USMLE NBME 18 - Questions and Answers - Discussions & Explanations

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TheAberrantGene

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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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34 year old man with progressive rash on his feet. HIV antibody test is positive. What do you give him in addition to HAART?
Antibacterial
Antineoplastic

I thought antibacterial since it could be bacillary angiomatosis. Why is it antineoplastic? I guess they were going for kaposi sarcoma here, but how were we supposed to know which one without biopsy? Also, sketchymicro and wiki say that treatment of kaposi is HAART. why would you give an antineoplastic?


thanks in advance for all of the help!!
 
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3. A 25 yo man just returned from work as worker from Africa begins oral chloroquine therapy for malaria caused by Plasmodium vivax. His initial therapeutic response is good, but he develops recurrent parasitemia 2 months later. Which of the following best explains the recurrence ?
a. Chloroquine is ineffective as oral therapy for P. vivax malaria (WRONG)
b. Chloroquine is ineffective on the exoerythrocytic malaria tissue stages
c. Chloroquine is only effective against P. vivax when combined with metronidazole
d. The patient has a second previously occult malaria infection
e. The patient is inefected with a chloroquine-resistant strain of P.vivax

why is A wrong? chloroquine would not target the hyponozoites, correct? is exoerythrocytic just a fancy name for that stage of hypnozoite? wouldn't the inability to target the hypnozoites make chloroquine ineffective for vivax?

1. a 35 yo woman with infertile, receive injection of contrast material into cervix. on hysterosalpingogram, contrast material also seen in peritoneal cavity, which explain this finding
a) rupture of the fallopian tube
b) rupture of the uterine body
c) spillage of contrast, which an artifact
d) spillage of contrast which normal

why do the tubes spill (d)? Are they normally not connected at all to the ovary? they just float there? This is definitely news to me if so :-O

3. A lab tech wipes doiwn the workbench with alcohol after an experiment. This treatment will successfully inactivated viruses with which of the following characteristics?
A- DNA genome
B- enveloped virion
C- helical capsid
D- icosahedral capsid
E- naked virion
F- RNA genome

33-year-old man dx with epilepsy age 10 years. Most recent generalized tonic-clonic was 5 years ago. Medication was adjusted. Current meds include carbamazepine. He's never had any collisions while driving his motor vehicle. Patient's status with respect to driving?
why is he medically qualified to drive? What is the cutoffs/regulations with this? never heard of this before

5. there was a celiac question.. why did they have pale stools? I thought pale stool tends to happen if you aren't excreting bile into the GI tract, sicne that is what gets converted to stercobillin that gives it the color.

39yo man with polycystic kidney disease has 6 mo hisory of intermitent blood in urine. T 37C, pulse 100, resp 24, BP 160/90. physical shows no other abnormality. his serum urea concentration is 100 mg.ml, creatinine 8mg.dl. urinalysis shows blood. arterial gas would be:
pH pCO2 HCO3
a)7.22/28/11
b)7.32/64/32
c)7.38/40/23
d)7.46/19/13
e)7.49/50/37

I understand why people say A since it was renal failure > metabolic acidosis. I think the way I was thinking about this was that i thought also in PKD people get hypertension from increased renin release due to the cysts blocking blood flow (hence why you give them ACE/ARBs).. so i was thinking E because high RAAS would cause lots of H+ to be excreted, creating the metabolic alkalosis. why is this wrong?

A 40 year old man has had orthostatic hypotension and loose stools for 1 year, 26 years of T1DM. What is causing the loose stools?
Exudation
Malabsorptioni
Motility disorder
Osmosis
Secretoin

Why motility? Somebody said previously it was a neuropathy from diabetes, why wouldn't that cause constipation instead?

5. 18 month old girl with 2 days of cough and hoarseness. 102 fever. Harsh, barking cough. Mild erythema of the oropharyngeal and laryngeal mucosa but no exudate. Rapid strep test is negative. Condition improves within 4 days. What was the cause?
Influenza A, Parainfluenza, RSV, S. aureus, C. diptheriae

I said influenza but it was wrong. Was it RSV? How can I tell what is was just based on "harsh barking cough" I didn't think it was parainfluenza since no inspiratory stridor. I was thinking flu since the erythema in the throat which is where influenza invades, right?


