Nbme 12 Block 1-4 (with Answers) 2y5k6x

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NBME 12 BLOCK 1

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ARR=2.3-1.3 =1%, 1% is equal to .01 so no needed to treat equal to 1/.01=100 so ans is F

Klienfelter

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ACE is present abundantly in the pulmonary vasculature, and it converts Angiotensin I to the physiologically active Angiotensin II

E... AKA Nursemaid s elbow... One of the mc injury in children between the age of 1-5 years..occurs when children are lifted or pulled by the hand or arm causing radial head to slip throughout part of the annular lig..manual reduction of the annular lig is DG... Hope it helps..

you are right here is the explanation . 48 F (weekness = motor, atrophy = lower MN . left =left because decussation of pyramidal tract is in the medullae) http://usmleforum.com/files/forum/2011/1/584961.php

Yes djt it is lateral horn unfourtunely . going back to the image after the mistake you will see that the F is between the gray and the white matter right on the edge so I assumed that it is the gray matter because of the question stem , Actually in the cervical and lumbar segment theris an enlaregent of the ventral horn laterally . because of the motor innervation of the limbs. We should recognise that this was a cervical section, it is not very tuph question but it is tricky . reference: http://.videohelp.com/vitualis/med/spinal_cord_2.htm

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NBME 12 BLOCK 2

single gene mutation in the receptor caused hyperthyroidism....means pth receptors on the osteoblasts of the metaphysis are independently activated (gain of function) despite the low levels of PTH(due to the hypercalecemia)

Yolk sac

Loading... Cut larva migrans Anclystoma necator

Candida endophthalmitis

Disseminating Candidiasis

But on the picture, you can clearly see narrow based budding.

‫خيال علمي‬

( I suspect Cryptococcus neoformans. The retinitis and endophthalmitis is due to CMV, which he got because of AIDS, the chronic illness)

MS

presentation of acoustic neuroma.The tumor mass of Rt. vestibulocochlear nerve will compress cerebellopontine angle if it's large enough. answer is the structure A (inferior cerebellar peduncle). The following link shows clear anatomic structure at that region

- b/c serine is usually the phosphorylation site for lots of signaling pathway. like MAPK. INSULINE().- the question is testing u on phosphorylation de phosphorylation of serine residues in cytoplasmic enzymes (EX: Glycogen phosphorylase) so here mutation has replaced serine with alanine so no serine no phosphorylation no activation of that enzyme

Acne mechanica Sweat produced by anything, including workouts, may cause acne -- but American Academy of Dermatology advises that it usually needs to be combined with friction on the skin. For example, high school and college football players who wear helmets during their workouts are prone to pimples on their foreheads due to friction at that spot where the headgear fits tightly. Players in this age group already have a high risk because of high hormone levels that contribute to acne, even without other factors. People who work out by jogging or biking with a backpack may get pimples in the spots under the straps

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NBME 12 BLOCK 3

Toxoplasmosis

Thank you and sorry for delay I think B is the correct answer, ...As you know beta thalassemia is due to mutation in splicing sites...so we should looking for a mutation before the splicing site...(lower cases are introns and upper cases are exons).... the start codon is located at position 154...ATG, and stop codon is located at position 1575...we should find a mutation between start and stop codon... the only base (g) mutation that can play role in changing and/or making a new splicing site is located at position 246

Hypersplenism. Only thought this because the other things didn't fit and enlarged spleen= more space to store blood cells --> decreased peripheral counts. I learned in heme that enlarged spleens can cause thrombocytopenia so it seemed close enough.

Hypersplenism is a condition in which the spleen becomes increasingly active and then rapidly removes the blood cells. It can result from any splenomegaly. It is most common with splenomegaly

False VC---Lined by Resp.Epithelium (Pseudostrat.Ciliated Columnar) True VC----Lined by Stratified Squamous Epithelium

False vocal cords lined by respiratory epi - pseudostratified ciliated columnar. True vocal cords- stratified squamous. The transitional zone between these two is a common site for development of laryngeal ca. That's all I know. Anyone else?

H3/483 True Vocal cords>dna virus(papillomas>hoarseness>stidor)affinity for stratified squamous epithelium(tvcords+only oro+layngopharynx, anterior epiglottis, upper ½ of posterior epiglottis) not nose paranasal sins, nasopharynx>most of larynx and tracheobronchial tree>pseudostatified columnal mucus secreting epith. not vestibule>space at top of larynx bordered by lowe ½ post epiglottis asup and by vestibular folds(false vocal cord) inferiorly.

n aprosodia is an acquired or developmental impairment in comprehending or generating the emotion conveyed in spoken language. This is seen sometimes in persons with Asperger syndrome.[5] Producing these nonverbal elements requires intact motor areas of the face, mouth, tongue, and throat. This area is associated with Brodmann areas 44 and 45 (Broca's area) of the left frontal lobe. Damage to areas 44/45 produces motor aprosodia, with the nonverbal elements of speech being disturbed (facial expression, tone, rhythm of voice).

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NBME 12 BLOCK 4

Von geirke

Dandy

Hyperchloremic Met Acidosis

C The diseased gene has a cross linkage with that rare allele. This cross linkage can be broken by recombination. segregartion is for the alleles of the same gene on two chromosome.

- Q4: Matrix metalloproteinases, which are secreted by macrophages, digest the extracellular proteins and produce a microenvironment that is more permissble for invasion and metastasis. Loss of E-cadherin and activation of a2b1 integrins are related with the invasive potential, but they are not secreted by macrophages. GNEF and tyrosine kinase is responsible for signal transduction, but again not secreted by macrophages. (Choice D)

- Q5: Since the boy has DMD, it means the mother is a carrier. So one of the X chromosomes she carries has the DMD mutation. If the normal X chromosome becomes inactivated in her muscle cells (so-called "unfavorable lyonization"), she would display the phenotypical features of the disease. (Choice D)