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 +0  (nbme21#48)

Seems like he has pyelonephritis because of the systemic symptoms (e.g. fever). The most common causes of that are E. coli (90%) followed by Enterococcus faecalis and Klebsiella. The only one that fits under "gram positive chains" is Enterococcus faecalis. // Pathoma pg. 132





Subcomments ...

submitted by hungrybox(1048),
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ywh lessmhioy si :worgn

eTehr usodlh osamtl vnree eb argithts pu rnlbubiii ni the neur.i In ,syholesim teh esxsec rniiubbil si xredteec ni het i.ebl frAet berlaiact icsornnvoe nad p,rueetka moes ilwl eb ceredetx in teh iernu sa ibnoliur. r,Heeowv in busotircetv rdsrsedo,i eth augetjcndo blnuiibir wlli vneer aehv eht rotiypptoun to gdnruoe ectalbair evoncroisn to /csornru.biltioe nI siht ,yaw teh uedcjnatog iburinlib ash on eroht ayw to be dcrxeete htoer ahtn dyclirte ni the niuer.

iesdcrt ot n/ca7al/63aur no edtidr

skip_lesions  Found a good pic showing bilirubin metabolism +  


submitted by amarousis(23),
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os ofr sthi eon yuo hvae ot loko ta the oiaitclds dloob usperesr and 'tasht hte auevls 'eoyur opdpuess ot ar.ed not eth erubmns ni eht o.lusncm iLke gopur Xs' dmoe si 07 eauebsc ti sha hatt uvale 32 semti. rupgo s'y mdeo si 80 eceubsa ti aprspea 20 .smtei rof daine,m uoy luodw ehav to retiw eht tsoidlica breumn 10502- how erev naym steim it arasepp nad nhte nifd het ddim.le ckiytr .istunoqe

sahusema  Wow. I hate this. I only looked at the number of participants and completely ignored the Diastolic BP readings +5  
ma_rad  Everyone commented how to get the mode right. But there is an easier way to realize that the median in Y is higher without all the calculations. If you see, the last Diastolic BP in group X is 110 (as there are ZERO people with 120). While group Y has 8 people with 120 DBP. This automatically shifts the median to the higher side. I got this wrong though at first I didn't pay attention to the "0" number at group X for 120 DBP +9  
brasel  I think there's another easy way to find the median without writing out every value. There are 100 total people in each group, so that means the median (if the DBPs are written in ascending order, which they are) is the 50th person. Group X: 8 + 12 + 30 = 50, so median is 70 Group Y: 2 + 8 + 10 + 20 +10 = 50, so median is 90 +8  
mangotango  I did it the way @brasel explained. The way @ma_rad did it could give the incorrect answer in some cases (e.g. Group X had 0 ppl with 120 BP but a ton of ppl for 110 BP etc. + Group Y had 10 ppl with 120 BP but basically none with 110 BP etc.). In this question that way worked but it's not always guaranteed since median doesn't sway with outliers, but mean does. // FA 2019 pg. 261 +  


submitted by chillqd(39),
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Teh mteS si niicsbgder thrs,smmoheoacoi erecczaitdhra by nrloamba roni egsinsn dna icdearnse anteiltisn ornpbiosta. siTh rcesinesa orI,n neinrascig .rinitfer nI serpnseo, BICT si dcaeesder, whhci rescseian airrnstnerf aiartonsut as ehret is sels cgtlarinuic recrair olml.ueces

hWit sxecse nroi in het bo,old it wlil cautcuealm in sisseut nlcnuidgi teh iv,erl snki, rpa.cesan Se eeuqla cedlniu addetil hromoycp,atdiya ogo,daimpshny ies,edbat yptoratahrh 2/2 lcmcaui hyaptohseppro oioi,netdsp nd leclplaurtHeoa oairanmCc

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 nwinkelmann(295),
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nI acse eannoy is a ndsee sa I am and utjs tddn'i em/srdnarbemrdeteun wath axlyect petioryarx folw is = .1EVF In rettirievsc o,cidinnost FVE1 is maronl ro sarndicee deu to ceeadrdes .FCV tsliitraInte sbfiorsi = rensdaice iyrwaa nechypraam slcfdafo druoan het ,iarywas hihcw si tawh oviderps ladari tto.nriac The aeergtr eht raalid ,antrciot het rwleo het iopnsglalc rfec,o nad so pxrietyaor lowf si r.iedcsnea

