NBME 16 help

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shubz123

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Took NBME 16 today and learned again that feeling "good" about a test doesn't always reflect in the score. I took the one without expanded feedback, so I can't help much, but in any case, after reading the posts on here, I got to wondering: Would y'all say a lower score on this test than other NBMEs or UWorld self assessments, is a common occurrence?
 
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1) 19 yr old girl withdrawn and isolated since graduating high school. stays in room and rarely sees friends. not interested in old friends or activities. very anxious and depressed by listening to radio that only she can hear. thinks about a government scheme to control the psychic pain people feel. she’s disheveled and malodorous. normal vital signs no abnormalities. mentally she’s distracted. she has sad mood and anxious, sad, blunted affect. best therapy? I’m stuck b/w buspirone and trazodone



buspirone, donepezil, lithium carbonate, risperiode, trazodone

She needs risperidone; she has schizophrenia. Risperidone is an atypical antipsychotic. "radio that only she can hear" is an auditory hallucination. She also has emotional blunting, a negative sign. This was a very kind question since only one antipsychotic was one of the answers.

2) 3 yr old boy, pain in arm after sister ran into him, third time he had to go to hospital for this “seems like he’s always in a vast” blue sclerae and normal teeth, upper extremity shows erytheme edema and tenderness to palpation. abnormal bruises suggestive of trauma. X-ray of right upper extremity shows fracture of humerus and osteopenia. defect in what?

answer is probably pro collagen synthesis isn’t it? since its a defect in type 1 collagen smh silly mistake by me



elastinfibrillin interaction, endocytosis of transferrin receptor, fibroblast growth factor receptor signaling, mature metallproteinase activation, procllaen synthesis, transforming growth factor beta secretion

Procollagen synthesis. This is osteogenesis imperfecta; he has a collagen type I mutation.



3)Fanconics syndrome, what are the Amino Acids, HC03, Phosphate and Glucose levels ? Increased or decreased for each. Its a disease of the proximal renal tubules of the kidney in which glucose, amino acids, uric acid, phosphate and bicarbonate are passed into the urine, instead of being reabsorbed, so everything(amino acids, Glucose, phosphate, HCO3) will be decreased right?

Don't remember. Fanconi's (both of them) is one of those syndromes I'm taking a hit on. I don't care about it, and I don't remember the answer.

4)55 yr old lady 3 month history of shortness of breath. Takes daily multivitamin. Leukocyte count 8000 , ca2+ 12 mg, urea nitrogen 10 mg, creatinine 1 mg, phosphorus 4.2 mg, X-ray shows enlarged hilar lymph nodes and reticulonodular infiltrates in upper lung fields. Analysis of biopsy specimen shows noncaseating granulomas. What are serum values?

PTH 1,25 dihydroxycholecalciferol

up up

up normal

up down

down up

down normal

down down



If i had to guess, i’d say pth is down and 1,25 dihyr is up(cuz increased activity of 1 alpha hydroxyls activity in sarcoidosis right?)

You're right. It's sarcoidosis.

5)68 yr old lady cystitis caused by vancomycin resistant enterococcus faecalis. which of the following mechanisms best explains the antibiotic resistance of this organism? i think its substitution of d-lac for d-aka in peptidoglycan(rmr this from dit but wanna double check)

alteration of outer membrane porin proteins, capsule production, b lactamase production, substitution of d-lac for d-aka in peptidoglycan, up regulation of a rapid efflux pump

Vanco resistance is d-ala d-ala substituted for d-ala d-lac, yes.

6) 24 yr old dude w nasal congestion, watery nasal discharge, sneezing. Says symptoms happen each spring, when grass and tree pollens are abundant. Which type of duds is likely to be effective in relieving these symptoms in the short term? help w this please. I think its a adrenergic agonist cuz phenylephrine is great for these situations but i dunno :( “a stands for alpha and b for beta”

a-adrenergic agonist, a-adrenergic antagonist, b- adrenergic agonist, b-adrenergic antagonist, nicotinic cholinergic agonist, nicotinic cholinergic antagonist

Alpha agonist will vasoconstrict vessels of the nose. since he's only having upper respiratory symptoms, it's an appropriate treatment.

7) an investigator is conducting a study of antiretroviral agents. The plan is to identify which agents inhibit entry of the HIV virus into the CD4+ T lymphocytes. Which of the following antiretroviral agents is likely to be identified in this study? Isn’t this a fusion inhibiter so enfuvirtide?

didanosine(ddi), enfuvirtide, lamivudine(3tc), nevirapine, tenofovir

Yes, en - fu - virtide inhibits fusion.
 
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@afrothunderman1 and @tantacles
The question of Fanconi syndrome above. Its a problem with reabsorption in the PCT.
Every thing that's supposed to be reabsorbed will be excreted in the urine instead.
So, serum conc. of amino acids, glucose, phosphate and HCO3 will all be decreased (and urine concentration is increased).
 
