USMLE NBME 18 - Questions and Answers - Discussions & Explanations

[TheAberrantGene]

NBME 18 has been released and is available on regular and extended feedback.
I will be taking it fairly soon as my exam is around the corner.
Let's continue the great trend on this forum and start a discussion once people start taking it,

Best of luck fellas !

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[tennischicnikki]

@Crdioman
1. I can't remember the exact answer but heparin is used in addition to beginning warfarin because of the half lives of coagulation factors II, VII, IX, X... they have to be cleared from the system before an effect is seen since warfarin inhibits vit k epoxidase during the production of coagulation factors. It doesn't affect any of the coagulation factors already present. PT/INR for warfarin, aPTT for heparin.
2. We discussed this one somewhere. Correct answer is he is allowed to drive.

@study03
1. BPH (obstruction ---> increased hydrostatic pressure in BS due to back pressure of urine)
2. C

For the driving question, are you talking about the guy with the seizure who recently changed his meds to Carbamezapine? I got it wrong, but when I looked up the drug, it was saying that they don't recommend driving while taking Cabamezapine. So I thought the answer would be that he can't drive as long as he's on that drug. Someone correct me if I'm mistaken please.

 

[tennischicnikki]

Answer is hypertension. Hypertension increases the pressure within the ventricle, and this pressure overload eventually results in diastolic heart failure, which is associated with concentric enlargement. Myocardial cells hypertrophy and develop "boxcar nuclei" when having to generate increased pressure due to hypertension.

Another way to look at it: concentric hypertrophy in an older person --> AS --> MCC of AS in elderly is HTN

 

[tennischicnikki]

maybe he is living in a group home because of preexisting condition

I agree. The questions says that his condition was worsening....as in this isn't a new onset. And he's obviously unable to care for himself, so he's in a group home. With no other hx of illness, I assumed he already was dx with SCH.

 

[tennischicnikki]

in anti cancer drug mediated myelosuppression which of the following needs to be monitored?
A) cytotoxic T cells
B) neutrophils
C) serum complement conc
D) serum immune globulin conc

is the answer B ?

I was also thinking about it in terms of what the myeloid cells gives rise to vs lymphoid cell. Lymphoid cells: B & T cells. Myeloid cells: magakaryocytes, RBC, monocytes, neutrophils, etc. And that lead me to the correct answer: B

 

[MissNomer]

A 19-year-old man is evaluated for signs of gastrointestinal bleeding. At laparotomy, a 5-cm blind outpouching on the antimesenteric side of the terminal ileum, about
15 cm from the ileocecal valve, is resected. Pathologic examination of the resected segment will most likely show which of the following?

Answer was meckels diverticulum(well, the actual words are heterotopic tissue). If the q would have said young kid, I would have been all about it. So adults can have meckel's diverticulum? Interesting.I don't think any question I've ever seen about meckel's involved a kid older than like 4

Bleeding blind outpouching on the antimesenteric side of the terminal ileum, 15 cm from the ileocecal valve can't be anything else and they can present at any age although more common in young.

 

[MissNomer]

2-44. Question about 28 yr old woman with PCOS. what's the best way to make her comply with her plan...
i was torn between referring to a support group and follow up appointments. Just following up a patient on their progress doesn't inherently motivate them to follow their treatment plan while not at the doctors office. Can someone give me a rationale here? I usually think uworld ethics q are okay, but some NBME ethics q's are just bogus.

Since you made the treatment plan it's your responsibility to follow her up as you are the one in charge.
This in contrast to the teenage pt who is non-compliant with his insulin injections and you need to have him see other "cool" kids injecting themselves with insulin. So you use peer pressure.
Also, support groups are helpful in patients with chronic conditions.

 

[KEMU163]

Hi there people,so i've searched the thread and couldn't find the answer to these:
1. Lab studies in bulimic patient with recurrent vomiting, what happens to K, HCO3, pH and anion gap?

