NBME 13 discussion

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Are we allowed to talk about this topic? There's a NBME 12 discussion that has a lot of full questions posted but there are sticky posts that seem to say don't talk about the NBMEs. Thank you for any clarification!

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Are we allowed to talk about this topic? There's a NBME 12 discussion that has a lot of full questions posted but there are sticky posts that seem to say don't talk about the NBMEs. Thank you for any clarification!

I'm guessing this refers to the real deal.
 
1. A 62-year-old man is brought to the emergency department because of a 3-hour history of progressive difficulty breathing and mild left shoulder pain. His symptoms began after he ran up several flights of stairs. He has poorly controlled hypertension and mild angina pectoris. He has smoked one-half pack of cigarettes daily for 40 years. He appears uncomortable and has labored breathing. Diffuse crackles, ronchi, and scattered wheezing on auscultation of the posterior lung fields. His arterial PO2 is 58 mm Hg. Which of the following is the most likely diagnosis?
A. Cardiac tamponade
B. Pneumonitis
C. Pneumothorax
D. Pulmonary edema
E. Pulmonary embolism


My answer was C. pneumothorax and that was wrong. I figured that his emphysema destroyed the lung parenchyma, thus increasing his risk of spontaneous pneumothorax (consistent with mild pain and hypoxemia). Although I wasn't happy with that choice because he has crap in his lungs which made me think pulmonary edema, but I figured a 40 year smoker is almost always going to have crap in his lungs. What do you guys think? We never really learned about acute episodes of pulmonary edema from simply walking up stairs in angina pectoris. Does that commonly happen?

2. An investigator is studying the human immune response to tumor antigens in malignancies. Which of the following sets of cancer types and tumor antigens is most likely to produce the highest antibody titer?
Cancer type; Tumor antigen
A. B-cell lymphoma; CD19
B. Breast cancer; HER2/neu
C. Cervical cancer; HPV type 16 E6 protein
D. Melanoma; tyrosinase
E. Prostate cancer; prostatic acid phosphatase


I picked B. Breast cancer; HER2/neu and that was wrong. I didn't even know where to begin on this one. I went with which cancer has a monoclonal antibody treatment, since I figured that means that the cancer was immunogenic enough for labs to create a synthetic drug (perhaps by studying cancer patient's serum antibodies?). Obviously not. What principles are going on here that I am totally missing? Is it something like HPV E6 is a viral component, therefore it's more immunogenic than any cancer that over expresses self-antigen? Is it some principle of which antigen is sitting on the cell membrane thus most accessible to circulating antibodies?

3. A 42-year-old man comes to the physican because of a 4-week history of muscle cramping and pain. Two months ago, he began treatment with simvastatin (80 mg daily) for hypercholesterolemia. After 1 month, marked improvement was noted in his serum LDL-cholesterol concentration, but serum triglyceride concentration remained increased. At that time, gemfibrozil was added to his regimen to decrease his triglyceride concentration. Physical examination today shows no abnormalities. This patient's myalgia is most likely related to which of the following effects of gemfibrozil on simvastatin?
A. Decreased bioavailability
B. Increased absorption
C. Inhibition of cytochrome P450 metabolism
D. Inhibition of hepatic glycosylation
E. Inhibition of hepatic sulfation


I picked D. inhibition of hepatic glycosylation and that was wrong. This question really ticked me off. I asked two professors at my school's pharmacology department and they said they couldn't find a source that could support any of those five answer choices. I mean maybe they didn't search that exhaustively, but it just seems silly that two PhD pharmacologists can't find the answer. What do you guys think? I remember from the Kaplan videos that gemfibrozil inhibits excretion of statins but Raymond never specifies the exact mechanism beyond that it's NOT P450 inhibition. I presume it's by inhibiting glucuronidation? Anyway, that's not an answer choice (on the exam when I saw glycosylation, I read glucuronidation... oops). Is it sulfation?

4. A 52-year-old man comes to the physician because of a 3-month history of epigastric abdominal pain; he also has had an unintentional 6.8-kg (15-lb) weight loss during this period. He has osteoarthritis treated with naproxen as needed. He has immigrated to the UsA from Japan 6 months ago. He eats mostly traditional Japanese food prepared by his wife. He has smoked 2 packs of cigarettes daily for 30 years and drinks three to four glasses of wine daily. He is 170 cm (5 ft 7 in) tall and now weighs 82 kg (180 lb); BMI is 28 kg/m^2. Physical examination shows epigastric tenderness. Upper gastrointestinal endoscopy shows a 4-cm ulcer in the stomach. Examination of a biopsy specimen of the lesion confirms adenocarcinoma. Which of the following is the strongest predisposing risk factor for the patient's condition?
A. Alcohol use
B. Diet
C. Ethnicity
D. Naproxen
E. Tobacco use


Okay so we have a male Japanese who eats nitrosamines, smokes, drinks, and uses NSAIDS. My answer was C. ethnicity and that was wrong. All I remembered when doing this question was that Japanese have a 3x elevated rate of occurrence of gastric adenocarcinoma vs whites in the US. I know that H. pylori causes most gastric adenocarcinoma, but that's not an answer choice unless I'm totally missing something. So the SECOND most common cause is what? Am I going to feel really dumb because I didn't habitually guess smoking?

