NBME 16 help

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shubz123

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Hi all,

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Kid with sickle cell anemia, prophylaxis with penicillin. This decreases infection for which of the following:

E coli
H. flu
N. meningiditis
Salmonella
S. pneumoniae

Looks like the answer is Strep pneumo. How can you eliminate N. meningitidis since penicillin can be used for that as well?

This is an epidemiology question. S. pneumo is MCC of infection in kids with sickle cell disease.
 
I forgot, one more Q:

54y F admitted with acute MI, at which point there were no murmurs or signs of heart failure; but 2 days later, she has acute SOB and sweating; HR 100, RR 24, BP 160/98. Crackles bilaterally, +murmur. Which murmur is most likely?

(then they basically gave a descriptor for each murmur type "grade x/6, diastolic decrescendo murmur heard best at Y")

I have no idea what this is... is she having heart failure 2 days after her MI...?

maybe papillary muscle rupture so mitral regurg?

that would be what, systolic murmur heard best at the apex, radiating to axilla?
 
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Just to confirm... the old man with HTN living in a farm in central Cali who distills his own liquor, worked in hat factory, textile factory, smoker... comes in with gout - most likely cause of his gout is "drinking home-distilled liquor"? I think I got distracted and wondered if this guy somehow has bladder cancer (perhaps he was exposed to something at his factory + his smoking hx), and what the relationship of that would be to gout. But now I wonder if it's as simple as alcohol -> risk factor for gout.

Also, would love any input on that question with the sheep blood agar plate image. (Refresher: 70y F with eprsistent fever despite IV broad-spectrum abx 3 days post-operation. She has a central venous cathether and a well-healing surgical wound. Gram stain shows 4um elliptical purple budding org. Candida, Cryptococcus, Ecoli, Sporothrix schenckii, Staph aureus).

Thanks!!!
 
Just to confirm... the old man with HTN living in a farm in central Cali who distills his own liquor, worked in hat factory, textile factory, smoker... comes in with gout - most likely cause of his gout is "drinking home-distilled liquor"? I think I got distracted and wondered if this guy somehow has bladder cancer (perhaps he was exposed to something at his factory + his smoking hx), and what the relationship of that would be to gout. But now I wonder if it's as simple as alcohol -> risk factor for gout.

Also, would love any input on that question with the sheep blood agar plate image. (Refresher: 70y F with eprsistent fever despite IV broad-spectrum abx 3 days post-operation. She has a central venous cathether and a well-healing surgical wound. Gram stain shows 4um elliptical purple budding org. Candida, Cryptococcus, Ecoli, Sporothrix schenckii, Staph aureus).

Thanks!!!
You were right in your initial thoughts of alcohol --> gout.

The second one was Candida. Unresponsive to broad spectrum abx, budding pattern, and had white colony formations.
 
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Not sure if I've skimmed over these questions in the forum and they have already been answered but can someone help me out with these:

1-27: 79 y/o woman who gets a hip fracture. She swims, knits, gardens. What is most likely to decrease the patient's risk for additional fractures?
a) Discontinue alcohol
b) Discontinue gardening
c) Walk every day
d) Go to swimming exercise class 3x's/week
e) Lose weight

I put D, but I got that wrong.

1-33: 12 y/o boy with difficulty walking, atrophy of lower extremities, hammer toes and high stepping gait. What would you find?
- Not even sure what disease this is. The one place I found that talks about hammer toes in First Aid is Friedreich's ataxia. So is the answer absence of Schwann cells?

1-39:
Woman w/ type 1 diabetes and has episodes of fainting during past 3 weeks. What is the mechanism of the drug to give as an injection during these hypoglycemic episodes?
a) decrease intestinal absorption of glucose
b) enhanced metabolism of insulin
c) promotion of peipheral insulin uptake
d) promotion of skeletal muscle glucose release
e) stimulation of hepatic glucose production

1-47: 27 y/o woman with left sided chest pain radiating to back and gets worse when she reaches over her head or behind her back. No abnormalities on cardiopulmonary exam, xray or ECG.

I put down a stupid answer, but now I'm thinking it is costochondritis. Thoughts?

2-23: 8 year old girl with breast buds and some public hair. What should you tell the mother about her development?
a) she might have precocious puberty
b) she is going to start menstruating soon (wrong, this is what i put)
c) need to order labs
d) development is less than where she should be <-- pretty sure this is wrong
e) development is normal

2-31: Retired boxer that gets mask like face, rigid movements, shuffling gait, resting tremor. What is the cause of this?

I can remember learning during school year that boxers get some kind of amyloid deposition leading to dementia... but amyloid angiopathy was wrong.

2-35: 25 y/o woman w/ history of irregular menstrual periods, deep voice, hirsutism, acne. Serum studies of insulin, testosterone, and lutenizing hormone show what?

This is PCOS right?? I know LH will be increased b/c of lack of feedback, not sure about insulin or testosterone.

2-47: 64 y/o man with abnormal densities in hilar region. Biopsy shows round cells with little cytoplasm that are 2x's size of lymphocytes. Which abnormality would you find?

Knee jerk reaction was sarcoidosis, but then biopsy suggests lymphoma?? I put hypermagnesemia but that is wrong

3-8: 23 y/o difficulty maintaining erection b/c of MVA that damaged thoracic spinal cord. He can get erection if stimulated physically --> the reflex arc involved between what nerve and the sacral parasympathetic nerves ?

I put genitofemoral which is wrong

3-15: 32 y/o woman who has multiple spontaneous abortions before giving birth to a baby with dysmorphic features and multiple organ anomalies.

I put gonadal mosaicism, thinking there is something wrong with a line of germinal cells, but now I'm think the answer could be "unbalanced chromosome rearrangement". I remember reading somewhere that chromosomal abnormalities are most common reason for spontaneous abortion.