champagnesupernova3  FEV1 is increased due to greater recoil of the lung tissue. FEV1/FVC is increased bc of that and bc of decrease in FVC +  
mangotango  But I thought with restrictive diseases, the FEV1 dec a little and FVC decreases a lot, yielding an FEV1/FVC ratio that's normal or increased?? +1  
an_improved_me  Yea the OP is wrong here. FEV1 does NOT equal expiratory flow rate. FEV1 is not a really a rate; its a volume of air pushed out in 1 second specifically. This will be decreased in a pt with ILD. This is because the volume of the lung decreases (due to increased elastic recoil). Expiratory flow rate (in this question) will be elevated, b/c of the answer stated. From uworld: "[fibrosis] causes increased lung elastic recoil, as well as airway widening due to increased outward pulling (radial traction) by surrounding fibrotic tissue. The resulting decrease in airway resistance leads to supernormal expiratory flow rates (higher than nromal when corrected for lung volume)". +  


submitted by notadoctor(159),
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Ualsu iranisetttli tspiuioennm si eht lihtglocaios efdtiinoni fo iIaoctphdi arlpouymn sfios.bir eW nkow ttha ihts ttnapie has umlranpyo oibsfirs bcaeesu teh oqstuine sttaes hatt ehter si isorbfu theiinncgk fo hte lrvaolea tes.ap ihsT estounqi asw tujs sittgen taht ew kenw eth toreh nasem rof roPumlany iob.sirsF

aneurysmclip  Nbme back at it again +27  
pg32  Is it still considered idiopathic pulmonary fibrosis is it appears to have been caused by an atypical pneumonia? +1  
zevvyt  Why not Sarcoidosis? Wouldn't Sarcodosis also be a chronic inflamation with fibrous thickening? +2  
swagcabana  UIP is a better answer. Sarcoid is a leap in logic, usual interstitial pneumonitis is textbook histological definition of idiopathic pulmonary fibrosis. The biopsy has no mention of noncaseating granulomas and the clinical picture is not consistent with an inflammatory process. You have to focus on the better answers, try not to get caught up in the "why nots?" Calling this sarcoidosis is like someone coming in with prototypical asthma and jumping to eosinophilic granulomatous with polyangiitis. Sure its a possibility but its definitely not likely. +6  
mangotango  I picked “diffuse alveolar damage” with Pulmonary Fibrosis in mind but these are actually key words for ARDS :/ +3  
zevvyt  thank you swagcabana! Very good explanation and strategy! +  


submitted by uslme123(66),
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revy tusidp tiu.noseq hTe suvri wsa hdinlea -- stab nhga udpeis hnew teyh lpees and do.lro So ti spsedar ot the banir rdcelyit ormf teh yrfaootlc tmsyes avi ratdergeor aponrtrst thurohg e.verns

niboonsh  yea, aeresol transmission via bat poop in caves +  
len49  How do you know the virus was inhaled? Doesn't mention it. Moreover, non-bite/scratch transmission is extremely rare. +  
makinallkindzofgainz  You get rabies by being bitten, not by inhaling it +  
drzed  She was probably bitten by a bat; many times the bite is not recognized ('unapparent bites'), and thus the CDC recommends that even if you think you have been bitten by a bat (or that you COULD have been bitten), you should go and get active/passive immunization immediately. +  
mangotango  Sketchy (and Zanki) says you can get rabies via animal bites OR aerosol transmission. In the U.S. it's most commonly through bats. It could also be through skunks (Western U.S.) or foxes/raccoons (Eastern U.S.). I remember this by thinking about how skunks smell so bad! +  
shieldmaiden  But the question is "how it got to the brain" not how she got it, so the best answer is through the nerves +  


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i lfle orf ilndbege fmro iensol ta ehsoc pisosaris tub ipsaosris stp inereceexp gincti.h s,Alo the ontstuiirbid si otn h.rrestciactaci

makinallkindzofgainz  Yes it is. These areas are all sun-exposed areas, and he is a farmer. Multiple years of sun-exposure can lead to Actinic Keratosis, a precursor of SCC. +3  
mangotango  @makinallkindzofgainz -- I think cry2mucheveryday means "distribution is not characteristic" of psoriasis +1  


submitted by pparalpha(85),
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EBV )4HVH(- stfceni B lelc orhhtgu .21CD

cplAayti eslycymotph no iaepehrplr bldoo seamr nt(o dcfeitne B lelcs, tbu vcreitae oxttciyco T s)lcle.