3. B. "Tissue stages" = hypnozoites in the liver.


1. D. Yes, the tubes open right into the peritoneal cavity. The egg is released into the peritoneal cavity and somehow gets into the tubes. That blew my mind when I learned it during MCAT studying. (The tubes opening into the peritoneal cavity is the basis of the “retrograde menstruation” hypothesis of how endometriosis works - shedded endometrial tissue migrates through the tubes and exits into the peritoneal cavity to be deposited somewhere.)


3. B, I believe. The alcohol interrupts lipid bilayers (i.e. envelopes)


33-year-old man dx with epilepsy: you can drive after you’re seizure-free for 6 months (in real life it varies by state, but I think the USMLE goes by 6 months)


5. I think you get pale stools with celiac because you fail to absorb fat due to the eroded villi.


39yo man with polycystic kidney disease: People with renal failure always have acidosis, not alkalosis, because they fail to excrete organic acids.


T1DM and loose stools: I got motility by the process of elimination. And if you google it, diabetic diarrhea is apparently a thing.


5. As far as the USMLE goes, “barking cough” is pathognomonic for paraflu.
 
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3. A 25 yo man just returned from work as worker from Africa begins oral chloroquine therapy for malaria caused by Plasmodium vivax. His initial therapeutic response is good, but he develops recurrent parasitemia 2 months later. Which of the following best explains the recurrence ?
a. Chloroquine is ineffective as oral therapy for P. vivax malaria (WRONG)
b. Chloroquine is ineffective on the exoerythrocytic malaria tissue stages
c. Chloroquine is only effective against P. vivax when combined with metronidazole
d. The patient has a second previously occult malaria infection
e. The patient is inefected with a chloroquine-resistant strain of P.vivax

why is A wrong? chloroquine would not target the hyponozoites, correct? is exoerythrocytic just a fancy name for that stage of hypnozoite? wouldn't the inability to target the hypnozoites make chloroquine ineffective for vivax?

1. a 35 yo woman with infertile, receive injection of contrast material into cervix. on hysterosalpingogram, contrast material also seen in peritoneal cavity, which explain this finding
a) rupture of the fallopian tube
b) rupture of the uterine body
c) spillage of contrast, which an artifact
d) spillage of contrast which normal

why do the tubes spill (d)? Are they normally not connected at all to the ovary? they just float there? This is definitely news to me if so :-O

3. A lab tech wipes doiwn the workbench with alcohol after an experiment. This treatment will successfully inactivated viruses with which of the following characteristics?
A- DNA genome
B- enveloped virion
C- helical capsid
D- icosahedral capsid
E- naked virion
F- RNA genome

33-year-old man dx with epilepsy age 10 years. Most recent generalized tonic-clonic was 5 years ago. Medication was adjusted. Current meds include carbamazepine. He's never had any collisions while driving his motor vehicle. Patient's status with respect to driving?
why is he medically qualified to drive? What is the cutoffs/regulations with this? never heard of this before

5. there was a celiac question.. why did they have pale stools? I thought pale stool tends to happen if you aren't excreting bile into the GI tract, sicne that is what gets converted to stercobillin that gives it the color.

39yo man with polycystic kidney disease has 6 mo hisory of intermitent blood in urine. T 37C, pulse 100, resp 24, BP 160/90. physical shows no other abnormality. his serum urea concentration is 100 mg.ml, creatinine 8mg.dl. urinalysis shows blood. arterial gas would be:
pH pCO2 HCO3
a)7.22/28/11
b)7.32/64/32
c)7.38/40/23
d)7.46/19/13
e)7.49/50/37

I understand why people say A since it was renal failure > metabolic acidosis. I think the way I was thinking about this was that i thought also in PKD people get hypertension from increased renin release due to the cysts blocking blood flow (hence why you give them ACE/ARBs).. so i was thinking E because high RAAS would cause lots of H+ to be excreted, creating the metabolic alkalosis. why is this wrong?