Thanks for any feedback!
 
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1. A 62-year-old man is brought to the emergency department because of a 3-hour history of progressive difficulty breathing and mild left shoulder pain. His symptoms began after he ran up several flights of stairs. He has poorly controlled hypertension and mild angina pectoris. He has smoked one-half pack of cigarettes daily for 40 years. He appears uncomortable and has labored breathing. Diffuse crackles, ronchi, and scattered wheezing on auscultation of the posterior lung fields. His arterial PO2 is 58 mm Hg. Which of the following is the most likely diagnosis?
A. Cardiac tamponade
B. Pneumonitis
C. Pneumothorax
D. Pulmonary edema
E. Pulmonary embolism


My answer was B. pneumothorax and that was wrong. I figured that his emphysema destroyed the lung parenchyma, thus increasing his risk of spontaneous pneumothorax (consistent with mild pain and hypoxemia). Although I wasn't happy with that choice because he has crap in his lungs which made me think pulmonary edema, but I figured a 40 year smoker is almost always going to have crap in his lungs. What do you guys think? We never really learned about acute episodes of pulmonary edema from simply walking up stairs in angina pectoris. Does that commonly happen?

2. An investigator is studying the human immune response to tumor antigens in malignancies. Which of the following sets of cancer types and tumor antigens is most likely to produce the highest antibody titer?
Cancer type; Tumor antigen
A. B-cell lymphoma; CD19
B. Breast cancer; HER2/neu
C. Cervical cancer; HPV type 16 E6 protein
D. Melanoma; tyrosinase
E. Prostate cancer; prostatic acid phosphatase


I picked B. Breast cancer; HER2/neu and that was wrong. I didn't even know where to begin on this one. I went with which cancer has a monoclonal antibody treatment, since I figured that means that the cancer was immunogenic enough for labs to create a synthetic drug (perhaps by studying cancer patient's serum antibodies?). Obviously not. What principles are going on here that I am totally missing? Is it something like HPV E6 is a viral component, therefore it's more immunogenic than any cancer that over expresses self-antigen? Is it some principle of which antigen is sitting on the cell membrane thus most accessible to circulating antibodies?

3. A 42-year-old man comes to the physican because of a 4-week history of muscle cramping and pain. Two months ago, he began treatment with simvastatin (80 mg daily) for hypercholesterolemia. After 1 month, marked improvement was noted in his serum LDL-cholesterol concentration, but serum triglyceride concentration remained increased. At that time, gemfibrozil was added to his regimen to decrease his triglyceride concentration. Physical examination today shows no abnormalities. This patient's myalgia is most likely related to which of the following effects of gemfibrozil on simvastatin?
A. Decreased bioavailability
B. Increased absorption
C. Inhibition of cytochrome P450 metabolism
D. Inhibition of hepatic glycosylation
E. Inhibition of hepatic sulfation


I picked D. inhibition of hepatic glycosylation and that was wrong. This question really ticked me off. I asked two professors at my school's pharmacology department and they said they couldn't find a source that could support any of those five answer choices. I mean maybe they didn't search that exhaustively, but it just seems silly that two PhD pharmacologists can't find the answer. What do you guys think? I remember from the Kaplan videos that gemfibrozil inhibits excretion of statins but Raymond never specifies the exact mechanism beyond that it's NOT P450 inhibition. I presume it's by inhibiting glucuronidation? Anyway, that's not an answer choice (on the exam when I saw glycosylation, I read glucuronidation... oops). Is it sulfation?

4. A 52-year-old man comes to the physician because of a 3-month history of epigastric abdominal pain; he also has had an unintentional 6.8-kg (15-lb) weight loss during this period. He has osteoarthritis treated with naproxen as needed. He has immigrated to the UsA from Japan 6 months ago. He eats mostly traditional Japanese food prepared by his wife. He has smoked 2 packs of cigarettes daily for 30 years and drinks three to four glasses of wine daily. He is 170 cm (5 ft 7 in) tall and now weighs 82 kg (180 lb); BMI is 28 kg/m^2. Physical examination shows epigastric tenderness. Upper gastrointestinal endoscopy shows a 4-cm ulcer in the stomach. Examination of a biopsy specimen of the lesion confirms adenocarcinoma. Which of the following is the strongest predisposing risk factor for the patient's condition?
A. Alcohol use
B. Diet
C. Ethnicity
D. Naproxen
E. Tobacco use


Okay so we have a male Japanese who eats nitrosamines, smokes, drinks, and uses NSAIDS. My answer was C. ethnicity and that was wrong. All I remembered when doing this question was that Japanese have a 3x elevated rate of occurrence of gastric adenocarcinoma vs whites in the US. I know that H. pylori causes most gastric adenocarcinoma, but that's not an answer choice unless I'm totally missing something. So the SECOND most common cause is what? Am I going to feel really dumb because I didn't habitually guess smoking?

Thanks for any feedback!

E A B B would be my answers.
 
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So what's the principle behind question #2? The most immunogenic antigen is the non-self antigen?
 
I also have some questions. changes in CREST syndrome

Esophageal peristalsis lower esophageal sphincter tone

Is the answer both decreased?
 
I also have some questions. changes in CREST syndrome

Esophageal peristalsis lower esophageal sphincter tone

Is the answer both decreased?

