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Contributor score: 83


Comments ...

 -2  (nbme24#29)

Up to 80 percent of aortic aneurysms are caused by "hardening of the arteries" (atherosclerosis). Atherosclerosis can develop when cholesterol and fat build up inside the arteries. ... Elevated blood pressure through the aorta can then cause the aortic wall to expand and bulge.

https://www.uwhealth.org/heart-cardiovascular/aortic-aneurysm-causes-symptoms-and-concerns/10971

Also, FA 2019 pg300 says complications of atherosclerosis includes aneurysm

almondbreeze  I was dumb and went for marfan.. +1
llamastep1  Wrong question lol +4

 +2  (nbme23#4)

FA2019 pg.479 + spina bifida occulta: failure of cudal neuropore to close, but no herniation + anencephaly: failure of rostral peuropore to close --> no forebrain, open calvarium


 +1  (nbme23#49)

Testosterone--> dihydrotestosterone (DHT)

DHT + early - differentiation of penis, scrotum, prostate + late - prostate growth balding, sebaceous gland activity


 +4  (nbme23#22)

other answer choices

black fly - onchocera volvulus (river blindness) tsetse fly - trypanosoma brucei (african sleepling sickness) deer fly - F. tularensis

peridot  Also, deer fly can transmit loa loa (FA 2019 p.159) in addition to F. tularensis +

 +1  (nbme22#20)

FA 2019 pg 455 on avascular necrosis of bone: Infarction of bone and marrow, usually very painful. Most common site is femoral head (watershed zone) (due to insufficiency of medial circumflex femoral artery). Causes include Corticosteroids, Alcoholism, Sickle cell disease, Trauma, SLE, "the Bends" (caisson/decompression disease), LEgg-Calve- Perthes disease (idiopathic), Gaucher disease, Slipped capital femoral epiphysis- CASTS Bend LEGS.


 +1  (nbme22#34)

uw: EBV commonly infects B cells, stimulating them to enter the cell cycle and proliferate continuously ("transformation or "immortalization"). this is accomplished when EBV-encoded activate proliferative and anti-apoptotic signaling pathways w/i the infected B cell. ... the immortalized B cells maintain the ability to secrete Ig and B-cell activation products (eg. CD23), with very few of them releasing virus particles at any one time.


 +2  (nbme22#28)

UW: the short gastric vv drain blood from the gastric funds into the splenic vein, pancreatic inflammation (e.g. pancreatitis, pancreatic ca.) can cause a blood clot w/i the splenic vein, which can increase pressure in the short gastric veins and lead to gastric varies only in the funds

almondbreeze  b/c pancreatic causes can form blood clot in splenic v, b/c splenic v runs behind pancreas +


 +2  (nbme20#14)
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r'nu,od pnmsranetariets d'loensu

9F02A1 p734. sasy CBCs rae ,wxya n,ikp arpyel ledonus





Subcomments ...

submitted by karljeon(118),
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A amn iwht a Hx of HtEO npdeeecden dna icncohr dba apin as lewl sa yraX- sfngdini of ficlsatnioi"acc in eth puei-pmrd em"aobnd si stom lelyki iererrngf ot a crhconi .tsicatpaienr

hTis eldsa to a akcl of ilepas neoierstc hnec,e aelp, fusenlogillm- otossl twih lio ptroesdl pre tp .Hx Tish ts'p paansrce also eston'd rceetse rothe eyns,mze ucsh as saslemy,a a,sepsrote nro yornnpsietg to( aacevtit rohet ,nsezye)m os hte aenrws si nizegraled"e t"obriaalmpso.n

karljeon  p. 367 (FA 2018) +11  
usmlecrasherss  pancreatic insufficiency FA 2019 p375 , +2  
almondbreeze  FA 2019 p391 on chronic pancreatitis +  
almondbreeze  UW: in chronic alcoholic pancreatitis, alcohol induced secretion of protein rich fluid precipitates in pancreatic duct--> forms ductal plugs that calcify +3  


submitted by karljeon(118),
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A mna ihtw a xH of EOtH epdnedence dna inhccro bda naip sa wlel sa ayXr- infsgdni fo nctiasfcoiaic"l in eht meppdr-ui n"boeamd is msot elyilk rernfrgei ot a richcon itcept.iansra

ihTs sdela ot a aclk of plasei nsretcoie ,eechn ,aepl iuml-oenllgfs osostl hwti oli lsroetpd rpe tp Hx. ihTs 'tsp acsanpre laso sentd'o ercsete trheo esezm,yn uhcs sa slse,myaa epoa,rsset onr gostpniyner ot( ivcettaa otrhe ,znemyes) so the eawrns si alzeerdeg"in psmab.nlitoroa"

karljeon  p. 367 (FA 2018) +11  
usmlecrasherss  pancreatic insufficiency FA 2019 p375 , +2  
almondbreeze  FA 2019 p391 on chronic pancreatitis +  
almondbreeze  UW: in chronic alcoholic pancreatitis, alcohol induced secretion of protein rich fluid precipitates in pancreatic duct--> forms ductal plugs that calcify +3  


submitted by mousie(216),
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te"da"nrso aer tspoaispheoB,shn lomconym desu to rtvpentaet/re itssosoeproo. Mots nmomoc serdvae fseceft ear oighEsisatp p(seiattn uhlods keta htwi eatrw and be prguiht rof at selta usmet,0)n3i esreisosOcnto of het ajw, dan ctpylaia rmeaofl etrsss frsc.teura k-tena rithg rmof FA 0821 gp 741

almondbreeze  FA 2019 pg 248 pill-induced esophagitis : bisphosphonates, ferrous sulfate, NSAIDs, potassium chloroide, tetracyclines +3  


submitted by neonem(570),
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I hintk mteatsasis was the btes poniot reeh aeucseb eehtr rea lpiemtlu agmitnnla ao.m.slpe.ns myriapr crneasc edtn to rtast as a gleins ssam in eht stisue of i.rgion In eth u,nlg stsastemae ear erom omnomc hatn mrapiry snspa.mloe

dbg  I seriously could not figure out whether those white opacities were actual lesions or reflections from the actual picture (flash light) ... mind went all the way maybe this is the shiny pleura so they're going after mesothelioma. smh +6  
dbg  shiny pleura with tiiiiny granulations if you look closely. but obviously was far off +  
et-tu-bromocriptine  "Multiple cannonball lesions" is indicative of a metastatic cancer. I think if they were leaning towards a mesothelioma, they'd show the border/edge of the lung ensheathed by a malignant neoplasm (see image): https://library.med.utah.edu/WebPath/jpeg1/LUNG081.jpg +4  
bullshitusmle  guys something I learned from NBMEs is that if there is a clinical vignette dont even look at the images they give you ,they are all useless and time-consuming +1  
goaiable  The way i narrowed it down was that the patient had signs of weight loss since three months whereas her cough developed recently (3 weeks). If the cancer arose in the lung then I think the cough or other pulmonary symptoms should emerge earlier. +1  
almondbreeze  FA2019 pg 669 in the lung, metastasis (usually multiple lesions) are more common the primary neoplasms. most often from breast, colon, prostate, and bladder ca. +1  


submitted by colonelred_(105),
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doLkeo it up and onfud htat usceaeb yoeur’ ni a esipnu iipsonot rfo a olng meit oryue’ ngigo ot evah enrcdsiea osneuv enturr iwhhc delsa ot rdsiaence OC. siTh iltnyvgeae abfeescdk no SRA,A galdnie to dreacesed des.aoertlon sA a rtesul, ryoe’u giogn to evha idasencer usrdisie hwihc esdla to edcserdae dlboo and malpas ume.olv