A 40 year old man has had orthostatic hypotension and loose stools for 1 year, 26 years of T1DM. What is causing the loose stools?
Exudation
Malabsorptioni
Motility disorder
Osmosis
Secretoin

Why motility? Somebody said previously it was a neuropathy from diabetes, why wouldn't that cause constipation instead?

5. 18 month old girl with 2 days of cough and hoarseness. 102 fever. Harsh, barking cough. Mild erythema of the oropharyngeal and laryngeal mucosa but no exudate. Rapid strep test is negative. Condition improves within 4 days. What was the cause?
Influenza A, Parainfluenza, RSV, S. aureus, C. diptheriae

I said influenza but it was wrong. Was it RSV? How can I tell what is was just based on "harsh barking cough" I didn't think it was parainfluenza since no inspiratory stridor. I was thinking flu since the erythema in the throat which is where influenza invades, right?

Can you double check on the pale stools description with that Celiac's question? IIRC they just described it as fatty bulky stools.
 
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last questions i swear..

i think one said something about the PMI being felt subxiphoid area.. does that just mean right ventricular hypertrophy is happening?

i think another one the answer was alport syndrome but it said it was an "x linked recessive", although I'm pretty sure FA has it as x linked dominant. what's up with that?

waht is c-Jun and is it important at all for boards? there was like 1 tiny thing on it in UW just with regards to southwestern blotting and that it's a transcription factopr
 
Can you double check on the pale stools description with that Celiac's question? IIRC they just described it as fatty bulky stools.
it was certainly described as pale. it was in a baby though if that makes any difference..

i mean fatty stool is probably still "pale" but not pale when you compare it to a biliary problem i'm thinking
 
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b descending colon. The trick is to know the major branches off the aorta. So pancreas spleen and stomach= celiac trunk first major offshoot (mostly, the pancreas has some help by the SMA if I remember right? W/e). Then you have the SMA giving you the rest of the intestines up until the distal 1/3 of the transverse colon. Then the IMA giving you the descending colon, etc. the adrenals get their blood supply pretty high up actually, I think between the Celiac trunk and SMA can't remember for sure. Anyway I remember this one as IMA because the fused horse shoe kidneys get caught up on the IMA, it is the most inferior major branch (and the question of course is talking about the most inferior part of the AA before it bifurcates.


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44yo woman at 15 wks gestation has a uterus consistent in size with gestational age. Amniocentesis shows increased a-fetoprotein concentration. Pts at risk for which defect?
congenital heart defect, horseshoe kidney, hypergonadism, malrotation of gut, spina bifida
Is it spina bifida? First Aid says a-fetoprotein is elevated in all NTD except spina bifida so I thought that's what separates it from the other NTDs
 
44yo woman at 15 wks gestation has a uterus consistent in size with gestational age. Amniocentesis shows increased a-fetoprotein concentration. Pts at risk for which defect?
congenital heart defect, horseshoe kidney, hypergonadism, malrotation of gut, spina bifida
Is it spina bifida? First Aid says a-fetoprotein is elevated in all NTD except spina bifida so I thought that's what separates it from the other NTDs

Yup it's spina bifida. First aid says Alpha-fetoprotein elevated except spina bifida occulta, which is slightly different than regular spina bifida. I made a similar mistake when I saw the question.
 
5. Man comes to doc for cast removal. Fracture of left humerus that required open reduction, internal fixation, cast immobilization. Muscle strength is 2/5 with extension of elbow and 1/5 with extension of wrist and fingers. Patient most likely sustained a fracture at (which location in humerus)?

A. Coronoid fossa
B. Distal shaft
C. Medial epicondyle
D. Radial groove
E. Surgical neck

I know the answer is radial groove, but can someone explain why there's weakness extending the elbow as well as wrist? I was under the impression that the radial groove was below the level of the nerve supplying the triceps, so the lesion would have to be above that.
 
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Dead space has to do with areas that are ventilated but not perfused (more or less). A shunt is the opposite-- not ventilated, but perfused. D should be the answer.

If everything else stays the same, except for the decreased number of measurements (smaller sample size), the width of the confidence interval will increase. Two ways to get this answer: look at the formula for a confidence interval or use logic.