Yeah, both are decreased.
 
A 40yr old woman with a 25yr history of seizures. Picture shows a collection of hole-like lesions in a coronal section of the brain and asks what the most likely cause of her seizure disorder is.

Glioblastoma multiforme
HSV encephalitis
Medial Temporal Sclerosis
Vascular malformation

I put GM...which was wrong. I'm assuming Vascular malformation is the correct answer but can anyone confirm that or explain it?
 
Yup it was an AVM. I think you can eliminate GBM because that would be a solid (versus swiss cheese) necrotic mass with hemorrhage.
 
Regarding the seizure question.

25year history would mean she was 15. GM is usually adults (and supratentorial)

HSV is temporal lobes...

I dont know what the other thing is

And AVM....sure why not?
 
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also GBM is malignant brain tumor, I do not think she could live for that long with it.

Yup it was an AVM. I think you can eliminate GBM because that would be a solid (versus swiss cheese) necrotic mass with hemorrhage.
 
1. A 62-year-old man is brought to the emergency department because of a 3-hour history of progressive difficulty breathing and mild left shoulder pain. His symptoms began after he ran up several flights of stairs. He has poorly controlled hypertension and mild angina pectoris. He has smoked one-half pack of cigarettes daily for 40 years. He appears uncomortable and has labored breathing. Diffuse crackles, ronchi, and scattered wheezing on auscultation of the posterior lung fields. His arterial PO2 is 58 mm Hg. Which of the following is the most likely diagnosis?
A. Cardiac tamponade
B. Pneumonitis
C. Pneumothorax
D. Pulmonary edema
E. Pulmonary embolism


I edit! I'm changing my mind here. I originally suggested E, however i think you can also make the case for pulmonary edema (D). a Pulmonary embolus would be much more abrupt in onset (not progressively worse for 3 hours).....also the has left shoulder pain/history of mild angina pectoris so he is probably now having unstable angina --> which is causing the pulmonary edema & the pulmonary edema explains all of his respiratory symptoms

4. A 52-year-old man comes to the physician because of a 3-month history of epigastric abdominal pain; he also has had an unintentional 6.8-kg (15-lb) weight loss during this period. He has osteoarthritis treated with naproxen as needed. He has immigrated to the UsA from Japan 6 months ago. He eats mostly traditional Japanese food prepared by his wife. He has smoked 2 packs of cigarettes daily for 30 years and drinks three to four glasses of wine daily. He is 170 cm (5 ft 7 in) tall and now weighs 82 kg (180 lb); BMI is 28 kg/m^2. Physical examination shows epigastric tenderness. Upper gastrointestinal endoscopy shows a 4-cm ulcer in the stomach. Examination of a biopsy specimen of the lesion confirms adenocarcinoma. Which of the following is the strongest predisposing risk factor for the patient's condition?
A. Alcohol use
B. Diet
C. Ethnicity
D. Naproxen
E. Tobacco use


I think answer is B. nitrosamines in japanese food. I don't think tobacco/alcohol use are major risk factors for gastric adenocarcinoma. especially considering that this cancer has been increasing in incidence in the japanese
 
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Tobacco use definitely raises the rate of gastric adenocarcinoma. Cancer.org says: "Smoking increases stomach cancer risk, particularly for cancers of the upper portion of the stomach closest to the esophagus. The rate of stomach cancer is about doubled in smokers."

They don't put a % increase in cancer risk with nitrosamines. I guess it has to be more than doubled since the NBME says that "diet" is the correct answer but I haven't seen a source giving a definitive number. From the searches I've done it sounds like the dietary link to gastric adenocarcinoma is weaker than the smoking link. Wonder what's up with that?
 
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4. A 52-year-old man comes to the physician because of a 3-month history of epigastric abdominal pain; he also has had an unintentional 6.8-kg (15-lb) weight loss during this period. He has osteoarthritis treated with naproxen as needed. He has immigrated to the UsA from Japan 6 months ago. He eats mostly traditional Japanese food prepared by his wife. He has smoked 2 packs of cigarettes daily for 30 years and drinks three to four glasses of wine daily. He is 170 cm (5 ft 7 in) tall and now weighs 82 kg (180 lb); BMI is 28 kg/m^2. Physical examination shows epigastric tenderness. Upper gastrointestinal endoscopy shows a 4-cm ulcer in the stomach. Examination of a biopsy specimen of the lesion confirms adenocarcinoma. Which of the following is the strongest predisposing risk factor for the patient's condition?
A. Alcohol use
B. Diet
C. Ethnicity
D. Naproxen
E. Tobacco use


I think answer is B. nitrosamines in japanese food. I don't think tobacco/alcohol use are major risk factors for gastric adenocarcinoma. especially considering that this cancer has been increasing in incidence in the japanese

I agree w/ iCY, it's definitely the nitrosamines in smoked food and Japanese background (japanese background to support the nitrosamines in smoked food, not choice c)
 