2. 95y/o with multiple ecchymoses in various stages of healing. Meds include metoprolol, HCTZ, metformin and glipizide. No chest pain or SOB. Walks two miles a day and lives with 75y/o daughter and 50y/o grandson. BMI is 15 and 6.3 kg weightloss since last visit
what to ask on interview?
do you feel safe at home?
change in stool (wrong)
exercising too much
eating okay
chewing problem

 

[lana62]

1. Metabolic alkalosis with hypokalemia
2. Do you feel safe at home?

 

[KEMU163]

Thanks @lana62

 

[Champagne_Tap]

Bringing this thread back to life for a quick Q, regarding --

41. 45-year-old man bmi 26, total cholesterol 200, HDL 50, triglycerides 550. Which drug to prescribe?
- Fenofibrate
​

I recall from UW that statins are given no matter what the lipid panel is to someone who has hypercholesterolemia. Can someone provide some reasoning why fibrates is a better answer than statins for this Q? Thanks!

 

[el_duderino]

Bringing this thread back to life for a quick Q, regarding --
.

41. 45-year-old man bmi 26, total cholesterol 200, HDL 50, triglycerides 550. Which drug to prescribe?
- Fenofibrate.
.​

I recall from UW that statins are given no matter what the lipid panel is to someone who has hypercholesterolemia. Can someone provide some reasoning why fibrates is a better answer than statins for this Q? Thanks!.

His problem is triglycerides, and fibrates lower triglycerides more.

 

[Champagne_Tap]

His problem is triglycerides, and fibrates lower triglycerides more. ....

Right, I understand that. His total cholesterol is high, however - 1st-line treatment would be statin therapy for that...right?

 

[el_duderino]

200 isn't even high, it's barely borderlime. 550 triglycerides is off the carts.

 

[Champagne_Tap]

OK, fair enough. Thanks!

 

[WeedForLunch]

Guys any help with explanation for this ?
Cholera toxin catalyzes transfer of ADP-ribose to an arginine residue in stimulatory G protein resulting in inhibition of GTPase activity. Which increases in cells as a result?


Answer is : Concentration of cAMP


But how does that happen ? :-/

 

[Step1stepper]

@usmle2016

1. Pre/postcentral gyrus - motor/sensory cortex (medial---> leg, foot) = A
2. Definitely Kaposi sarcoma so antineoplastic. As far as differentiating them there was no mention of a cat scratch = D
4. Smoker, peripheral edema/congested liver (RHF), distant heart sounds ---> cor pulmonale = C

N#3 answer is a little tricky
Transcription of the reductase gene is enhanced by the sterol regulatory element binding protein (SREBP). This protein binds to the sterol regulatory element (SRE), located on the 5' end of the reductase gene. When SREBP is inactive, it is bound to the ER or nuclear membrane with another protein called SREBP cleavage-activating protein (SCAP). When cholesterol levels fall, SREBP is released from the membrane by proteolysis and migrates to the nucleus, where it binds to the SRE and transcription is enhanced. If cholesterol levels rise, proteolytic cleavage of SREBP from the membrane ceases and any proteins in the nucleus are quickly degraded

 

[CT doc]

Guys any help with explanation for this ?
Cholera toxin catalyzes transfer of ADP-ribose to an arginine residue in stimulatory G protein resulting in inhibition of GTPase activity. Which increases in cells as a result?


Answer is : Concentration of cAMP


But how does that happen ? :-/

I'm not positive but I'm thinking inhibition of GTPase results in GTP not being broken down, which results in permanant Gs activation, which activates adenylate cyclase via permanent Gs activation, increasing cAMP

 

[chickensoupdr]

Yup!

Why is it Heterotopic Gastric Mucosa...? Why can't it be Crohn's?

 

[shygirl1987]

1. D (the lower the blood:gas coefficient, the faster the induction rate)
2. I think I put E, only one that made sense to me since the right kidney is fine and the left ureter isn't dilated.
3. B
4. E
5. D

(Someone correct me if I'm wrong on the first 2 cause my memory is shot)

Hi, can you clarify why number 5 is D please. Thanks

 

[Pam Platense]

Hope this help u. It's from Am Fam Physician. 1999 Feb 1;59(3):635-646.

 

[Inventor of Post-Its]

Why is it Heterotopic Gastric Mucosa...? Why can't it be Crohn's?

Crohn's can cause fistulas, but this question describes a 5 cm outpouching, which is definitely a diverticulum (ie Meckel).