The formula: x-bar +/- (t critical)*(standard error of the mean) where standard error of the mean is equal to the sample standard deviation, s, divided by the square root of the sample size, n. In the first case, n=20 so 8/(sq.rt.20) is smaller than 8/(sq.rt. 4). Therefore, when n is reduced from 20 to 4, we can see the mean has a larger value added/subtracted from it, making the interval wider when n=4 instead of 20.

The other way to approach that is from a qualitative perspective. The width of a confidence interval represents our uncertainty concerning the estimate. If we have a larger sample, we should be less uncertain about our estimate (narrower interval). Similarly, if we have a smaller sample, we will be more uncertain about our estimate (again, assuming that the only change is sample size). This should make sense, because we would like to have all possible information (no uncertainty), but we can't usually get all the information (so we're left with uncertainty). Simply put, larger samples (more information) get us closer to the truth and reduce our uncertainty about our estimate of that truth (the mean, in this case).
B should be correct.

Digging up this old post, but I think this answer is wrong. It is likely that the 95% CI will increase, but it may not. The original set of 20 measurements had an SD of 8 mm Hg. It's possible your new set of 4 measurements have an SD of 1 mm Hg, in which case the 95% CI will be +/- (1/2) instead of +/- 8/sqrt(20). In this case the 95% CI will be smaller.
 
44yo woman at 15 wks gestation has a uterus consistent in size with gestational age. Amniocentesis shows increased a-fetoprotein concentration. Pts at risk for which defect?
congenital heart defect, horseshoe kidney, hypergonadism, malrotation of gut, spina bifida
Is it spina bifida? First Aid says a-fetoprotein is elevated in all NTD except spina bifida so I thought that's what separates it from the other NTDs
It is spina bifida. FA says AFP is elevated in all NTD except spina bifida OCCULTA. Meningocele/myelomeningoceles are types of spina bifida- and you'll see elevated AFP with those.
 
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Think about it like this. If you know that the radial groove is below the level, then sure as hell the distal shaft is below the level. So why pick that answer to begin with?
 
Think about it like this. If you know that the radial groove is below the level, then sure as hell the distal shaft is below the level. So why pick that answer to begin with?

I picked surgical neck. I had just copied and pasted the question and answer from a previous poster. I'll go edit for clarity.
 
Oh and to answer your question, the weakness in the elbow is due to muscle atrophy. The trick is to see that there is a relative decrease with just finger and wrist extension. That is why it's radial nerve at the groove.
 
Digging up this old post, but I think this answer is wrong. It is likely that the 95% CI will increase, but it may not. The original set of 20 measurements had an SD of 8 mm Hg. It's possible your new set of 4 measurements have an SD of 1 mm Hg, in which case the 95% CI will be +/- (1/2) instead of +/- 8/sqrt(20). In this case the 95% CI will be smaller.

This questions hinges on a fundamental statistical concept: increasing the sample size boosts statistical power. This increases confidence in the test results and reduces the influence of outlying values. While it may be possible that 4 measurements have the same (or very similar) values, there would be little reason to believe that these 4 values are, themselves, representative of the sample population as a whole. But as we increase the number of measurements, we gain confidence that the values are representative of the population of interest.
 
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Question about the 2 month old with vomiting and diarrhea....how do we differentiate rotavirus vs. norovirus (besides that "wheel shaped virus" idea which I didn't know). In the US, we don't have much rotovirus due to vaccines, so I thought this child would have norovirus.
 
5. Man comes to doc for cast removal. Fracture of left humerus that required open reduction, internal fixation, cast immobilization. Muscle strength is 2/5 with extension of elbow and 1/5 with extension of wrist and fingers. Patient most likely sustained a fracture at (which location in humerus)?

A. Coronoid fossa
B. Distal shaft
C. Medial epicondyle
D. Radial groove
E. Surgical neck

I know the answer is radial groove, but can someone explain why there's weakness extending the elbow as well as wrist? I was under the impression that the radial groove was below the level of the nerve supplying the triceps, so the lesion would have to be above that.