"onsi:nMluosceo" + omspnoto etst (tibisaenod ctetedde by aongaititlnug fo hpsee ro soreh CBsR)

sbryant6  Atypical lymphocytes are CD8+ T cells, not CD4+. Remember that. +15  
mangotango  I remember this because Infectious Mononucleosis is caused by a virus (mostly EBV, sometimes CMV) and MHC Class I functions to present endogenous antigens (e.g. viral or cytosolic proteins) to CD8+ T cells. In comparison, MHC Class II is more involved with presenting exogenous antigens (e.g. bacterial proteins) to CD4+ T cells. // FA 2019, pg 100 +1  


submitted by qfever(48),
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Pmhaato 2018 diontie paeg a4tpreh c 1 - arluCell jyurIn - III. Resblviere am;p& eerbselrviir ealullrc inurjy - B1..

I ahd iiyfultdcf rtnyig ot uirfeg otu wath pcoyhrid cagehn manse .u.hgtho.

bharatpillai  i swear i've done the same question before on uworld/ one of the previous NBMEs and the answer to that was intracellular Ca accumulation. +1  
mangotango  @bharatpillai that's also true! Dec ATP >> dec activity of Ca2+ and Na+/K+ pumps >> cellular swelling (earliest morphologic manifestation of reversible cell injury), mitochondrial swelling --- FA, pg 207 Na+/K+ ATPase inhibited >> inc intracellular Na+ >> dec activity of Ca2+/3Na+ exchange pump >> inc intracellular Ca2+ --- this is the same way digoxin works in the heart! +  


submitted by nwinkelmann(295),
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shTi npxlisea ti ylreal well htwi a tei:ucpr m2lf/nyiloatl.ohtasm:sttt0.gtsp/oA/maah1lPAued/l.wh.wpwh//idtesil.

oHpciyrd ceganh = one fo teh erlay nsgis fo lcerulla enrngdoaeeti in srsnepeo to yrjnui htta uerslst in aoutmailuncc fo rtaew ni eht clel. Hoe/xaamisyipcih eslad to eedeacs ni irceabo trrnipoiaes ni het iatohmndocri nad rsecaeedd PTA rnotupocid deu ot ulirafe of teh Na/++K asATeP geindal ot aN+ dan retaw isffnidou itno eth lle.c aIvldiniud etbluu lsecl ppraae llsenow adn t"ye"pm whti osmtal eoccdlud nlme,u grmouesull is lle.plahreucyr

dickass  it's basically from pathoma chapter 1: cellular injury causes swelling +5  
md_caffeiner  @dickass you why arent you on every q stem? +1  
mangotango  do you mean "causing failure of the Na+/K+ ATPase" instead of "due to failure of Na+/K+ ATPase..." ? The low ATP is due to dec aerobic respiration, I believe. +1  
fatboyslim  @Mangotango yes exactly. Na/K ATPase stops working due to the lack of ATP. I think nwinkelmann mixed it up +  


submitted by xxabi(260),
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oengnchoBrci omircacna = gnul ceanrc

tTah ibgen sd,ia nlgu arncnoiocedmaa lplcyasiifec si tsdaasoeic twhi peyrhcrhotip otaysphrho,aerott cwhhi is a rnaaitasoelcpp omrdensy tczareahecird yb itldaig bn,igculb agai,ratlhr ontji ni,foessfu adn iterpsissoo of btaluru snobe

luke.10  why not systemic scleroderma since i did this question wrong and i chose systemic sclerosis scleroderma , can someone explain that ? +2  
kernicterusthefrog  My best guess answer to that @luke.10 is that: a) there's no mention of any skin involvement (which there would be in order to be scleroderma) b) Scleroderma shows pitting in the nails, not clubbing c) There would be collagen deposition with fibrosis, not hypertrophy of the bone at joints Saying that, I also got this wrong! (but put RA...) so I'm not claiming to "get this" Hope my thought process helps, though! +6  
yotsubato  This is in FA 2019 page 229 +10  
larascon  I agree with @kernicterusthefrog on this one, Bronchogenic carcinoma = lung cancer. Squamous cell carcinoma gives you hypercalcemia (new bone formation; maybe?), commonly found in SMOKERS ... +3  
waterloo  the clubbing is the symptom that takes out alot of the answer choices. It's super tricky. +  
jawnmeechell  Plus the patient has an 84 pack-year smoking history, super high risk for lung cancer +  
veryhungrycaterpillar  FA 2019 pg 229 is all paraneoplastic syndromes. There is no mention of bronchogenic carcinoma in any of them. There is adenocarcinoma, but that is most likely in non smokers, not in someone with 84 pack year of smoking history. Why does he have 5 upvotes for referencing first aid here, what am I missing? +3  
jakeisawake  @veryhungrycaterpillar sounds like bronchogenic carcinoma is a general term for lung cancer. You are right that if a non-smoker gets lung cancer it is most likely adenocarcinoma as non-smokers rarely get small cell. However, smokers can get adenocarcinomas as well. The oncologist that I shadow sees this frequently. Adenocarcinoma of the lung causes hypertrophic osteoarthropathy per 229 in FA2019 +2  
mangotango  @verhungrycaterpillar @jakeisawake Adenocarcinoma is the most common tumor in nonsmokers and in female smokers (like this patient), so adenocarcinoma would still be the most likely cancer for this pt over the others. Pathoma Pg. 96. +3  
fatboyslim  Apparently bronchogenic carcinoma is basically an umbrella term for lung cancer. Source: https://radiopaedia.org/articles/lung-cancer-3 +  
lifeisruff  bronchogenic is another term for adenocarcinoma in situ according to pathoma +  
topgunber  With the exception of mesothelioma- 95% are bronchogenic +  


