NBME 12 discussion

[titan25]

1 v max 1 enzyme is 300 and 2 nd 30 compare the Km values

km1 is 10 times km 2
km1 is 1/10 km2
we cant compare


2 upregulation of which protects from ARDS is IL 10

3 which anti hypertensive restores back potassium other k sparing

4 a 14 years old brougt to physian because mostly sleeping withdrawn and complaining of abdomen pain 3 weeks , what history will u take first...should we recretion drug history....options school history , devlopmental, family history

5 a drug given in two patients obese and normal given same doses graph ploted with conc on y axis and time on x , slope of normal person is greater
compared to normal person drug x in obese has

greater VD/ lower bioavailability / higher clearance/ shorter absorption

6 pedigree given four genrations AD 1st genration gene seq 4 5 6 changes to 156 cause...is it recombination

7 cytoplasmic enzyme mutated at 127 alanine replaced by serine why reduction of enzyme activity

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[HelpPleaseMD]

I'd say ure lacking FA knowledge. it is explicitly stated in FA that Chlamydia is intracellular. its also why doxy works really well on it cause that antibiotic tends to accumulate within cells.

 

[RedSoxSuck]

two quick questions that havent been covered, thanks in advance:



2.) man with premature ejaculation: do you give him an ssri or viagra?

Well i thought problem is due to SSRI so perhaps give him cyproheptadine since its serotonin antagonist. Damn!

 

[RedSoxSuck]

I'd say ure lacking FA knowledge. it is explicitly stated in FA that Chlamydia is intracellular. its also why doxy works really well on it cause that antibiotic tends to accumulate within cells.

Yea, it is and i remembered but just failed to think about it.

 

[RedSoxSuck]

Is anyone else categorizing their mistakes? I am trying to limit the categories to failed integration, didn't know, careless mistake/faulty recall and WTF? Suggestions. Thanks

 

[RedSoxSuck]

4. 70 y/o male with 6 month history of abnormal sleep behavior, punches at the air and yells as if acting out his dreams but doesn't wake up, and often falls on the floor; no abnormality on neuro exam, what would you find in patient?

Answers: absent muscle atonia in REM, anterior cingulate mass lesion, major depressive disorder with psychotic features, left temporal EEG spikes, nocturnal hypoglycemia (no clue about this, i said left temporal EEG, but it could also be muscle atonia absent in REM)

[/QUOTE]

I put Left temporal lobe as well. So if he has muscle atonia during REM, then why is he able he is able to punch at the air...this threw me off. Thanks

 

[HelpPleaseMD]

giving viagra for premature ejac is just lol.

 

[HelpPleaseMD]

4. 70 y/o male with 6 month history of abnormal sleep behavior, punches at the air and yells as if acting out his dreams but doesn't wake up, and often falls on the floor; no abnormality on neuro exam, what would you find in patient?

Answers: absent muscle atonia in REM, anterior cingulate mass lesion, major depressive disorder with psychotic features, left temporal EEG spikes, nocturnal hypoglycemia (no clue about this, i said left temporal EEG, but it could also be muscle atonia absent in REM)

I put Left temporal lobe as well. So if he has muscle atonia during REM, then why is he able he is able to punch at the air...this threw me off. Thanks[/QUOTE]

"absent muscle atonia = has tone"

 

[RedSoxSuck]

In a patient with chronic peripheral neuropathy, enzyme histochem staining showed fiber grouping. Why?

Altered expression of muscle enzyme due to damage nerve fibers.
altered trophic substance from the innervating neurons.
Regeneration of muscle fibers ( wrong )
Reinnervation of muscle fibers by regen. axons (correct according to other posts). Why is this correct?

 

[RedSoxSuck]

Yeah limited to the forehead definitely points to helmet

I got this wrong. I chose allergy to family pet. How can this trap be avoided? Perhaps reading the question more carefully and realizing that problem is only on a particular part of the body? These kind of questions are gimme's are shouldnt be missed. Thanks folks!

 

[RedSoxSuck]

Hey GTFOOMICT, I just took NBME 12 today too.. what a blow to my confidence. A week ago I got a 232 on UWSA#2 and NBME 12 took me down to a 205! What gives?