N#3 answer is a little tricky
Transcription of the reductase gene is enhanced by the sterol regulatory element binding protein (SREBP). This protein binds to the sterol regulatory element (SRE), located on the 5' end of the reductase gene. When SREBP is inactive, it is bound to the ER or nuclear membrane with another protein called SREBP cleavage-activating protein (SCAP). When cholesterol levels fall, SREBP is released from the membrane by proteolysis and migrates to the nucleus, where it binds to the SRE and transcription is enhanced. If cholesterol levels rise, proteolytic cleavage of SREBP from the membrane ceases and any proteins in the nucleus are quickly degraded

You don't have to know all this to get the question right, though - just understand that the cell has regulatory mechanisms so that if the cholesterol level gets too low, the cell will try to raise it back up. Increase LDL-R to bring more cholesterol into the cell, and increase HMG-CoA to make more new cholesterol.

 

[Inventor of Post-Its]

One question of my own - 6 year-old boy with vomiting, and clumsiness, PE shows papilledema, impaired upward gaze, pupil response to the right, and broad-based gait. CT shows enlarged lateral and third ventricles, 2-cm mass.

I realize now that this is a pinealoma, but the cerebellar signs tripped me up (and also just knowing the cerebellum is a really common location for childhood brain tumors). Is the broad-based gait supposed to be from the tumor compressing the cerebellum like it is with the colliculi? Also, what's up with "pupil response to the right"? Do they mean light?

 

[Dr. Edd P.]

1/4 it is!

Isn't this supposed to be 1/2? because whats asked in the question is just the male fetus?

 

[Inventor of Post-Its]

Isn't this supposed to be 1/2? because whats asked in the question is just the male fetus?

But we don't know whether the mother is a carrier or not. 1/2 chance she is * 1/2 chance that, if she is, her male fetus will get that allele --> 1/4 chance overall.

 

[unicorn416]

One question of my own - 6 year-old boy with vomiting, and clumsiness, PE shows papilledema, impaired upward gaze, pupil response to the right, and broad-based gait. CT shows enlarged lateral and third ventricles, 2-cm mass.

I realize now that this is a pinealoma, but the cerebellar signs tripped me up (and also just knowing the cerebellum is a really common location for childhood brain tumors). Is the broad-based gait supposed to be from the tumor compressing the cerebellum like it is with the colliculi? Also, what's up with "pupil response to the right"? Do they mean light?

Not sure what "pupil response to the right" means, but I thought of it as impaired upward gaze --> parinaud syndrome --> usually pinealoma or something compressing dorsal midbrain area (might compress cerebellum as you suggested). Wouldn't overthink it, especially with the other answer choices.

 

[OlgaW007]

Hi everyone! I just did my NBME 18. I already found an answer for this question but there was no explanation. If anybody knows please reply.

A 68-year-old man comes to the physician because of a 1-month history of light-headedness and tightness in his chest with exertion. He adds that the pain is worse after arguing with his wife, and the symptoms resolve with rest. He has a past history of lower gastrointestinal bleeding; evaluation at that time was negative on upper endoscopy and colonoscopy. His temperature is 37°C (98.6°F), pulse is 85/min, respirations are 15/min, and blood pressure is 110/75 mm Hg. Physical examination shows no abnormalities. His hemoglobin concentration is 8.2 g/dL, and hematocrit is 24%. Test of the stool for occult blood is positive. An ECG shows no abnormalities. Repeat colonoscopy shows no abnormalities. Which of the following is the most likely cause of this patient's gastrointestinal symptoms?
A
) Adenocarcinoma of the colon
B
) Angiodysplasia
C
) Diverticulitis
D
) Peutz-Jeghers syndrome
E
) Ulcerative colitis (WRONG)

Goljan says (p.453) that diagnosis angiodysplasia made with colonoscopy. Here they did not find anything.

 

[OlgaW007]

B, C, E, C, F

58 yo man, 4 year history of productive cough and increased sputum. smoker, T 37º, HR 72, RR 18. Physical exam cyanosis, diffuse wheezing. Which of the pulmonary cell types most likely to be abnormal?
A. Alveolar endothelial cells
B. Alveolar macrophages
C. Pseudostratified columnar epithelial cells
D. Type I pneumocytes
E. Type II pneumocytes.