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1. A 62-year-old man is brought to the emergency department because of a 3-hour history of progressive difficulty breathing and mild left shoulder pain. His symptoms began after he ran up several flights of stairs. He has poorly controlled hypertension and mild angina pectoris. He has smoked one-half pack of cigarettes daily for 40 years. He appears uncomortable and has labored breathing. Diffuse crackles, ronchi, and scattered wheezing on auscultation of the posterior lung fields. His arterial PO2 is 58 mm Hg. Which of the following is the most likely diagnosis?
A. Cardiac tamponade
B. Pneumonitis
C. Pneumothorax
D. Pulmonary edema
E. Pulmonary embolism


My answer was C. pneumothorax and that was wrong. I figured that his emphysema destroyed the lung parenchyma, thus increasing his risk of spontaneous pneumothorax (consistent with mild pain and hypoxemia). Although I wasn't happy with that choice because he has crap in his lungs which made me think pulmonary edema, but I figured a 40 year smoker is almost always going to have crap in his lungs. What do you guys think? We never really learned about acute episodes of pulmonary edema from simply walking up stairs in angina pectoris. Does that commonly happen?

2. An investigator is studying the human immune response to tumor antigens in malignancies. Which of the following sets of cancer types and tumor antigens is most likely to produce the highest antibody titer?
Cancer type; Tumor antigen
A. B-cell lymphoma; CD19
B. Breast cancer; HER2/neu
C. Cervical cancer; HPV type 16 E6 protein
D. Melanoma; tyrosinase
E. Prostate cancer; prostatic acid phosphatase


I picked B. Breast cancer; HER2/neu and that was wrong. I didn't even know where to begin on this one. I went with which cancer has a monoclonal antibody treatment, since I figured that means that the cancer was immunogenic enough for labs to create a synthetic drug (perhaps by studying cancer patient's serum antibodies?). Obviously not. What principles are going on here that I am totally missing? Is it something like HPV E6 is a viral component, therefore it's more immunogenic than any cancer that over expresses self-antigen? Is it some principle of which antigen is sitting on the cell membrane thus most accessible to circulating antibodies?

3. A 42-year-old man comes to the physican because of a 4-week history of muscle cramping and pain. Two months ago, he began treatment with simvastatin (80 mg daily) for hypercholesterolemia. After 1 month, marked improvement was noted in his serum LDL-cholesterol concentration, but serum triglyceride concentration remained increased. At that time, gemfibrozil was added to his regimen to decrease his triglyceride concentration. Physical examination today shows no abnormalities. This patient's myalgia is most likely related to which of the following effects of gemfibrozil on simvastatin?
A. Decreased bioavailability
B. Increased absorption
C. Inhibition of cytochrome P450 metabolism
D. Inhibition of hepatic glycosylation
E. Inhibition of hepatic sulfation


I picked D. inhibition of hepatic glycosylation and that was wrong. This question really ticked me off. I asked two professors at my school's pharmacology department and they said they couldn't find a source that could support any of those five answer choices. I mean maybe they didn't search that exhaustively, but it just seems silly that two PhD pharmacologists can't find the answer. What do you guys think? I remember from the Kaplan videos that gemfibrozil inhibits excretion of statins but Raymond never specifies the exact mechanism beyond that it's NOT P450 inhibition. I presume it's by inhibiting glucuronidation? Anyway, that's not an answer choice (on the exam when I saw glycosylation, I read glucuronidation... oops). Is it sulfation?

4. A 52-year-old man comes to the physician because of a 3-month history of epigastric abdominal pain; he also has had an unintentional 6.8-kg (15-lb) weight loss during this period. He has osteoarthritis treated with naproxen as needed. He has immigrated to the UsA from Japan 6 months ago. He eats mostly traditional Japanese food prepared by his wife. He has smoked 2 packs of cigarettes daily for 30 years and drinks three to four glasses of wine daily. He is 170 cm (5 ft 7 in) tall and now weighs 82 kg (180 lb); BMI is 28 kg/m^2. Physical examination shows epigastric tenderness. Upper gastrointestinal endoscopy shows a 4-cm ulcer in the stomach. Examination of a biopsy specimen of the lesion confirms adenocarcinoma. Which of the following is the strongest predisposing risk factor for the patient's condition?
A. Alcohol use
B. Diet
C. Ethnicity
D. Naproxen
E. Tobacco use


Okay so we have a male Japanese who eats nitrosamines, smokes, drinks, and uses NSAIDS. My answer was C. ethnicity and that was wrong. All I remembered when doing this question was that Japanese have a 3x elevated rate of occurrence of gastric adenocarcinoma vs whites in the US. I know that H. pylori causes most gastric adenocarcinoma, but that's not an answer choice unless I'm totally missing something. So the SECOND most common cause is what? Am I going to feel really dumb because I didn't habitually guess smoking?

Thanks for any feedback!
(1) D. symptoms suggestive of acute MI or unstable angina => heart failure = up hydrostatic pressure in pulmonary veins = pulmonary edema

(2) C. All of the other answer choices are "self" proteins that are normally made by the body and thus will be poorly immunogenic. Only HPV/E6 is an example of a foreign antigen that will induce a vigorous immune response

(3) The answer was CYP450 inhibition, but that was a guess. Fibrates aren't on the list of any CYP450 inhibitors i've seen.

(4) Diet. Japonese get gastric cancer due to heavy nitrosamine intake.

I actually got all of the above right, so those are the answers.