Same here. But i did not do as well as you on UWSA 2 because i made around 14 silly, slap me now kinnda mistakes. I thought NBME 12 was little more tricky.

 

[RedSoxSuck]

Would anyone mind expanding on the following setup/explanation? Kind of still confused as to why 2.3 - 1.3.

Here is the question:

The other one regarding the NNT was 100

The question asked "how many women need to have babies and treated to prevent a woman from getting ANY development disorder"

Using trace metals as the control group, it would have been"

2.3% - 1.3% = 1.0% absolute risk reduction

Then 1/0.01 = 100

Thanks

 

[ijn]

In a patient with chronic peripheral neuropathy, enzyme histochem staining showed fiber grouping. Why?

Altered expression of muscle enzyme due to damage nerve fibers.
altered trophic substance from the innervating neurons.
Regeneration of muscle fibers ( wrong )
Reinnervation of muscle fibers by regen. axons (correct according to other posts). Why is this correct?

So normally you have type 1 and 2 muscles fibers evenly distributed in a muscle biopsy. Let's say you have a disease like ALS where you have death of peripheral neurons. The body tries to compensate via axonal regeneration. The regenerating axon will then innervate the muscle fibers in a given area of deinnervation. All muscle fibers will assume either type 1 or type 2 depending on what type of muscle the neuron originally innervated. On biopsy you no longer have a checkboard appearance of type 1 and 2 fibers. They'll either be pure type 1 or pure type 2.

The other test question they really like related to this topic are giant motor unit action potentials (MUAPs).

 

[ijn]

I got this wrong. I chose allergy to family pet. How can this trap be avoided? Perhaps reading the question more carefully and realizing that problem is only on a particular part of the body? These kind of questions are gimme's are shouldnt be missed. Thanks folks!

I think one way to think about it is this - the NBME isn't like Kaplan or UWorld. The NBME (and STEP 1) is extremely straight forward. They don't play tricks. If they include BMI in the question prompt, it's for a reason (99% of the time you can probably guess it's a question on PCOS or degenerative joint disease without reading anything else lol). If they tell you it's limited to a specific part of the body, it's for a reason. Like let's say she has a rash, but it's only on her arms or only on her legs (and they'll probably throw in it's linear in distribution) - that's a huge buzz phrase for poison ivy.

Sure, they include superfluous lab information all of the time, but when it's there's something unique or odd in the patient presentation then they are looking for a unique or odd answer. They aren't playing mind games.

 

[HelpPleaseMD]

ijn is right as usual, but I'd like to qualify that a bit. I had quite a few questions on the uslme exam where they would deliberately make you think one answer but then ask something totally different to confuse you

 

[RedSoxSuck]

1.There was a question about an elderly woman with Alzheimer’s and they wanted to know where the lesion was. I guess the answer was hippocampal formation. Why not mammillary bodies? Or for answer to be mammillary body, there had to some sort of thiamine/alcohol clue? Or is it just based on age and going for the better answer?

2.Question about a 38 year old man showing small testes and no sperm. Was the answer Chromosomal analysis of lymphocyte?

3.27 year old man had recurrent vesiculoulcerative lesions of vermillion borders of the lips for last 6 months. Virus remains latent where? Answers: Endothelial cells, epithelial cells, macrophage, myocyte, neurons and osteoclast. I thought it was herpes 1 which is latent in trigeminal ganglia so answer is: Neurons?

4. Diagnosis of Ehrlichiosis is made. Mechanism of antibiotic? Binding to folic acid, binding to glycoprotein, hydrogen ion, inhibition of glucose syn, inhibit of peptioglycan sys or protein syn, inhibit of water uptake..

5. 51 yo female visits doctor because of a firm lump in her neck for 5 months. PE: modest symmetric enlargement of the thyroid gland. Her serum T4 (1.8). What additional serum findings? Decreased TSH, decreased thyrotropin release hormone, increased thyroxine binding globulin, presence of anti thyroid peroxidase ab or presence of TS antibodies (my answer).

I was thinking its graves. So i think most likely (best answer) is probably decreased TSH?