3-34: The cough question with whether the vocal cords are open/closed during swallowing, immediately after laryngeal irritation, and while coughing.

Please a definitive answer, the previous posts were confusing me.

4-25: Patient undergoes radical prostatectomy. Which of following is at risk of injury?
a) dome of bladder
b) obturator nerve
c) pelvic parasympathetic nerve
d) penile urethra
e) ureterovesical junction (wrong)

4-36: AA man with CHF and ejection fraction of 30%. What drug is contraindicated?

I could have sworn Beta-blockers were contraindicated in decompensated in CHF.

4-42: 2 y/o boy who has developmental delay. Mother has hearing loss. Older sister has delayed speech. Maternal Uncle has stroke like episodes.

So I didn't put heteroplasmy because that has to do with inheriting good and bad copies of mitochondrial DNA. And I know mitochondrial diseases have things to do with myopathies. Wasn't really sure how those symptoms related so I put autosomal dominant (wrong). Can someone explain.
 
Not sure if I've skimmed over these questions in the forum and they have already been answered but can someone help me out with these:

1-27: 79 y/o woman who gets a hip fracture. She swims, knits, gardens. What is most likely to decrease the patient's risk for additional fractures?
a) Discontinue alcohol
b) Discontinue gardening
c) Walk every day
d) Go to swimming exercise class 3x's/week
e) Lose weight

I put D, but I got that wrong.

1-33: 12 y/o boy with difficulty walking, atrophy of lower extremities, hammer toes and high stepping gait. What would you find?
- Not even sure what disease this is. The one place I found that talks about hammer toes in First Aid is Friedreich's ataxia. So is the answer absence of Schwann cells?

1-39:
Woman w/ type 1 diabetes and has episodes of fainting during past 3 weeks. What is the mechanism of the drug to give as an injection during these hypoglycemic episodes?
a) decrease intestinal absorption of glucose
b) enhanced metabolism of insulin
c) promotion of peipheral insulin uptake
d) promotion of skeletal muscle glucose release
e) stimulation of hepatic glucose production

1-47: 27 y/o woman with left sided chest pain radiating to back and gets worse when she reaches over her head or behind her back. No abnormalities on cardiopulmonary exam, xray or ECG.

I put down a stupid answer, but now I'm thinking it is costochondritis. Thoughts?

2-23: 8 year old girl with breast buds and some public hair. What should you tell the mother about her development?
a) she might have precocious puberty
b) she is going to start menstruating soon (wrong, this is what i put)
c) need to order labs
d) development is less than where she should be <-- pretty sure this is wrong
e) development is normal

2-31: Retired boxer that gets mask like face, rigid movements, shuffling gait, resting tremor. What is the cause of this?

I can remember learning during school year that boxers get some kind of amyloid deposition leading to dementia... but amyloid angiopathy was wrong.

2-35: 25 y/o woman w/ history of irregular menstrual periods, deep voice, hirsutism, acne. Serum studies of insulin, testosterone, and lutenizing hormone show what?

This is PCOS right?? I know LH will be increased b/c of lack of feedback, not sure about insulin or testosterone.

2-47: 64 y/o man with abnormal densities in hilar region. Biopsy shows round cells with little cytoplasm that are 2x's size of lymphocytes. Which abnormality would you find?

Knee jerk reaction was sarcoidosis, but then biopsy suggests lymphoma?? I put hypermagnesemia but that is wrong

3-8: 23 y/o difficulty maintaining erection b/c of MVA that damaged thoracic spinal cord. He can get erection if stimulated physically --> the reflex arc involved between what nerve and the sacral parasympathetic nerves ?

I put genitofemoral which is wrong

3-15: 32 y/o woman who has multiple spontaneous abortions before giving birth to a baby with dysmorphic features and multiple organ anomalies.

I put gonadal mosaicism, thinking there is something wrong with a line of germinal cells, but now I'm think the answer could be "unbalanced chromosome rearrangement". I remember reading somewhere that chromosomal abnormalities are most common reason for spontaneous abortion.

3-34: The cough question with whether the vocal cords are open/closed during swallowing, immediately after laryngeal irritation, and while coughing.

Please a definitive answer, the previous posts were confusing me.

4-25: Patient undergoes radical prostatectomy. Which of following is at risk of injury?
a) dome of bladder
b) obturator nerve
c) pelvic parasympathetic nerve
d) penile urethra
e) ureterovesical junction (wrong)

4-36: AA man with CHF and ejection fraction of 30%. What drug is contraindicated?

I could have sworn Beta-blockers were contraindicated in decompensated in CHF.

4-42: 2 y/o boy who has developmental delay. Mother has hearing loss. Older sister has delayed speech. Maternal Uncle has stroke like episodes.

So I didn't put heteroplasmy because that has to do with inheriting good and bad copies of mitochondrial DNA. And I know mitochondrial diseases have things to do with myopathies. Wasn't really sure how those symptoms related so I put autosomal dominant (wrong). Can someone explain.
1-27: C, needs to be weight-bearing
1-39: E, glucagon stimulates hepatic glucose release
1-47: It was costochondrotis.
2-23: E, she has normal development
2-31: It was neuronal degeneration from chronic traumatic encephalitis (since he was a pro boxer, he got hit in the head a bunch of times)
2-35: It is PCOS, don't recall the answer choices. In general, LH:FSH ration >2.0, insulin increased, glucose increased
2-47: The answer was hyponatremia, I think, because of SIADH from a small cell carcinoma
3-8: pudendal nerve
3-15: unbalanced chromosomal translocation is the only good explanation for 3 abx and 1 badly deformed full-term child.
3-34: closed during swallowing, closed during irritation, open during coughing
4-25: C, pelvic parasympathetics
4-36: Can you put the drug list again? I got it right, but I can't recall what I picked.
4-42: Has to be heteroplasmy, because it appears to be one gene that's causing multiple phenotypes. Inheritance might be autosomal dominant, but that isn't what the question asked. The question asked what explains the different presentations.
 