I agree...i thought the same exact thing and got it wrong. Did you ever find an answer? I also thought the lesion would have to be higher up.
 
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.
 
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
 
very stupid question about genetics ( weakest subject): okay, so this pertains to that question about the girl with cystic fibrosis. Her brother is healthy. I get how to do the punnett square thing and that autosomal recessive is 25% with 2 carrier parents, etc. What I don't get is why the boy's chance of being a carrier has anything to do with any other pregnancy the mom had. if she has 1,000 babies, doesn't each new baby present with a fresh new chance of getting, not getting, or being a carrier? If not, I'm prepared to say " oh, well, person in question already has CF, so i guess she can be marked off the punnett square, leaving us with only 3 possibilities left...but then again, why are there only 3 possibilities left?"
 
very stupid question about genetics ( weakest subject): okay, so this pertains to that question about the girl with cystic fibrosis. Her brother is healthy. I get how to do the punnett square thing and that autosomal recessive is 25% with 2 carrier parents, etc. What I don't get is why the boy's chance of being a carrier has anything to do with any other pregnancy the mom had. if she has 1,000 babies, doesn't each new baby present with a fresh new chance of getting, not getting, or being a carrier? If not, I'm prepared to say " oh, well, person in question already has CF, so i guess she can be marked off the punnett square, leaving us with only 3 possibilities left...but then again, why are there only 3 possibilities left?"

The brother doesn't have cystic fibrosis, so he's either a carrier or homozygous normal. So out of the 4 genetic possibilities (CC, Cc, Cc, cc) we can eliminate cc. That leaves 3 possibilities.
 
The brother doesn't have cystic fibrosis, so he's either a carrier or homozygous normal. So out of the 4 genetic possibilities (CC, Cc, Cc, cc) we can eliminate cc. That leaves 3 possibilities.

I thought it meant in terms of before he was born and in the womb. Of course in retrospect we can mark off aa since we know he doesn't have it. Thanks


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I agree...i thought the same exact thing and got it wrong. Did you ever find an answer? I also thought the lesion would have to be higher up.

The branch to the lateral head of the triceps comes off a bit later right before the groove, but it's just the most likely location, and if you break your humerus in half at the midline intuitively speaking you're going to have trouble extending your forearm, regardless of whether you are an inch distal to the branching off point of the nerves to the triceps.
 
Digging up this old post, but I think this answer is wrong.
I did put the qualifier that everything stays the same, except for the sample size, so the answer is correct. I didn't see the actual question, but it doesn't appear that the original post had any information to indicate some other factor changing in addition to the sample size.

It is likely that the 95% CI will increase, but it may not.
See my previous point. If the sample size decreasing is the only change (constant critical value, constant sample statistic [sample mean, for example], constant sample standard deviation), then the CI will necessarily increase in width due to a larger standard error.

The original set of 20 measurements had an SD of 8 mm Hg. It's possible your new set of 4 measurements have an SD of 1 mm Hg, in which case the 95% CI will be +/- (1/2) instead of +/- 8/sqrt(20). In this case the 95% CI will be smaller.
Again, it's been a while, but I believe the original post said only the sample size was changing (or it's implied by the nature of the question). I don't believe this is what the question was asking.
 
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This questions hinges on a fundamental statistical concept: increasing the sample size boosts statistical power. This increases confidence in the test results and reduces the influence of outlying values. While it may be possible that 4 measurements have the same (or very similar) values, there would be little reason to believe that these 4 values are, themselves, representative of the sample population as a whole. But as we increase the number of measurements, we gain confidence that the values are representative of the population of interest.
I don't remember the exact question, but I don't believe it's primary (most direct) purpose was directed towards an understanding of statistical power, but rather, it was aimed at directly assessing your understanding of how an estimate's precision (as represented by the the width of a confidence interval or size of the standard error) is impacted by a change in sample size. Statistical power is more directly related to hypothesis testing rather than using confidence intervals to estimate parameter values. I'm also unsure if your use of the word "confidence" is in reference to a confidence interval, but keep in mind that the confidence level is independent of a sample size. But, I think you were gearing more towards the idea that we feel more assured that we're getting "closer to the truth" with a larger sample size.
 