6. 70 yo female crying and difficulty sleeping because her husband died 3 weeks ago. No suidical ideas. What is the appropriate initial action by doc? Encouraging the patient to live with a relative (wrong), provide supportive counseling ( eliminated bc you are handing her off to someone else), recommend cognitive behav, antidepress, long acting benzo?

7. 16 yo girl with type 1 dm, she is happy to have lost weight and would like to lose more, hb a1c is 8.4%...Whic of her behavior led to her weight loss? Decrease amt of self administered insulin (seems like a right answer after re reading and realizing diff hb a1c compare to what it was 6 months ago), overuse of laxatives, restricting calorie consump (wrong), self induced vomitting, starting an intense exercise program.

8. 22 yo male cant conceive for 2 years. His wife has kids from previous marriage. His PE shows well developed muscle mass, thick beard, profuse body hair, NO GYNECOMASTIA, bilateral testicular atrophy, no sperm, high testosterone, and no serum LH. Reason for azoospermia? Androgen insensitivity (wrong), hypo pit, non fucn testicular tumor, klinefelter, testosterone adminstration ( this seems correct bc of exogenous testoterone leading to negative feed back inhibition etc)

9. 24 yo male with 1 month history of recurrent episodes of headaches, palpitations, sweating. Last for 15 minutes. Has a large supra renal mass on the right side. Tissue involved arose from? ectoderm outpouching, ectodermal retention, endodermal invagination, mesodermal clustering (wrong), neural crest migration.

I think it has to do with pheochromocytoma so neural crest migration?


Thank you!

 

[RedSoxSuck]

I think one way to think about it is this - the NBME isn't like Kaplan or UWorld. The NBME (and STEP 1) is extremely straight forward. They don't play tricks. If they include BMI in the question prompt, it's for a reason (99% of the time you can probably guess it's a question on PCOS or degenerative joint disease without reading anything else lol). If they tell you it's limited to a specific part of the body, it's for a reason. Like let's say she has a rash, but it's only on her arms or only on her legs (and they'll probably throw in it's linear in distribution) - that's a huge buzz phrase for poison ivy.

Sure, they include superfluous lab information all of the time, but when it's there's something unique or odd in the patient presentation then they are looking for a unique or odd answer. They aren't playing mind games.

Good point. Thanks

 

[HelpPleaseMD]

1) dont remember the question. 2) yes- its the easiest to access cell 3) neurons 4) inhibit protein synthesis-- doxycycline is the doc for all these buggers. u gotta remember that. 5) I think I put presence of antithyroid peroxidase ab. DEF not Graves. Look at the T4 levels dude. 6) provide supportive counseling. How is that handing off to anyone else? 7) decrease amount of self administered insulin 8)Testosterone administration. 9) classic for pheo so yes neural crest.

Gotta review FA bro.

 

[RedSoxSuck]

1) dont remember the question. 2) yes- its the easiest to access cell 3) neurons 4) inhibit protein synthesis-- doxycycline is the doc for all these buggers. u gotta remember that. 5) I think I put presence of antithyroid peroxidase ab. DEF not Graves. Look at the T4 levels dude. 6) provide supportive counseling. How is that handing off to anyone else? 7) decrease amount of self administered insulin 8)Testosterone administration. 9) classic for pheo so yes neural crest.

Gotta review FA bro.

Yea, i agree. I seriously thought that 1.8 (T4) was elevated. I even looked it during the nbme. STUPID CARELESS mistakes cost me around 22 questions and thats a big chunk to give away. Thanks for your help.

 

[Boardz]

45 yo man has severe, substernal, crushing chest pain for the past 2 hours. His pulse is 100/min, respirations are 14/min, and blood pressure is 170/100 mmHg. A grade 3/6 holosystolic murmur is heard best over the cardiac apex. After treatment with oxygen, aspirin, nitroglycerin,morphine, and a thrombolytic, the chest pain resolves, and his blood pressure decreases to 120/60mmHg. Repeat auscultation of the chest does not detect a cardiac murmur.

Which of the following is the most likely cause of the murmur?

A: Acute aortic valve insufficiency
B: aortic dissection
C: atrial septal defect
D: Papillary muscle ischemia
E: Patent Ductus arteriosus
F: Ventricular Septal Defect (wrong)

Could someone tell me what the answer is and why?

