolepsy!

 

[JooceMan137]

Shigella is inflammatory and the kid had mucous and WBCs in his stool as well. E-Coli doesn't have inflammatory diarrhea. I too picked E-Coli but going back through it there really wasn't anything in the stem that screamed e-coli outside of a kid with bloody diarrhea.

Awesome, thank you. I don't have the exact question so I can't recall all the details they mentioned. So E.coli doesn't have inflammatory diarrhea? I don't want to sound like i'm doubting you, but can you provide some sort of source? It'll help it stick in my mind better if I get the full story

 

[AnatomyGrey12]

Awesome, thank you. I don't have the exact question so I can't recall all the details they mentioned. So E.coli doesn't have inflammatory diarrhea? I don't want to sound like i'm doubting you, but can you provide some sort of source? It'll help it stick in my mind better if I get the full story

Well apparently I was wrong according to the poster above. I actually can't find data either way for it. I just know in the sketchy vid on E coli there is no fire, and in the shigella vid there is fire lololol.

 

[popopopop]

Look under "enteroinvasive e coli" in first aid. I didn't know off the top of my head hehe.

 

[confused_and_tired]

An investigator is studying patients w/ West Nile, data collected on 25 patients Dx. Collected demographic information and possible infection source. What type of study design is this? The answer case series. Why is it not cross-sectional? It sounded like they were trying to figure out risk factors for WNV.

A 52yo M in ED for 4h h/o severe headache, anxiety, sweating, and palps. 2y h/o HTN controlled well w/ clonidine and HCTZ but ran out of Rx 3d ago. HR 120, PE shows diaphoresis, what happens when you give propanolol? Okay, obviously cardiac output decreases by why does TPR increase?

A 56yo M w/ 20y h/o chronic back pain undergoes placement of an electrode in the midbrain for pain management. Previous physicial and neuro exam WNL. When implant activated, there is a marked decrease in pain. Admin of which of the following substances would most likely result in the result in return of the pain? I put enkephalin (it was a guess but sounded fun) and other choices = beta-endorphin, morphine, oxycodone, but naloxone was the correct answer. Did they want us to assume he was using opioids for his pain? And still, w/ the electrode, shouldn't he be feeling better? I have no idea what they were going for in this question.

A 51yo M has acute onset of fever and resp. failure 6 weeks after cadaveric renal transplant, is on cyclosporine, prednisone, and TMP-SMX. Vitals: temp 101F, HR 120, RR 40, BP 110/60. No rash, diffuse inspiratory and expiratory crackles, no gallop/murmur, labs = low leukocytes, high BUN and Cr, normal WBCs and RBCs in urine. CXR = "white out?" I can't post it, sorry. Most likely cause? Answer: CMV. I had no idea how to approach this question. Is there some key association that I am missing here? Should we just essentially assume PNA assoc. w/ lung transplantation is CMV until proven otherwise? (I put P. jiroveci infection but it was a complete guess).

92yo F recently admitted to nursing home b/c progressive dementia has large purpuric lesions on dorsa of both forearms and hands. +H/o these things occuring in past, no evidence of abuse. Normal platelet count. Most likely cause? Answer: atrophy of dermal collagen. I put platelet dysfunction because I thought they were going for a qualitative PLT disorder which often presents w/ normal PLT counts. How does atrophy of dermal collagen --> purpura? I thought that it was just wrinkles that the atrophy would cause.

A 62yo M comes to MD for 1 week h/o muscle cramps assoc. w/ painful spasms in arms and legs. Tells MD that for past 4mo. he has had trouble opening jars and using silverware. PE = m. weakness, exaggerated DTRs. Appropriate Tx of spasms includes systemic administration of drug w/ following MOA? Answer: GABA-B R agonist. I now know that is is baclofen but I have no idea what the condition is. Any thoughts?