medstruggle  Doesn’t supine position compress IVC leading to decreased venous return? (This is the pathophys of supine hypotension syndrome.) There was a UWorld questions about this ... +4  
tea-cats-biscuits  @medstruggle *Supine position* decreases blood pooling in the legs and decreases the effect of gravity. *Supine hypotension syndrome*, on the other hand, seems specific to a pregnant female, since the gravid uterus will compress the IVC; in an average pt, there wouldn’t be the same postural compression. +8  
welpdedelp  this was the exact same reasoning I used, but I thought the RAAS would inactivate which would lead to less aldosterone and less sodium retention +3  
yotsubato  You gotta be preggers to compress your IVC +5  
nwinkelmann  Could you also think of it in a purely "rest/digest" vs "fight/fright/flight" response, i.e. you're PNS is active, so your HR and subsequently your CO is less? But the explanation given above does make sense. Also because I think just saying someone is one bed rest leaves a lot up for interpretation, maybe not with this patient because his pelvis is broken, but lots of people on bed rest aren't lying flat.... ? +1  
urachus  wouldnt low aldosterone cause low plasma sodium? choice B +5  
kpjk  could it be that, while low aldosterone levels decrease plasma sodium levels- there is also decrease in blood volume(plasma),so there wont be a decrease in the "concentration" of sodium +4  
almondbreeze  FA 2019 pg 306 on Lt heart failure induced orthopnea - Shortness of breath when supine: increased venous return from redistribution of blood +  
almondbreeze  if there was no HF, it would lead to increased CO --> decreased aldosterone +  
theunscrambler  @peqmd thanks for sharing that. According to the presentation, the diuresis via ANP occurs (along with sodium), which is followed up by an increased in RAAS --> maintains sodium levels. This cycle can then continue. Slide 13. +  
jj375  @urachus - Either BB or Sattar taught me this but I feel like it is often forgotten. "RAAS/Aldosterone affects blood volume, and ADH affects Na level". So Increasing aldosterone will increase blood levels however water follows the sodium so you will not get a change in sodium levels. ADH however does affect Na since aquaporins are bringing in water without affecting sodium levels. +  


submitted by colonelred_(105),
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Ledook it pu nad nduof hatt cbseaue yueor’ in a pinseu nsptooii fro a long etmi rye’ou onigg to ahve adisecrne vneosu nrtuer cwhih sedla ot rnsdaeeci .OC Tsih aynlgteive dbseafcke no ARA,S enadilg ot caeersdde dtoenslraeo. As a rsluet, yeour’ gngio ot hvae eaedrnics irdsuise hhwic deasl ot erdeecdas odbol dna amlasp .mvoeul

medstruggle  Doesn’t supine position compress IVC leading to decreased venous return? (This is the pathophys of supine hypotension syndrome.) There was a UWorld questions about this ... +4  
tea-cats-biscuits  @medstruggle *Supine position* decreases blood pooling in the legs and decreases the effect of gravity. *Supine hypotension syndrome*, on the other hand, seems specific to a pregnant female, since the gravid uterus will compress the IVC; in an average pt, there wouldn’t be the same postural compression. +8  
welpdedelp  this was the exact same reasoning I used, but I thought the RAAS would inactivate which would lead to less aldosterone and less sodium retention +3  
yotsubato  You gotta be preggers to compress your IVC +5  
nwinkelmann  Could you also think of it in a purely "rest/digest" vs "fight/fright/flight" response, i.e. you're PNS is active, so your HR and subsequently your CO is less? But the explanation given above does make sense. Also because I think just saying someone is one bed rest leaves a lot up for interpretation, maybe not with this patient because his pelvis is broken, but lots of people on bed rest aren't lying flat.... ? +1  
urachus  wouldnt low aldosterone cause low plasma sodium? choice B +5  
kpjk  could it be that, while low aldosterone levels decrease plasma sodium levels- there is also decrease in blood volume(plasma),so there wont be a decrease in the "concentration" of sodium +4  
almondbreeze  FA 2019 pg 306 on Lt heart failure induced orthopnea - Shortness of breath when supine: increased venous return from redistribution of blood +  
almondbreeze  if there was no HF, it would lead to increased CO --> decreased aldosterone +  
theunscrambler  @peqmd thanks for sharing that. According to the presentation, the diuresis via ANP occurs (along with sodium), which is followed up by an increased in RAAS --> maintains sodium levels. This cycle can then continue. Slide 13. +  
jj375  @urachus - Either BB or Sattar taught me this but I feel like it is often forgotten. "RAAS/Aldosterone affects blood volume, and ADH affects Na level". So Increasing aldosterone will increase blood levels however water follows the sodium so you will not get a change in sodium levels. ADH however does affect Na since aquaporins are bringing in water without affecting sodium levels. +  


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bnrcietnoFi si an reualcaxtlrle trmxia tcnooiypr,elg eihwl lmain is na ieaitmdetenr mineftla atht yiafclsicpel iorvpsde sruppto ot eth elcl luseu.nc noD’t oncesuf mainl ithw nlaniim enescc(i ehats us ;elyclr)a linnmia si leki tcriieof,bnn na CME elptoiyrgnoc dan a omarj oneptcomn of eht aslab ilaanm of btsemena nmrsema.be

masonkingcobra  Lamin looks like a "cross" and held up Jesus and the basal lamina is super important just like jesus (you bet there are people who believe this) https://answersingenesis.org/biology/microbiology/laminin-and-the-cross/ +34  
dr.xx  blasphemy @masonkingcobra +1  
luciana  I clearly confused lamin with laminin, now I know +3  
almondbreeze  FA 2019 pg 48 lamin +1  
almondbreeze  picked tubulin but i guess tubulin makes up microtubules and therefore is spherical +  
abkapoor  Also remember progeria is due to lamin a dysfunction, and progeria patients have messed up nuclei +  
brise  @abkapoor the f is progeria? and do we need to know it for step? +  
brise  @abkapoor omg jk jk wow +  


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teiFnobcrni is na rrxlcteualael atrmix geyotopircl,n iehlw lamin si an eimdinttaeer tieafmln hatt lscfylicipea pdvoeris otruspp to teh cell elucsnu. ot’Dn eosnufc inmal wthi inminal e(icscen steha su alcle;y)r imainln si ekil ,ociinftenbr na ECM eycnoirlopgt dan a aorjm octopnmen of the alabs maanli of tseenmab msnbmeea.r

masonkingcobra  Lamin looks like a "cross" and held up Jesus and the basal lamina is super important just like jesus (you bet there are people who believe this) https://answersingenesis.org/biology/microbiology/laminin-and-the-cross/ +34  
dr.xx  blasphemy @masonkingcobra +1  
luciana  I clearly confused lamin with laminin, now I know +3  
almondbreeze  FA 2019 pg 48 lamin +1  
almondbreeze  picked tubulin but i guess tubulin makes up microtubules and therefore is spherical +  
abkapoor  Also remember progeria is due to lamin a dysfunction, and progeria patients have messed up nuclei +  
brise  @abkapoor the f is progeria? and do we need to know it for step? +  
brise  @abkapoor omg jk jk wow +  


Up to 80 percent of aortic aneurysms are caused by "hardening of the arteries" (atherosclerosis). Atherosclerosis can develop when cholesterol and fat build up inside the arteries. ... Elevated blood pressure through the aorta can then cause the aortic wall to expand and bulge.

https://www.uwhealth.org/heart-cardiovascular/aortic-aneurysm-causes-symptoms-and-concerns/10971

Also, FA 2019 pg300 says complications of atherosclerosis includes aneurysm

almondbreeze  I was dumb and went for marfan.. +1  
llamastep1  Wrong question lol +4  


submitted by famylife(93),
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nteerInvsa" hte ecmussl fo teh iaeldm rnmtaetocpm fo eth hitgh t(ootuabrr uee,trsnx rdcuatod lusogn, trddoacu sib,erv uacoddrt nmsagu dan glr)aic"s.i

c/eh:ofyrvoti./n/epnehvaeit-tmbwnloaer/oertuslmb/aaetnro/mtr-s

almondbreeze  FA 2019 pg 444 +2  


submitted by docred123(6),
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Cna yonane tfrheur pnxleia s!?thi I oulcd tleaimeni a wef temi ihsoecc dna I sseugde ,eorcclytr tusj eedn emro mntifoanrio! Tsnakh

wired-in  Patient has 5 yr h/o hep C, so it is chronic. Chronic inflammation is characterized by presence of lymphocytes & plasma cells while neutrophils is more characteristic of acute inflammation (Pathoma Ch. 2). AFP is within reference range so probably not HCC. Choice D, palisading lymphocytes & giant cells suggests granuloma which isn't typical of hep C. +42  
almondbreeze  Fa2019 pg 215, 217 on acute/chronic inflammation +1  
popofo  But doesn't AFP has not-so-high sensitivity for hepatocellular carcinoma (HCC)? If so, a negative result shouldn't be able to rule out HCC? +  
popofo  But doesn't AFP has not-so-high sensitivity for hepatocellular carcinoma (HCC)? If so, a negative result shouldn't be able to rule out HCC? +  