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15 yr old boy, 6’3 and weights 165 lb, BMI 21 kg, pulse is 85/min and bounding/ bp is 110/40. dislocation of right lens. Pectus excavatum. grade 3/6 decrescendo diastolic murmur heard at aortic area. Wide mediastinum. Genetic defect in what? so this is marfans so fibrillin correct?? Sometimes I read it has to do w/collagen and sometimes fibrillin so whats the right choice???

collagen type 2, elastin, fibrillin, hyaluronate, proteoglycan
 
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Last set of questions. Would you be able to help me out with these/check my answers. Ty!

1. Liver showing centrilobular pallor and swelling of hepatocytes and kidneys showing proximal convoluted epithelial cells. Which is the mechanism?



A) activation of aspartate-spcific caspase

B) Binding of Fas ligand to receptor

C) Decreased function of Na/K ATPase

D) Ribosomal degradation

E) Stimulation of PFKase





is it decreased function of NA/K Atpase, since its a reversible cellular injury first of all(cellular swelling is classic for reversible injury) so the NA/K being screwed up means sodium will accumulate and water will follow and so swelling? Agree, and its specifically because there is insufficient ATP due to decreased oxidative phosphorylation





2) 26 yr old dude has tenesmus and bloody diarrhea. Apppearance of intestine from rectum to mid ascending colon shown in pic. Terminal ileum is normal(so we know its not chrons!) biopsy shows micro abscesses within the crypts and depletion of mucus from goblet cells? diagnosis? Is this ulcerative colitis? Sounds like it.
Yep


amebic sysentery, collagenous colitis, crohn disease, ischemic bowel disease, ulcerative colitis





3)60 yr old woman has 2 history of hypertension comes to doc for follow up examination. Hypertension has been poorly controlled during the past six months despite availability of appropriate pharmacotherapy. which of the following statements by the physician is most appropriate to begin a discussion about this patients possible noncompliance w her medication regimen?

Is it “it is hard to take pills every day for a condition that has no symptoms” i think its this..other choices That's what I put

“i will arrange for nurse to visit to make sure you’re taking meds properly”

“I’m sorry but i must say missing your meds can kill you”

“you clearly have not been taking your meds. you must be more responsible”

“you realize that your high blood pressure could have been avoided”



4) 38 yr old lady w/ 10 wk history of epigatric pain and frequent stool. She had two episodes of renal calculi during the past 2 yrs. Physical exam shows multiple superficial lipomata and mild epigastric tenderness. Upper endoscopy show two large non bleeding duodenal ulcers. her gastric pH is 2.3, and serum gastrin concentration obtained immediately after the procedure is 2000 pg/ml(N<100). Proton pump inhibitor therapy is begun. measurement of which of the following is the most appropriate next step in management?



serum calcium concentration, serum cortisol concentration, serum tissue transglutaminase activity, stool alpha 1 antitripson concentration, urine 5 hydroxyindoleacetic acid concentration

Because she has renal calculi and gastrinoma, so you have to consider Multiple Endocrine Neoplasia (MEN) syndrome (most likely MEN1)


5) 12 year old with walking abnormality for 6 months. mild atrophy and hammer toes.nerve biopsy shows

abnormal myelin sheaths

absence of shwann cells

lymphycytic infiltrate

abnormal astrocytes

abnormal oligodendrocytes


is this abnormal myelin sheaths(charcot marie tooth disease)? I didn't get this one, but based off of other posts, yes.


6) 54 yr old man w/ aneurysm in distal portion of his abdominal aorta. Estimated cross-sectional area of the aneurysm is 2 cm^2 and the mean velocity of blood flow thru the aneurysm is 20cm/sec. which of the following best represents the flow rate in L/min thru the aneurysm? Can someone please help me out with this?


1.0, 2.4, 3.2, 3.6, 4.0

Flow = Area x Velocity = (2 cm^2) x (20 cm/sec) = 40 cm^3/sec = 40 mL/sec
Then convert to L/min


7)55 yr old dude w contipationsine taking meds for chronic persistent cough n sinus congestion. which ingredient in this med most likely cause of this patients new symptom? dextromethorphan right?


acetaminophen, dextromethorphan, guafenesin, loratidine, phenylephrine
Not exactly sure about this one, but I put phenylephrine because it is an alpha adrenergic agonist
Actually now I'm thinking it is dextromethorphan because it is a codeine analog and opiates cause constipation


8) It was about the niacin cholesterol mechanism. Which one is the better answer? antagonizes VLDL cholesterol secretion or inhibits cholesterol uptake

I'm guessing the cholesterol uptake is referring to absorption in the gut? (e.g. ezetimibe) Inhibiting uptake by the liver wouldn't make sense. Cardiovascular system section in FA (lipid-lowering agents chart at the end of the section) refers to reduction of VLDL secretion

9) 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 searched this up and someone said that the best answer is 4/6 holosystolic murmur heard best over lower left sternal border and cardiac apex. What do you think about this one? Agree. My thinking (at the last second of answering this question) was a papillary muscle rupture resulting in mitral regurgitation (holosystolic murmur heard best at apex). Even though FA says rupture (of wall or papillary muscle) occurs from 3-14 days, pathoma says 4-7 days, and Goljan says it's impossible to put numbers on it, I guess 2 days is not terribly unreasonable? In any case, free wall rupture would present with cardiac tamponade (pulsus paradoxus and signs of shock: tachycardia, low BP, decreased level of consciousness)