 

[confused_and_tired]

HELLO
I HAVE SOME QUESTIONS
1- the question on tryptohan synthase ? why is it missense mutation . why not deletion ?
2- the boy with ankyrin gene mutation ( hereditary spherocytoces) why is he heterozygous but not homo ?
3-the question on vitamin D deficeny ? why is the answer cholecalciefrol but not 7 hydroxycholesterol ?

Regarding item 2, I am not sure if this is correct but according to Medscape, "Defects of beta-spectrin are more likely to be expressed in the heterozygous state because synthesis of beta-spectrin is the rate-limiting factor." (Hereditary Spherocytosis: Practice Essentials, Pathophysiology, Etiology). Nothing about the genetics of hereditary spherocytosis that I can find in First Aid or Pathoma so this is the best that I got.

 

[YoungDoc25]

An investigator is studying patients w/ West Nile, data collected on 25 patients Dx. Collected demographic information and possible infection source. What type of study design is this? The answer case series. Why is it not cross-sectional? It sounded like they were trying to figure out risk factors for WNV.

A 52yo M in ED for 4h h/o severe headache, anxiety, sweating, and palps. 2y h/o HTN controlled well w/ clonidine and HCTZ but ran out of Rx 3d ago. HR 120, PE shows diaphoresis, what happens when you give propanolol? Okay, obviously cardiac output decreases by why does TPR increase?

A 56yo M w/ 20y h/o chronic back pain undergoes placement of an electrode in the midbrain for pain management. Previous physicial and neuro exam WNL. When implant activated, there is a marked decrease in pain. Admin of which of the following substances would most likely result in the result in return of the pain? I put enkephalin (it was a guess but sounded fun) and other choices = beta-endorphin, morphine, oxycodone, but naloxone was the correct answer. Did they want us to assume he was using opioids for his pain? And still, w/ the electrode, shouldn't he be feeling better? I have no idea what they were going for in this question.

A 51yo M has acute onset of fever and resp. failure 6 weeks after cadaveric renal transplant, is on cyclosporine, prednisone, and TMP-SMX. Vitals: temp 101F, HR 120, RR 40, BP 110/60. No rash, diffuse inspiratory and expiratory crackles, no gallop/murmur, labs = low leukocytes, high BUN and Cr, normal WBCs and RBCs in urine. CXR = "white out?" I can't post it, sorry. Most likely cause? Answer: CMV. I had no idea how to approach this question. Is there some key association that I am missing here? Should we just essentially assume PNA assoc. w/ lung transplantation is CMV until proven otherwise? (I put P. jiroveci infection but it was a complete guess).

92yo F recently admitted to nursing home b/c progressive dementia has large purpuric lesions on dorsa of both forearms and hands. +H/o these things occuring in past, no evidence of abuse. Normal platelet count. Most likely cause? Answer: atrophy of dermal collagen. I put platelet dysfunction because I thought they were going for a qualitative PLT disorder which often presents w/ normal PLT counts. How does atrophy of dermal collagen --> purpura? I thought that it was just wrinkles that the atrophy would cause.

A 62yo M comes to MD for 1 week h/o muscle cramps assoc. w/ painful spasms in arms and legs. Tells MD that for past 4mo. he has had trouble opening jars and using silverware. PE = m. weakness, exaggerated DTRs. Appropriate Tx of spasms includes systemic administration of drug w/ following MOA? Answer: GABA-B R agonist. I now know that is is baclofen but I have no idea what the condition is. Any thoughts?