submitted by neovanilla(39),

A = Maybe the superficial dorsal vein

B = Areolar tissue

C = Urethra (surrounded by corpus spongiosum)

D = Corpus cavernosum (correct answer)

Sildenafil increases blood flow to the penis by dilating the corpus cavernosum (increased NO via inhibition of PDE5 --> cGMP --> smooth muscle relaxation). It doesn't actually affect the blood vessels supplying the corpus cavernosum, I believe

mangotango  This pathway causes relaxation of vascular smooth muscle so it causes vasodilation and increased blood flow to the corpus cavernosum, causing an erection. +  


submitted by madan(-4),

hey!!! its delayed heamolytic reactio occur in the amneastic antibody in the host

usually present with mild type of heamolyis after two week. mechanisms, host already had made antibody against the donar antigen.

mangotango  But wouldn't you want to use the Indirect Coombs Test, since it measures whether there's anti-donor antibodies within the serum? +  


submitted by strugglebus(165),
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odenaHdrhecMeto/noyod nca dale ot udednye-epecon- iadvo in glon rmte .sue SDAsNI you oals odavi due to aprtali ffcseinveeintes in erpuitanoch npai sa llew as ceurl .kirs sT'AC era wonnk to terta tcuineahopr naip yevr lwle .ie(. ibse,dtae ATR praeyht)

champagnesupernova3  Drugs for neuropathic pain: TCAs, gabapentin and pregabalin +1  
mangotango  SNRIs +  
mangotango  also SNRIs* +1  
zevvyt  methadone isn't a pain med(even though it's an opiate), it's used for opiate addiction. And hydrocodone is used for "moderate" pain and this person is in "severe" pain. +  


submitted by strugglebus(165),
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cderoHh/nedytdneMoooa anc aedl ot eceydunn-oeed-p idoav in nlog remt s.ue sIDSAN you alos vidoa eud ot lritapa eiicstvneneeffs in toahcurienp npai as elwl sa ulrec ki.rs 'CsTA ear wknno ot rteta uericopahnt nipa yvre lwel e.i(. bd,tsaeei ATR yp)rtaeh

champagnesupernova3  Drugs for neuropathic pain: TCAs, gabapentin and pregabalin +1  
mangotango  SNRIs +  
mangotango  also SNRIs* +1  
zevvyt  methadone isn't a pain med(even though it's an opiate), it's used for opiate addiction. And hydrocodone is used for "moderate" pain and this person is in "severe" pain. +  


submitted by hayayah(1080),
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heT wot smot aritmopnt MI onicptmcsoial tath ccour iwntih a 2-5 ady nsap ear lyaiaprpl smlecu pureutr nda triunrtlnvreiaec muepst eut.rur

iaylalrPp leumsc rrupuet slead ot svreee atirlm itg,nrtagireuo daerh sa a sslcyito mmruur at eth a.epx

dulxy071  I disagree. any sort of rupture is usually the result of the action of macrophages (to eat away dead, necrotic tissue) which come in on day 3. This was merely a word game to get the time line right. They said "TWO DAYS LATER" (keeping in mind our time line starts 16 hours after the first symptoms appeared in this stem) which actually turns out to be day 3 +5  
leaf_house  Wouldn't necrosis of the interventricular septum create a VSD, which would also produce a loud, (holo)systolic apical murmur? I don't get how we're supposed to differentiate, here. +1  
mangotango  A VSD produces a holosytolic, harsh-sounding murmur loudest at the tricuspid area, not the mitral (apex) area -- FA, pg. 288, 289. +4