You answered C. Could you explain why?

 

[Inventor of Post-Its]

Hi everyone! I just did my NBME 18. I already found an answer for this question but there was no explanation. If anybody knows please reply.

A 68-year-old man comes to the physician because of a 1-month history of light-headedness and tightness in his chest with exertion. He adds that the pain is worse after arguing with his wife, and the symptoms resolve with rest. He has a past history of lower gastrointestinal bleeding; evaluation at that time was negative on upper endoscopy and colonoscopy. His temperature is 37°C (98.6°F), pulse is 85/min, respirations are 15/min, and blood pressure is 110/75 mm Hg. Physical examination shows no abnormalities. His hemoglobin concentration is 8.2 g/dL, and hematocrit is 24%. Test of the stool for occult blood is positive. An ECG shows no abnormalities. Repeat colonoscopy shows no abnormalities. Which of the following is the most likely cause of this patient's gastrointestinal symptoms?
A
) Adenocarcinoma of the colon
B
) Angiodysplasia
C
) Diverticulitis
D
) Peutz-Jeghers syndrome
E
) Ulcerative colitis (WRONG)

Goljan says (p.453) that diagnosis angiodysplasia made with colonoscopy. Here they did not find anything.

I guess you might be able to pick up angiodysplasia on a colonoscopy, but you would DEFINITELY see any of the others - that was my reasoning. And FA says the diagnosis is confirmed by angiography, not colonoscopy.

 

[tarsuc]

52 yo man is brought to er 30min after the onset of chest pain and shortness of breath. He had played tennis all day and he does not remember how much fluid he had consumed. His temperature is 36.7 oC, pulse 122min, respirations 28min and BP 90/50 mmHg. PE shows dry skin and decreased capillary refill. cardiac normal. Which of the following findings in the nephron best describes the tubular osmolarity, compared with serum in this patient?
PT //macula densa //medullary collection duct
- Isotonic, hypotonic, hypertonic (?)


can someone explain please

 

[Makaar]

52 yo man is brought to er 30min after the onset of chest pain and shortness of breath. He had played tennis all day and he does not remember how much fluid he had consumed. His temperature is 36.7 oC, pulse 122min, respirations 28min and BP 90/50 mmHg. PE shows dry skin and decreased capillary refill. cardiac normal. Which of the following findings in the nephron best describes the tubular osmolarity, compared with serum in this patient?
PT //macula densa //medullary collection duct
- Isotonic, hypotonic, hypertonic (?)


can someone explain please

My understanding: Fluid entering the pct is isotonic, fluid at top of dct is hypotonic (and this is sensed by macula densa), fluid leaving is hypertonic

 

[Makaar]

68-year-old man with creatinine 2.3 due to chronically increased hydrostatic pressure in Bowman space. Cause?

Anyone understand why it's BPH and not diabetes (which specifically targets efferent arteriole)? Won't both cause a chronic increase in hydrostatic pressure in Bowmans space?

 

[Anti-PD1]

68-year-old man with creatinine 2.3 due to chronically increased hydrostatic pressure in Bowman space. Cause?

Anyone understand why it's BPH and not diabetes (which specifically targets efferent arteriole)? Won't both cause a chronic increase in hydrostatic pressure in Bowmans space?

Bowman's space is part of the tubule. The efferent arteriole is in parallel with the glomerular capillaries. Two very different sides of the equation.

 

[Makaar]

Bowman's space is part of the tubule. The efferent arteriole is in parallel with the glomerular capillaries. Two very different sides of the equation.

Thanks man. So simple. Definitely over thought that one.

 

[premedstud101]

56g x 4 cal/g = 224 cal (so he has 2000 - 224 = 1776 left to eat in one day). 630 + 1146 = 1776 and 630/1146 = 30/55

I don't understand this calculation. How did you arrive at the 630 and 1146 numbers?

 

[Rahas]

I don't understand this calculation. How did you arrive at the 630 and 1146 numbers?

Don't remember the exact question, but I believe of the 2000 cal, 224 were acquired via dietary protein, leaving 1776 to be split between carbs and fats in a 30:55 ratio.