4-36: Can you put the drug list again? I got it right, but I can't recall what I picked.

4-36: 58 y/o African American man with CHF has a S3 sound & left ventricular ejection fraction of 30%. What treatment is contraindicated?
a) Amiodarone
b) Diltiazem
c) Lisinopril
d) Metoprolol (incorrect)
e) Sildenafil

Appreciate the answers btw. Any thoughts about 1-33 (the hammer toe and high stepping gait kid)
 
4-36: 58 y/o African American man with CHF has a S3 sound & left ventricular ejection fraction of 30%. What treatment is contraindicated?
a) Amiodarone
b) Diltiazem
c) Lisinopril
d) Metoprolol (incorrect)
e) Sildenafil

Appreciate the answers btw. Any thoughts about 1-33 (the hammer toe and high stepping gait kid)
It was E, because as part of your initial rx, you gave him a nitrate.

Someone else here answered 1-33, I think it was myelin degeneration by Friedrich's ataxia. Can't remember exactly.
 
Girl broke tibia and now has cast removed. Calf smaller. What happened to myocytes? Is it glycogenolysis

Onset of anesthesia is group Y faster than group x. Group X is isoflurane at 1.5x MAC. Group Y is isoflurane and nitrous oxide at .75x MAC. What explains the diff in response rates?

Is there a consensus on the smoking and alveolar macrophage question?

Thanks!
 
Girl broke tibia and now has cast removed. Calf smaller. What happened to myocytes? Is it glycogenolysis
For got the exact wording, but which ever choice had to do w/ Protein loss (I think it might've been ubiquination? )

Onset of anesthesia is group Y faster than group x. Group X is isoflurane at 1.5x MAC. Group Y is isoflurane and nitrous oxide at .75x MAC. What explains the diff in response rates?
Blood:gas coefficient (low blood solubility --> faster onset , high blood solubility --> slower onset)

Is there a consensus on the smoking and alveolar macrophage question?

Got it wrong.. (wanted to pick Up, down, up, but that wasn't an option. I then picked all Up, thinking 1 week of exposure may --> more acute issues...that was wrong)

Thanks!
 
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a thrombosis in the SMA would cause ischemia in the... jejunum?

the question w/ drug X and ang-ii, was it a part agonist?

the picture with the parasite with the little spike coming off the side, what was the treatment? it wasn't metro.

what does niacin do in terms of cholesterol? FA says it inhibits adipose lipolysis and hepative VLDL synth but that wasn't an answer choice.

the kid who dove into the shallow swimming pool.. where was the lesion?

girl w/ CF who doesn't take her meds. has basically peripheral neuropathy - what vitamin is deficient?

what's wrong with occult blood for colon cancer screening?

old man w/ DOE who has enlarged R and L ventricles and a holosystolic apical murmur. wasn't aortic stenosis... he also had lung crackles and an axillary PMI.

what changes occur after you return to sea level and have greater oxygen delivery?
 
a thrombosis in the SMA would cause ischemia in the... jejunum? Yea, I think that was the only one that was supplied by SMA

the question w/ drug X and ang-ii, was it a part agonist? Part agonist

the picture with the parasite with the little spike coming off the side, what was the treatment? it wasn't metro. Praziquantel.

what does niacin do in terms of cholesterol? FA says it inhibits adipose lipolysis and hepative VLDL synth but that wasn't an answer choice. It was the one that had VLDL in it.

the kid who dove into the shallow swimming pool.. where was the lesion? Was this the ques with ruptured herniated disc as answer choice.

girl w/ CF who doesn't take her meds. has basically peripheral neuropathy - what vitamin is deficient? Vit E. Got this wrong as well, but looks like it is vit E based on FA

what's wrong with occult blood for colon cancer screening? Not sensitive

old man w/ DOE who has enlarged R and L ventricles and a holosystolic apical murmur. wasn't aortic stenosis... he also had lung crackles and an axillary PMI. Dont remember this ques. Need more of ques stem

what changes occur after you return to sea level and have greater oxygen delivery? Inc hematocrit
 
thanks! for the praziquantel one, what was the parasite??
swimming pool wasn't the ruptured disc- he can't move his right upper and lower extremities and it had a spinal cord X section.

i ALWAYS forget that vitamin E deficiency can cause neuropathies!

the the cardiac Q - the only detail i left out was decreased systolic function. ans choices were AS, CAD, DCM, htn dz, tamponade. was it DCM?
 
Thank you!

I would seriously appreciate anyone who can help w/ the spinal cord lesion. Can't move his right upper & lower extremities ... where will the lesion be and will it be on the L or the R? I assumed R because I assumed LMN lesion.
 
51 y/o man with HBV negative PAN has proximal muscle weakness and myalgia. What will biopsy show?

Was this inclusion body myositis? If so would it be central vacuolization with glycogen accumulation? Or with lipid accumulation? Other options are mucopolysaccharide deposition, or ischemic necrosis.

Thanks!
 
yes, that was the answer. i got it right. it was a wordy but straightforward question.

Great, I appreciate your help!

Could you or anyone else please explain the albinism question? I picked "inability to produce melanin" which is correct, but can't 100% say why "aberrant migration of neural crest" is a bad answer, as this is also listed as a cause of albinism since melanocytes are derived from the neural crest. I'm guessing it has something to do with the eyes being blue.
 
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Great, I appreciate your help!

Could you or anyone else please explain the albinism question? I picked "inability to produce melanin" which is correct, but can't 100% say why "aberrant migration of neural crest" is a bad answer, as this is also listed as a cause of albinism since melanocytes are derived from the neural crest. I'm guessing it has something to do with the eyes being blue.

I think if it was failure of neural crest cell migration there would be more problems than just albinism. Or inability to produce melanin is a more common cause of albinism.
 