submitted by notadoctor(159),
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oAidgccrn to loj,nGa hmytpyocilea erva is eno of the smot omncmo saesuc fo ui-hiCddarB srmyon.de dicAgrocn to ,FA irhBau-diCd is teicdasaso ermo agrlenlye whit cugarbllyoheeap e,stsat yameitlhopyc vea,r ttoppasrmu as,sett adn H.CC

tHaepci isohcirrs nac eb luder uot sadbe no the tmei cesour of het a'tpnties etrintospnea - he asw nfei 2 esekw oga dna teh nadaimolb aipn dtsaret an orhu g.ao

krewfoo99  Also in cirrhosis, the liver wont be enlarged or tender on palpation +1  
almondbreeze  @krewfoo99 Good job. accoring to FA2019 pg.368, congestive liver disease (hepatomegaly, ascites, varices, abdominal pain, liver failiure) seems to be the key in Budd-Chiari SD +2  


submitted by sajaqua1(532),
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ru-ChdiiBda ysndemor uccros henw hreet is loisoncuc fo het ciahept niev or het ctapihe vien fslia ot irnad tion eht .IVC Tihs nac be udeasc yb tsorsimhbo fo hte ehcpiat ,eivn ro by htrig deisd ehtra elurafi (ucsgnai bldoo ot k'cab 'up ev,wrreheye btu tis titnfiseaamon gohurht teh heaictp inve rae all the isgsn fo Bdi-ahrdiCu snem)r.oyd inAtygnh atht nca esacenri hte ksir fo rsosmthoib acn hetn rcenaeis het rkis of diCa-Bhidru mdnse.oyr Thsi nedclisu oempyicaytlh erv,a a heuroygplleaacb s.atte urO ptienta adn VP but edmiss ihs ptiampntoen wot wskee go.a He own epesnrst wtih casrlle ,reicuts na ergladne v,elri dan meos ssgni of rptlao eoyne.rthpnis Tsiomrohsb of eth loyn mticlnoaaa oionpt tperdesne ahtt rcoesv lla of tshi si het tciapeh nive ei ruo tpniate sha .ua-iCiBhrdd embReerm ttha udhriCiaBd- iwll vahe a ntgme"u vle"ri prpecaanea no rosgs gplo.yhota

B) tpaHeic orhcirssi- sit' reetiynl slipoesb uro tpnieta sedo aveh aetipch rhsisoicr for rletdauen ,nesasor ehwerov eth uaect nteos kasme tsih less llek.yi C) carPcneati co-amiarnc catiapencr imaroccan ouisonrbttc of het cnommo ielb utcd olcdu scuae a c'abk up' of eb,li ttyeiumlal sauicgn eoms rlvie degmaa and cralsel scrit.ue orHewve enco inaga eth tmiing mseka shit inllyke.u D) olrtaP vein -rimohsbtos aprtol evin shibstmroo lcduo cuesa moes pscinle enemlagrnte nad oltpra npyths.ieroen wovreH,e ist isttnoruboc dowul ont saeuc a etdern, ledregna velir ueascbe it si emtrsa.pu )E mriyPar hethsarmmi-osoco ued ot a tecdfe in hcdpenii corpntiud,o hsit inor drvolaoe tsneerps wthi edadrenk k,ins linnius dnaliu,retigos cetihap adgame tw(ih hte eailtnotp for ehpertuaalcllo nrac)caoim adn etahr eesdasi rtei(srivtec or dialtde ,yripmtahocdoay ipngededn on yoru ueo.)rcs heT loyn eon of esteh gnsis ttha our itnpaet ash si an aregndle .vierl

almondbreeze  FA 2019 pg 386 +  


submitted by defalty98(3),
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hyW ear we icpntgliocma ?itgnsh hCgnea in het asseb wlil ordeyst eht ciipoadrnlm equeencs qeierudr ofr nya trrsieticno deuecnlsaeno to krw.o ithetMnoaly is teh onyl oipotn atht meaks eses.n

arcanumm  This makes sense have reading what your comment. I overlooked this and just assumed the GATC was a mutation that allowed the restriction enzyme to work on the mutant only. +2  
arcanumm  it makes even more sense when looking at "numerous small fragments." Methylation is truly the obvious answer here in retrospect. +1  
bgiri  DNAse can also cause a change in base by breaking down dna at the GATC sequence? +  
almondbreeze  @bgiri Had the same reasoning - according to wiki, DNase catalyzes the hydrolytic cleavage of phosphodiester linkages in the DNA backbone, thus degrading DNA. +  


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itPaten is utnrerc rdbe,fae-ts os ew can ieamntile scotrefu esof(turc is udfno in ehyno nda tirfus dna esmo lof,uarm btu tno ni stbera imkl). ttiPaen ash curndgei nscbasstue btu on gcleuso in the niue,r os he must oems -eocgsonlnu sar.gu yM rtelaeffdiin fro dungirce ncoo-nslgeu rasgus ni eth eunri si rroeissdd ucetfros eobstlimma ro oclgsaate ismot.aeblm eW have eedatmiinl usr,ctfoe so ttah slveae us hwit oktsealaignac eifeyincdc ro cssilca mosg.alctaaei

sympathetikey  & Galactokinase deficiency would be much milder. +6  
smc213  Big was soybean formula not giving any issues. Soy-milk can be used as a substitute formula in patients with Classic Galactosemia since it contains sucrose (->fructose and glucose). +1  
oslerweberenu  Why can't this be glucose 6 phosphatase deficiency Confused me +  
almondbreeze  @oslerweberenu G6PD - increased RBC susceptibility to oxidant stress (eg, sulfa drugs, antimalarials, infections, fava beans) -> hemolysis; has nothing to do with presence of reducing sugar +1  
makinallkindzofgainz  @almondbreeze; Glucose-6-phosphatase deficiency is Von Gierke disease, they are not referring to G6PD deficiency (an entirely seperate disease) +7  


submitted by lfsuarez(141),
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Tshi ostqeniu saks bauto eht ieshcnmma fo thyarteopoph sa ti teleasr ot eontlnaa jecun.ida Whti oepoht,yhatrp libbiinur is iyslmp otcerdenv to retaw uloebls oriemss taht rae tneh albe to eb eexrcedt yb hte ykined. shTi hwoeerv edso otn njoaugtec hte biiinbr.lu

almondbreeze  FA 2019 pg 387 +  
abhishek021196  Physiologic neonatal jaundice At birth, immature UDP-glucuronosyltransferase = unconjugated hyperbilirubinemia = jaundice/ kernicterus (deposition of unconjugated, lipid-soluble bilirubin in the brain, particularly basal ganglia). Occurs after first 24 hours of life and usually resolves without treatment in 1–2 weeks. Treatment: phototherapy (non-UV) isomerizes unconjugated bilirubin to water-soluble form. +  


submitted by nwinkelmann(292),
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g98@8h ee"uBsca het onrobuticst si obave hte lovelara nrsgoei trehe is a edseaecr in ria wlof, otn glun vm,esluo whhic lwodu aemk ihst na etvbrucoist loptyhg"oa is the msto pleuflh nxnaoilptea. If yuo kwno teh smto acsbi /iyopoigtfoisthoepyahdinln fo urtecbvtois vs vtreiteicrs c(whih I od, stju 'dndit in ttha mtos iismflidpe awy), hetn ouy nac freiug angnhity tu.o fI hmsnoteig is agmitcpin ayaiwr owlf = u,rtbtiovcse if shoetnimg si pnitagcmi aiywar mvolue = trcevi.tires HTAKN !OUY

burningmoon  How about emphysema? airway volume changed but it's obstructive. +2  
almondbreeze  i think OP meant to say that something DECREASING airway volume = restrictive +3  
jgraham3  I think they mean if something is impacting LUNG volume (ie. expansion/compliance) = restrictive Airway disorder --> obs. / Parenchymal disorder --> res. With emphysema the airway collapses (obs.) before they are able to exhale fully thus the air is trapped +  
dna_at  Just to be clear, this is not a classical obstructive lung disease affecting the small airways, as it is above the carina (trachea). This is better classified as a fixed upper airway obstruction. See the flow loop here for "fixed obstruction" - it came up in IMED UWorld so maybe familiarize yourself with the image since it is unique! https://www.grepmed.com/images/2948 +4  


