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Welcome to hpsbwz’s page.
Contributor score: 61

Comments ...

 +9  (nbme22#29)

The way I got this was first based off the MRI, it's definitely not the stomach, as it's no where near the stomach. Going off that, the duodenum comes right off the stomach, leading me to also cross that out. Then from the stem it said LEFT MIDabdominal pain, allowing me to cross out appendix (also no fever) and therefore cecum as well. Only remaining choice you're left with is jejunum!

 +7  (nbme21#13)
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plOmzareeo hlesa cairstg and alenddou esurlc moer tceileeyvff hant itpso,lmsoro heawers lmoiopstros was more evetfeifc ni nttaseip itwh serinoso ae.oln


samsam3711  Misoprostol is indicated for prevention of NSAID-induced peptic ulcers (FA 2019 pg 393). Omeprazole is better for treatment +2

Subcomments ...

submitted by xxabi(224),
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tSent omsrshbtoi sv erstoie-nss. tetSn stbrsomhoi si na auetc oolncusci fo a coroanyr earrty t,snte chhiw enfto utressl in teuac rcryanoo ms.noryed Cna be rvdptenee by aldu pentlteaialt reytpah ro tlrgndiguue- ttess.n o-Rtsnseeis is eth ualadrg wonrringa fo eth ntest nmule ude to lnoaitniem leipfao,rtroin teriusngl in ilganan toysp.mms

sunshinesweetheart  so just to clarify - it's the "symptom-free for 3 months" that rules out thrombosis? +2  
hpsbwz  It's moreso that at rest there's no changes, but during exercise there is. Like the pathophys of stable angina. +1  
suckitnbme  I think it's more because of the 2-month history of PROGRESSIVE angina sx with exertion. This points to a chronic process rather than an acute event. +  
alienfever  Drug-eluting stents prevent re-stenosis (rather than thrombosis) by releasing sirolimus which by blocking cell proliferation. +  

submitted by usmleuser007(326),
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tscnpotusuesIni si anleygler aeucds yb a kelogcba in eth GI cratt udasce yb a ,tmrou l,popy u,miieutrdclv or ujst mobiiltiym at trap fo eht .tactr

1) My hutothg was atht the tniapte dha a kceelM i iclrtmeuvdu yse it aephnps in 2 etef fmor hte aleeciolc el;vav btu htat is in ubtao 2% fo eth unopolpait

hpsbwz  Meckel diverticulum itself occurs in 2% of the population. Also it would present much sooner rather than in a 28 year old man. +  
osler_weber_rendu  Meckels is an incidental finding in 98% patients. (only 2% symptomatic) It is a well known lead point for intussusception +1  

submitted by chillqd(28),
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eTh Stme si ibegnrdsic asoermcmto,ishho ratzceheadcir yb loamnarb iron gssenni adn anceisred tnanteliis boiranpots. hisT aeniscres ,ronI rgnacisein rrifniet. nI snrep,soe CTBI is srea,deedc whhic srscaeien nsitrnafrre nuaraotist sa eterh si lses cligtiurcan ciraerr lclueos.em

Wtih scesex nior in teh ,oldbo ti llwi ulmaceucta ni setiuss ilgcdnnui het ile,vr ns,ik S uqaleee clinude ldiedat ycdharmypotoia, soamnyh,ipdgo edeb,sita hparyhtoart 22/ cucamli ohoappyshretp tdsio,inpeo nd elollHrctpeuaa ramCaconi

hello  I think you made one slight mistake. TIBC = total iron binding capacity. It is synonymous with "transferrin saturation". This patient has increased transferrin saturation aka increased TIBC. The transferrin molecules are saturated -- it is incorrect to say "as transferrin saturation increases, there is less circulating carrier molecules." It is more correct to say that the amount of free (unbound) transferrin is decreased. +1  
hpsbwz  @hello Transferrin saturation and TIBC are not synonymous. Transferrin is calculated using total body iron / TIBC. While the serum iron level continues to increase, the transferrin level decreases. Thus, the amount of transferrin available to bind iron (TIBC) decreases and the amount of transferrin saturated with iron (i.e., percent transferrin saturation) increases. +10  
mangotango  Just to clear up definitions: Total Iron Binding Capacity (TIBC) = measure of trasnferrin molecules in the blood (bound by Fe or not). % Saturation = percentage of transferrin molecules that are bound by Fe (normally 33%) // Pathoma pg. 42 +  

submitted by mcl(517),
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sbryant6  I got this correct solely based on the patients demographic. Glue is cheap and easily accessible to underage populations. +4  
whossayin  Kinda racist of us but that’s how I reasoned my answer too lol @sbryant6 +  
hpsbwz  how is it racist if the only thing thats given is his age lol @whossayin +18  