10) 28 yr old lady w/ 1 month history of pelvic pain that has become increasingly severe during the past week. Her mensrual flow has been unusually heavy during her last three menstrual periods. Menses have occurred at 24-28 day intervals since menarche at the age of 12 years. Phys exam shows a palpable mass in the left adnexa. Serum studies show an increased CA 125 concentration. Vaginal ultrasonography shows an 8 cm mass in the left ovary. During surgical removal of the ovary, which of the following structures passing inferior to the ovary must be protected? I think its ureter but wanna double check w you



external iliac artery, internal iliac artery, ovarian ligament, round ligament of the uterus, ureter
I put ureter too, but I'm also wondering about this one



11) 18 yr old dude w acute lymphblastic leukemia has 3 day history of intermittent fever and left sided chest pain. He’s in 5th week of induction chemotherapy consisting of asparaginase, daunorubicin, prednisone, and vincristine. His absolute neutrophil count has been less than 500/mm for the past month. Temp is 102 F and he has dullness to percussion and decreased breath sounds on the left side. Chest X-ray shows a left lower lobe infiltrate and a moderate pleural effusion on the left. Photo of pas-stain of pleural fluid shown in the pic of the question. Whats the appropriate therapy? I need help w this one



amphotericin B, Ertapenem, Ganciclovir, Infliximab, Rituximab
I don't know either, but the patient has neutropenia and a lobar pneumonia with pleural effusion, so I'm guessing its either a fungus or a bacteria, so one of the first two answer choices?


12) 16 yr old boy dove into pool, unable to move right upper and lower extremities. Most likely cause of movement deficits in this patient is damage to which region of the spinal cord? Is it G, by the ventral cord of the spinal cord?

If I recall correctly its the lateral corticospinal tract, which runs in the lateral-most portion of the spinal cord. But I'm not sure if its on the left or right, since the pt has upper and lower extremity motor loss and CST fibers decussate in the medulla. Image of labeled spinal cord section:
http://flylib.com/books/2/426/1/html/2/spinal cord disorders_files/da1cspinal_cord_disordersff12.png


a,b,c,d,e,f,g,h



13) a previously healthy 27-year-old woman comes to physician because of a 3 week history of episodes of left sided chest pain and tenderness. the pain radiates to the back and is exacerbated when she reaches over her head or behind her back. she has not had shortness of breath, sweating, or light-headedness. her temperature is 37.1 pulse is 92/min, respirations are 14/min, and blood pressure is 130/86 mm Hg. Cardiopulmonary examination shows no abnormalities. examination shows tenderness to palpation 2 cm lateral to the midline and 10 cm below the clavicle on the left. an x-ray of the chest and ECG show no abnormalities. Which of the following is most likely diagnosis?


A) Achalasia - Would probably have difficulty swallowing

B) Acute pericarditis - ECG would probably show something

C) Costochondritis

D) Dissecting aortic aneurysm - Would probably have hemodynamic issues, although the pain radiating to back got me thinking about this one

E) Gastroesophageal reflux disease - Pain would be less localized and would be exacerbated with eating/drinking, not just movement

F) pleurisy - Apparently this is another term for 'pleuritis'; the pain would be less localized and exacerbated with breathing

G) pneumothorax - Would show something on x-ray and pt would have changes in breathing pattern

H) Stable angina pectoris

Costochondritis is known to be one of the great mimickers of stable angina, similar to GERD

14) 23 yr old diagnosed w sjoren syndrome has burning pain in her toes for past month. rates pain 3 on 10 point scale. she uses capsaicin cream for pain which produces partial relief. Neuro exam shows decreased perception of temperature over feet bilaterally. Sensation to vibration, proprioception, reflexes, muscle strength, muscle tone, and bulk are normal. Which neurotransmitter mediating pain? Is it substance P? Yep



gamma minobutyric acid, dopamine, enkephalin, serotonin, substance P



15) 15 yr old boy, 6’3 and weights 165 lb, BMI 21 kg, pulse is 85/min and bounding/ bp is 110/40. dislocation of right lens. Pectus excavatum. grade 3/6 decrescendo diastolic murmur heard at aortic area. Wide mediastinum. Genetic defect in what? so this is marfans so fibrillin correct?

collagen type 2, elastin, fibrillin, hyaluronate, proteoglycan
This is Marfan's

My answers are in bold above. For those of you who have the 'extended feedback' version of the test, please please please correct me on anything that is wrong.
 
