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NBME 11 block 2 q 1 to 50 - maryam2009
#81
hmm..i think i got it now,thanx maryam.
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#82
20 is d .. I did this test online
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#83
23---DD
we need to cut 2lb=7000 cal (3500*2)
1 hr walk/d will cut 3500 cal
In the meanwhile she is also getting 1800*7 calories=12600 in a week
decrease intake for 500 cal /d * 7 days=3500 cal
so 3500+3500=7000
hope i m ryt ??
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#84
hy maryam, i am a week away from my exam, i wanted to know if you by any chance have the questions of the NBME 11 in the order they are answered in the forum pleaase pleasee
Smile thanxss a looot Smile
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#85
29.C

PaCO2=metabolic CO2 production/Va
So if Ventilation increases to match up with CO2 production, PCO2 remains the same.

posted by Saye

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#86
Explanation ......Q4

-Statistical significance= Is determined by P value.....and as see the p value is less than .05....hence for sure there is a difference between the two interventions (NOT BY CHANCE ALONE).....If the P Value is greater than .05 u can SAY the difference in the two interventions is due to CHANCE ALONE .....So A is out

-Practical Importance means CLINICAL SIGNIFICANCE not Statistical....and clinical significance MUST ANSWER THE QUESTION ...how effective is the intervention or treatment in the CLINICAL SETTING....And the doctor made the CALL in this case not the researcher....And the way u measure CLINICAL SIGNIFICANCE IS by some of the following methods...EFFECT SIZE ,Number Needed to treat,and Preventive fraction.....


-Already in the question u stated the magnitude of the difference was so small....How do they know ? They calculated NNT....

as u know NNT= 1/49%-45 %=1/4%=25.....Taking Program A as a control (as u know control groups can get placebo or as in this case STANDARD CARE)....

-This means if the health official decided to change Program B as a STANDARD of CARE .....to treat HYPERCHOLSTEROLEMIA in 1 patient 25 should be INVOLVED .....

---NNT=25 is not clinical significant.....hence choice B......


about the other choices....


Choice D....once you find the difference is STATISTICALLY SIGNIFICANT ...the sample size should be assumed LARGE and Enough...Only question sample size if the STUDY is not STATISTICALLY SIGNIFICANT....i.e When Calculated P Value is greater than .05.....

Choice C....Many times the investigator will report the lowest COMPUTED P Value ....In general the smaller the p the BETTER......

And I remember a question on NBME 7 where the computed P value was greater than .05.....and the answer was ....Due to chance alone....but the scenario was almost the same as this question.....

is posted by yeabiruh

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#87
****Q20 explanation:
D-Noncompetitive Antagonist

This is the case on the concept of "Spare Receptors"

Assume ...100% receptor occupancy required by an Agonist to exert Maximum Effect (Emax) /Optimal effect.

and now consider, if Emax is achieved with result

*Efficacy of Drug X decreases
*5 of the spare receptors are still Unoccupied

Now if we raise the drug "X" dosage.....it will bind to the remaining unoccupied spare receptors and brings it Efficacy back to to the Emax.

there for "No Change in Efficacy" , only "Potency decreases"(as needed higher dose of Drug X)


---------------------------------Graph on the Right--------------------------

But at "High Dose" of of NCA (Drug Y), it will bind to e.g all the 10 spare receptors---->result

*Efficacy(Emax) of Drug X decreases
*there are non of the spare receptors left unoccupied

since there are no extra receptors left, even if we raise the Drug "X" dosage, it won't be able to increase it's Efficacy back to Emax.


is posted by Sarim
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#88
48....to add

Thalamic syndrome (or thalamic pain syndrome)It is also known as "Dejerine-Roussy disease"

is a condition that can be associated with inadequate blood supply from the posterior cerebral artery. It is a rare neurological disorder in which the body becomes hypersensitive to pain as a result of damage to the thalamus, a part of the brain that affects sensation. The thalamus has been described as the brain’s sensory relay station. Primary symptoms include pain and loss of sensation, usually in the face, arms, and/or legs.

Pain or discomfort may be fel after being mildly touched or even in the absence of a stimulus. The pain associated with thalamic syndrome may be made worse by exposure to heat or cold and by emotional distress. Sometimes, this may include even such emotions as those brought on by listening to music.


Gerstmann's syndrome
is a cognitive impairment that results from damage to a specific area of the brain -- the left parietal lobe in the region of the angular gyrus. It may occur after a stroke or in association with damage to the parietal lobe. It is characterized by four primary symptoms: a writing disability (agraphia or dysgraphia), a lack of understanding of the rules for calculation or arithmetic (acalculia or dyscalculia), an inability to distinguish right from left, and an inability to identify fingers (finger agnosia). The disorder should not be confused with Gerstmann-Sträussler-Scheinker disease, a type of transmissible spongiform encephalopathy.



Lateral medullary syndrome (also called Wallenberg syndrome and posterior inferior cerebellar artery syndrome) is a disease in which the patient has a constellation of neurologic symptoms due to injury to the lateral part of the medulla in the brain, resulting in tissue ischemia and necrosis.

This syndrome is characterized by sensory deficits affecting the trunk (torso) and extremities on the opposite side of the infarction and sensory deficits affecting the face and cranial nerves on the same side with the infarct. Specifically, there is a loss of pain and temperature sensation on the contralateral (opposite) side of the body and ipsilateral (same) side of the face. This crossed finding is diagnostic for the syndrome.

Clinical symptoms include swallowing difficulty, or dysphagia, slurred speech, ataxia, facial pain, vertigo, nystagmus, Horner syndrome, diplopia, and possibly palatal myoclonus.

http://en.wikipedia.org/wiki/File:Gray700.png


Weber's syndrome (superior alternating hemiplegia) is a form of stroke characterized by the presence of an oculomotor nerve palsy and contralateral hemiparesis or hemiplegia.

Structure damaged Effect

substantia nigra

contralateral parkinsonism because its dopaminergic projections to the basal ganglia innervate the ipsilateral hemisphere motor field, leading to a movement disorder of the contralateral body.

corticospinal fibers:
contralateral hemiparesis and typical upper motor neuron findings

corticobulbar tract:
difficulty with contralateral lower facial muscles and hypoglossal nerve functions

oculomotor nerve fibers:
ipsilateral oculomotor nerve palsy with a drooping eyelid and fixed wide pupil pointed down and out. This leads to diplopia

It is caused by midbrain infarction as a result of occlusion of the paramedian branches of the posterior cerebral artery or of basilar bifurcation perforating arteries.

http://en.wikipedia.org/wiki/File:Weber%...ndrome.svg

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#89
hi meryam,

i want ur guidance.. i just hav finished kaplan lectures videos n notes for the frst tym. i have purchased 3month uw questions now. i havnt done questions or fa before. at ths point,is gud to do uw ques +fa for the frst tyme? i want to b ready by feb.

looking forwards to ur reply,
thanx
n gudluk for ur exam
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#90
pls people pass me nbme 11 ialready have taken it online but would like to review my answers and contribute to this post. dont be stingy. just mail me and help a fellow future doc of america



dominicanak
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