I had a few questions though. Is Acute intermittent porphyria autosomal dominant? CO inhibits cytC. I'm assuming it inhibits transport of electrons to cytC and not from cytC (I put transfer from and got it wrong)

Then there was some neuroanatomy one where I must have mis-identified which line was the central sulcus.
 
(1) D. symptoms suggestive of acute MI or unstable angina => heart failure = up hydrostatic pressure in pulmonary veins = pulmonary edema

(2) C. All of the other answer choices are "self" proteins that are normally made by the body and thus will be poorly immunogenic. Only HPV/E6 is an example of a foreign antigen that will induce a vigorous immune response

(3) The answer was CYP450 inhibition, but that was a guess. Fibrates aren't on the list of any CYP450 inhibitors i've seen.

(4) Diet. Japonese get gastric cancer due to heavy nitrosamine intake.

I actually got all of the above right, so those are the answers.

I had a few questions though. Is Acute intermittent porphyria autosomal dominant? CO inhibits cytC. I'm assuming it inhibits transport of electrons to cytC and not from cytC (I put transfer from and got it wrong)

Then there was some neuroanatomy one where I must have mis-identified which line was the central sulcus.

Yes AIP is AD. Dont get mixed up with the cytochrome business - just know CO, CN, N3 block electron transfer to O2 - that is the cytochrome you should have chosen.
 
I had a few questions though. Is Acute intermittent porphyria autosomal dominant? CO inhibits cytC. I'm assuming it inhibits transport of electrons to cytC and not from cytC (I put transfer from and got it wrong)

Then there was some neuroanatomy one where I must have mis-identified which line was the central sulcus.

Carbon monoxide inhibits Cyt a+a3 => O2, answer choice "E". I think I confused myself on that one too by thinking it was cytochrome C that's inhibited by carbon monoxide, when really it's cytochrome C oxidase that is inhibited by carbon monoxide. Also if they asked about cyanide then it'd be the same answer.

The answer to the neuroanatomy one w/ left hand weakness was "B" (somatosensory cortex), with "C" being the motor cortex, and "D" being the premotor.
 
hii..exm in three days nbme 13
a mouse melanoma b13 is injected to its tail,tumors are formed at liver ,lung,ovaries..another mouse initially injected with antibody to liver surface antigen no nodules are present in liver,but are present in lung and ovaries,
in vitro the antibody doesnt show any cyto toxic affect,which of the following process most likely affected
1)homing
2)initiation
3)invasion(wrong)
4)motility
5)progression
6)invasion
 
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How are y'all able to see which individual questions you got wrong? Is that included in the extended feedback option? The description I read implied that you would not be told which specific questions you got wrong.
 
In the one with the 77 year old lady where they show the picture of her spine and she has osteoporosis, which is elevated? Is it IL-1? cus that's the only one I'm left with but I've never heard that IL-1 is increased in osteoporosis.
 
In the one with the 77 year old lady where they show the picture of her spine and she has osteoporosis, which is elevated? Is it IL-1? cus that's the only one I'm left with but I've never heard that IL-1 is increased in osteoporosis.

Another name for IL-1 is osteoclast activating factor. I think Goljan mentioned it somewhere. There was another question about the pathophys of multiple myeloma and the TNF alpha / IL-1 pathway was the answer to that too.
 
How are y'all able to see which individual questions you got wrong? Is that included in the extended feedback option? The description I read implied that you would not be told which specific questions you got wrong.

It doesn't tell you the right answer but it does tell you which questions you specifically got wrong.

The statins/fibrates question really ticked me off. I can't believe that CYP450 inhibition was the right answer since I can't find any evidence of that anywhere in my books or on the 'net. Eh, whatever.

This one was tough -- really didn't see much improvement from NBME 12 last week. Anatomy and genetics killed me on this one.

Did anyone get the question right about the thalassemia and mRNA changes? I thought it was a splicing defect but got it wrong.
 
It doesn't tell you the right answer but it does tell you which questions you specifically got wrong.

The statins/fibrates question really ticked me off. I can't believe that CYP450 inhibition was the right answer since I can't find any evidence of that anywhere in my books or on the 'net. Eh, whatever.

This one was tough -- really didn't see much improvement from NBME 12 last week. Anatomy and genetics killed me on this one.

Did anyone get the question right about the thalassemia and mRNA changes? I thought it was a splicing defect but got it wrong.

I felt the same one about the fibrate one too - wiki apparently says it's CYP 450 inhibitor though. Oh well. Hopefully it's on my test because I'll never forget it!

I got that thalassemia one wrong too. The correct answer was "cleavage and polyadenylation." The person had a mutation in AATAAA=>AACAAA which is the sequence required to initiate mRNA adenylation.
 
A 43 year old man comes to the ED because of a 1-year history of low back pain. Before this examination, the patient says, "My physician is arrogant and insensitive. He never returns my phone calls, i always have to wait forever to be seen, the tests he orders are painful and unnecessary, and he can never tell me what is causing my back pain or how to treat it." Which of the following is the most appropriate response by the ED physician about this patient's complaint?

A. Reassure the patient that his physician's behavior is not unusual, and that low back pain can be difficult to assess
B. Encourage the patient to make an appointment with his physician to communicate his concerns.
...
... (not great answer choices)
E. Telephone the patient's physician to make him aware that the patient is very dissatisfied with treatment.