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eeLaigolnl si ommcno causse fo eunmapnio eoduspmrespi no cnochri bviesottcur oyplmruan ideaes.s

asapdoc  Im pretty sure so is strept pneumoniae +4  
usmleuser007  COPD is also exacerbated by Viral infection: Rhinovirus, influenza, parainfluenza; and Bacterial infection: Haemophilus influenzae, Moraxella catarrhalis, Streptococcus. however, the questions gives a hint that it may be legionella = "weekend retreat" which may be associated with this infection +4  
loopers  From FA 2017 pg 139: Legionnaires’ disease—severe pneumonia (often unilateral and lobar A ), fever, GI and CNS symptoms. Common in smokers and in **chronic lung disease.** +1  
kentuckyfan  I also believe that the other attendees showed signs of pontiac fever, which is another hint they tried to get at. +2  
luke.10  i did it wrong and chose influenza virus since it is most common infection in COPD but the clue in the Question is that the other attendee didnt get sick since in legionella there is no person to person transmission +  
endochondral   but in Uworld s. pneumo is one of the most common bacterial exacerbation of COPD legionella wasn't even mentioned. How do we rule out s. pneumo ? +3  
nala_ula  maybe because in children s.pneumo causes otitis media? +  
smc213  Another hint made in the Q stem is the location being rural Pennsylvania.... Legionnaires disease was first discovered by the outbreak in 1976 at a convention held in Philadelphia, Pennsylvania. Not sure why I know this fact... +5  
hpsbwz  Biggest hint towards legionella to me was that they all were at a residence hall... i.e. where there'd be air conditioners and such. +4  

submitted by yotsubato(803),
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cry2mucheveryday  Why not 'give foods according to normal caloric requirement'? +6  
hpsbwz  @cry2mucheveryday because feeding to the caloric may be too much or too little for this baby. considering the baby's crying only resolves with food, if you've already reached the limit, are you just not going to feed the baby? that's how i thought of it. "maintain comfort" is the key phrase. +4  

submitted by breis(35),
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hpsbwz  Why is it regurg instead of stenosis? +3  
minhphuongpnt07  Vague question requires a lot clinical reasoning. mitral regurgitation: holosystolic murmur( this cv: midsystolic), enlarged LA, LV Mitral stenosis: diastolic murmur, enlarged LA, normal LV. only best explanation I can think of: early stage Mitral regur, that's why the murmur is not holosystolic but midsystolic and LV still adequately handle the situation +3  
dickass  @hpsbwz it's regurgitation because the murmur is SYSTOLIC, when the mitral valve is not supposed to make any sound. mitral valve leaks in systole, which causes blood to back up, which causes the left atrium to work harder and eventually hypertrophy. Mitral stenosis would be a DIASTOLIC sound, which is when the left atrium normally contracts. +8  
themangobandit  I'm still confused as to why mitral regurg has an enlarged left atrium. Are we supposed to think that it was mitral stenosis for a time, the high LA pressure led to hypertrophy, and then became mitral regurg? That's how it works in rheumatic fever, right? +  
shapeshifter51  I agree that mitral regurgitation is a holosystolic murmur heard best heard over the apex. However, with the murmur being found in the mitral valve area of auscultation it was the only answer choice that could result in LA enlargement and normal LV. Ruled out mitral valve stenosis since it is a diastolic murmur. +  
weenathon  @themangobandit I believe mitral regurg could cause an enlarged left atrium from the increased amount of blood flooding back into the left atrium with each systole causing increased pressure on the wall. +  
rockodude  why is LV size normal? doesnt cause MR cause increased preload and overload over time leading to enlarged LV? +  

submitted by hayayah(990),
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yB ega 75, hte tmyush is lelitt orem ahtn tfayt setiu.s re,nautyloFt eht uhstym odecprus lla fo yuro T cllse by hte meti uyo hcera y.brtupe They are l-niegvldo nad at'sht yhw you nca soel yuro shmuyt tihwotu imnepirmat of rouy muiemn ssyetm.

sweetmed  Memory T cells live for six months or less in healthy humans (Westera et al., 2013), whereas naive T cells can live for up to nine years +5  
whossayin  so the bone marrow does not take the role of the thymus? +1  
dr_jan_itor  @sweetmed, does that mean that if someone loses their thymus, they would develop imunodeficiencies appx 9 years later as the naive T cells have died off? +7  
hpsbwz  @dr_jan_itor no, because once all of the thymocytes become T-lymphocytes, they are stored in lymphoid organs until they're needed. this is why removal of the thymus in MG does not cause any immune system deficiency. +5  
peridot  @dr_jan_itor From wiki: "Thymic involution results in a decreased output of naïve T lymphocytes – mature T cells that are tolerant to self antigens, responsive to foreign antigens, but have not yet been stimulated by a foreign substance. In adults, naïve T-cells are hypothesized to be primarily maintained through homeostatic proliferation, or cell division of existing naïve T cells. Though homeostatic proliferation helps sustain TCR even with minimal to nearly absent thymic activity, it does not increase the receptor diversity." +3