I’ll take a stab on these (mainly just my thought process)

1) I don’t remember the exact question, but I don’t think it was over a specified time, so I ruled that out and case series fit.
2) clonidine = sympatholytic so he’s going to have reflex hypertension and all propranolol did was exasterbate the a1 receptor action by selectively blocking b1&2
3) missed this and had the same thought process haha
4) pneumonia in a transplant pt is most commonly CMV unless something specifically rules that out (I think it’s in FA, but I could be mistaken)
5) Senile purpura results in thin skin and weak blood vessels which leads to easy bruising. The patient being really old made me lean more towards this as a simpler explanation, but I definitely see your point. That probably would have been the answer on UWorld haha
6) I honestly pick baclofen for any sort of spasticity if that’s an answer choice. Not 100% sure what he has though

 

[AnatomyGrey12]

A 52yo M in ED for 4h h/o severe headache, anxiety, sweating, and palps. 2y h/o HTN controlled well w/ clonidine and HCTZ but ran out of Rx 3d ago. HR 120, PE shows diaphoresis, what happens when you give propanolol? Okay, obviously cardiac output decreases by why does TPR increase?

Propranolol is non-selective B blocker. B2 causes vasodilation, so if you block it you get constriction => increased TPR. The B1 obviously drops the CO.

A 51yo M has acute onset of fever and resp. failure 6 weeks after cadaveric renal transplant, is on cyclosporine, prednisone, and TMP-SMX. Vitals: temp 101F, HR 120, RR 40, BP 110/60. No rash, diffuse inspiratory and expiratory crackles, no gallop/murmur, labs = low leukocytes, high BUN and Cr, normal WBCs and RBCs in urine. CXR = "white out?" I can't post it, sorry. Most likely cause? Answer: CMV. I had no idea how to approach this question. Is there some key association that I am missing here? Should we just essentially assume PNA assoc. w/ lung transplantation is CMV until proven otherwise? (I put P. jiroveci infection but it was a complete guess).

In UW, the NBME's, and basically any Qbank if the patient had a recent transplant you should always think CMV first because of it's association with transplantation.

A 56yo M w/ 20y h/o chronic back pain undergoes placement of an electrode in the midbrain for pain management. Previous physicial and neuro exam WNL. When implant activated, there is a marked decrease in pain. Admin of which of the following substances would most likely result in the result in return of the pain? I put enkephalin (it was a guess but sounded fun) and other choices = beta-endorphin, morphine, oxycodone, but naloxone was the correct answer. Did they want us to assume he was using opioids for his pain? And still, w/ the electrode, shouldn't he be feeling better? I have no idea what they were going for in this question.

I think, big I think here, is that they were going for the simple fact that you would likely be blocking their pain in the same way opioids do. So naloxone would reverse that.

92yo F recently admitted to nursing home b/c progressive dementia has large purpuric lesions on dorsa of both forearms and hands. +H/o these things occuring in past, no evidence of abuse. Normal platelet count. Most likely cause? Answer: atrophy of dermal collagen. I put platelet dysfunction because I thought they were going for a qualitative PLT disorder which often presents w/ normal PLT counts. How does atrophy of dermal collagen --> purpura? I thought that it was just wrinkles that the atrophy would cause.

Basically she's just old and her skin is thinner which leads to easy bruising/purpura

 

[confused_and_tired]

I’ll take a stab on these (mainly just my thought process)

1) I don’t remember the exact question, but I don’t think it was over a specified time, so I ruled that out and case series fit.
2) clonidine = sympatholytic so he’s going to have reflex hypertension and all propranolol did was exasterbate the a1 receptor action by selectively blocking b1&2
3) missed this and had the same thought process haha
4) pneumonia in a transplant pt is most commonly CMV unless something specifically rules that out (I think it’s in FA, but I could be mistaken)
5) Senile purpura results in thin skin and weak blood vessels which leads to easy bruising. The patient being really old made me lean more towards this as a simpler explanation, but I definitely see your point. That probably would have been the answer on UWorld haha
6) I honestly pick baclofen for any sort of spasticity if that’s an answer choice. Not 100% sure what he has though

Thanks for the help, any thought processes outside of mine are greatly appreciated!

 

[confused_and_tired]

please can someone explain this;
23 year old woman with fever DIC hypotension.
Hx: splenectomy after trauma. Which bacteria is cause of sepsis?