 

[dendrites]

45 yo man has severe, substernal, crushing chest pain for the past 2 hours. His pulse is 100/min, respirations are 14/min, and blood pressure is 170/100 mmHg. A grade 3/6 holosystolic murmur is heard best over the cardiac apex. After treatment with oxygen, aspirin, nitroglycerin,morphine, and a thrombolytic, the chest pain resolves, and his blood pressure decreases to 120/60mmHg. Repeat auscultation of the chest does not detect a cardiac murmur.

Which of the following is the most likely cause of the murmur?

A: Acute aortic valve insufficiency
B: aortic dissection
C: atrial septal defect
D: Papillary muscle ischemia
E: Patent Ductus arteriosus
F: Ventricular Septal Defect (wrong)

Could someone tell me what the answer is and why?

Papillary muscle ischemia

 

[anamika t]

could someone explain how did we reach answer b? i m tired of applying my brains in this.. feel like don't have any brains now !!

 

[anamika t]

papillary muscle ischemia cos myocardial infarction could lead to papillary muscle ischemia, which can present with pan systolic murmur of mitral regurgitation at cardiac apex, rest all are signs of MI itself, and it resolves with treatment.. therefore AMI --> papillary muscle ischemia --> functional MR

 

[anamika t]

Papillary muscle ischemia

papillary muscle ischemia cos myocardial infarction could lead to papillary muscle ischemia, which can present with pan systolic murmur of mitral regurgitation at cardiac apex, rest all are signs of MI itself, and it resolves with treatment.. therefore AMI --> papillary muscle ischemia --> functional MR

 

[anamika t]

can someone tell me q 16 block 2

54 yr old woman with hypertension started on hydrochlorthiazide, now has low potassium, what can raise potassium and lower blood pressure further ?
a) atenolol
b)nifedipine
c) losartan

 

[Boardz]

can someone tell me q 16 block 2

54 yr old woman with hypertension started on hydrochlorthiazide, now has low potassium, what can raise potassium and lower blood pressure further ?
a) atenolol
b)nifedipine
c) losartan

Losartan. Angiotensin II stimulates adrenal release of aldosterone. ACEI and ARBs block this.

 

[eastcoastdr]

4. 55 y/o male who was shoveling snow and collapsed. He had weakness and tingling in upper and lower extremities before he collapsed. Now he has positive Babinski on left. CT shows brain bleed on the right. What’s the strongest predisposing risk factor?

Answer choices: cholesterol plaque, cigarette smoke, DVT, hypertension, vasculitis

Okay so the answer is Hypertension according to a previous poster. But this is a concept I am struggling with..I seem to always miss the stroke questions no matter how many times I review neuro. I'm looking at the section on Ischemic Brain Disease in FA 2012 (pg447) and from questions like this how do you differentiate between what caused his stroke (i.e. atherosclerotic vs. embolic vs. lacunar). I'm assuming since the answer is hypertension, the stem was trying to point at a lacunar stroke..which I know usually affects lenticulostriate arteries in internal capsule and causing contralateral hemiparesis. is that what this stem is getting at? It can't be embolic bc there is no Hx of afib, right? But how do we absolutely rule out cholesterol plaque? Is it becuase there's no Hx of high LDL levels or whatever? I guess HTN is just the better answer, huh?

 

[Boardz]

Okay so the answer is Hypertension according to a previous poster. But this is a concept I am struggling with..I seem to always miss the stroke questions no matter how many times I review neuro. I'm looking at the section on Ischemic Brain Disease in FA 2012 (pg447) and from questions like this how do you differentiate between what caused his stroke (i.e. atherosclerotic vs. embolic vs. lacunar). I'm assuming since the answer is hypertension, the stem was trying to point at a lacunar stroke..which I know usually affects lenticulostriate arteries in internal capsule and causing contralateral hemiparesis. is that what this stem is getting at? It can't be embolic bc there is no Hx of afib, right? But how do we absolutely rule out cholesterol plaque? Is it becuase there's no Hx of high LDL levels or whatever? I guess HTN is just the better answer, huh?