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Ans in blue
+kween and +afrothunderman1, I was wondering about the question with diabetic pt taking hydrochlorothiazide whose BP doesn't go down, and what additional drug to use. I would also use an ACE or an ARB, but in this case the pt has renal dz (diabetes and microalbuminuria), and I looked up Clonidine, which turns out it (along with alpha-methyldopa) is best for treating pts with HTN who have renal disease (because they are centrally-acting alpha2-agonists; the renal dz is probably what is preventing the effects of other HTN drugs like diuretics, ACEIs, etc)
 
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+kween and +afrothunderman1, I was wondering about the question with diabetic pt taking hydrochlorothiazide whose BP doesn't go down, and what additional drug to use. I would also use an ACE or an ARB, but in this case the pt has renal dz (diabetes and microalbuminuria), and I looked up Clonidine, which turns out it (along with alpha-methyldopa) is best for treating pts with HTN who have renal disease (because they are centrally-acting alpha2-agonists; the renal dz is probably what is preventing the effects of other HTN drugs like diuretics, ACEIs, etc)

Wasn't it the sartan drug because ace/arbs are renoprotective(specifically protect against the damage caused by activation of RAAS)? Am I talking about the right question?
 
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Wasn't it the sartan drug because ace/arbs are renoprotective(specifically protect against the damage caused by activation of RAAS)? Am I talking about the right question?
Actually you are probably correct. Clonidine is down the line. I just thought since the diuretic didn't work, then centrally acting might be best. But just saw an article detailing hierarchy of pharmacologic intervention in diabetics with proteinuria: "The first line pharmacologic intervention should be an angiotensin converting enzyme inhibitor or angiotensin II type 1 receptor blocker in those with diabetes or non-diabetics with more than 200 mg protein/gram creatinine on a random urine sample. For non-diabetics with less than 200 mg protein/gram creatinine on a random urine sample, no specific first-line drug class is recommended. After initial dosing with an ACEi, ARB or other drug, a diuretic should be added to the regimen. Thereafter, beta-blockers, calcium channel blockers, apha blockers and alpha 2 agonists (e.g. clonidine) and finally vasodilators (e.g. minoxidil) should be added to achieve blood pressure goal. Combinations of ACEi and ARB are helpful in reducing proteinuria and may also lower blood pressure further in some some cases." http://www.ncbi.nlm.nih.gov/pubmed/16298269
 
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Actually you are probably correct. Clonidine is down the line. I just thought since the diuretic didn't work, then centrally acting might be best. But just saw an article detailing hierarchy of pharmacologic intervention in diabetics with proteinuria: "The first line pharmacologic intervention should be an angiotensin converting enzyme inhibitor or angiotensin II type 1 receptor blocker in those with diabetes or non-diabetics with more than 200 mg protein/gram creatinine on a random urine sample. For non-diabetics with less than 200 mg protein/gram creatinine on a random urine sample, no specific first-line drug class is recommended. After initial dosing with an ACEi, ARB or other drug, a diuretic should be added to the regimen. Thereafter, beta-blockers, calcium channel blockers, apha blockers and alpha 2 agonists (e.g. clonidine) and finally vasodilators (e.g. minoxidil) should be added to achieve blood pressure goal. Combinations of ACEi and ARB are helpful in reducing proteinuria and may also lower blood pressure further in some some cases." http://www.ncbi.nlm.nih.gov/pubmed/16298269

thank you for sharing that!
 
15 yr old boy, 6’3 and weights 165 lb, BMI 21 kg, pulse is 85/min and bounding/ bp is 110/40. dislocation of right lens. Pectus excavatum. grade 3/6 decrescendo diastolic murmur heard at aortic area. Wide mediastinum. Genetic defect in what? so this is marfans so fibrillin correct?? Sometimes I read it has to do w/collagen and sometimes fibrillin so whats the right choice???

collagen type 2, elastin, fibrillin, hyaluronate, proteoglycan

Marfans = fibrillin. There's a type of ehlers danlos that has marfanoid features, which would be caused by a defect in collagen, but ehlers danlos is caused by type 3 or type 5 collagen, depending on the variant, not type 2, so fibrillin is the best answer.
 
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5) 12 year old with walking abnormality for 6 months. mild atrophy and hammer toes.nerve biopsy shows

abnormal myelin sheaths

This is right, but i don't think it's Chacort marie tooth. I think this is friedriechs ataxia
hammer toes is a key word


10) 28 yr old lady w/ 1 month history of pelvic pain that has become increasingly severe during the past week. Her mensrual flow has been unusually heavy during her last three menstrual periods. Menses have occurred at 24-28 day intervals since menarche at the age of 12 years. Phys exam shows a palpable mass in the left adnexa. Serum studies show an increased CA 125 concentration. Vaginal ultrasonography shows an 8 cm mass in the left ovary. During surgical removal of the ovary, which of the following structures passing inferior to the ovary must be protected? I think its ureter but wanna double check w you

external iliac artery, internal iliac artery, ovarian ligament, round ligament of the uterus, ureter
I put ureter too, but I'm also wondering about this one

This is right as well.
Remember the mneumonic. "Water (ureters) under the bridge (uterine artery). In first aid.

the question with diabetic pt taking hydrochlorothiazide whose BP doesn't go down, and what additional drug to use. I would also use an ACE or an ARB, but in this case the pt has renal dz (diabetes and microalbuminuria)