Thats 85 (30 + 55) ratio points for a total of 1776 cals. So 1 ratio point equals 1776/85 = 20.89.

30 x 20.89 = 627
55 x 20.89 = 1149

 

[dontwantaids]

it's actually a case of cryoglobinuria due to hep c, which typically presents with arthralgia, purpura, nephritic syndrome

 

[403710]

Looked through here and couldn't find the answers to these- help a brotha out!

Q. 58-year-old man comes to the physician because of a 4-year history of recurrent cough productive of increased sputum. Use of over-the-counter cough suppressants has not resolved his symptoms. He has smoked 2 packs of cigarettes daily for 35 years. He has no family history of lung disease. His temperature is 37°C (98.6°F), pulse is 72/min, and respirations are 18/min. Physical examination shows cyanosis. Diffuse wheezing is heard on auscultation. Which of the following pulmonary cell types is most likely to be abnormal in this patient?

- Answer: Pseudostratified columnar epithelial cells (Other options: Alveolar Endothelial cells, Alveolar Macrophages, Type I or Type II pneumocytes)

I get that this is more likely Chronic Bronchitis with metaplasia of the pseudostratified columnar epithelium to stratified squamous, but would i be wrong in thinking of this as also having a component of centrilobular emphysema with alveolar endothelial cell damage ("abnormality")?



Q. A 25-year-old man is admitted to the hospital because of severe crush injuries to the chest and extensive burns over 30% of his body surface area. Three hours later, he develops tachypnea and dyspnea. Arterial blood gas analysis on room air shows a decreased Po2 and Pco2. A chest x-ray shows bilateral interstitial and alveolar infiltrates. The patient is intubated and mechanically ventilated. Damage to which of the following is most likely to preclude restoration of normal tissue architecture and pulmonary function in this patient?

- Answer: Basement membranes (Other options: Capillaries, Fibroblasts, Macrophages, Mast Cells, Type I pneumocytes)

If I'm correct and this is ARDS, why would there not be capillary and even type I pneumocyte damage? From Goljan re ARDS: "Capillary damage causes leakage of a protein-rich exudate producing hyaline membranes. Neutrophils damage type I and II pneumocytes."



Q. 60-year-old man for routine health examination. Has had normal blood pressure measurements. BP today 170/95mmHg. Physical examination shows no other abnormalities. Serum show hypokalemia and metabolic alkalosis. Plasma renin activity and serum aldosterone concentrations are increased. Following the administration of captopril, there is a marked increase in plasma renin activity. Which of the following is the most likely cause of the findings in this patient?
- Renal artery stenosis (Other options: Aldosterone-secreting tumor, Chronic glomerulonephritis, Cushing Syndrome, Essential Hypertension)

Couldn't the etiology of essential hypertension be idiopathically increased renin secretion? Given that, wouldn't it increase further with administration of an ACE-I?



Q. 24-year-old man with 3-day progressive numbness of both feet ascended to thighs. Last 24 hours, numbness and tingling of hands. PE ataxic gait. Deep tendon reflexes diminished in upper extremities and absent in knees and ankles. Vibration and joint position absent in fingertips and feet bilaterally. Mild weakness distal upper extremities ad moderate weakness of lower extremities. Structure involved?
- Myelinated primary afferents

Is this just GBS?

 

[wickey4083]

Looked through here and couldn't find the answers to these- help a brotha out!

Q. 58-year-old man comes to the physician because of a 4-year history of recurrent cough productive of increased sputum. Use of over-the-counter cough suppressants has not resolved his symptoms. He has smoked 2 packs of cigarettes daily for 35 years. He has no family history of lung disease. His temperature is 37°C (98.6°F), pulse is 72/min, and respirations are 18/min. Physical examination shows cyanosis. Diffuse wheezing is heard on auscultation. Which of the following pulmonary cell types is most likely to be abnormal in this patient?

- Answer: Pseudostratified columnar epithelial cells (Other options: Alveolar Endothelial cells, Alveolar Macrophages, Type I or Type II pneumocytes)

I get that this is more likely Chronic Bronchitis with metaplasia of the pseudostratified columnar epithelium to stratified squamous, but would i be wrong in thinking of this as also having a component of centrilobular emphysema with alveolar endothelial cell damage ("abnormality")?