submitted by asapdoc(63),
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ln.jaGrDo eanpxsli ti rleyla ewll on eht d.aiou I ilwl just eigv het icsba .edia llA eth boneglohsim aevh haalp in ti thoerfeer oyu nntoac ictnoe ti on oigeolbnhm crotorpilssehee

someduck3  Just to add to this; a-thal is due to a deletion. While b-thal is due to a mutation. If they had a b-thal there would be target cells. a-thal just presents as microcytic & hypochromic. +9  
almondbreeze  looks like a-thal can have target cells too. Individuals with alpha thalassemia trait (-α/-α or --/αα) are asymptomatic, with a normal CBC. The peripheral blood smear typically shows hypochromia, microcytosis, and target cells. (emedicine.medscape.com › article › 955496-clinical) +  


submitted by krewfoo99(93),
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oS laascbyil ahtw hits si iagsyn atht ADN liwl eb tdtemisrnta ot het gropney not RNSo.A ADN illw receatlip ni eth G2 epash and aesrrtfn fo ADN liaermta to nrogype lilw crcou in eth M hap.se eTh RAN mya eb etumtda adn mnkagi iecfdetve r,ctpodsu but tshi lilw nto ttmasirn ntio eth eopry,ng shtu otn iagnefcft esesicp vlavsriu sbdae no NRA sitnaum.to

bk2458  makes sense!! +  
almondbreeze  good work +1  
tyrionwill  the question asks the reason of no impact on its survival. if a protein translated from a wrong mRNA loses its function, how can we say the bacteria will still survive well? if there is always fatal error happened during mRNA transcription, and always leading to fatal dysfunctional protein, how can the bacteria and its progeny still survive? so the point will be whether the fatal errors will always happen during transcription? I dont know... +  
tyrionwill  actually FA and NBME seem to have made a wrong statement that RNA polymerase has no proofreading function. RNA polymerase has more fidelity to DNA than DNA polymerase by 2 ways: 1) highly selection of correct nucleotide, and 2) proofreading. (Jasmin F Sydow and Patrick Cramer, RNA polymerase fidelity and transcriptional proofreading: https://pure.mpg.de/rest/items/item_1940413/component/file_1940417/content) however, if survival of the species refers only to the reproduction of progeny, mRNA mutation has nothing with the progeny. +1  


submitted by keycompany(310),
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iTsh tnuoqsie si gsddiu.esi ahWt htey aer ylearl ksigan si "thwa is het seol endneaitmtr of psceies uvvsaril?" ehT noyl srnwea is teh byaitli ot .errpceaot cBaeseu NDA eesmyaPlro ash aopird-gofern itav,tyci nepryog lwil be nauefftdec by ANR eParsmesloy klca fo rodp-aogiernf tic.yativ

ls3076  the phrasing of this explanation doesnt make sense to me. +4  
ls3076  oh wait sorry i just read it again. So instead of proofreading how are errors handled with RNA? +  
thomasburton  Think the point is basically although errors with RNA polymerase make make the bacterium not very good at infecting or killing or whatever it does not affect replication as it is not used during replication! +5  
almondbreeze  common sense asked in a very very convoluted way.. +  


submitted by monkd(18),
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mA I czyar or did owrdUl not heav a qoieustn htta attesd Snattis rae het msto fevtfeiec rudg elrrsaegds fo ebisaenl dilps.i Tsih iogcl whetr my f.fo

adisdiadochokinetic  You are not crazy. I got this question wrong for the same reason but here's why I think NBME was going with fibrates. You can use the Friedewald equation to calculate LDL cholesterol from the values they give. This equation is LDL= Total Cholesterol-HDL Cholesterol-(Triglycerides/5). The Triglycerides/5 term is an estimate for VLDL. If you calculate it in this case you get an LDL of 120 which is firmly normal and thus the patient would ostensibly not benefit from statin therapy. +14  
hello36654  omg when the hell am I going to remember this equation? Jesuusssssss, this kind of details makes me want to give up on STEP +4  
almondbreeze  Her goal LDL should still be <100, bc she has 3 CHD risk equivalents (https://www.aafp.org/afp/2002/0301/p871.html#afp20020301p871-t3) CHD risk equivalent=the major risk factors that modify LDL goals 1) age(M>45, F>55), 2) smoking status, 3) hypertension(>140/90), 4) ow HDL level (<40), and 5) family history. (https://www.aafp.org/afp/2002/0301/p871.html#sec-4) +  
almondbreeze  *low HDL level (refer to table 3 of the article) +  
makinallkindzofgainz  These guys are hitting up attending-level cardiovascular risk factor calculations, meanwhile I picked statins because I think I remember that they help the heart +12  
jimdooder  So I ended up going with fibrates because of her age (39). I vaguely remember being taught that statins are really only recommended for patients >40 because the big study that came out about them was in the 40-75 age group. I think this might contribute to the question but I'm not totally sure. https://en.wikipedia.org/wiki/Statin#Primary_prevention +  
ytho  This question inspired my screen name +2  
cbreland  "Statins are always the answer", "Fat Female 40 Fertile", "Fibrates can cause gallstones". I feel lied to +  
brise  I'm not sure if this question is correct. I chose statins according to what an attending told me and UWOLRD 2, I just went back to check and on uworld 2, you only consider giving fibrates if their TG levels are above 1,000. So idk what the nbme is smoking. Or if doctors actually write these questions. +  


submitted by monkd(18),
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mA I cyarz or ddi dwlUor otn eahv a squentoi thta ttdeas sittnSa ear het tsmo iceefetfv rdug delrsasrge fo eibnelsa siilpd. siTh oigcl wther ym ff.o

adisdiadochokinetic  You are not crazy. I got this question wrong for the same reason but here's why I think NBME was going with fibrates. You can use the Friedewald equation to calculate LDL cholesterol from the values they give. This equation is LDL= Total Cholesterol-HDL Cholesterol-(Triglycerides/5). The Triglycerides/5 term is an estimate for VLDL. If you calculate it in this case you get an LDL of 120 which is firmly normal and thus the patient would ostensibly not benefit from statin therapy. +14  
hello36654  omg when the hell am I going to remember this equation? Jesuusssssss, this kind of details makes me want to give up on STEP +4  
almondbreeze  Her goal LDL should still be <100, bc she has 3 CHD risk equivalents (https://www.aafp.org/afp/2002/0301/p871.html#afp20020301p871-t3) CHD risk equivalent=the major risk factors that modify LDL goals 1) age(M>45, F>55), 2) smoking status, 3) hypertension(>140/90), 4) ow HDL level (<40), and 5) family history. (https://www.aafp.org/afp/2002/0301/p871.html#sec-4) +  
almondbreeze  *low HDL level (refer to table 3 of the article) +  
makinallkindzofgainz  These guys are hitting up attending-level cardiovascular risk factor calculations, meanwhile I picked statins because I think I remember that they help the heart +12  
jimdooder  So I ended up going with fibrates because of her age (39). I vaguely remember being taught that statins are really only recommended for patients >40 because the big study that came out about them was in the 40-75 age group. I think this might contribute to the question but I'm not totally sure. https://en.wikipedia.org/wiki/Statin#Primary_prevention +  
ytho  This question inspired my screen name +2  
cbreland  "Statins are always the answer", "Fat Female 40 Fertile", "Fibrates can cause gallstones". I feel lied to +  
brise  I'm not sure if this question is correct. I chose statins according to what an attending told me and UWOLRD 2, I just went back to check and on uworld 2, you only consider giving fibrates if their TG levels are above 1,000. So idk what the nbme is smoking. Or if doctors actually write these questions. +  


submitted by hipster_do(6),
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Im’ ggnio to yas ’ist X kledni amiemblalgmgniouaa taherr tnah SDCI, tbu eth fndicerefe etnweeb teesh owt era tniy tbu sith is wyh I nhtki ’sit hte rfr:oem

  • yoB eirseadcn( kisr ubt bhto AB dan SICD ear x de)nikl
  • ucrRnetre airaetblc neonifstci ubt dtn’o ontinme edahrrai ro trsuhh ihwhc is ni SCID
  • emilnieT is etafr 6 ,tmoshn so het re’sthmo sintadeiob erow off.