According to FA, ist line for HTN and diabetes is ACEi/ARB, then Ca channel blockers, then diuretics, beta blockers and alpha blockers
Clonidine is very short acting and cause cause severe rebound hypertension when a dose is skipped. so I think its only used in severe hypertensive emergency
 
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The question about lady stung by bee 30 minutes ago She develops urticarial lesion. 6 hours later the area becomes underrated and firm. What explains the induration at the site of the sting? Someone said the answer was "influx of macrophages producing IL1, IL6, TNF alpha. But that doesn't make sense because that describes DELAYED HYPERSENSITIVITY and bee stings are type 1 hypersensitivity. Please help.

decrease in expression of adhesion molecules on vascular endothelial cells, decrease in serum C reactive protein concentration, influx of macrophages producing IL1, IL6, and TNF alpha, Lysis of endothelial cells by the alternative compliment pathway, vasoconstriction

Thanks!
 
I believe the question with the diabetic Pt. also said African American, so angioedemia was a risk there. Therefore the choice would be ARB
 
Can anyone help me out with this question I can't seem to find the answer:

The investigator studying bacterial virulence factors: Fur protein that binding increases as the concentration of iron in the culture media increases. Fur most likely regulates which of the following processes in these bacteria: a). methylation, b) post-transcriptional modification c) splicing d) transcription e) translation

Thanks!
 
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The question about lady stung by bee 30 minutes ago She develops urticarial lesion. 6 hours later the area becomes underrated and firm. What explains the induration at the site of the sting? Someone said the answer was "influx of macrophages producing IL1, IL6, TNF alpha. But that doesn't make sense because that describes DELAYED HYPERSENSITIVITY and bee stings are type 1 hypersensitivity. Please help.

decrease in expression of adhesion molecules on vascular endothelial cells, decrease in serum C reactive protein concentration, influx of macrophages producing IL1, IL6, and TNF alpha, Lysis of endothelial cells by the alternative compliment pathway, vasoconstriction

Thanks!

The first part of the reaction is mediated by histamine. Six hours later, your body essentially has a foreign body reaction to the venom, which is why macrophages are the likely answer.
 
Can anyone help me out with this question I can't seem to find the answer:

The investigator studying bacterial virulence factors: Fur protein that binding increases as the concentration of iron in the culture media increases. Fur most likely regulates which of the following processes in these bacteria: a). methylation, b) post-transcriptional modification c) splicing d) transcription e) translation

Thanks!

Got this one right, the answer is transcription.
A) DNA methylation is normally for telling the difference between the daughter and parent strands during DNA rep...can be used to shut off DNA transcription too, but even if fur is methylating its still regulating transcription
B) Unlikely, the question mentions nothing about phosphorylation, etc
C) Doesnt occur in prokaryotes
E) Control of gene expression is almost always at the transcriptional level not tranlsation

Hope that helps
 
11) 18 yr old dude w acute lymphblastic leukemia has 3 day history of intermittent fever and left sided chest pain. He’s in 5th week of induction chemotherapy consisting of asparaginase, daunorubicin, prednisone, and vincristine. His absolute neutrophil count has been less than 500/mm for the past month. Temp is 102 F and he has dullness to percussion and decreased breath sounds on the left side. Chest X-ray shows a left lower lobe infiltrate and a moderate pleural effusion on the left. Photo of pas-stain of pleural fluid shown in the pic of the question. Whats the appropriate therapy? I need help w this one



amphotericin B, Ertapenem, Ganciclovir, Infliximab, Rituximab
I don't know either, but the patient has neutropenia and a lobar pneumonia with pleural effusion, so I'm guessing its either a fungus or a bacteria, so one of the first two answer choices?

So for this one I just did process of elimination. I agree...I got down to ampho B and Ertapenem, so its either bacterial or fungal. The picture to me looked like Blasto, but it was definitely too big in comparison to the cells around it to be bacterial, so regardless of which fungal infection is was, he's immunosuppressed due to chemo so I picked ampho B. I got the extended feedback and I didn't get this one wrong
 
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What is absolute risk reduction in woman?
recurrent stroke standard treat. new antiplatel.drug
Women 12 .04
Man 24 .08
Overall 18 .06
 
A case control study is conducted possible association between herbicide and diagn. non-Hodgkin lym. Control are match to case by age,gender and race. On match pare analysis, the odd ratio= 3.2 (95% CI 1,4-5-4). Which one affect Validity? 1.Based measurem.of condition.2.Based meas.of exposure.3. confounding by age. 4.type1 error. 5.type2 error.
 
A 60 y.o wom. with 2 years history of hypertension come to PH.Her BP has been poorly control, despite appropriate pharmatherapy. Which one statement aapropr. to begin discussion about noncompliance? 1.I'll range a nurse to visit you.... 2.I must tell you that missing you medication would kill you. 3. it's hard to take pills every day for condition without symptoms. 4. you not been taking a medication,you must be more responsible. 5.you realize that your HB could have been avoided?
 