Q. A 25-year-old man is admitted to the hospital because of severe crush injuries to the chest and extensive burns over 30% of his body surface area. Three hours later, he develops tachypnea and dyspnea. Arterial blood gas analysis on room air shows a decreased Po2 and Pco2. A chest x-ray shows bilateral interstitial and alveolar infiltrates. The patient is intubated and mechanically ventilated. Damage to which of the following is most likely to preclude restoration of normal tissue architecture and pulmonary function in this patient?

- Answer: Basement membranes (Other options: Capillaries, Fibroblasts, Macrophages, Mast Cells, Type I pneumocytes)

If I'm correct and this is ARDS, why would there not be capillary and even type I pneumocyte damage? From Goljan re ARDS: "Capillary damage causes leakage of a protein-rich exudate producing hyaline membranes. Neutrophils damage type I and II pneumocytes."



Q. 60-year-old man for routine health examination. Has had normal blood pressure measurements. BP today 170/95mmHg. Physical examination shows no other abnormalities. Serum show hypokalemia and metabolic alkalosis. Plasma renin activity and serum aldosterone concentrations are increased. Following the administration of captopril, there is a marked increase in plasma renin activity. Which of the following is the most likely cause of the findings in this patient?
- Renal artery stenosis (Other options: Aldosterone-secreting tumor, Chronic glomerulonephritis, Cushing Syndrome, Essential Hypertension)

Couldn't the etiology of essential hypertension be idiopathically increased renin secretion? Given that, wouldn't it increase further with administration of an ACE-I?



Q. 24-year-old man with 3-day progressive numbness of both feet ascended to thighs. Last 24 hours, numbness and tingling of hands. PE ataxic gait. Deep tendon reflexes diminished in upper extremities and absent in knees and ankles. Vibration and joint position absent in fingertips and feet bilaterally. Mild weakness distal upper extremities ad moderate weakness of lower extremities. Structure involved?
- Myelinated primary afferents

Is this just GBS?

yes, it's GBS

 

[yankees527]

Anyone else get tripped up about the radial groove question? The question specifically states their triceps strength is 2/5, and injury at the radial groove is beyond the point where the triceps gets its innervation fibers.

 

[wickey4083]

Don't remember the exact question, but I believe of the 2000 cal, 224 were acquired via dietary protein, leaving 1776 to be split between carbs and fats in a 30:55 ratio.

Thats 85 (30 + 55) ratio points for a total of 1776 cals. So 1 ratio point equals 1776/85 = 20.89.

30 x 20.89 = 627
55 x 20.89 = 1149

it's bc protein=4cal, fat=9cal, then you can get the answer

 

[Rahas]

I don't remember very well, but I think distal muscles were weaker than the triceps? Being in a cast --> disuse --> triceps weakness; since the distal muscles were weaker, something other than disuse was also part of the pathology.

Again, I don't remember this quesiton so I could be totally off...

 

[wickey4083]

52 yo man is brought to er 30min after the onset of chest pain and shortness of breath. He had played tennis all day and he does not remember how much fluid he had consumed. His temperature is 36.7 oC, pulse 122min, respirations 28min and BP 90/50 mmHg. PE shows dry skin and decreased capillary refill. cardiac normal. Which of the following findings in the nephron best describes the tubular osmolarity, compared with serum in this patient?
PT //macula densa //medullary collection duct
- Isotonic, hypotonic, hypertonic (?)


can someone explain please

bc, PT reabsorb the Na and H2O together, macular densa is around the distal convoluted tubule, which is the lowest conc of the tubule (check the FA), and the collection duct's conc is hyper due to the ADH's effect

 

[Rodeo clown]

Quick question. What did you guys put for the question about a 16 year old boy who masturbates and has sexual fantasies about girls and etc?

just schedule a follow up or suggest he calm down and reduce the frequency of masturbation? Sorry the the options are in my own words. Obviously, the NBME options were more formal. Lol.

 

[GBurdell]

Quick question. What did you guys put for the question about a 16 year old boy who masturbates and has sexual fantasies about girls and etc?

just schedule a follow up or suggest he calm down and reduce the frequency of masturbation? Sorry the the options are in my own words. Obviously, the NBME options were more formal. Lol.

schedule next visit. I put that and it wasn't in my incorrects.