I picked A but clearly was wrong. I think it might be B. Did anyone get it right?
 
I picked A too, but I think it's probably E. Telling the patient to do something seems like it's less likely to be the right answer than taking charge doing it yourself.
 
A 43 year old man comes to the ED because of a 1-year history of low back pain. Before this examination, the patient says, "My physician is arrogant and insensitive. He never returns my phone calls, i always have to wait forever to be seen, the tests he orders are painful and unnecessary, and he can never tell me what is causing my back pain or how to treat it." Which of the following is the most appropriate response by the ED physician about this patient's complaint?

A. Reassure the patient that his physician's behavior is not unusual, and that low back pain can be difficult to assess
B. Encourage the patient to make an appointment with his physician to communicate his concerns.
...
... (not great answer choices)
E. Telephone the patient's physician to make him aware that the patient is very dissatisfied with treatment.

I picked A but clearly was wrong. I think it might be B. Did anyone get it right?

B - always advise patient to discuss issues with his physician directly.
 
I'm clearly missing something (most likely brain cells): what's the difference btw pulmonary and bronchial arteries? I believe the question was like what is more indicative of pulm vs bronchial...
 
22 y/o woman develops right flank pain 3 days after undergoing appendectomy and right ovarian resection because of appendiceal abscess. Vital signs are normal. On exam, she has mild right flank tenderness. Most likely cause of this patient's pain is accidental ligation of which of the following structures on the right?

Ovarian Artery
Ovarian Vein
Renal Artery
Renal Vein
Ureter
Uterine ligament

Correct answer is apparently Ureter. Why wouldn't there be a stronger physiologic response beyond mild flank pain if the ureter was ligated? What would happen if the Uterine ligament was ligated?
 
This is a clinical question. Not all of Step 1 is basic science. This just happens to be the most common error during this kind of surgery.
 
22 y/o woman develops right flank pain 3 days after undergoing appendectomy and right ovarian resection because of appendiceal abscess. Vital signs are normal. On exam, she has mild right flank tenderness. Most likely cause of this patient's pain is accidental ligation of which of the following structures on the right?

Ovarian Artery
Ovarian Vein
Renal Artery
Renal Vein
Ureter
Uterine ligament

Correct answer is apparently Ureter. Why wouldn't there be a stronger physiologic response beyond mild flank pain if the ureter was ligated? What would happen if the Uterine ligament was ligated?

No, because you are thinking the Cardinal ligament (contains uterine vessels) NOT the uterine ligament (which is the Broad ligament) and does not contain vessels. Acute hydronephrosis via ureter ligation would cause these symptoms.
 
This is a clinical question. Not all of Step 1 is basic science. This just happens to be the most common error during this kind of surgery.

No, because you are thinking the Cardinal ligament (contains uterine vessels) NOT the uterine ligament (which is the Broad ligament) and does not contain vessels. Acute hydronephrosis via ureter ligation would cause these symptoms.

Thanks for the input/help.
 
Increase of Beta chains of fetal hemoglobin will increase the affinity of Hb for what
Any input guys.
 
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What do you mean by PFK-1? I'm not sure which question you're referring to. There was one question about using hydroxyurea in sickle cell anemia to increase HbF, in which case the answer is that you get an increase in affinity for oxygen.
 
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Increase of Beta chains of fetal hemoglobin will increase the affinity of hemoglobin for which of the following substances? The options are CO2,Chloride ions,0xygen,Protons,PFK 1?
Any input guys.

What was the wrong answer that you picked? If I had to GUESS, I'd guess proton. Compared to HbF, it would have a lower affinity for O2, so it should theoretically bind to H+ more

Are you sure that's what the question said? Fetal hemoglobin should not express beta chains at all so is it asking if beta chains are expressed alongside fetal Hb?

Why I don't think its the other choices:
PFK1 is an enzyme and is nonsense (probably to throw you off into thinking 23BPG), you see a Cl shift but it shouldnt bind Hb, CO2 does not bind Hb but will dissociate to bicarb and H+ where bicarb is part of the Cl shift and H+ can be buffered by binding Hb, HbF is left shifted so it has HIGHER affinity for O2 than HgB which is how the baby gets o2 from mom. When Hg binds O2 in the lungs, it kicks off H+ to reform CO2 to be breathed out

But again, are you sure that's the way the questioned was stated because it sounds like a poorly worded question as is...
 
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I see all the above questions have been clarified :)

I made mistakes in the following. Any suggestions regarding the correct choice?
Any explanations would be much appreciated

1. An autopsy is done on a 50-year-old man who died of pneumonia despite 5 days of antibiotic therapy in the intensive care unit. He had a 15-year history of
alcoholism. A photograph of a sagittal section of the brain is shown. Based on this pathology, which of the following findings was most likely present on
neurologic examination of the patient prior to his death?
A) Dysdiadochokinesia WRONG :(
B) Dysmetria on finger nose testing
C) Essential tremor
D) Gait ataxia
E) Present Romberg sign