last questions i swear..

i think one said something about the PMI being felt subxiphoid area.. does that just mean right ventricular hypertrophy is happening?

i think another one the answer was alport syndrome but it said it was an "x linked recessive", although I'm pretty sure FA has it as x linked dominant. what's up with that?

waht is c-Jun and is it important at all for boards? there was like 1 tiny thing on it in UW just with regards to southwestern blotting and that it's a transcription factopr

PMI is sub xiphoid because i think that question had to do with COPD (Flattening of diaphragm pulls the heart down is how I think about it)
 
Thank you that makes sense! I was wondering why none of the drugs aren't swapped out if the pt develops resistance?

They swapped but that question is worded terribly. I had to read it like four times to make sure I had it straight but they describe her viral load decreasing and CD4 count increasing not the other way around
 
So, if we weren't told she had a maternal uncle with the disease the answer would be 1/8, right?

It would be:
Probability she inherited the disease from her dad 1/2
probability she inherited the disease from her mother 1/2
probability her baby is diseased 1/2

No, inheritance is maternal for X-linked recessive. The 4 yo has Duchenne which is X-linked recessive. The mother of the 4 yo and 20 yo is definitely a carrier. If we didn't know about the uncle you could still get the answer. Now, if they hadn't told us the 4 yo had the disease then it would be 1/8 because we wouldn't know the carrier status of the mother.

So it's:
Probability 20 yo sister is a carrier: 1/2
Probability 20 yo sister's male fetus has the disease: 1/2

Without knowing about the 4 yo (but still knowing about maternal uncle):
Probability mother of 4 yo and 20 yo is a carrier: 1/2
Probability 20 yo sis is carrier: 1/2
Probability 20 yo sis' male fetus has disease: 1/2
 
please help on this!!!

21 year old man loses 15% of his total blood volume within 2 minutes after a motor vehicle collision. Which of the following findings is most likely?

A. chemoreceptor mediated vasoconstriction>> marked this and was wrong.
B. decreased sympathetic nerve activity to the veins
C. increased sympathetic nerve traffic to the SA node
D. increased tonic release of ANP from the atria
E. increased vagal efferent nerve activity to the SA node
 
In case anyone is still wondering about the man with diabetes and diarrhea, the way I approached was I didnt even really worry about the diabetes. I just connected his orthostatic hypotension and diarrhea and assumed that it had to be do to overactive parasymp, or too little symp, which would cause an increased motility. I know this explanation may not satisfy everyone but its how I thought of it.
 
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I was thinking the same thing... how to differentiate a prospective, cohort study, which would measure the incidence of the MI's from the randomized control trial
It comes down to study design. The RCT involves randomization of patients into treatment arms, but the prospective cohort study does not. The prospective cohort study is more observational in that manner (RCT is more of a controlled experiment).

In the cohort study, for example, you try to find groups that are nearly identical except for the fact that one group consists of smokers without any cancer and the other group is made up of non-smokers without any cancer--then, follow them over time. A (highly unethical) RCT would randomize patients to smoke or not smoke-- clearly, one option is more appropriate/practical than the other (in some cases).

Edit: I hadn't seen the original question, so here it is below. Notice what's bold/italic/underlined-- They start by talking about comparing outcomes in 3 groups of patients (Angio 1, Angio2, and operative). Then, they use the words "chance process" & "assigned" to tell you there is a random assignment of participants. These features should set your sights on the RCT study design.

17. A study is conducted to compare the incidence of myocardial infarction in patients undergoing two different types of angioplasty or an operative procedure to manage single-vessel coronary artery disease. A total of 1000 patients are enrolled. Through a chance process, 500 are assigned to undergo the operative procedure, 250 are assigned to undergo one type of angioplasty, and 250 are assigned to undergo a second type of angioplasty. All patients are followed for 3 years to determine the incidence of myocardial infarction. Which of the following best describes this study design?
A) Case-control study
B) Community intervention trial
C) Ecological study
D) Historical cohort study
E) Prospective cohort study
F) Randomized clinical trial
 
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It comes down to study design. The RCT involves randomization of patients into treatment arms, but the prospective cohort study does not. The prospective cohort study is more observational in that manner (RCT is more of a controlled experiment).