play odds. just like the number one cause of a heart attack is an in situ thrombosis of the coronary arteries (not emboli, etc.) --> atherosclerosis.

for subarachnoid hemorrhage, it isn't emboli, or a ruptured plaque... it's hypertension, slowly owning the vasculature up there (ADPKD, renal artery stenosis, aortic stenosis, etc. ALL of these have to do with increasing the blood pressure in the vasculature in your dome-piece predisposing you for subarachnoid hemorrhages.) (marfan's and ehler's make the vasculature weaker further predisposing you to ownage from hypertension)

aortic dissection? answer depends on if it's thoracic vs. abdominal.

if the dude was shoveling snow and had a thoracic dissection, play odds = hypertension was the #1 risk factor.

if the dude was shoveling snow and had an abdominal dissection, play odds = atherosclerotic plaque

pathoma was good for this.

 

[eastcoastdr]

thank you Boardz, you are right. Sometimes when I'm in exam mode I forget to stop and think about what is the BEST answer, not just what is a possible explanation. I'm taking Step 1 for real on Friday and I'm planning on spending the rest of my time reading Pathoma and my marked questions on uworld.

 

[Boardz]

thank you Boardz, you are right. Sometimes when I'm in exam mode I forget to stop and think about what is the BEST answer, not just what is a possible explanation. I'm taking Step 1 for real on Friday and I'm planning on spending the rest of my time reading Pathoma and my marked questions on uworld.

that's pretty much exactly what i'm doing. I play on doing all of pathoma again, all my incorrects (about 500), then the entire uworld qbank again, plus however many NBMEs I can throw in there. I have about 10 days. :I

edit: p.s. i was totally channeling goljan up there

 

[medstudentASY]

A 60-year old man with stable angina pectoris begins treatment with a medication that decreases ventricular preload and increases coronary artery blood flow. This medication is most likely to be effective because it acts on which of the following?

• Calcium conductance
• cAMP synthesis
• cGMP synthesis
• Potassium conductance
• Prostaglandin synthesis
• Sodium conductance

Was this cGMP synthesis, i.e. nitrates? I got stuck on trying to figure out how this would increases coronary blood flow. Venodilation --> Decreased VR --> Decreased CO --> SNS activation --> Increase contractility....?.. Increased CBF?

Probably a brain fart on my part but any explanation on this question would be appreciated.

 

[Boardz]

A 60-year old man with stable angina pectoris begins treatment with a medication that decreases ventricular preload and increases coronary artery blood flow. This medication is most likely to be effective because it acts on which of the following?

• Calcium conductance
• cAMP synthesis
• cGMP synthesis
• Potassium conductance
• Prostaglandin synthesis
• Sodium conductance

Was this cGMP synthesis, i.e. nitrates? I got stuck on trying to figure out how this would increases coronary blood flow. Venodilation --> Decreased VR --> Decreased CO --> SNS activation --> Increase contractility....?.. Increased CBF?

Probably a brain fart on my part but any explanation on this question would be appreciated.

Yeah it's cGMP. It's talking about drugs like nitroglycerin that are venodilators. I believe most, if not all, venodilators work through cGMP and they're popular in treating angina because they decrease the WORK & OXYGEN DEMAND of the heart.

Since they venodilate, that decreases the preload, which decreases the work the heart has to do, which decreases the OXYGEN DEMAND, which alleviates the angina.

Coronary blood flow occurs in diastole and when the heart is not contracting. Thus, coronary blood flow is increased. I forget if the coronary arteries are dilated themselves...

 

[medstudentASY]

Thanks. I just spoke to a friend about this and he mentioned that nitrates DO have a coronary vasodilatory effect. Was reading here http://cvpharmacology.com/vasodilator/nitro.htm and they mention too that even though nitrates are primarily venodilators, they do cause mild coronary vasodilation.
I got too caught up on whether nitrates cause coronary artery vasodilation that I didn't pick cGMP when I should've. Ah well.