I had no idea what was wrong in the cerebellum. Looked fine to me :(


2. A 76-year-old woman is brought to the emergency department because of a 3-hour history of severe headache, slurred speech, and confusion. She has a 2-year history of atnal fibrillation. She has difficulty
understanding and answering questions, but she is cooperative. Ophthalmologic examination shows hemianopia and a tendency to gaze to the right. The pupils are normal sized and reactive to light. Neurologic
examination shows left-sided numbness and paralysis that are more severe In the face and upper extremity than In the lower extremity. Which of the following arteries is most likely Involved in this patient's condition?
A) Anterior cerebral
B) Anterior spinal
C) Middle cerebral artery. right?
D) Posterior cerebral WRONG :(
E) Vertebral

Visual problems -> post cerebral artery right? :(


3. A 54-year-old man has a squamous cell carcinoma of the right lung. Analysis of his germline DNA shows two alleles. m and n, at the microsatellite locus Z tightly linked to the p53 gene. Similar analysis of the
neoplastic cells shows the presence of the m allele only. These findings are most likely due to which of the following processes?
A) Germline mosaicism
B) Loss of heterozygosity. right?
C) p53 Gene amplification
D) Pericentric inversion involving p53 and locus Z
E) Point mutation of allele n WRONG

WTF was this? What is germline DNA?

4. An 18-year-old woman with mild mental ******ation is brought to the physician because of a 3-day history of decreased ability to see in reduced light. She has a lifelong history of chronic diarrhea. Two years ago,
she developed a lack of muscle control of her arms and legs, and generalized weakness. Her 16-year-old brother has had similar symptoms. Ophthalmologic examination shows bilateral retinitis pigmentosa. There
is ataxia and loss of deep tendon reflexes. Laboratory studies show erythrocytes with spiny projections and a serum total cholesterol concentration of 40 mg/dL. Which of the following apolipoproteins is most likely
deficient in this patient?
A) ApoA-l
B) Apo A-Il
C) ApoB
D) ApoC
E) ApoE WRONG :(

:(

5. A 43-year-old man comes to the physician for a routine health maintenance examination. He is 170 cm (5 ft 7 in) tall and weighs 86 kg (188 lb); BMI is 30 kg/rn2. Physical examination and laboratory studies show no
other abnormalities. He tells the physician. "My older brother just got diagnosed with diabetes. I don't want that to happen to me. What should I do?" Which of the following diets is most likely to be effective in
decreasing this patient's risk for type 2 diabetes mellitus?
A) Low-calorie. right?
B) Low-carbohydrate WRONG :(
C) Low-cholesterol
D) Low-protein
E) Low-sodium

:(

6. A 7-year-old girl is brought to the physician by her parents because of a 3-year history of temper tantrums when her parents leave her. She refuses to sleep alone and recently would not attend her friend's birthday
slumber party. She calls to her mother If she is In another room of the house. Each morning, the patient's teacher has to carry her Into school crying. Her mother recently returned to work full-time and says that she
is quite angry that her daughter is behaving in such a defiant way. Her father recalls that he behaved the same way when he was her age. Which of the following is the most likely explanation for this patient's
behavior?
A) Conduct disorder
B) Oppositional defiant disorder
C) Post-traumatic stress disorder
D) Separation anxiety disorder Right?
E) Normal behavior WRONG

I thought the kid was too old to have separation anxiety disorder :(

7. A female newborn is delivered at 34 weeks' gestation in an advanced-care setting where special delivery systems are available. The diagnosis of persistent pulmonary hypertension is made. Considering that the
newborn can be carefully monitored for methemoglobinemia, which of the following is the most appropriate therapy?
A) Desflurane
B) Hyperbaric oxygen
C) Nitric oxide
D) Nitrous oxide WRONG.
E) Oxygen diluted with helium

WTF was this about?
 
1. Alcoholics --> cerebellar atrophy --> gait ataxia

2. That sounds like a classic MCA stroke. You can get contralateral hemianopia with a MCA.

3. LOH sounds right, but I'm not 100%

I see all the above questions have been clarified :)

I made mistakes in the following. Any suggestions regarding the correct choice?
Any explanations would be much appreciated

1. An autopsy is done on a 50-year-old man who died of pneumonia despite 5 days of antibiotic therapy in the intensive care unit. He had a 15-year history of
alcoholism. A photograph of a sagittal section of the brain is shown. Based on this pathology, which of the following findings was most likely present on
neurologic examination of the patient prior to his death?
A) Dysdiadochokinesia WRONG :(
B) Dysmetria on finger nose testing
C) Essential tremor
D) Gait ataxia
E) Present Romberg sign

I had no idea what was wrong in the cerebellum. Looked fine to me :(


2. A 76-year-old woman is brought to the emergency department because of a 3-hour history of severe headache, slurred speech, and confusion. She has a 2-year history of atnal fibrillation. She has difficulty
understanding and answering questions, but she is cooperative. Ophthalmologic examination shows hemianopia and a tendency to gaze to the right. The pupils are normal sized and reactive to light. Neurologic
examination shows left-sided numbness and paralysis that are more severe In the face and upper extremity than In the lower extremity. Which of the following arteries is most likely Involved in this patient's condition?
A) Anterior cerebral
B) Anterior spinal
C) Middle cerebral artery. right?
D) Posterior cerebral WRONG :(
E) Vertebral

Visual problems -> post cerebral artery right? :(
 
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5 is a low-calorie diet. He doesn't have Diabetes Type II yet (based on the absence of any other abnormalities) so he only needs to lower his weight. Lowering weight requires low-calorie not low-carb.