 

[HopesandDreams]

Hi everyone! I just did my NBME 18. I already found an answer for this question but there was no explanation. If anybody knows please reply.

A 68-year-old man comes to the physician because of a 1-month history of light-headedness and tightness in his chest with exertion. He adds that the pain is worse after arguing with his wife, and the symptoms resolve with rest. He has a past history of lower gastrointestinal bleeding; evaluation at that time was negative on upper endoscopy and colonoscopy. His temperature is 37°C (98.6°F), pulse is 85/min, respirations are 15/min, and blood pressure is 110/75 mm Hg. Physical examination shows no abnormalities. His hemoglobin concentration is 8.2 g/dL, and hematocrit is 24%. Test of the stool for occult blood is positive. An ECG shows no abnormalities. Repeat colonoscopy shows no abnormalities. Which of the following is the most likely cause of this patient's gastrointestinal symptoms?
A
) Adenocarcinoma of the colon
B
) Angiodysplasia
C
) Diverticulitis
D
) Peutz-Jeghers syndrome
E
) Ulcerative colitis (WRONG)

Goljan says (p.453) that diagnosis angiodysplasia made with colonoscopy. Here they did not find anything.

angiodysplasia is more often in the right colon which you can't see with colonoscopy. everything else you would be able to see

 

[HuskyPride149]

Just took this today and got a 207.....only NBME i took and im aiming for at least a 220. Got a 215 and a 228 on uworld assessments. My exam is in 2 days ie Thursday. For ppl who took this and the real exam any thoughts on how comparable youre score was? Should I reschedule my exam? HELP!!

 

[Rodeo clown]

Just took this today and got a 207.....only NBME i took and im aiming for at least a 220. Got a 215 and a 228 on uworld assessments. My exam is in 2 days ie Thursday. For ppl who took this and the real exam any thoughts on how comparable youre score was? Should I reschedule my exam? HELP!!

I take the exam on Thursday as well. In my opinion, you are more likely to shoot above your NBME score since the NBMEs are known to underpredict notoriously. If you are looking for opinions you'll probably hear a lot of different things (overpredict, underpredict, same score) which will only confuse you more. Only you can be your best Judge. Just my observation- apparently UWSA2 has been very predictive off late. Good luck! Just walking into the exam center not freaking out can probably fetch you an additional 10 points. Lol. You can do this!

 

[Lostinoblivion]

FYI for anyone who felt cruddy after this test, I took it 8 days before my exam and scored a 228 and wasn't very happy, since my goal was higher and I thought my UWorld progress reflected something in the 230s. Well, my actual score came back today and I managed a 240 on the real thing. So anyway, if you didn't feel wonderful after this test, you do have hope of still doing much better on the actual exam, and I'm saying that as someone who normally does better on practice than the real thing.

OMG I wish I had seen this earlier. Just cancelled my test because I got 225 on this one. Really disappointed in myself

 

[MedGrl@2022]

GB syndrome--> Immune response against MYELIN due to molecular mimckery between the bug and myelin. (against gangliosides of myelin mostly) Answer is D

I understand why it could be GB but why can't his symptoms be to a Vitamin b12 deficiency... is it definitely GB because of the fast progression???

 

[MedGrl@2022]

section 3, 29/50:
Healthy 5yo boy comes for motion sickness. Parents want to give dyphenhydramine before a trip. Whats the mecanism of action of the drug - for motion sickness :
a) agonist alpha1 adrenoreceptors
b) agonist beta1 adrenoreceptors
c)agonist N-methyl-D-aspartate receptors
d)antagonist histamine 2 receptors (I know its H1, but thats the closest I figure out - wrong)
e) antagonist M3 receptors (is this one?)
f) antaagonist serotonin receptors

Thanks a lot!

okay I understand that 1st generation antihistamines have antimuscarinic effects but how does antagonism of M3 help with motion sickness. To the best of my knowledge, it does not. Antagonism of M1 could help with motion sickness but not M3. Can someone please help me out here? Why did NBME choose this as their answer???