I know that strep pneuomoniae is common with splenectomized patient and they need vaccination against strep to prevent infection but I think sepsis and DIC common with gram negative septicemia. So It confused me and I choosed E. coli.

Is DIC also common with gr + bacterial sepsis?

I got this one incorrect as well with the same logic, DIC is more likely w/ E. coli than S. pneumoniae. But, it is possible that you can have DIC w/ S. pneumoniae and so I think what the question really was assessing was to see if you knew which pathogens are the more dangerous post-splenectomy which are: S. pneumoniae, H. influenzae, and N. meningitidis. Yes, E. coli is encapsulated but it is not the leading pathogen of concern in post-splenectomy patients. So basically, this is a terribly done "most likely" question meant to trick you.

I hope this makes sense.

 

[star050]

Q about male with 6 mo hx of burning abdominal pain 1-2 hours after he eats. Black stool for 2 days. Use of antacids and H blockers not effective. Sweating profusely and has light-headedness when he stands. BP 105/70 while sitting. Epigastric tenderness. CT show 1-cm mass in pancrea. IHC labeling of neoplastic cells in a biopsy would involve use of antibodies directed to which?
answer was gastrin.
Can someone explain why? I thought it would be one of the pancreatic hormones (glucagon, insulin and somatostatin were also there as well as a few others.)

 

[confused_and_tired]

An investigator compares DNA sequences of a group of newborns w/ acondroplasia w/ the sequences from healthy newborns. DNA sequence shows a G --> C mutation in FGFR3 on chrom. 4. Sequences for 2 groups: Achondroplasia: 5'-TACCGGGT-3'; healthy: 5'-TACGGGGT-3'. As a result of the mutation, Mspl (restriction enzyme) is created that allows for a convenient Dx test. Which of the following represents the substrate specificity of Mspl? Answer: 5'CCGG. I have no idea what is going on here with this one. Any help please?!?!

 

[confused_and_tired]

Q about male with 6 mo hx of burning abdominal pain 1-2 hours after he eats. Black stool for 2 days. Use of antacids and H blockers not effective. Sweating profusely and has light-headedness when he stands. BP 105/70 while sitting. Epigastric tenderness. CT show 1-cm mass in pancrea. IHC labeling of neoplastic cells in a biopsy would involve use of antibodies directed to which?
answer was gastrin.
Can someone explain why? I thought it would be one of the pancreatic hormones (glucagon, insulin and somatostatin were also there as well as a few others.)

The patient has Zollinger-Ellison syndrome which causes many ulcers in the upper GI tract (stomach, duodenum, and jejunum). It is due to a gastrin-secreting tumor which causes massive amounts of acid release and thus causes the ulcers. Therefore, to assess for the presence of gastrin, the antibodies should target gastrin and none of the other hormones as they are unrelated to the pathology. Hope this helps!

 

[star050]

The patient has Zollinger-Ellison syndrome which causes many ulcers in the upper GI tract (stomach, duodenum, and jejunum). It is due to a gastrin-secreting tumor which causes massive amounts of acid release and thus causes the ulcers. Therefore, to assess for the presence of gastrin, the antibodies should target gastrin and none of the other hormones as they are unrelated to the pathology. Hope this helps!

Ah yes, the one disease that always seems to slip my mind. Thank you!

 

[AnatomyGrey12]

An investigator compares DNA sequences of a group of newborns w/ acondroplasia w/ the sequences from healthy newborns. DNA sequence shows a G --> C mutation in FGFR3 on chrom. 4. Sequences for 2 groups: Achondroplasia: 5'-TACCGGGT-3'; healthy: 5'-TACGGGGT-3'. As a result of the mutation, Mspl (restriction enzyme) is created that allows for a convenient Dx test. Which of the following represents the substrate specificity of Mspl? Answer: 5'CCGG. I have no idea what is going on here with this one. Any help please?!?!