In the cohort study, for example, you try to find groups that are nearly identical except for the fact that one group consists of smokers without any cancer and the other group is made up of non-smokers without any cancer--then, follow them over time. A (highly unethical) RCT would randomize patients to smoke or not smoke-- clearly, one option is more appropriate/practical than the other (in some cases).

Edit: I hadn't seen the original question, so here it is below. Notice what's bold/italic/underlined-- They start by talking about comparing outcomes in 3 groups of patients (Angio 1, Angio2, and operative). Then, they use the words "chance process" & "assigned" to tell you there is a random assignment of participants. These features should set your sights on the RCT study design.

17. A study is conducted to compare the incidence of myocardial infarction in patients undergoing two different types of angioplasty or an operative procedure to manage single-vessel coronary artery disease. A total of 1000 patients are enrolled. Through a chance process, 500 are assigned to undergo the operative procedure, 250 are assigned to undergo one type of angioplasty, and 250 are assigned to undergo a second type of angioplasty. All patients are followed for 3 years to determine the incidence of myocardial infarction. Which of the following best describes this study design?
A) Case-control study
B) Community intervention trial
C) Ecological study
D) Historical cohort study
E) Prospective cohort study
F) Randomized clinical trial

Thanks so much
 
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can someone please help me with this question?

A 45 year old man comes to the physician for an annual maintenance examination. he is 183 cm tall and weighs 86 KG BMI is 26 Kg/m2. CBC shows no abnormalities. The avg of 2 fasting serum lipid studies shows a total cholestrol of 200 mg/dl. HDL is 50 mg/dL, and triglycerides of 550 mg?dL. In addition to suggesting lifestyle changes it is most appropriate for the physician to prescribe which of the following drugs?
A) Colestipol
B) Ezetimibe
C) Fenofibrate
D) Orlistat
E) Simvastatin
 
can someone please help me with this question?

A 45 year old man comes to the physician for an annual maintenance examination. he is 183 cm tall and weighs 86 KG BMI is 26 Kg/m2. CBC shows no abnormalities. The avg of 2 fasting serum lipid studies shows a total cholestrol of 200 mg/dl. HDL is 50 mg/dL, and triglycerides of 550 mg?dL. In addition to suggesting lifestyle changes it is most appropriate for the physician to prescribe which of the following drugs?
A) Colestipol
B) Ezetimibe
C) Fenofibrate
D) Orlistat
E) Simvastatin

Fibrates are used for Triglycerides... which seems to be very high in this patient.
 
Is there a specific reason we were supposed to be led to Kaposi's sarcoma (vs. BA) for the dude's foot rash? I chose antibiotic because I remember Sattar saying all you need for KS is HAART, so I didn't figure you'd need anything else. Several sources have said the only way to differentiate is based on the presence of neutros in BA and lymphos in KS, but we weren't given that info.
 
An experimental animal is created that has a defect in an innate gastrointestinal defense mechanism. Organism is found to have decreased HCl prod. After 2 months on biopsy gastric fundus and body show decreased mucosal thickness and hyperplasia of enterochromaffin like cells. This closely resembles?
- Chronic gastritis is the answer
But why not Peptic ulcer disease - Gastric ulcer type ?
 
1. An 8 year old girl is brought to the physician by her mother because of a 3 week history of poor feeding chronic diarrhea and pale foul smelling stools.
Mother says the symptoms began with colicky abdominal pain following introduction of solid food to the infant;s diet. There is hsitory of gluten senstivity. She is 60th percentile and 25th percentile for length and weight.
P/E Normal

Which cell is dysfunctional:
a. enterocyte
b. goblet
c. paneth (x incorrect)
d. parietal
e. serosal


I don't think it's in my list of questions I got wrong. And I believe I chose a) enterocyte. I'm not sure if my thinking is correct, but I was thinking gluten sensitivity...celiac dz & absorption problems...and absorption of nutrients is by the enterocytes in the villi.
 
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