A 60 y.o wom. with 2 years history of hypertension come to PH.Her BP has been poorly control, despite appropriate pharmatherapy. Which one statement aapropr. to begin discussion about noncompliance? 1.I'll range a nurse to visit you.... 2.I must tell you that missing you medication would kill you. 3. it's hard to take pills every day for condition without symptoms. 4. you not been taking a medication,you must be more responsible. 5.you realize that your HB could have been avoided?

"it's hard to take pills..." is apparently a good way without being confrontational.
 
A case control study is conducted possible association between herbicide and diagn. non-Hodgkin lym. Control are match to case by age,gender and race. On match pare analysis, the odd ratio= 3.2 (95% CI 1,4-5-4). Which one affect Validity? 1.Based measurem.of condition.2.Based meas.of exposure.3. confounding by age. 4.type1 error. 5.type2 error.

Was this the question where the patients self-reported their exposure? If so, the answer has to do with self-reporting because they'll be more likely to claim exposure if they've been diagnosed with the disease in question.
 
Was this the question where the patients self-reported their exposure? If so, the answer has to do with self-reporting because they'll be more likely to claim exposure if they've been diagnosed with the disease in question.
I got it, thank you!
 
What about question with spinal cord pictures, the boy after he dove into 3 foot swimming pool.Unable to move his right upper and lower extremities. I think it's corticospinal track, but left or right?
 
What about question with spinal cord pictures, the boy after he dove into 3 foot swimming pool.Unable to move his right upper and lower extremities. I think it's corticospinal track, but left or right?

My best guess for that one is that the CST was damaged.
 
He's unable to move his R extremities, so I think it's a R sided lesion since the decussation was above.

I got it wrong so I'm not too sure about this one.
 
18 y/o man w/ ALL c/o intermittent fever & L sided CP. on chemo. absolute neutrophil count is 500. CXR left lower lobe infiltrate and a moderate pleural effuction. a photomicrograph of a periodic acid-schiff stain of the pleural fluid obtained via thoracentesis is shown. which of the following is the most appropriate pharmacoptherapy for this pt?
a) amphotericin b
b) ertapenem
c) ganciclovir
d) infliximab
e) rituximab
 
18 y/o man w/ ALL c/o intermittent fever & L sided CP. on chemo. absolute neutrophil count is 500. CXR left lower lobe infiltrate and a moderate pleural effuction. a photomicrograph of a periodic acid-schiff stain of the pleural fluid obtained via thoracentesis is shown. which of the following is the most appropriate pharmacoptherapy for this pt?
a) amphotericin b
b) ertapenem
c) ganciclovir
d) infliximab
e) rituximab

I don't remember the image specifically, but let's look at the clues.
Chemo: decreased immune function; neutropenic
CXR: lobar infiltrate
Histology: I'm guessing PAS has relevance here
All of this leads me to think a fungal infection, for which A would be correct.

Viral is typically not related to neutropenia and lobar infection.
Rheumatoid arthritis not suggested by given history.
Bacterial infection possible but the picture probably rules this in/out.
 
I don't remember the image specifically, but let's look at the clues.
Chemo: decreased immune function; neutropenic
CXR: lobar infiltrate
Histology: I'm guessing PAS has relevance here
All of this leads me to think a fungal infection, for which A would be correct.

Viral is typically not related to neutropenia and lobar infection.
Rheumatoid arthritis not suggested by given history.
Bacterial infection possible but the picture probably rules this in/out.

thanks. sorry, i forgot to post the pic. here it is: http://imgur.com/CtEmUqA -- to me it was looking kinda CMVesq but histo is my weak point.
 
thanks. sorry, i forgot to post the pic. here it is: http://imgur.com/CtEmUqA -- to me it was looking kinda CMVesq but histo is my weak point.

CMV would be intracellular inclusions, these are extracellular, about the size of the neutrophils. They kind of look like budding yeast. Couldn't tell you which specifically, but it points to amphotericin B as the answer.
 
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Hey guys, just a doubt:

in MS, are oligodendrocytes of the CNS destroyed, right?


Thanks
 
CST = CorticoSpinal Tract. In the spinal cord, for all practical purposes, motor deficit is ipsilateral. Right sided paresis is due to right sided lateral corticospinal tract involvement.
That's assuming the lesion is below the CST pyramidal decussation. This would be based on knowledge of mechanism of injury as well as spinal cord vs. brainstem histology, both of which I am still unsure about. Was the injury due to diving? And if he has upper and lower extremity motor deficit, the lesion would have to be pretty high up (cervical or above, probably). Anyone who has the extended feedback version get this right/wrong and know what answer they chose? Thanks.
 
Few questions on this:

1) In the rats that are exposed to cigarette smoke, what are the changes in mucous production and secretions, cilia activity, and macrophage activity? I had put increased across the board -- I believe you eventually get cili dysfunction with smoking, but I thought a week was much too short for that to take place. Had no idea about macrophage activity, but I figured it would be increased due to the acute irritation.