Hello all, Sorry if these have been asked before. I’ve tried to find reputable answers for them, with not much luck.

1. Could someone expand upon what structural feature of poliovirus mRNA is the reason why it can be translated without a 5’-cap? (choices: Absence of 3’-UTR, absence of 5’-UTR, absence of polyA tail, presence of internal ribosome entry site, short open reading frame)

2. For the graph about ghrelin and consumption of a meal, would its concentration drop after the meal, and if so do any of you remember where on the curve it would be?

3. Basic question. Would faulty p53 in Li-Fraumeni lead to impaired regulation of apoptosis? :confused:

4. The different response rate between the 2 drugs X and Y and induction of anesthesia, is it due to the difference in the blood-gas partition coefficients (because lipid solubility is more associated with potency and MAC)?

5. What is the brain tumor that was the malignant, small blue neoplasm that expressed cytokeratin, chromogranin, and synaptophysin (I keyed off the last 2 and put neuroblastoma, :()? Is it the small cell met to the brain because she has Lambert-Eaton symptoms?

Thanks everyone. Really appreciate all the prior discussions. :)
 
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Hello all, Sorry if these have been asked before. I’ve tried to find reputable answers for them, with not much luck.

1. Could someone expand upon what structural feature of poliovirus mRNA is the reason why it can be translated without a 5’-cap? (choices: Absence of 3’-UTR, absence of 5’-UTR, absence of polyA tail, presence of internal ribosome entry site, short open reading frame) I believe this was the presence of internal ribosome entry site. The others seemed to be options that would reduce translation.

2. For the graph about ghrelin and consumption of a meal, would its concentration drop after the meal, and if so do any of you remember where on the curve it would be? Don't know; got it wrong

3. Basic question. Would faulty p53 in Li-Fraumeni lead to impaired regulation of apoptosis? :confused: Think this is correct; faulty p53 -> cells that should be sent to die are not and are instead allowed to continue through the cell cycle.

4. The different response rate between the 2 drugs X and Y and induction of anesthesia, is it due to the difference in the blood-gas partition coefficients (because lipid solubility is more associated with potency and MAC)? Got this wrong but someone above said it was due to the blood-gas partition coefficient. Basically, high partition coefficient -> high solubility in blood -> slow onset of action; therefore the drugs must differ in solubility/coefficient to have such drastic changes in onset

5. What is the brain tumor that was the malignant, small blue neoplasm that expressed cytokeratin, chromogranin, and synaptophysin (I keyed off the last 2 and put neuroblastoma, :()? Is it the small cell met to the brain because she has Lambert-Eaton symptoms? Small cell carcinoma - and yes as far as I can find in FA, Lambert-Eaton is associated with SCC, so that's what I went with.

Thanks everyone. Really appreciate all the prior discussions. :)
 
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Thanks for the response. I think your right on number 1 with the poliovirus as I found on http://en.wikipedia.org/wiki/Poliovirus it mentioning the internal ribosome entry site (IRES).
For number 2, I think it might have been the peak of the graph. Looks kind of like this: http://www.diabesity.eu/images/ghrelinfluctuation.gif

I think you are right for the last 2 as well. Thanks!

Yes it is the peak of the graph. Ghrelin stimulates hunger "Ghrelin makes your stomach GROWL (TM-Matteo)" and therefore it would subsequently decrease post-consumption
 
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Yes it is the peak of the graph. Ghrelin stimulates hunger "Ghrelin makes your stomach GROWL (TM-Matteo)" and therefore it would subsequently decrease post-consumption

Yeah thanks. I see that now. I just wasn't sure how fast it would decrease. Oh well. Nice mnemonic. :)
 
Girl broke tibia and now has cast removed. Calf smaller. What happened to myocytes? Is it glycogenolysis

Onset of anesthesia is group Y faster than group x. Group X is isoflurane at 1.5x MAC. Group Y is isoflurane and nitrous oxide at .75x MAC. What explains the diff in response rates?

Is there a consensus on the smoking and alveolar macrophage question?

Thanks!


For the smoking one the answer that people are saying is right (mucus up, cilia down, macrophage up) isn't even a choice!

The only 3 choices that have mucus up (which is obvious) are A) cilia up, macrophage up....B) cilia up, macrophage down......C) cilia down, macrophage down

I put A and was wrong. So I guess the answer is either B or C and both have them have macrophage down. So I guess the answer is C then since that's the one with cilia down? I still don't get why macrophage activity is down though.

choices D-F have mucus production down which i highly doubt (but could be wrong so correct me if i am!)
 
For the smoking one the answer that people are saying is right (mucus up, cilia down, macrophage up) isn't even a choice!

The only 3 choices that have mucus up (which is obvious) are A) cilia up, macrophage up....B) cilia up, macrophage down......C) cilia down, macrophage down

I put A and was wrong. So I guess the answer is either B or C and both have them have macrophage down. So I guess the answer is C then since that's the one with cilia down? I still don't get why macrophage activity is down though.

choices D-F have mucus production down which i highly doubt (but could be wrong so correct me if i am!)

I got that question right. The answer was mucus up, cilia activity down, and macrophage function down. I just reasoned that the smoke/toxins would impair the macrophage functioning, but would be happy to hear a more detailed explanation if someone wanted to.
 
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Couple (possibly stupid) questions:

1. 28 y/o AA male with 3mo hx of fatigue, weakness, significant weight loss, 6mo hx of dry cough, chest pain, SOB. Works as carpenter, has pets, went to mexico 1 yr ago. 5 pack year smoking hx. CXR shows bilateral hilar adenopathy and right paratracheal node enlargement. Bx results show noncaseating granulomas that are AFB negative and fungi negative. What's the strongest predisposing risk factor for this pt's condition?
--> Employment, Ethnicity, Gender, Living with pets, Recent travel to Mexico, Smoking Hx

2. 56 y/o F with 3wk hx of dysphagia for solids and then solids and liquids. Irregular mass at GE junction. Chronic infection with which pathogens most likely causes the path findings?
-->Clonorchis, CMV, E. Histolytica, H. Pylori, M. TB
Was it H.Pylori leading to esophageal adenocarcinoma?