The way it was explained to me is that restriction enzymes bind palindromes. All the other details were essentially fluff and they were just using it to distract from the basic concept they were getting at. So both 5'CCGG or 3'GGCC would have been acceptable in that scenario. Obviously the latter wasn't a choice.

 

[Drdrmd509]

Little finger = ulnar nerve. D is the root of the ulnar nerve, which is a branch of the medial cord. C isn't right because the carpal tunnel contains the median nerve.

It's like lower trunk compression klumpke palsy and I'm only know seeing it bc it's both hands it doesn't specify right or left its both hands and fingers

 

[Drdrmd509]

A 77 yr old has difficulty fastening buttons, weakness in intrinsic muscles of hands, loss of sensation in little fingers. What is the cause?

A. Chronic lunate subluxation w/ Median N compression.
B. Compression of radial N. in spiral groove.
C. Compression of ulnar N. in carpal tunnel
D. C7-T1 foraminal stenosis.

Why D? And what did you do to rule out the others?

It's klumpke palsy I believe, intrinsic muscles of the hand and parasthesias

 

[Drdrmd509]

The propranolol questions deals with rebound hypertension, if you block beta, you get un opposed alpha agonist effect of the sympathetic rebound, it increases your tpr and ur cardiac output has to go down bc how would it push against that

 

[Drdrmd509]

30 yr old man w/ 3 month hx of jaw and left arm pain. Increased thirst, increased urination. Peptic ulcer 2 months ago. Elevated calcium, elevated PTH. X-ray w/ normal humerus. What is the best mechanism for explaining the impaired homeostasis in this patient?

A. Decreased Ca+2 reabsorption by renal tubules.
B. Decreased expression of PTH hormone receptors on osteoblasts
C. Decreased hydroxylation of Vit D. by renal tubule epithelial cells.
D. Increased calcitonin secretion by thyroid.
E. Increased motility of monocytes in bone marrow.
F. Increased osteoclast maturation and activity.

Why F? Is this primary hyperparathyroidism? Osteitis fibrosa cystica? And why is a decrease/defected in hydroxylase in kidney to get active Vit D not correct? Not sure where I am not connecting something! Thank you!

He has men 1 i believe, the polydipsa is from hypercalcemia from a parathyroid adenona and an ulcer from zollinger Ellison

 

[Dr.Bruh]

What’s the consensus on 20 in terms of being and under or over predictor? Used it for my baseline and got rocked haha. Been hearing it the toughest of the new nbmes. Does that seems to be the case for those who have taken them all and the real thing??

 

[AnatomyGrey12]

What’s the consensus on 20 in terms of being and under or over predictor? Used it for my baseline and got rocked haha. Been hearing it the toughest of the new nbmes. Does that seems to be the case for those who have taken them all and the real thing??

I dunno, NBME 20 and 21 have been my highest so far. I felt like they were of equal difficulty. I like them way better than the old ones lol, 17 rocked me.

 

[YoungDoc25]

What’s the consensus on 20 in terms of being and under or over predictor? Used it for my baseline and got rocked haha. Been hearing it the toughest of the new nbmes. Does that seems to be the case for those who have taken them all and the real thing??

If you haven’t done any of the old ones, it’s consistently a low ball score from what I’ve seen. Learn what you can from it and just keep grinding!

 

[watermelon master]

The way it was explained to me is that restriction enzymes bind palindromes. All the other details were essentially fluff and they were just using it to distract from the basic concept they were getting at. So both 5'CCGG or 3'GGCC would have been acceptable in that scenario. Obviously the latter wasn't a choice.

What? Isn't a palindrome read the same forward to backward as backward to forward? I still don't understand why the answer is what it is

 

[AnatomyGrey12]

What? Isn't a palindrome read the same forward to backward as backward to forward? I still don't understand why the answer is what it is

That is correct. The section with the mutation was like 5'CCGG and if you convert it you also get 5'CCGG. A palindrome.