SCID ohdslu be aiitdleymem cuesbea thye stju ’ndto aveh eht I2L rteercosp. CVDI osshw pu when reyet’h 200-4 ysera l.do Yuo etg neatbs aligrenm rstceen in hb.ot No ienmotn fo besnta mtciyh owsadh cwhhi si ni ISC.D

placebo079  “Uniformly” low is also a clue; in CVID they are not. +4  
tea-cats-biscuits  This makes sense, though what really threw me off was that in Classic Bruton’s Agammaglobulinemia there’s near-zero B counts though (or at least that’s what FA and UTD says, “Absent B cells in peripheral blood” FA 116, 2018). The Q says the leukocyte count was normal though. Wouldn’t the leukocyte count include lymphocytes in the differential? And wouldn’t lymphocytes be low due to the near complete lack of B cells in peripheral circulation if it was BA? +2  
partybrockk  @tea-cats-biscuits Bruton’s is a failure of B cells to /MATURE/. So you get normal lymphocyte counts, decreased levels of immunoglobulins, and absent germinal centers. +5  
tea-cats-biscuits  @partybrockk That makes sense to me, but I keep getting hung up on how that’s not what either FA or UTD says about the classic lab findings of XLA. UTD specifically says this: “Laboratory findings include hypogammaglobulinemia/agammaglobulinemia, deficient antibody responses to immunizations, and absent or markedly reduced B cells in the blood,” and I previously quoted FA. I suppose it doesn’t really matter, but it’s definitely a bit frustrating unless I’m missing something about how absent B cells in the blood wouldn’t correlate to a decreased lymphocyte count ... +3  
temmy  please correct me if i am wrong cos i might be but my logic was there is decreases immunoglobulin uniformly meaning the B cells are uniformly absent and since they develop in the germinal center, the germinal center will be absent. +2  
almondbreeze  Picked 'decreased # of CD4 lymphocytes'.. ->Both CD4 and CD8 T lymphocytes were affected; the decrease was most pronounced for naïve T cells. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1809006/) +  


submitted by meningitis(540),
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zholrioodahyhcrtedoi is DCO rof rioepNgehnc ietDseba sisdiunpi csbeeua it daiclpaaryxol csaseu an esricnea in BP by nrginesaic midous oiporsbnta and utsh wtaer oitrspb,ona Paaomht ilnapexs htis eiylnc.

ponssrseDeim is tcirneorc suaeceb upon gistnfa udlf(i est)nrroiitc ADH si sndicraee ningema HAD is engbi aerldese llynarteC tub is not gnkwiro ni hte kdseiny ta eth 2V errpscteo of eht ipelelaith ralen lslce at nlClgieoct ucdt.

On ahtt n,oet eriiAomdl si duse for huitimL cniedud pncehginore D.I

hello  Where in Pathoma? I couldn't find it. +1  
almondbreeze  also sketchy says that thiazide s decrease the amount of lithium cleared--> lithium toxicity +1  
paperbackwriter  Agh confused as well because FA2019 (pg 562) says that thiazides are implicated in lithium toxicity D: +  
paperbackwriter  OOPS, please ignore last comment. I just realized that this Q stem never mentioned lithium. And on top of that @meningitis mentioned that amiloride is used if lithium induced. Apologies. +  
jaramaiha  Question is nephrogenic DI. ADH is increased but kidney's aren't reacting, mutated receptors. In which the Tx is HCTZ +  


submitted by gh889(127),
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nidrogcca ot aodpettu tizsaiedh scuea a limd iypevolmhoc astte huts ruyo CTP will ese omer aN adn HO2 g;-&-t by liprnipce ahtt the TPC aswayl bbersosra 0%6 fo hawt ti ee,ss it ilwl ebsarrbo meor earwt nad .Na

almondbreeze  in sketchy as well +  


submitted by imgdoc(135),
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I nthki aotl of peoepl ightm have vroe edshamzipe woh orpamttin NPA dan PBN rlaeyl ea,r yse it si mopitatnr ot owkn steeh edspitep tge retcesde by eth ltraar/ilvnituarce rumcamydoi nguidr treah lu.fraie evwrHoe itrhe vleoarl tevescesfneif ni tgeriant arteh fraeuli is lic,hz a crepertop ltod me ahtt fi APN nda NPB erwe os ufuels in tiiansersru enth wyh do we igev dirt?eiusc tsI' aesbeuc ARSA vworerseop itsh tyesms ehecn ugsicna vgnetaie csftfee dna the lnessde polo of earth lefua.ri AKA hwy ew evgi EAC hiibtni.sro

wKnigno taht APN etsg ezuleanrdit yb the RASA s,semyt we anc htfsi oru osfuc acbk to ehtar ielfaru in htis tna,tpie rweeh iadcrac ptuotu is ,eareddesc aidleng ot HAD rsiteonce dna yflilna ualdinotli iph.yatmaeorn

almondbreeze  a concept continuously emphasized by uw, but I get always wrong :'( +2  
almondbreeze  good work done! +  
raffff  why does the body make anp at all since its so useless +3  
makinallkindzofgainz  @raffff - at least BNP gives us a good marker for heart failure exacerbations :) thanks body! +  
mannan  Yeah it's important clinically because it has a high sensitivity (if negative, rule out) for Heart failure. +  
alimd  At the same time ANP inhibits renin release? +  


submitted by imgdoc(135),
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I tnhki ltoa fo elppeo itgmh haev vero sdhaiezepm hwo ottmainpr PAN nad NBP lleyar r,ea yse ti is atnirmpto ot wnok teshe ppsdiete teg sdteeecr yb eth rvltairacl/urneita myidruocam uignrd trahe .ailfuer eervHow eihrt laroelv efevnftieecss in itneargt aerth laiufre is ihzl,c a treprpoec odtl em tath fi NPA dna NPB were so lusefu in aenusrsriit hten ywh od ew ivge diut?rscie 'tsI acesbeu SARA reroweopsv htsi temssy hceen unicsga vaengeit eescfft adn the ssleden loop fo reath uliar.fe AAK wyh ew giev ECA iorsbh.niit

nowniKg htta NPA tsge eldiatrunez by hte AASR es,symt we nac isthf our cufso akbc ot herta lrefaiu in tshi t,itpnae erhwe adcraic otputu is ed,adeersc liaegnd ot DAH scerteoni dan anilfyl iotniullad ramoithnpey.a

almondbreeze  a concept continuously emphasized by uw, but I get always wrong :'( +2  
almondbreeze  good work done! +  
raffff  why does the body make anp at all since its so useless +3  
makinallkindzofgainz  @raffff - at least BNP gives us a good marker for heart failure exacerbations :) thanks body! +  
mannan  Yeah it's important clinically because it has a high sensitivity (if negative, rule out) for Heart failure. +  
alimd  At the same time ANP inhibits renin release? +  


submitted by hayayah(1076),
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siTh is a tenatpi seac of putmrotspa .isdtyihotri aCn rseai pu ot a yrae teafr dilryeev dna ahs tcoimycyhpl ttilna.irfe

almondbreeze  FA 2019 pg 338 +1  
waterloo  Although history seems to point towards that, she has an enlarged thyroid, and in postpartum thyroiditis, thyroid usually normal in size (from FA). regardless either would have lymphocytes infiltrating. +  