3. 9 y/o M w/ hx of mild mental ******ation, motor seizures, systolic ejection murmur, pink-yellow papules in butterfly distribution on nose bridge-nasolabial folds. Multiple calcified nodules on subependymal regions. LVH on echo with aortic outflow narrowing from subvalvular septal mass. Dx?
--> Familial hypertrophic myopathy, Gardner syndrome, Glycogen storage disease 1, MEN 1, Tuberous sclerosis

4. Point tenderness lateral to acromion over humeral head. Full passive shoulder motion. Pain reproduced with resisted abduction of shoulder when shoulder's abducted 90 degrees and arm is giving thumb's down sign. Full sensation intact. What was damaged?
--> Deltoid, Infraspinatus, Subscapularis, Supraspinatus, Teres major, Teres minor

5. 35 y/o M w/ 6mo hx of burning abdominal pain after eating, 2day hx of black stools. No sx relieved with OTC antacids and H2 blockers. Sx also includes orthostatic hypotension. PE reveals epigastric tenderness and 1cm pancreatic mass. Immunohistochemical labeling of neoplastic cells will use antibodies directed against what?
--> Amylase, Gastrin, Glucagon, Insulin, HPP, Lipase, Serotonin, Somatostatin, VIP

6. 26 mo M w/ 3day hx of cough, SOB, 1wk hx of fever. 9mo hx of multiple cutaneous S. Aureus abscesses rxed with systemic antibiotics. Displays failure to thrive. Left posterior lung crackles. CXR reveals left lingula cavitary infiltrates. Cultures show filamentous g+ rod. Most likely organism?
--> B. Anthracis, Nocardia asteroides, P. Jirovecci, S. Bovis

7. Would a PE count as dead space or a shunt?

8. Excessive morphine would cause tox how?
--> Chronic dosing decreasing bioavailability
--> Chronic dosing increasing bioavailability
--> Morphine downregulating mu-opioid receptors with chronic dosing
--> Morphine inhibiting its own metabolism
--> Morphine metabolized to active metabolites that accumulate

9. Stool occult blood testing has:
--> Low sensitivity, low specificity, potential for false positive, uncertain NPV, uncertain PPV

10. To strengthen infraspinatus and teres minor, what movements should be done against resistance?
--> Abduction, adduction, extension, lateral rotation, medial rotation

11. 66 y/o M w/ 6mo hx of decreased exercise tolerance and SOB on exertion. Pulse 92bpm, RR 22/min, BP 120/80. Bilateral basilar crackles, 2/6 holosytolic murmur at apex, and S3 gallop on auscultation. Echo reveals L & R ventricular enlargement, decreased systolic function. Dx?
--> Aortic valve stenosis, CAD, Dilated cardiomypoathy, Hypertensive HD, Pericardial tamponade

12. Sigmoid colon mass revealing adenocarcinoma. Which LNs would it mets to?
--> Inferior mesenteric, Internal iliac, Left colic, Pararectal, Superficial inguinal

13. Initial screening shows 500/2500 pts with c. trachonatis infections. 1yr later, screening shows an additional 200 students with infection. Annual incidence in this population?

14. X-linked recessive disease in 1/100,000 Ms. Expected prevalence in heterozygous Fs?
Would someone mind explaining their rationale?

15. FHx of fragile X syndrome. The pedigree question of likelihood of 3rd generation individual having the gene expansion?
Idk if I can show the pedigree chart here, but could someone explain it if they remember it?

16. 2wks post-transplant pt w/ erythematous, maculopapular rash, diarrhea, increased LFTs and bilirubin. What caused his sx?
--> Donor macrophages secreting cytokines
--> Donor plasma cells
--> Donor T lymphocytes
--> Host macrophages
--> Host plasma cells
--> Host T lymphocytes

17. 6mo M w/ hx of recurrent upper and lower resp tract infections, hypocalcemia rxed with Ca2+ supplementation, surgical repair of aortic coarctation. PE reveals broad nasal bridge and dysplastic pinnae. Cause of recurrent infections?
--> Hyper IgM, Hypocellular marrow, IgE deficiency, IgG deficiency, T Lymphocyte deficiency?
Mind explaining what this pt has?

18. 18mo M with lethargy for 3hrs unresponsive on arrival. 10mo ago had hypoglycemia and diarrhea followed by cardioresp arrest. PE reveals hepatomegaly. Decreased serum glucose, ketones, carnitine. Decreased urine ketones and presence of urine dicarboxylic acids. Pt responds with IV glucose. Medium chain TAGs administered for 6mos with normal serum glucose levels. Pt has what deficiency?
--> G6Phosphatase, HMG CoA lyase, Hormone sensitive lipase, LPL, Long chain acyl CoA DH, PEPCK

19. 10y/o F anemic with hx of splenectomy, recent cholecystectomy. CBC: low Hb, normal MCV, PC, increased Reticulocyte Count. Peripheral smear shows pale RBCs. Underlying abnormality?
--> Hb structure, Iron absorption, Erythrocyte spectrin, Oxidative enzyme function, EPO production

20. Cholesterol emboli on funduscopic exam. Likely origin of embolus?
--> Abdominal aorta, L common carotid, R anterior cerebral, R middle cerebral, R ophthalmic

21. Heterogenous pedunculated mass in L atrium in 19y/o M.
--> Hemangiopericytoma, Lipoma, Myxoma, Rhabdomyosarcoma, Teratoma

22. Cystic Fibrosis = defect in what in bronchial epithelium?
--> Adrenocreceptors, Membrane receptors, Nuclei receptors, Protein regulation, Protein structure

23. Pink rods on Gram stain. Pink =
--> Endoplasmic reticulum, Outer membrane, PG cell wall, Polysaccharide capsule

24. Alcohol + Acetaminophen. Alcohol causes increased risk of liver injury bc?
--> Decreased acetaminophen clearance via glucuronidation
--> Increased acetaminophen bioavailability
--> Induced CYP450 that activate acetaminophen to hepatotoxic metabolites
--> Met acidosis due to increased NADH/NAD+ ratio

thanks a lot!
 
