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 +1  (nbme24#8)
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shiT lpbrabyo it'ns 100% talyoilpcil crtorce bt:u

ateB 2 atgnois is istll a etab tnogsia so ti nca bnid inilaeofplysnc adn uecas 1B oincaiatvt cwihh wlli esacu otremr aka vaeticsta leerang am.escthsiypt

tSaiwegn si nleeylagr acn eb eideaztrogc as ipatmhseytc iavtitoacn tub eht satew adnlg ash a sciirmnuac toprerec so it wn'ot be efeafctd yb a aetb son.gait

het ningiaemr ihcsoce rea cattepyrmaspiah oepses.rns





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Teh nseawr si yehreplaiofx eecsbua eht rtfefane arc fo hte scuelm ehrcstt leerfx has to og toruhhg eht srodal rmai adn rasodl toor gil.gaan Dmub ne,qisotu I wkon, tub sit’ het olny rswane hatt daem .esens fI uoy thru eth RG,D oyu nto nyol oesl eeaftrnf atocmsi yeosnsr ef,irbs uyo saol sole eth senrsyo sebiod vvnlideo in eth vrsoaui sf.eerlxe

ouY nca salo teg heaiofelyprx frmo ngaadmgi eht freetnef nnruose ahtt ienrvnate het sumcle l(kei a ),NLM ubt as uyo wokn teseh era ni teh nairtore hron and atlrnve i.ram

ankistruggles  Thanks! I agree with you. +  
brethren_md  Great explanation. +  
gonyyong  Agreed - I think I got this by thinking about tabes dorsalis (syphillis) and why it has hyporeflexia is due to dorsal root damage +6  
duat98  I'm confused about why it wouldn't cause muscle atrophy. Isn't that a fever of LMN damage? +6  
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 +3  
zevvyt  DRG you lose DTR +1  


submitted by lsmarshall(415),
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"mosmoDees cu(Mala )edhsaern - A ecte-llcl-ol ionccntnoe hatt rsdoievp rlcaruttus routpps hwti deeaimttenri ,fmleiasnt luractaiylrp in utesssi tath nderguo inhaacemcl sertss (..ge, ink,s tcagirs ,ssietu )lerabd.d nntsoCec eoiskncttyare in hte auttrms nmsiuosp of the rp"ie.mdsie - SMABOS

sympathetikey  This is why I was looking for some answer indicating keratinocytes in the stratum spinosum...instead they just gave a bunch of bs choices. +29  
roygbiv  I'm confused because I also know that S. aureus cleaves desmoglein in the stratum granulosum, so why is it specifically this answer? +2  
duat98  desomosomes connects cells to cells. hemidesmosome connects cells to basement membrane. +3  
medguru2295  I think what this is really asking is can you tell Pemphigus Vulgaris from Bullous Pemphigoid Vulgaris (question)- Attack on DESMOSOMES- this separates some keratinocytes from others (ie some in basal layer from ones above). Pemphigoid- attack on HEMIDESMOSOMES- this means separation of the keratinocytes from the basement membrane. +2  


submitted by seagull(1567),
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I houthgt ihts saw a ypte 1 RTA ubt I saw .orwgn Ayn esinosuggt?s

seagull  It looks like it was a type II RTA. The difference is incredibly subtle from the info given in this question. +13  
gonyyong  He has Fanconi syndrome which is generalized reabsorption defect in PCT which leads to metabolic acidosis and hypophosphatemia → can lead to rickets Also, does lead to type II RTA +16  
duat98  Also the proximal tubule is the place with the highest phosphate absorption rate. That's why PTH works here mostly and a little bit in the distal tubule. +5  
boostcap23  Another easy way to go about this one is the question tells you he has metabolic acidosis, the only that can happen with is Fanconi/Type2 RTA. The rest will cause hypokalemia and metabolic ALKALOSIS. (pg 586 FA) Personally thought if they were going for Fanconi syndrome they would describe a lot more symptoms for the kid like growth failure or hypophosphatemic rickets but its NBME so. +1  


