NBME Answers : consistentwrongdoer3's page

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+0 visit this page (nbme23#38)

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What are we supposed to be looking at? I see multinucleated giant cells. I also see infiltrate (can’t tell if this is mononuclear or not).

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methylased Young child following URI with TCP is pretty classic ITP. Sometimes they throw in extra stuff on purpose, but I didn’t see much on the bone marrow aspirate either. +9

mousie I was also thinking ITP but the bone marrow image kind of threw me off too, not sure what I'm supposed to see but still think ITP is best choice ... +

meningitis It also almost threw me off, but then I remembered he had low platelet count and I guessed those multinucleated cells were Megakaryocytes (I looked for Megakaryocyte Bone Marrow Biopsy in google and they are the same). +1

what Bone marrow shows increased megakaryocytes -> ITP +

+0 visit this page (nbme23#16)

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Why does methylation cause loss of resistance to GATC restriction endonuclease? Does this have to do with methylation of U to T?

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methylased GATC related to methylase --> https://en.wikipedia.org/wiki/Dam_methylase +10

sympathetikey Dam methylase, alright +2

yogi https://www.neb.com/tools-and-resources/usage-guidelines/dam-and-dcm-methylases-of-e-coli +3

+0 visit this page (nbme23#49)

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I thought that the primary sympathetic innervation to the heart was through T1-T4. Why would stimulation of this ganglion not affect skin vessels in the upper limb?

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methylased Stellate ganglion --> sympathetics for sweat to skin in UE + head. Apparently also to increase HR (some cardiologists ablate stellate ganglion for tachy that cant be controlled by beta blockers). +

tea-cats-biscuits The stellate ganglion is a sympathetic ganglion, so it wouldn’t increase vasodilation in the skin of the upper extremity. Also in most people, the inferior cervical ganglion is fused with the first thoracic ganglion (T1), forming the stellate ganglion. +39

sympathetikey Got this wrong too. I think upper extremity skin vasodilation (which I picked) is probably more due to local metabolites. +

+21 visit this page (nbme24#10)

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The answer is hyporeflexia because the afferent arc of the muscle stretch reflex has to go through the dorsal rami and dorsal root ganglia. Dumb question, I know, but it’s the only answer that made sense. If you hurt the DRG, you not only lose afferent somatic sensory fibers, you also lose the sensory bodies involved in the various reflexes.

You can also get hyporeflexia from damaging the efferent neurons that innervate the muscle (like a LMN), but as you know these are in the anterior horn and ventral rami.

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ankistruggles Thanks! I agree with you. +1

brethren_md Great explanation. +1

gonyyong Agreed - I think I got this by thinking about tabes dorsalis (syphillis) and why it has hyporeflexia is due to dorsal root damage +10

duat98 I'm confused about why it wouldn't cause muscle atrophy. Isn't that a fever of LMN damage? +8

charcot_bouchard Muscle atrophy wont occur because alpha motor neuron is intact. Motor control of Corticospinal tract on this is intact. so no atrophy. u can move shiti/ But remeber muscle spindle that is responsible for INITIATING stretach reflex send Ia fibre to DRG from where it synapse with Alpha motor neuron. if DRG is damage ur muscle is fine but u cant initiate strech reflex. areflexia +5

zevvyt DRG you lose DTR +2