2) At what age is it normal to begin puberty in girls? There was a question of an 8 year old girl whose started to develop breast buds and pubic hair. I thought this was precocious puberty and you would want to do laboratory studies to confirm. Apparently the correct answer is to tell the worried mother that this is normal? It just seems awfully early to be so nonchalant about a girl entering puberty, and not want to do any testing.

3) 20 year old girl with servere dysuria and a painful vulvar lesion -- vesicual lesions on a erythematous base. Which organism? I had it between Candida and HSV. It was HSV. I've never heard of dysuria in an HSV infection, seeing as the bladder and most of the urethra is not stratified squamous, I didn't think it could be HSV. I know the lesion is classic of HSV is a vesicular rash on erythematous base, but candida also commonly infects the vulva and can cause a painful, red lesion with sores.

4) Do you form immunity against chlamydia? I didn't think you did. There was a stats question where you screened freshman girls for chlamydia and 500 out of 2500 tested positive. Then a year later you tested them again and there were an additional 200 positives, and it then wants you to find the incidence. I thought you would divide 200/2500 as it's a year later and one of the original 500 girls could have been infected again. The correct answer is 200/2000 as you subtract the original 500 girls from the population, so I'm assuming there is immunity? And even if you do have immunity, there are multiple types of chlamydia (D-K), so what if an original girl was infected with D strain and then a year later with F strain? This question seems flawed to me.
 
Hey guys, just a doubt:

in MS, are oligodendrocytes of the CNS destroyed, right?


Thanks
Yes. I was wondering about this too and confirmed it in uworld, pathoma, FA. Don't forget that you also see lipid laden macrophages on histo, and increased lymphocytes and protein (myelin basic protein and oligoclonal IgG) in the CSF. Treatment is beta-interferon and steroids.
 
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Few questions on this:

1) In the rats that are exposed to cigarette smoke, what are the changes in mucous production and secretions, cilia activity, and macrophage activity? I had put increased across the board -- I believe you eventually get cili dysfunction with smoking, but I thought a week was much too short for that to take place. Had no idea about macrophage activity, but I figured it would be increased due to the acute irritation.
mucus secr. UP, macr. and cilia-Down.

2) At what age is it normal to begin puberty in girls? There was a question of an 8 year old girl whose started to develop breast buds and pubic hair. I thought this was precocious puberty and you would want to do laboratory studies to confirm. Apparently the correct answer is to tell the worried mother that this is normal? It just seems awfully early to be so nonchalant about a girl entering puberty, and not want to do any testing. Don't remember.

3) 20 year old girl with servere dysuria and a painful vulvar lesion -- vesicual lesions on a erythematous base. Which organism? I had it between Candida and HSV. It was HSV. I've never heard of dysuria in an HSV infection, seeing as the bladder and most of the urethra is not stratified squamous, I didn't think it could be HSV. I know the lesion is classic of HSV is a vesicular rash on erythematous base, but candida also commonly infects the vulva and can cause a painful, red lesion with sores. HSV

4) Do you form immunity against chlamydia? I didn't think you did. There was a stats question where you screened freshman girls for chlamydia and 500 out of 2500 tested positive. Then a year later you tested them again and there were an additional 200 positives, and it then wants you to find the incidence. I thought you would divide 200/2500 as it's a year later and one of the original 500 girls could have been infected again. The correct answer is 200/2000 as you subtract the original 500 girls from the population, so I'm assuming there is immunity? And even if you do have immunity, there are multiple types of chlamydia (D-K), so what if an original girl was infected with D strain and then a year later with F strain? This question seems flawed to me.
200/2000=10
 
Why is that correct though? Why are you subtracting 500 from the original 2500? Chlamydia is not a chronic condition, and the question asks for annual incidence, so why is it not 200/2500? It stated that the 200 girls were tested a year after to first girls, so the original 500 girls should be apart of the normal population again.

If you're subtracting them because of immunity, I think that's a flawed question then, because as I stated there are multiple subtypes of chlamydia and you can become infected multiple times.
 
Why is that correct though? Why are you subtracting 500 from the original 2500? Chlamydia is not a chronic condition, and the question asks for annual incidence, so why is it not 200/2500? It stated that the 200 girls were tested a year after to first girls, so the original 500 girls should be apart of the normal population again.

If you're subtracting them because of immunity, I think that's a flawed question then, because as I stated there are multiple subtypes of chlamydia and you can become infected multiple times.
....
 