 

[gatorbate3]

Hey Y'all,

My exam is tomorrow & I'm trying to find the right answers to some questions I got wrong on NBME 12. I'm new to SDN, so I hope I'm even posting the right way

Q. A man collapses while shoveling snow. Before collapsing, his wife said he complained of tingling & weakness of his left upper and lower extremities. He has a (+) Babinski on the left. There's a picture of a noncontrast CT with a big white area in the R hemisphere. Which is the strongest predisposing risk factor?
A. Cholesterol plaques (wrong)
B. Cigarette smoking
C. DVT
D. HTN
E. Vasculitis

Sorry I don't have the picture. I am not very good at reading scans, so I'm not even sure what it's showing. It's white, which means it's denser than what's surrounding it, is that assumption correct? The only thing I could think of while taking the exam was maybe stroke? & high cholesterol was a risk factor for strokes? but so is HTN & the other things listed. Maybe HTN is the stronger risk factor? I'm not sure. If someone has the correct answer & explanation I'd be grateful. I'm sure it's something simple & I'm so stressed from my test being tomorrow I'm losing info! Lol. I'm sure everyone knows how that goes.

 

[Belleza156]

Noncontrast CT scan was showing a hyperdense (bright white) hemorrhage in the basal ganglia region. These are due to HYPERTENSION. Here is a link: http://emedicine.medscape.com/article/338055-overview

The vignette described what appeared to be a stroke so you could have been swayed to choose atherosclerosis, but they key was knowing that whenever you see hyperdensity indicating a hemorrhage in basal ganglia area the cause is always hypertension.

So far what I have gathered from the Qbanks is the following:

Problem: Intracerebral hemorrhage in basal ganglia area --> cause: Hypertension
Problem: Cystic looking cavity in brain associated with stroke --> cause: atherosclerosis
Problem: Abdominal aortic aneurysm--> cause: atherosclerosis
Problem: Aortic dissection (false lumen formed aorta in CT scan)--> cause: hypertension, (cystic medial degenration in those with Marfans is also a cause but minor # of cases in comparison to HTN)

 

[Dallas]

Hey Y'all,

My exam is tomorrow & I'm trying to find the right answers to some questions I got wrong on NBME 12. I'm new to SDN, so I hope I'm even posting the right way

Q. A man collapses while shoveling snow. Before collapsing, his wife said he complained of tingling & weakness of his left upper and lower extremities. He has a (+) Babinski on the left. There's a picture of a noncontrast CT with a big white area in the R hemisphere. Which is the strongest predisposing risk factor?
A. Cholesterol plaques (wrong)
B. Cigarette smoking
C. DVT
D. HTN
E. Vasculitis

Sorry I don't have the picture. I am not very good at reading scans, so I'm not even sure what it's showing. It's white, which means it's denser than what's surrounding it, is that assumption correct? The only thing I could think of while taking the exam was maybe stroke? & high cholesterol was a risk factor for strokes? but so is HTN & the other things listed. Maybe HTN is the stronger risk factor? I'm not sure. If someone has the correct answer & explanation I'd be grateful. I'm sure it's something simple & I'm so stressed from my test being tomorrow I'm losing info! Lol. I'm sure everyone knows how that goes.

Stroke is a family name
First you want to know is this 1) a hemorrhagic stroke where the vessel is ruptured, or is this a 2) ischemic stroke where either A) systemic circulation has failed to deliver oxygen to the brain or B) A blockage of the vessel by a thrombus has cut off oxygen supply to that part of the brain.

Now the first 3 answer choices point to some form of thromboembolic stroke and you have not been given enough information to differentiate the etiology of a thromboembolism, so that makes A,B and C improbable right off the bat.

So 50/50 your first life line has been used.

Vasculitis or HTN. Well he is an old dude, there is nothing in there hinting to vasculitis (pain when eating, other autoimmune or neurological stuff), he is doing strenous work, HTN seems much more probable than vasculitis. Plus if the image shows the white opacity in the basal ganglia (somewhere around the lacunar striate) you know for sure this is HTN over vasculitis.

This is just my thinking. Dont know if it is the correct answer.

 

[Luliba]

Its early diastole. Think about when the pressure at the base of the aorta is highest. It is during early diastole before the pressure has a chance to be distributed to the rest of the vasculature.

Someone help me on this one:

Experiment measuring right coronary blood flow, when is the maximum flow?

