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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://download.videohelp.com/vitualis/med/spinal_cord_2.htm
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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
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Cut larva migrans
Anclystoma necator
Candida endophthalmitis
Disseminating Candidiasis
But on the picture, you can clearly see narrow based budding.

( 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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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 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 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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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)