Couple (possibly stupid) questions:

1. 28 y/o AA male with 3mo hx of fatigue, weakness, significant weight loss, 6mo hx of dry cough, chest pain, SOB. Works as carpenter, has pets, went to mexico 1 yr ago. 5 pack year smoking hx. CXR shows bilateral hilar adenopathy and right paratracheal node enlargement. Bx results show noncaseating granulomas that are AFB negative and fungi negative. What's the strongest predisposing risk factor for this pt's condition?
--> Employment, Ethnicity, Gender, Living with pets, Recent travel to Mexico, Smoking Hx

it's sarcoidosis and biggest predisposing factor is AA race

2. 56 y/o F with 3wk hx of dysphagia for solids and then solids and liquids. Irregular mass at GE junction. Chronic infection with which pathogens most likely causes the path findings?
-->Clonorchis, CMV, E. Histolytica, H. Pylori, M. TB
Was it H.Pylori leading to esophageal adenocarcinoma?

i believe so because i put CMV and got it wrong and none of the other ones are related to the esophagus.

3. 9 y/o M w/ hx of mild mental ******ation, motor seizures, systolic ejection murmur, pink-yellow papules in butterfly distribution on nose bridge-nasolabial folds. Multiple calcified nodules on subependymal regions. LVH on echo with aortic outflow narrowing from subvalvular septal mass. Dx?
--> Familial hypertrophic myopathy, Gardner syndrome, Glycogen storage disease 1, MEN 1, Tuberous sclerosis

hamartomas, ash-leaf spots, seizures = tuberous sclerosis

4. Point tenderness lateral to acromion over humeral head. Full passive shoulder motion. Pain reproduced with resisted abduction of shoulder when shoulder's abducted 90 degrees and arm is giving thumb's down sign. Full sensation intact. What was damaged?
--> Deltoid, Infraspinatus, Subscapularis, Supraspinatus, Teres major, Teres minor

empty can test

5. 35 y/o M w/ 6mo hx of burning abdominal pain after eating, 2day hx of black stools. No sx relieved with OTC antacids and H2 blockers. Sx also includes orthostatic hypotension. PE reveals epigastric tenderness and 1cm pancreatic mass. Immunohistochemical labeling of neoplastic cells will use antibodies directed against what?
--> Amylase, Gastrin, Glucagon, Insulin, HPP, Lipase, Serotonin, Somatostatin, VIP

ZE syndrome


6. 26 mo M w/ 3day hx of cough, SOB, 1wk hx of fever. 9mo hx of multiple cutaneous S. Aureus abscesses rxed with systemic antibiotics. Displays failure to thrive. Left posterior lung crackles. CXR reveals left lingula cavitary infiltrates. Cultures show filamentous g+ rod. Most likely organism?
--> B. Anthracis, Nocardia asteroides, P. Jirovecci, S. Bovis

nocardia. the only 2 g+ rods that are filamentous are nocardia and actinomyces israeli

7. Would a PE count as dead space or a shunt?

dead space because perfusion defect

8. Excessive morphine would cause tox how?
--> Chronic dosing decreasing bioavailability
--> Chronic dosing increasing bioavailability
--> Morphine downregulating mu-opioid receptors with chronic dosing
--> Morphine inhibiting its own metabolism
--> Morphine metabolized to active metabolites that accumulate



9. Stool occult blood testing has:
--> Low sensitivity, low specificity, potential for false positive, uncertain NPV, uncertain PPV

sensitivity = TP/TP + FN....the physician is worried about there being too many FN's that is patients who don't test positive but do have the disorder. generally physicians care more about specificity/sensitivity and patients care more about PPV/NPV.

10. To strengthen infraspinatus and teres minor, what movements should be done against resistance?
--> Abduction, adduction, extension, lateral rotation, medial rotation


11. 66 y/o M w/ 6mo hx of decreased exercise tolerance and SOB on exertion. Pulse 92bpm, RR 22/min, BP 120/80. Bilateral basilar crackles, 2/6 holosytolic murmur at apex, and S3 gallop on auscultation. Echo reveals L & R ventricular enlargement, decreased systolic function. Dx?
--> Aortic valve stenosis, CAD, Dilated cardiomypoathy, Hypertensive HD, Pericardial tamponade

S3 gallop, enlarged heart, mitral regurg, systolic dysfunction = dilated cardiomyopathy

12. Sigmoid colon mass revealing adenocarcinoma. Which LNs would it mets to?
--> Inferior mesenteric, Internal iliac, Left colic, Pararectal, Superficial inguinal

interial iliac

13. Initial screening shows 500/2500 pts with c. trachonatis infections. 1yr later, screening shows an additional 200 students with infection. Annual incidence in this population?

incidence = new cases/population at risk. population at risk is 2000 not 2500 since 500 already have it. so 200/2000 = 10%

14. X-linked recessive disease in 1/100,000 Ms. Expected prevalence in heterozygous Fs?
Would someone mind explaining their rationale?

i said 1/50,000 and got it right. because they have a 1/2 chance of giving it to their sons if they're heterozygous since it's X linked. so 1/50,000 * 1/2 = 1/100,000

15. FHx of fragile X syndrome. The pedigree question of likelihood of 3rd generation individual having the gene expansion?
Idk if I can show the pedigree chart here, but could someone explain it if they remember it?