I'd say low-carb would be suitable for someone thats already a diabetic, but low-calorie would work there as well.

6- would seem to be separation anxiety disorder. I think you're thinking of Separation Anxiety which is in infants whereas Separation Anxiety Disorder is normal in that age.

7- is Nitric Oxide. Nitrous Oxide is a general anesthetic whereas Nitric Oxide is the vasodilator. I might say hyperbaric O2, but they specifically mention methemoglobinemia which results from nitrate drugs so I guess its Nitric Oxide.
 
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I just finished nbme13 and man it was brutal, my scored dropped like 15 points compare to nbme12. Has anyone experienced this or is it just me damn
 
I just finished nbme13 and man it was brutal, my scored dropped like 15 points compare to nbme12. Has anyone experienced this or is it just me damn
I dropped 2 points from NBME 12, and 7 from NBME 7. The curve on these NBMEs is so tight that 1-2 questions causes quite a jump or decrease in scores.
 
I think the other Qs were covered/explained, but I figured I'd add to the pool of knowledge... at least, I hope I'm adding to it! :)

2. MCA is correct. What gave it away to me was the upper extremity and face numbness and paralysis, which on the motor and sensory homunculi corresponds to the lateral part of the brain (supplied by the MCA). The gaze going to the right indicates a frontal eye field defect, also in the lateral part of the brain. The hemianopia I am guessing is from knocking out both the Meyer's loop and dorsal optic radiations in the temporal and parietal lobes respectively (each one on their own would have the quadrantic anopia). A PCA lesion would have hemianopia with macular sparing since the macula has its own blood supply.

3. Loss of heterozygosity is definitely correct. I didn't really understand this one that well, but I used process of elimination. If you had a point mutation in n, you would still have m and p53 present on the gene. Pericentric inversion when the genes are tightly linked is unlikely and it also doesn't usually cause a loss of genes unless there is unbalance. Obviously not amplification of p53 since it was lost in the tumor cells. And since the tumor cells are not germ cells, you can rule out germline mosaicism. Germline DNA is in gonadal cells (sperm/ova).

4. Apo B. I think this is a weird presentation (at least according to what I read in First Aid) in terms of age, but I think this is abetalipoproteinemia. It's autosomal recessive though as far as I can tell and usually presents early. Symptoms fit though-- night blindness, ataxia, spiky RBCs. But I did process of elimination on this one since I didn't know that cluster of symptoms beforehand-- seemed to me that the neuro involvement was due to dysfunctional myelin production, the night blindness was due to low Vitamin A (and therefore low fat absorption, supported by the diarrhea), and really low cholesterol meant that either she wasn't absorbing it from her diet (which if I remember correctly only contributes to ~30% of total cholesterol anyway), wasn't synthesizing it, or it wasn't floating around in her blood. Since the answer choices were all Apo proteins, I deduced that it was either B or E like you did, but since E is really for the chylomicron remnants only and B was for actual uptake by the tissues, I assumed that B was the one that was defective.

I see all the above questions have been clarified :)

I made mistakes in the following. Any suggestions regarding the correct choice?
Any explanations would be much appreciated

...
 
Eek I should have saved this exam until a much later date. Any help is appreciated!!

1) 60 yo carpenter w/ difficulties using tools. Smoked for 45 yrs, drinks lots of alcohol. PE showed no lymphadenopathy. Decr strength in upper and lower extremities (4/5) and atrophy of hand muscles. Has diffuse hyperreflexia. Fasciculations in hands and upper extremity muscles. Sensory exam normal. What do you expect to find in future?
a. Dementia
b. Difficulties swallowing
c. Loss of facial sensation
d. Loss of peripheral vibratory sensation
e. Nystagmus

2) 55 yo recovers from stroke 2 yrs ago and lives alone. He has incr risk of what?
a) agoraphobia
b) major depressive disorder
c) obsessive compulsive disorder
d) PTSD
e) social phobia

3) Tracings of skeletal muscle responses to electrical stimulation and asked which one represented the highest amt of calcium sequestered in the SR

4) Woman on lithium. Tonicity in 3 tubule structures compared to serum (proximal tubule, JGA, medullary collecting duct). I thought it was iso, hypo, hyper but it's not that. Thanks!
 
1. ALS with both LMN (atrophy) and UMN (hyperreflexia) signs --> difficulties swallowing

4. Lithium acts as a ADH antagonist, so think about those effects.

Eek I should have saved this exam until a much later date. Any help is appreciated!!

1) 60 yo carpenter w/ difficulties using tools. Smoked for 45 yrs, drinks lots of alcohol. PE showed no lymphadenopathy. Decr strength in upper and lower extremities (4/5) and atrophy of hand muscles. Has diffuse hyperreflexia. Fasciculations in hands and upper extremity muscles. Sensory exam normal. What do you expect to find in future?
a. Dementia
b. Difficulties swallowing
c. Loss of facial sensation
d. Loss of peripheral vibratory sensation
e. Nystagmus

4) Woman on lithium. Tonicity in 3 tubule structures compared to serum (proximal tubule, JGA, medullary collecting duct). I thought it was iso, hypo, hyper but it's not that. Thanks!
 
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