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That's assuming the lesion is below the CST pyramidal decussation. This would be based on knowledge of mechanism of injury as well as spinal cord vs. brainstem histology, both of which I am still unsure about. Was the injury due to diving? And if he has upper and lower extremity motor deficit, the lesion would have to be pretty high up (cervical or above, probably). Anyone who has the extended feedback version get this right/wrong and know what answer they chose? Thanks.
The pyramidal decussation takes place at the caudal medulla, hence I said that CST lesion in the spinal cord is for all practical purposes always ipsilateral. The mechanism of injury in most spinal flexion/extension injuries (diving, whiplash, falling on one's head from a ladder) is injury to the cervical cord because it is contained in the most mobile part of the spine. You don't need histology here, you need gross anatomy to identify various sections, which is pretty important in neuroanatomy. The brainstem is usually identified by the presence of the various nuclei, peduncles and the the dorsal location of the spinal canal (apart from the distinctive shape of certain levels). The spinal cord can be identified by the expansion of the central grey matter especially at the cervical and lumbar levels, and the typical formation of posterior and anterior horns with a more central spinal canal. For it to be upper and lower motor deficit, you're right it has to be high up, i.e. between C1-c5 (after which the brachial plexus begins and some nerves branch off). A medullary lesion is highly unlikely due to mechanical injury. Vascular lesions or even mass effect will affect more than just the corticospinal tract in the medulla, and such signs will be mentioned (especially on the exam). Here is a link that you might find helpful with regards to gross neuroanatomy.

Few questions on this:

1) In the rats that are exposed to cigarette smoke, what are the changes in mucous production and secretions, cilia activity, and macrophage activity? I had put increased across the board -- I believe you eventually get cili dysfunction with smoking, but I thought a week was much too short for that to take place. Had no idea about macrophage activity, but I figured it would be increased due to the acute irritation.
There is a discussion about this question on page 4.

2) At what age is it normal to begin puberty in girls? There was a question of an 8 year old girl whose started to develop breast buds and pubic hair. I thought this was precocious puberty and you would want to do laboratory studies to confirm. Apparently the correct answer is to tell the worried mother that this is normal? It just seems awfully early to be so nonchalant about a girl entering puberty, and not want to do any testing.
The age threshold drops lower with time, right now for girls it is age 7 and boys, age 9.

3) 20 year old girl with servere dysuria and a painful vulvar lesion -- vesicual lesions on a erythematous base. Which organism? I had it between Candida and HSV. It was HSV. I've never heard of dysuria in an HSV infection, seeing as the bladder and most of the urethra is not stratified squamous, I didn't think it could be HSV. I know the lesion is classic of HSV is a vesicular rash on erythematous base, but candida also commonly infects the vulva and can cause a painful, red lesion with sores.
Painful vesicular lesions on the USMLE are HSV, no questions asked. Dysuria is definitely part of the HSV symptomatology. Vulvar pruritus is the chief complaint of most people with candidial vaginitis, and the USMLE almost always mentions a thick (curdy) whitish discharge.

4) Do you form immunity against chlamydia? I didn't think you did. There was a stats question where you screened freshman girls for chlamydia and 500 out of 2500 tested positive. Then a year later you tested them again and there were an additional 200 positives, and it then wants you to find the incidence. I thought you would divide 200/2500 as it's a year later and one of the original 500 girls could have been infected again. The correct answer is 200/2000 as you subtract the original 500 girls from the population, so I'm assuming there is immunity? And even if you do have immunity, there are multiple types of chlamydia (D-K), so what if an original girl was infected with D strain and then a year later with F strain? This question seems flawed to me.
What if the girls weren't treated after being screened? I haven't seen the question so I don't know what it says exactly.
 
I read here that the answer to the question about horskidney disease is 'many arteries' but i read in FA that horsekidney disease is due to stop by inferior mesentery artery


so?
 
53 yo alcoholic, homeless man comes to ed by police. appears cachectic, fever. clubbing of fingers, breath smells, missing teeth, numerous cavities. has increased fremitus, dullness to percussion, and tubular breath sounds in right lower lung. leukocyte count 11.4k. sputum grows purulence, gram + cocci in chains, and gram - bacilli. x ray shows cavitation in right lower lung lobe with surrounding infiltrate. sputum will likely grow which of the following?

chlamydophila pneumonia, haemophilus influenza, mycoplasma pneumonia, strep pneumon, normal oral flora

homeless -> aspiration pneumonia.
 
I read here that the answer to the question about horskidney disease is 'many arteries' but i read in FA that horsekidney disease is due to stop by inferior mesentery artery


so?

A horseshoe kidney is just a failure of the kidneys to develop into separate organs, and they are attached at one end to each other. This connection is what gets caught on the IMA. I believe the question was forcing you to infer why this would be a problem, and this is because the kidneys are much lower in the abdomen than they should be, the renal arteries are most likely to branch off the abdominal aorta at an abnormal place. Since the question was asking about a man with an abdominal aortic aneurysm undergoing repair, you'd definitely want to know the location of the renal arteries so you don't block their flow.
 
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Just did NBME 16 and had a question that I couldn't find a definitive answer to online -
The 5 year old who is treated with aspirin and then falls into a coma. I know they're getting at Reye's but none of the answers (cerebral edema, metabolic alkalosis (wrong, this is what I picked), SAH, venous sinus thrombosis or viral encephalitis) seemed to fit. I also considered viral encephalitis but wasn't sure…any thoughts?

Also, any thoughts on NBME 16 in regard to time management? I felt myself running much tighter on time on this NBME than on any other NBME I've taken so far (NBME 12, 13, 7)

Thanks for the help!
 
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