A) Early diastole
B) Early systole
C) Late diastole
D) Late systole

I put "late diastole" and it was wrong. Is it "early diastole"? This seemed like a very easy question

but the flow of the coronaries is not supposed to be in systole????

 

[Dallas]

but the flow of the coronaries is not supposed to be in systole????

Nope, nein, no, nie, nej, naw, nah, non etc

During systole the heart muscle is contracting effectively pressing on all its arteries.
When the heart muscle relaxes in diastole the coronary arteries expand and negative pressure sucks blood in from the aorta.

Negative pressure is lowest and flow is the highest in early diastole and tapers off as both the volume in the coronary arteries becomes occupied as well as outward swelling and pressure from the cardiac muscle begins to increase pressure in the coronary system.

 

[Belleza156]

A 56-year-old man with alcoholism comes to the physician because of a 2-month history of increasingly severe stomach pain and increased volumes of foul-smelling stool; he also has had a 9-kg (20..Jb) weight loss during this period. He has a history of multiple visits to the emergency department because of severe abdominal pain. He has consumed one bottle of red wine daily for 5 years. His temperature is 37"C (98.6"F). Physical examination shows epigastric tendemess. His fasting serum glucose is 150. CT scan shows pancreatic calcifications. The most likely cause of this patients current symptoms is a decrease of what?

a. bile acid synthesis
b. colonic bacteria
c. duodenal pH
d. fecal elastase
e. 7-alpha hydroxylase

What is the answer here? It's an alcoholic with chronic pancreatitis? It's not acute right? And he has steatorrhea. So is the answer duodenal pH or 7-alpha hydroxylase?

Is the patient lacking pancreatic secretions, HCO3- from the ductal cells of pancreas? So now he can't neutralize acidic chyme and the pancreatic enzymes can't be activated? Is that the cause of the steatorrhea?

Or are the bile acids not being reabsorbed so the patient is deficient so he can't digest fats-->steatorrhea. But would that cause compensatory synthesis of new bile so that is why 7-alpha hydroxylase isn't correct, it would be increased not decreased?

Any help with this one is very much appreciated!

 

[berry15]

Is the answer to this MHC1 since RSV is a virus and MHC1 mediates viral immunity? I'm not sure how the mediation of viral immunity is related to the clearance of virus infected cells. Any help is appreciated!

A 6-month-boy is diagnosed with respiratory syncytial virus infection. Which of the following cell surface protein complexes is most likely involved in recognition and clearance of virus-infected cells in this patient?
a fas ligand
b interleukin-2 (IL-2) receptor
c MHC I
d TNF receptor

 

[Myxedema]

Is the answer to this MHC1 since RSV is a virus and MHC1 mediates viral immunity? I'm not sure how the mediation of viral immunity is related to the clearance of virus infected cells. Any help is appreciated!

A 6-month-boy is diagnosed with respiratory syncytial virus infection. Which of the following cell surface protein complexes is most likely involved in recognition and clearance of virus-infected cells in this patient?
a fas ligand
b interleukin-2 (IL-2) receptor
c MHC I
d TNF receptor

Virus infects host cell --> Viral antigen is processed by the cell --> Viral antigen presented via MHC-I --> CD8+ T-cell recognizes MHC-I molecule loaded with viral antigen --> CD8+ T-cell kills the infected cell (via various mechanisms)

Also NK cells kill host cells that don't express their "self" antigens on MHC-I molecules.

Other choices are involved in the cell-mediated immunity as well, but MHC I is the one "most likely involved".

 

[berry15]

Awesome, thanks! It's right in FA too, sometimes the terminology used in the book throws me off.

 

[berry15]

Does anyone know the answer to this one?

A 39 year old woman with well-controlled type 1 DM has end stage renal disease. The serum concentration of which of the following is most likely to be increased?

1. 1,25-dihydroxycholecalciferol
2. EPO
3. Estrogen
4. PTH
5. TSH

 

[berry15]

And another ... TIA (is this lanosterol c14?)

A 20 yr old man treated with Miconazole for toe fungus. Mutation of which of the following fungal targets is the most likely cause of this resistance?