UW: the short gastric vv drain blood from the gastric funds into the splenic vein, pancreatic inflammation (e.g. pancreatitis, pancreatic ca.) can cause a blood clot w/i the splenic vein, which can increase pressure in the short gastric veins and lead to gastric varies only in the funds

almondbreeze  b/c pancreatic causes can form blood clot in splenic v, b/c splenic v runs behind pancreas +  


submitted by welpdedelp(226),
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It asw a suForgeuirn gis-et;d-ob& ss.sibtaeso oniugreuFrs edsiob era edibveel to eb reomfd by armpcgeasho tath aehv ocydshtegpoa dna ptatemdte ot gietds eht ie.frsb

almondbreeze  info about ferruginous bodies being mf can't be found on FA/UW :'( they just say it's 'material' +  
taediggity  FA 2020 677, FA 2019 659... mf?? mofos?? +3  
69_nbme_420  Just to add: The question asks what cell type initiated the Fibrosis → Alveolar macrophages engulf the particles and induce fibrosis (same pathophys for all Pneumoconiosis). Pathoma 2019 Pg 92 +7  


submitted by rogeliogs(9),
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yM hoarcppa to itsh iusqoten was eorm tsuj ocnifsug in hte inof they aer ign.igv neNo fo het trohe tnopio asmek nesse buscaee erthe si ton dcievnee ot lkat tobau emth. I aws rvye emtptde ot kicp het arceedes" ipnlte utconpord"i ubt I ermedemerb Dr aGnjlo igaysn hkn"iT ie,slmp nhtik cah,ep yeth are not trying to tkric u."yo S,o chbuyb arptsne = cbhbyu .disk

almondbreeze  thought his words on "think cheap" had to do with treatments - i.e. exercise +  
alimd  Yes they are. There are so many trick questions +  
skuutnasty  I chose leptin deficiency cuz I was tryna get fancy with it. For anyone who is interested, however... according to UpToDate: "Most people with obesity do not have any abnormalities in the leptin gene, their serum leptin concentrations are high reflecting their increased fat mass..." Peace +  


submitted by jooceman739(27),
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timsoenoa:lbatR

The aisypnchi asdi teh ybo is likneuly to eevlpdo yan orhte na,lpmosse so he sdt'oen heva teh rteiihedn bR amotitu.n

nI tshi ,esac eh has teh cdorspia roi.tobaalnsmet orcdpaSi rsblmaoetniaot uerqirse wot mitsoac auinstomt of Rb in eth same ailtnre lecl.

sJtu as a sdie note: eediIhrtn ostisnormabelat ednt ot be elaait.brl diporSca ear r.lineltuaa

carls14  aren't retinal cells a type of somatic cell? Why not is the mutation not considered in the somatic cell of the child? +9  
omerta  Although this mutation would be considered somatic, I believe the question is just asking you to be specific as to which cells. If you answered "somatic cells of the child," that's quite broad and could apply to almost anything. +12  
kernicterusthefrog  I had the same struggle and thought process. +1  
eacv  There is a Uworld qx that explain this in detail> ID: 863 +3  
arcanumm  I read the answer options too fast so got this wrong. It is a somatic cell type, but somatic in general implies a higher risk for developing other cancers. The hint here is that the physician stated he is unlikely to develop any other neoplasms, so it is a specific double hit mutation in the retina. +7  
almondbreeze  wouldn't she have any possibility of developing osteosarcoma as well? :( +  
almondbreeze  did some reading and it seems like osteosarcoma only occurs in familial retinoblastoma with RB mutation +  
brise  But how can a 5 year old get two mutations to get retinoblastoma? In 5 years?! Obviously doctor is probably wrong LOL +  
jaramaiha  The difference between familial and sporadic mutations dealing with Rb is that in this case he only had one hit so that only one eye is affected. In other words, if he would have been born with the familial type, he would present with Rb in both eyes and also be predisposed to osteosarcoma. In this instance he only has Rb in one eye having only a one hit mutation in his right eye. When the stem says this is the first mutation it's implying that he wasn't born with the familial type so to obtain a second mutation over the course of his lifetime would be rare. +  
brise  @jaramiaha I believe it still falls into a two hit mutation, but both were sporadic. But you are right about being unilateral. +  


submitted by jooceman739(27),
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etmaibtRao:nlso

hTe hisnacipy adsi teh boy si yuenllki ot evdpole any ertho n,moslseap so he sndto'e ahve het irnedeith bR uto.iatnm

In tish aesc, he sah eht rdaopcis tnmlaitosareo.b cadrpSoi italeotaorbmsn qisreeur owt mctiosa istnatoum fo Rb in teh maes lritaen .lelc

Just as a iesd en:to eenirIdth oasirmsotaletnb ntde to be et.irbalal cSpaodri era l.rlitnauae

carls14  aren't retinal cells a type of somatic cell? Why not is the mutation not considered in the somatic cell of the child? +9  
omerta  Although this mutation would be considered somatic, I believe the question is just asking you to be specific as to which cells. If you answered "somatic cells of the child," that's quite broad and could apply to almost anything. +12  
kernicterusthefrog  I had the same struggle and thought process. +1  
eacv  There is a Uworld qx that explain this in detail> ID: 863 +3  
arcanumm  I read the answer options too fast so got this wrong. It is a somatic cell type, but somatic in general implies a higher risk for developing other cancers. The hint here is that the physician stated he is unlikely to develop any other neoplasms, so it is a specific double hit mutation in the retina. +7  
almondbreeze  wouldn't she have any possibility of developing osteosarcoma as well? :( +  
almondbreeze  did some reading and it seems like osteosarcoma only occurs in familial retinoblastoma with RB mutation +  
brise  But how can a 5 year old get two mutations to get retinoblastoma? In 5 years?! Obviously doctor is probably wrong LOL +  
jaramaiha  The difference between familial and sporadic mutations dealing with Rb is that in this case he only had one hit so that only one eye is affected. In other words, if he would have been born with the familial type, he would present with Rb in both eyes and also be predisposed to osteosarcoma. In this instance he only has Rb in one eye having only a one hit mutation in his right eye. When the stem says this is the first mutation it's implying that he wasn't born with the familial type so to obtain a second mutation over the course of his lifetime would be rare. +  
brise  @jaramiaha I believe it still falls into a two hit mutation, but both were sporadic. But you are right about being unilateral. +  


submitted by armymed88(47),
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donuW leanihg amrfn aloitmy rfo up tli 3 sdya stolc,( MNPs, crrialia sPeot)rfmoev ya3ds tli wekes- ougnanltrai sis,eut wne evss,lse new ut,mleehpii ronttcncaio erraip( dan eetrgnrn)eaoi mRol dee 1kw til -6m reclape eocanlgl III iwth I, searcine nrsettgh (up to %00-67 rnilaoig enrshttg ibslo)spe

john055  it looks like the patient has new onset erythema which points to infection and I think neutrophils make sense. I myself have marked angiogenesis but I did it offline. Is angiogenesis the right answer ? +1  
almondbreeze  yup +  
almondbreeze  according to FA 2019 pg217, neutrophil is present during inflammatory phase- i.e. only up to 3d after the wound. After that we have the proliferative phase with granulation tiss. and angiogenesis, epithelial cell proliferation, dissolution of clot, and wound contraction (involved cells: fibroblasts, myofibroblasts, endothelial cells, keratinocytes, mf) +  
mitchell_to_lakers  why not fibrosis? +  
waterloo  mitchell_to_lakers They are asking why is the incision erythematous and slightly warm. When someone is red, Dr. Sattar says that's because blood is going there. Fibrosis isn't a mechanism where someone's tissue will appear red and warm, it's collagen deposition. +4  
juanca10  Very good! +  


submitted by armymed88(47),
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nduoW alhegni mtmyranfoali for up til 3 syad ,tlso(c sP,MN rfeormialeai vcPso)rt ays3d lit k-sewe nuratnialog isetus, wne sle,evss ewn pmt,ileieuh aionccortnt eparir( nda otgaerer)nine mReelod w1k lti m6- pealcre onegcall III whti ,I sneracie ngetrtsh pu( ot -0%076 niloairg rhetsngt spbio)lse

john055  it looks like the patient has new onset erythema which points to infection and I think neutrophils make sense. I myself have marked angiogenesis but I did it offline. Is angiogenesis the right answer ? +1  
almondbreeze  yup +  
almondbreeze  according to FA 2019 pg217, neutrophil is present during inflammatory phase- i.e. only up to 3d after the wound. After that we have the proliferative phase with granulation tiss. and angiogenesis, epithelial cell proliferation, dissolution of clot, and wound contraction (involved cells: fibroblasts, myofibroblasts, endothelial cells, keratinocytes, mf) +  
mitchell_to_lakers  why not fibrosis? +  
waterloo  mitchell_to_lakers They are asking why is the incision erythematous and slightly warm. When someone is red, Dr. Sattar says that's because blood is going there. Fibrosis isn't a mechanism where someone's tissue will appear red and warm, it's collagen deposition. +4  
juanca10  Very good! +  