0% because the daughter's father didn't have it and he only got 1 X from his mother. so he could only give that 1 X to his daughters so they can't have it.

16. 2wks post-transplant pt w/ erythematous, maculopapular rash, diarrhea, increased LFTs and bilirubin. What caused his sx?
--> Donor macrophages secreting cytokines
--> Donor plasma cells
--> Donor T lymphocytes
--> Host macrophages
--> Host plasma cells
--> Host T lymphocytes

GVHD

17. 6mo M w/ hx of recurrent upper and lower resp tract infections, hypocalcemia rxed with Ca2+ supplementation, surgical repair of aortic coarctation. PE reveals broad nasal bridge and dysplastic pinnae. Cause of recurrent infections?
--> Hyper IgM, Hypocellular marrow, IgE deficiency, IgG deficiency, T Lymphocyte deficiency?
Mind explaining what this pt has?

di george. hypocalcemia due to lack of parathyroid glands. T lymphocyte deficiency due to lack of thymus.


18. 18mo M with lethargy for 3hrs unresponsive on arrival. 10mo ago had hypoglycemia and diarrhea followed by cardioresp arrest. PE reveals hepatomegaly. Decreased serum glucose, ketones, carnitine. Decreased urine ketones and presence of urine dicarboxylic acids. Pt responds with IV glucose. Medium chain TAGs administered for 6mos with normal serum glucose levels. Pt has what deficiency?
--> G6Phosphatase, HMG CoA lyase, Hormone sensitive lipase, LPL, Long chain acyl CoA DH, PEPCK

none of the other ones are a fatty acid oxidation disorder

19. 10y/o F anemic with hx of splenectomy, recent cholecystectomy. CBC: low Hb, normal MCV, PC, increased Reticulocyte Count. Peripheral smear shows pale RBCs. Underlying abnormality?
--> Hb structure, Iron absorption, Erythrocyte spectrin, Oxidative enzyme function, EPO production

RBC's lacked central pallor = hereditary spherocytosis. i also think they mentioned her father had a splenectomy when he was young. it's an AD disease.

20. Cholesterol emboli on funduscopic exam. Likely origin of embolus?
--> Abdominal aorta, L common carotid, R anterior cerebral, R middle cerebral, R ophthalmic

the other ones would not end up in the right eye.

21. Heterogenous pedunculated mass in L atrium in 19y/o M.
--> Hemangiopericytoma, Lipoma, Myxoma, Rhabdomyosarcoma, Teratoma

buzzword. pedunculated mass in heart = probably myxoma


22. Cystic Fibrosis = defect in what in bronchial epithelium?
--> Adrenocreceptors, Membrane receptors, Nuclei receptors, Protein regulation, Protein structure

membrane channel protein has a deletion and is being degraded instead of expressed at the membrane

23. Pink rods on Gram stain. Pink =
--> Endoplasmic reticulum, Outer membrane, PG cell wall, Polysaccharide capsule

pink = gram negative = LPS from outer membrane

24. Alcohol + Acetaminophen. Alcohol causes increased risk of liver injury bc?
--> Decreased acetaminophen clearance via glucuronidation
--> Increased acetaminophen bioavailability
--> Induced CYP450 that activate acetaminophen to hepatotoxic metabolites
--> Met acidosis due to increased NADH/NAD+ ratio

alcohol upregualtes one of the CYP P450 enzmyes. taking acetominophen afterwards causes increased activation into hepatic metabolites. but if you drink after taking acetominophen then it's protective. i was confused about this also.

thanks a lot!
 
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any consensus on the cough/vocal cords question?

whether or not the vocal cords are open/closed

1) while swallowing
2) immediately after laryngeal irritation
3) while coughing
 
Just a quick clarification. I think the sigmoid adenocarcinoma would spread to the inferior mesenteric nodes (that's at least what I put and got it correct).

For the vocal cord one, I put closed while swallowing, closed after laryngeal irritation, and open while coughing (and it was correct).
 
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Just a quick clarification. I think the sigmoid adenocarcinoma would spread to the inferior mesenteric nodes (that's at least what I put and got it correct).

For the vocal cord one, I put closed while swallowing, closed after laryngeal irritation, and open while coughing (and it was correct).

yes you're right sorry! i got it right too not sure why i bolded the wrong answer this time.

i think there was another question on this nbme or another that asked for where cancer from the cervix would drain and i got confused.
 
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Not sure if I've skimmed over these questions in the forum and they have already been answered but can someone help me out with these:


1-33: 12 y/o boy with difficulty walking, atrophy of lower extremities, hammer toes and high stepping gait. What would you find?
- Not even sure what disease this is. The one place I found that talks about hammer toes in First Aid is Friedreich's ataxia. So is the answer absence of Schwann cells?

I don't think anybody has answered 1-33 yet. I got it right, and I think it's Charcot-Marie-Tooth disease (defective production of myelin and associated with scoliosis, foot deformities -- it says high or flat arches in FA, but I remember learning "hammer toes" as a buzzword). I can't remember what the exact answer options are, but I put down something to do with defective myelin (probably the Schwann cells that you mentioned).

Also, maybe this is a basic/obvious question because nobody seems to have asked about it yet, but I can't figure out the woman with anemia:

2-14: 38 yo woman comes to physician for pre-employment exam; she has no history of serious illness; she takes no meds; her vitals are normal; PE shows no abnormalities
Lab studies show: Hb 8.2, Hct 25%, MCV 69, leukocytes 5900, retic 0.8%, platelets 350K

Most likely DX = ?
Aplastic anemia
Iron-deficiency
Sickle cell
B-thal minor
B12 deficiency

So I was between iron deficiency and B-thal minor, and went with B-thal because people are usually asymptomatic and it was wrong; what am I missing here??
 