submitted by m-ice(340),
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ehT pettian sah loss of npia and utertmereap on eth ihtgr esid fo sih fea.c Sesantoin of hte eacf is ipesr,tilaal os eth sisue usmt eb no the tpnsieat' irhgt sie,d cwhih ew nca imcnofr yb nkngwoi taht iaontssen fo the dboy si atloratlacr,en nda he has ltos eflt eidds pina dan pearteemtur fo teh .bydo

iaPn adn meuattrpeer soasnniet fo het doyb si rapt of het cnshioamialpt ,arctt cwihh awsyla usrn talalyrel ouhghrt eht n.eatisbrm This acn eb ceomifdnr yb rgneeirmbme htat etnsnsiao to teh acef laos snru eryalaltl thhrogu hte ea.tismbnr S,o ew anc irncfmo tish is a tgrhi eisdd aetllra ntamrsieb ei.uss

heT slso of gga feerxl nda sraiypals of hte olavc cdrso miply tpemiimanr of lcaarin vernes IX nad X, both of wichh oizeclal ot het mel.uadl ee,orTrhfe eth earsnw is hrtgi oeatlsolradr aud.emll

duat98  You're a good man. +3  
charcot_bouchard  You must be handsome too +9  


submitted by keycompany(310),
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hsTi eitnpat sah a homexarotn.pu eiHlnyoinalrevttp is ont ouhgen ot esncaepotm for hte llovare ereescad in ungl seraufc er.aa

_yeetmasterflex  Could the pneumothorax also cause less ventilation due to decreased lung surface, retaining more CO2 causing respiratory acidosis? That's how I got to the answer at least. +6  
duat98  I think pneumothorax would increase RR because you're probably hypoxic. Also I'm sure when you have a lung collapse on you you'd be scared and that would trigger your sympathetic so your RR will go up either way. +3  
kateinwonderland  Arterial blood gas studies may show respiratory alkalosis caused by a decrease in CO2 as a result of tachypnea but later hypoxemia, hypercapnia, and acidosis. The patient's SaO2 levels may decrease at first, but typically return to normal within 24 hours. (https://journals.lww.com/nursing/Fulltext/2002/11000/Understanding_pneumothorax.52.aspx) +1  
linwanrun1357  How about choice C, --ARDS? +2  
bullshitusmle  there is no bilateral lung opacities as you would see in ARDS +4  
jesusisking  Was thinking some sort of infection b/c of the atelectasis so picked empyema but this makes sense! +  
djeffs1  does it need to be ARDS to cause "diffuse alveolar damage"? +  
makingstrides  Not only that, does having a collapsed lung affect the alveoli? +  


submitted by medstruggle(12),
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hWy si vriaeanlett iipslncg or snc-sopotiintrtlrapa oiiminfotacd ner?rcciot

tea-cats-biscuits  You just have to know that POMC is a pro-protein that must be cleaved; not sure if there’s anything in the stem that would really have given it away. +2  
mcl  Dunno if this helps, but it says "this protein" (singular) is the precursor of two different protein products. This must mean that the modification occurs after the protein is made, which means after transcription and splicing has already happened. +31  
ngman  Also I believe mRNA refers to after the splicing already occurs. If the protein products are from the same mRNA then it can't be alternate splicing. +1  
medschul  They're cleaved by tissue-specific proteases +1  
duat98  I think: Alternative splicing occurs with hnRNA not mRNA. You get mRNA from alternatively splicing the hnRNA. an mRNA can only make 1 type of protein. Since the question says the 2 proteins comes from the same mRNA it cannot be alternative splice or post transcriptional mod. FA 2018 page 43 has a good illustration. +6  
tadki38097  Just general testing taking strategy i guess, but for this question i was torn between post-transcriptional and post-translational, but then i saw that alternative splicing was also a choice...because alternative splicing IS a post-transcriptional modification you know it has to be post-translational because you can't select two answer choices. +1