submitted by calcium196(11),
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iadeiqbmduiniet-tU pyesstlioro si nto irlsevbeyr deteacff yb nin.lius Teh otsenqui asks rfo resrleevbi syaw hatt lnnuisi aetfscf ti, and atunbniuiiiqto woudl alde ot oaeiandrtdg avi s,oteapers hhwci si nto .rvereilbse yetucairslpa/Nocmlc sutingnh asmke essen casebue XOFO si a rsatrnopticin o,acftr so ti t’cna od sit job if ti si ni eht !lmctopsay

meningitis  Thank you for your explanation! One question: How about the serine phosphorylation? Is it answered by pure memorization that the FOXO TF is serine phosphorylated, or is it a general fact that all TF's are serine-threonine phosphorylated? +  
tsl19  I'm not sure, but it may be as simple as this: ubiquitin-mediated proteolysis is irreversible, but both N/C shuttling and phosphorylation are generally reversible processes. +  
didelphus  I also guessed that FOXO must be a part of the PI3K pathway, since insulin regulates metabolism through PI3K and the question stem specifically mentions that. Phosphorylation is a major part of that pathway, so even indirectly phosphorylation would regulate FOXO. Frustrating question. +18  
niboonsh  yes, FOXO is affected downstream of the activation of PI3K. This is a really good video that explains the whole cascade https://www.youtube.com/watch?v=ewgLd9N3s-4 +2  
alexb  According to wikipedia (https://en.wikipedia.org/wiki/FOXO1) phosphorylation of FOXO1 is irreversible. This is referring to phosphorylation of serine residues on FOXO by Akt, which occurs in response to insulin. But the NBME answer suggests it's reversible. What's up? +1  
almondbreeze  could wiki be wrong on phosphorylation being irreversible? according to this article, it is a reversible process: regulation of FoxO transcription factors by reversible phosphorylation and acetylation (https://www.sciencedirect.com/science/article/pii/S0167488911000735#s0010) some wiki info, however, is helpful : In its un-phosphorylated state, FOXO1 is localized to the nucleus, where it binds to the insulin response sequence located in the promoter for glucose 6-phosphatase and increases its rate of transcription. FOXO1, through increasing transcription of glucose-6-phosphatase, indirectly increases the rate of hepatic glucose production.[19] However, when FOXO1 is phosphorylated by Akt on Thr-24, Ser-256, and Ser-319, it is excluded from the nucleus, where it is then ubiquitinated and degraded. The phosphorylation of FOXO1 by Akt subsequently decreases the hepatic glucose production through a decrease in transcription of glucose 6-phosphatase. +  
leaf_house  It seems like the phosphorylation from Akt leads to destruction, but maybe the assumption is that that phosphorylation step (excluding every other step of ubiquitin-proteosome pathway) is reversible, where proteolysis is final. @niboonsh video is good but doesn't split this one. +  


submitted by assoplasty(93),
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taFs era cgeeknoit cepex(t odd achni ,A)F os ehyt drpuceo eksntoe rof rgeney ponoicurtd )ycoAA-(etlC htarre anht ocsgeul. fI hte uinsoqet seakd tahw het aiprmry cuorse of erngey topdnuiorc wsa, ti wudol tllsi be ngecylgo n(ad not ,entkso)e uebcsea this is inhtiw 42 uhsr.o eeHvwor freat 24 ouhsr teh swenar uoldc eb teeonk ise.dob Rsasged,erl eth seoitnuq lapfiyeclics dasi the tp dha a rumse olcgeus of ,010 nciniagtdi thta we ear onkglio ofr ehsotgnim htta peviodrs a attreussb ofr loesnecniuegogs.

rnuiDg pisodre of tna,avstori sstruebast rof egeoecunsonsilg come ofrm otw s:souerc (1) rnkwdaobe fo esiitgxn e,lmscu or ()2 avi idhaonc-d FA ugrtohh Cy-pAlpironoo. V*nlaei( saol deefs noit ypirponlo o,CA tub is nto devvionl urdgin vtraosanti gt-;&- ees b)lowe

(1) eTh rlutvape-nineyaa lecyc dvispero ihts t(ialeumgn ni lmecsu + raeytvup g-t;&- inleana t--;g& ogse ot elirv -;>- ntitnaonsraima ot gortaluoehlpea-tkat ;gt&-- uevartyp is rdpaestea rmof ulmegntai -&t;-g maenulgit soeg ot arue ,eccyl utpveray oegs no to geienl.noou)secsg ecataLt cna sola eb dsue hsit( oldcu vhae eenb a ithrg rsnawe fi ti rewe )detlis.

)2( ddO nihac sAF rae sola gieugnlocc, but casitre adci ird(epdvo in the arwnse ccioe)h s’nti dod ain,ch so ti is nylo ikegnocet adn acn be edrlu o.ut

ghlAothu vnleia an(d htreo ecdnabhr .)aa. edfe noit pnlorooCA-iy,P yhet rae not dsue in oitanrsavt ecesaub aoairttvsn lsrtiyct eislre no hteacip gisonec.sgeuleon eehTs ..aa aer ont aeloembtidz in teh vrile esucabe hte eirlv csakl dcchbhreann-ai ..aa taeasernrfs nzeey.m nI rFsti diA, omeiBhc enst,ico eunrd tovniStnFatari,gs/a in hbot teh fanst“gi ”taset icw(hh is wnhtii hte iemt famre of hist o,sq)nteiu or het ntosiaav“rt ate,”ts bhot iltizeu htceipa incoseoulgens.eg yM ostmipnuas is ttah vlanie si edsu gdiunr urrlgea e,asomtbiml nad tno indugr sdprioe fo rst.votaian

hello  I want to re-emphasize something that @assoplasty has already stated :). The Q-stem states serum glucose = 100, and the Q asks why the patient is able to maintain normoglycemia. Therefore, you can immediately eliminate choices A and C because acetoacetate and beta-hydroxybutyrate are sources of energy during ketogenesis -- ketogenesis does not provide glucose energy sources. +7  
chandlerbas  ^ this checks out: valine and isoleucine are broken down in the muscle into branched chain 2 oxo acid via branched chain aminotransferase (reversible) then the valine and isoleucine leave the muscle and swims to the liver to be acted on by branched chain 2 oxo acid DH (irreversible). So bascially the process from taking BCAA valine and isoleucine requires 2 enzymes. the first enzyme is in the muscle, and the second enzyme is in the liver (for simplification purposes --> both organs contain both enzymes but dont have the same affinity for their substrate). source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1147506/?page=4 so you're right to say that the liver +5  
toxoplasmabartonella  Thank you for such a great explanation. Isn't it glutamate instead of glutamine that combines with pyruvate in muscle to yield alanine for Cahill cycle? +1  
almondbreeze  @ toxoplasmabartonella think you are right +  
revanthshanmukh  its given that methionine histidine and valine are glucogenic AA.nso why not these form the glucose in the body first compared to alanine? +  


submitted by hayayah(1076),
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sniyytneee-sCcite knheomice prrotece 5 C)C5R( is a rtoinep onduf no eht uacfrse fo 4CD s.ellc

yotsubato  Note, this is NOT in FA +2  
sbryant6  It is in UWorld. +3  
almondbreeze  it's in FA2019 pg.110 +1  
almondbreeze  but missing the full name for CCR5 +4  
demihesmisome  CXCR4 is also a chemokine receptor. +2  
sononono  Uworld ID 953 +  


submitted by hayayah(1076),
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Ci-eeysysecitetnn keiemonhc oprrctee 5 )C5R(C si a tpeionr nuodf on eht efuacsr fo 4DC le.lcs

yotsubato  Note, this is NOT in FA +2  
sbryant6  It is in UWorld. +3  
almondbreeze  it's in FA2019 pg.110 +1  
almondbreeze  but missing the full name for CCR5 +4  
demihesmisome  CXCR4 is also a chemokine receptor. +2  
sononono  Uworld ID 953 +  