1. Cell wall 1,3-Beta-glucan synthase active site
2. DNA polymerase alpha
3. Lanosterol C 14 demethylase active site
4. RNA polymerase beta subunit
5. 50S ribosomal subunit binding site
6. Transpeptidase enzyme (PBP-2B) active site

 

[Myxedema]

Does anyone know the answer to this one?

A 39 year old woman with well-controlled type 1 DM has end stage renal disease. The serum concentration of which of the following is most likely to be increased?

Secondary hyperparathyroidism (typical lab: Increased PTH with normal calcium) is commonly caused by renal failure. --> PTH

A 20 yr old man treated with Miconazole for toe fungus. Mutation of which of the following fungal targets is the most likely cause of this resistance?

MOA of azole antifungals: 14-alpha-demethylation of lanosterol --> Mutation of demethylase enzyme can produce resistance

 

[pizzo]

You know what will cure acne on that girl's forehead right?

Vit A derivative or oxyclean

 

[pizzo]

Hey GTFOOMICT, I just took NBME 12 today too.. what a blow to my confidence. A week ago I got a 232 on UWSA#2 and NBME 12 took me down to a 205! What gives?

205 is a better predictor. Be happy, that's a pass!

 

[pizzo]

Idk...not trying to be a douche or anything, but was that question really so difficult? Acne on forehead and just started wearing a helmet=helmet causing it....ive heard chocolate can lead to acnebut that would prob be more widespread...

As far as if they will put difficult questions on there, hell yes, haha.

that chocolate thing is an old wive's tale and has been proven NOT to be true. Just think logically, easy question.

 

[phoenix89]

Hey guys I missed a really easy basic question, I would like some help if you remember it. It went something like:

1)Sympathetic stim to heart: what happens
I put in: Inc Heart Rate, Dec Afterload, Inc Preload

I thought the B1 would cause the heart rate inc, the b2 would cause dec afterload, and a1 would inc preload. But my concepts arent very clear as to which receptors get activated in vivo, can somebody help me out.

 

[arayoflight771]

hey, I cant seem to find the questions / answer's to nbme 12 ... if anyone has them I would GREATLY APPRECIATE IT!!
thanks
email me : [email protected]

 

[Corbac]

1. Klinefelter's, look for the Barr body in easily obtainable cells.

2. Pulm vasculature. I believe the idea is an outdated one (at least so we were told by lecturers), but ACE is present in high amounts at capillary beds. FA "covers" this in the renal chapter with a picture of the lungs in the AngII discussion. This was quite tricky, actually, and should serve as a reminder to read all choices.

3. That's Dandy-Walker and is from absent formation of the 4th vent. If I remember correctly, Met is the right answer. (e.g., no cerebellar vermis which arises from Met). Between Met and Myencephalon, I don't know how you would pick. Luckily Mye was not a choice.

4. No muscle atonia in REM. FA covers this fairly well in Behavioral chapter.

5. Took me a while to figure this one out, but you've copied it wrong. I had to go to my test to find this out. The boy has increased ketones and hepatosplenomegaly. Increased ketones rules out MCAD/LCAD and Carnitine transfer deficiencies. The time course is also much better for a disorder of gluconeogenesis than one of impaired FA oxidation.

6. Parasympathetic outflow is responsible for the vasovagal response (aka neurocardiogenic syncope), which is a fancy way of saying "fainting." People faint when anxious (giving blood, needles, etc.) and can experience warmth, nausea, and light-headedness prior to going out. Think about the important diagnostic points separating cardiac syncope (all the other causes listed) from fainting and seizures. This is more of a third year thing, admittedly. As a test taking skill, you should also note that all the others imply structural damage to the heart and would be unlikely in a young military recruit who is undergoing BT. Another place this skill is useful is in lung pathology questions: separate obstructive from restrictive answer choices, increased A-a gradient choices from normal A-a choices, increased AG met acidosis from normal AG choices, and so on.

Edit: Just wanted to add that these are tough questions and if you can minimize your careless errors on test day you'll likely do super. For my own education, what were you looking for with FISH of subtelomeres in the infertile man?

Dandy - Walker is failure of foramen of Luschka and Magendier to open causing Dilatation of IV ventricle and the cause is agenesis of cerebellar vermis and splenium of corpus calosum . Meten and Myelen both produce IV ventricle ..