Look at it this way: 5' CCGG
----------------------GGCC 5'

 

[watermelon master]

Regarding the HLA question: wouldn't the chance to have a sibling match be 25%? Isn't a 1:4 ratio 20%? Do I not understand basic math?

 

[OCAZSCButters]

From what I remember, the CD count was below 50 or something and it was a single enhancing lesion which points more towards lymphoma. Toxo is usually multi ring enhancing lesions. Correct me if im wrong

FA2019 - 177
EBV --> CNS lymphoma - ring enhancing solitary ddx w/toxo

 

[watermelon master]

Was wondering if somebody could explain the etiology behind "inflammatory diarrhea" what does it mean to be inflammatory?

 

[AnatomyGrey12]

Was wondering if somebody could explain the etiology behind "inflammatory diarrhea" what does it mean to be inflammatory?

Blood and pus in the stool essentially.

 

[watermelon master]

Blood and pus in the stool essentially.

And histologically? Don't you get blood and pus in the stool from ecoli? Why is Salmonella enteriditis inflammatory but not typhii?

 

[madidus]

And histologically? Don't you get blood and pus in the stool from ecoli? Why is Salmonella enteriditis inflammatory but not typhii?

In general, whether it will be an inflammatory/bloody diarrhea or non-inflammatory/watery diarrhea depends on the mechanism of the infecting organism. If the organism invades the mucosal cells and colonizes it will be inflammatory.

There are some strains of E. coli that cause bloody diarrhea. The one you need to know for step is EHEC O157:H7, but EHEC is transmitted through undercooked beef products and the history in the question was a young child and multiple infection in a day-care center which makes me think more "gross children" fecal-oral transmission.

S. typhi DOES invade but for some (low yield) reason doesn't stimulate a inflammatory response in the bowl. Instead, it enters the lymphoid tissue and causes a systemic infection.

I hope this makes sense and i didn't mess it up somehow

 

[watermelon master]

In general, whether it will be an inflammatory/bloody diarrhea or non-inflammatory/watery diarrhea depends on the mechanism of the infecting organism. If the organism invades the mucosal cells and colonizes it will be inflammatory.

There are some strains of E. coli that cause bloody diarrhea. The one you need to know for step is EHEC O157:H7, but EHEC is transmitted through undercooked beef products and the history in the question was a young child and multiple infection in a day-care center which makes me think more "gross children" fecal-oral transmission.

S. typhi DOES invade but for some (low yield) reason doesn't stimulate a inflammatory response in the bowl. Instead, it enters the lymphoid tissue and causes a systemic infection.

I hope this makes sense and i didn't mess it up somehow

And does this have anything to do with leukocytes in the stool? I know that S. enteriditis is inflammatory since the sketchy has the flame there - lol, but there isn't a flame for S. typhi. So does S. typhi cause leukocytes in the stool?

 

[madidus]

And does this have anything to do with leukocytes in the stool?

Yes, most of the time. If the pathogenesis is mucosal invasion it will also trigger an immune reaction and cause neutrophil transmigration and some will end up in the stool. I kind of lumped inflammatory and bloody together before but it doesn't always have to be true. In EHEC the pathogenesis is the shiga-like toxin and not invasion so I don't think you would see neutrophils in the stool.

I know that S. enteriditis is inflammatory since the sketchy has the flame there - lol, but there isn't a flame for S. typhi. So does S. typhi cause leukocytes in the stool?

Sketchy is correct. You won't see leukocytes in S. typhi. The reason is unclear but for some reason non-typhoid salmonella cause Il-8 dependent neutrophil transmigration when invading but S. typhi does not.

Source: Uptodate

 

[FutrDoc22]

On the question with 34 year old HIV positive man who had enlarged abdominal lymph nodes following antiretroviral therapy, how do we know this is due to CD4+ T lymphocytes ? Thanks in advance!