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I don't think anybody has answered 1-33 yet. I got it right, and I think it's Charcot-Marie-Tooth disease (defective production of myelin and associated with scoliosis, foot deformities -- it says high or flat arches in FA, but I remember learning "hammer toes" as a buzzword). I can't remember what the exact answer options are, but I put down something to do with defective myelin (probably the Schwann cells that you mentioned).

Also, maybe this is a basic/obvious question because nobody seems to have asked about it yet, but I can't figure out the woman with anemia:

2-14: 38 yo woman comes to physician for pre-employment exam; she has no history of serious illness; she takes no meds; her vitals are normal; PE shows no abnormalities
Lab studies show: Hb 8.2, Hct 25%, MCV 69, leukocytes 5900, retic 0.8%, platelets 350K

Most likely DX = ?
Aplastic anemia
Iron-deficiency
Sickle cell
B-thal minor
B12 deficiency

So I was between iron deficiency and B-thal minor, and went with B-thal because people are usually asymptomatic and it was wrong; what am I missing here??

I think it is an epi question. from the labs (as far as i can see), there is no way to tell the difference between B-thal and iron deficiency, but iron def. is way more common. Also, I'm not sure that the anemia is very marked in cases of B-thal minor
 
I got that question right. The answer was mucus up, cilia activity down, and macrophage function down. I just reasoned that the smoke/toxins would impair the macrophage functioning, but would be happy to hear a more detailed explanation if someone wanted to.

yea, can someone explain this? This seems to run contrary to what we learn about the pathogenensis of emphysema, for example.

I mean, here are some papers with >100 citations saying the exact opposite

http://www.ncbi.nlm.nih.gov/pubmed/16166618
http://www.ncbi.nlm.nih.gov/pubmed/14583334
http://molpharm.aspetjournals.org/content/68/5/1343.full
http://respiratory-research.com/content/7/1/66
 
Also, maybe this is a basic/obvious question because nobody seems to have asked about it yet, but I can't figure out the woman with anemia:
...
So I was between iron deficiency and B-thal minor, and went with B-thal because people are usually asymptomatic and it was wrong; what am I missing here??
Her reticulocyte count.

yea, can someone explain this? This seems to run contrary to what we learn about the pathogenensis of emphysema, for example.

I mean, here are some papers with >100 citations saying the exact opposite

http://www.ncbi.nlm.nih.gov/pubmed/16166618
http://www.ncbi.nlm.nih.gov/pubmed/14583334
http://molpharm.aspetjournals.org/content/68/5/1343.full
http://respiratory-research.com/content/7/1/66
Here are some supporting the answer:
...macrophages from smokers may be slightly suppressed in their responses.
...Our data thus suggest that smokers may have a limited ability to mount an effective pulmonary immune defense after anesthesia and surgery.
...Defective efferocytosis may perpetuate inflammation in smokers with or without chronic obstructive pulmonary disease (COPD).
 
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A 12 year old girl is brought to the physician for a follow up examination. Three months ago, she sustained a complex fracture of the left tibia, which required cast immobilization. The cast is removed. Examination of the calf shows that it is smaller than the right calf. Which of the following processes in this patient's myocytes is the most likely cause of these findings?

A) anaerobic glycolysis
B) fatty acid degradation
C) glycogenolysis
D) oxidative phosphorylation
E) polyubiquitination

I put C and I got wrong

what is the right answer?

Thanks
 
I think it was E. Muscle has atrophied, which involves cells breaking down their proteins and some organelles.
 
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A 35-year-old man comes to the physician because of a 3-year history of an enlarging nose, coarsening of his facial features, muscle weakness, and increased hand and foot size. Physical examination shows a large fleshy nose and prognathism. Serum studies show an increased insulin.lik growth factor-I concentration. An MRI of the brain shows a pituitary adenoma. Morphologic analysis of a biopsy specimen of the tumor shows a densely granulated somatotroph adenoma. Further studies show that the Gas subunit of G proteins in the tumor lack GTPase activity. The tumor cells in this patient most like have an increased activity of wich of the following enzymes?

A) Adenylyl cyclase
B) Guanylyl cyclase
C) Janus kinase
D) Phospholipase C
E) Tyrosine kinase

I put D and I got wrong. What is the correct answer?

They are asking about tumor (pit. adenoma) molecular changes, right?
 
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No the pituitary adenoma is distracting information. If a GTPase is missing, that means something is constitutively active. In this case, we are dealing with a Gs protein which activates adenylyl cyclase, so A is the correct answer.
 
A 62-year-old man with unstable angina pectoris undergoes coronary catheterization. In order to visualize the anterior interventricular (left anterior descending) artery, the tip of the angiographic catheter would need to be placed into the orifice of which of the following arteries?:

A) Circumflex
B) Left coronary
C) Left marginal
D) Right coronary
E) Right marginal

I put A and I got it wrong. What is the correct answer?

I think it is so specific! I don't do angioplastic everyday. Damn!
 
left main homie. it may be a little specific but if right main and left main are both answer choices, you KNOW one of those is right because they are proximal-est. then you have to know that left main does anterior circulation and right does posterior. don't mean sound condescending, but if you put cx, that's more an error in test-taking skill than knowledge base
 
A 62-year-old man with unstable angina pectoris undergoes coronary catheterization. In order to visualize the anterior interventricular (left anterior descending) artery, the tip of the angiographic catheter would need to be placed into the orifice of which of the following arteries?:

A) Circumflex
B) Left coronary
C) Left marginal
D) Right coronary
E) Right marginal

I put A and I got it wrong. What is the correct answer?

I think it is so specific! I don't do angioplastic everyday. Damn!

B) LCA. The LAD is a branch of the LCA, so to view the LAD you would need to advance the catheter to its orifice on the LCA. If you advance further, you would be in the L circumflex since the LCA bifurcates into the LAD and L circumflex.
 
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