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tieQsuon dsake rfo argm osiepvti occic ni CNH.IAS S. asueur sfmor t,clseusr inaiielgmtn .ti ihTs aevlse scooecucnrtE iesaafcl dna Gpuor A s.erpt E. aileacfs is soadsaicte ithw sT.IU

almondbreeze  get the clinicals but got thrown off by 'chain'. FA2019 pg.137 also says coccus = berry, strepto =twisted (chain), differentiating the two:( +2  


submitted by mcl(598),
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Paetnti yma aveh trraeyedhi m,aageidone icwhh si atsdisacoe tiwh trrureec"n cattaks of tn,einse vss,aiem eclzoalid bueounstuasc aedem nlinovvgi eth treeixm,esit lagiein,ta ac,ef ro ru,ktn or ouualbsmsc aeemd fo prepu iyaarw or sb"oe.lw Teh lcearti eogs no ot say r1-et"aesCse ontiibirh okwrs iecdtyrl no the tpnlmmecoe dna toacnct alpmsa cdsaseca to eeudcr nkibiynard reeslea" ihcwh is oals lyabporb ogod ot .nkwo

/t6cgPchhmci/lt//il3s.b1erMimvw.wn36nos/tp:a6w.8Cp/.n

notadoctor  Thought this was a trick question as C1 esterase deficiency also results in a decrease in C4. However, the second answer choice was not referring to C4 but to C4 binding protein, which I now know is different. I also didn't realize C1 esterase was technically a complement protein. +4  
youssefa  Based on many sources hereditary angioedema does NOT cause a rash (urticaria) which is a main differentiating point between angioedema and allergy. This mislead me in this question. Any clarification? +22  
ergogenic22  +1 on the above because uptodate states that c1 esterase inhibitor deficiency, both acquired and nonhereditary, are both non-urticarial, non-pruritic, and that is confirmed by the above linked article +2  
sahusema  Question writer probably didn't know the difference between cutaneous urticaria and subcutaneous edema. +3  
almondbreeze  same. got it wrong bc the pt didn't have sx of hereditary angioedema - swollen lips and eyelids +2  
teepot123  fa 19 pg 107 +  
beloved_bet  According to Amboss "Mast cell-mediated angioedema Often associated with urticaria and pruritus Other associated with clinical findings of allergic reactions (see type 1 hypersensitivity reaction) Presents within 30 minutes to 2 hours after exposure and resolves over hours to days" +1  


submitted by readit(14),
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hWy is is tno epsoud neysau?mr

rcA"iot mnesyodrpessuua atclpilyy cuorc sa a lutser of aramut /-+ ,ntinrntioeev a ideosecnrd ubstes fo armtatuic rtciao rjiuyn in hte roiymjat fo as.sce yhTe cna eb ceuta or "hccni.ro

sutporm=nt-aitaeyrua/psdsnpid/ee:cu/lsgiaror/l?oeiatgsaraoc.hd

readit  *same goes for saccular aneurysm, which also is usually 2/2 trauma +  
samsam3711  In the question stem there is no indication of trauma so it would be hard to just assume that +  
almondbreeze  see my comment above for marfan syndrome. might help +  
drzed  This is because a pseudoaneurysm is between the media and adventitia, and is incited by trauma; a dissection is between the intima and the media and is a result of hypertension causing an intimal tear. The history points toward cocaine -> hypertension rather than penetrating trauma. +  


submitted by neonem(570),
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jorMa sikr rfacot ofr iroatc snisocdeti is ,tyeninrhpeso dna ni stih ecas gtmih eb ued ot nieccoa s,ue hwihc usecas karemd hsipne.reoytn ciosintsesD ausec a tear ni the untiac maiitn -- doblo nca lwof cadrwkbsa tnoi eht iceirprduma dan cueas nedm.oapat ihTs etiafsnsm as ckcaelsr ni eht guln ued to roop tfle ieauvlnrctr fnocinut lnfidiilo(lscti/ga mlperbo due ot o.ricnoespm)s

forerofore  there is another clue, the man has diminished pulses in just one arm, which means that the left subclavian artery must be involved somehow, and an aortic dissection would be the best answer explaining this. +9  
temmy  please why is there where a diastolic mumur? +1  
whoissaad  @temmy Aortic dissection especially near the root of aorta can lead to dilatation of the aortic valves, which can lead to Aortic regurgitation (diastoic murmur at left sternal border) +8  
garibay92  Does anyone know why is this patient's tepmerature elevated? +1  
ratadecalle  @garibay92, not important for this question I think but cocaine can cause malignant hyperthermia +1  
almondbreeze  judging by his heart murmur, he probably has marfan syndrome. that's the only place where FA talks about dissecting aneurysm +  
almondbreeze  he's only 28 - another clue for marfan? +  
turtlepenlight  did anyone else think it was weird his only sx was SOB? I always think of radiating pain as being a good clue for dissection +2  
cmun777  @almondbreeze his heart murmur is at the LSB (aortic regurg) and not consistent with MVP plus no other sx/indication of Marfan. I think the only association of RF you should think about in this question is the cocaine use and consequent HTN. +1  
ibestalkinyo  @turtlepenlight I agree. I chose another answer because I was like, there's no way this guy doesn't hurt if he's got a dissection. +1  


submitted by neonem(570),
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Mrjoa krsi foract orf atrioc tosiceidns is tehrnnespoi,y and in hist acse mihgt eb ued ot eacoicn seu, wchih uaecss kdamre ese.nniophyrt csitsnioeDs euacs a reta in het nicuta inatim -- dlboo cna flwo dksbcawra niot eth pdirimeucra dna esuca tadapmon.e This fstsmiaen as kerlacsc ni the nlug ude ot poor elft lanerutirvc nnoiftuc oldgsaini/cllfi(it epobrlm ude ot poermo)snsic.

forerofore  there is another clue, the man has diminished pulses in just one arm, which means that the left subclavian artery must be involved somehow, and an aortic dissection would be the best answer explaining this. +9  
temmy  please why is there where a diastolic mumur? +1  
whoissaad  @temmy Aortic dissection especially near the root of aorta can lead to dilatation of the aortic valves, which can lead to Aortic regurgitation (diastoic murmur at left sternal border) +8  
garibay92  Does anyone know why is this patient's tepmerature elevated? +1  
ratadecalle  @garibay92, not important for this question I think but cocaine can cause malignant hyperthermia +1  
almondbreeze  judging by his heart murmur, he probably has marfan syndrome. that's the only place where FA talks about dissecting aneurysm +  
almondbreeze  he's only 28 - another clue for marfan? +  
turtlepenlight  did anyone else think it was weird his only sx was SOB? I always think of radiating pain as being a good clue for dissection +2  
cmun777  @almondbreeze his heart murmur is at the LSB (aortic regurg) and not consistent with MVP plus no other sx/indication of Marfan. I think the only association of RF you should think about in this question is the cocaine use and consequent HTN. +1  
ibestalkinyo  @turtlepenlight I agree. I chose another answer because I was like, there's no way this guy doesn't hurt if he's got a dissection. +1  


submitted by tissue creep(113),
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odtArrohp ofr ,reus tbu rfo teh oecrdr 'Im yrtept esur hsit swa Cnnuhyakugi irVu.s lOyn tgo siht orfm a drlWUo iuoesnqt as I ahnd't nees ti nulti eth,n but ytnraeappl eht iaarrlhtag is llryea ,dba ihwch si twha dewr em ot teh e.nasrw

:g/l/ihen/nygtht.hp/csdw.ucdacxmuwn.wikvto

meningitis  More like Zika Virus (Same a. aegypti vector) since it says she has rash associated to her bone and muscle pain. I had Zika one time (i live in Puerto Rico). Remember also dengue and Zika are Flavivirus. Dengue can cause hemolysis (hemorrhagic), and Zika is associated with Guillen Barre and fetal abnormalities. +12  
nala_ula  I'm shocked that I found a fellow puerto rican on this site! Good luck on your test! +2  
namira  dont be shocked! me too! exito! +2  
niboonsh  Dengue is also known as "bone break fever" which makes me think its more likely to be dengue due to the "excruciating pains in joints and muscles". https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4242787/ +21  
dr_jan_itor  I was thinking that its Murine typhus transmitted by fleas +  
monique  I would say this is more likely scenario of either Dengue or Chikungunya, not Zika virus. Excruciating pain is common in those, not in Zika. Zika has milder symptoms of those three infection. +2  
jakeperalta  Can confirm that Chikungunya's arthralgia is pretty horrible, from personal experience. +  
almondbreeze  UW: co-infection with chikungunya virus with dengue virus can occure bc Aedes mosquito is a vector of both Chiungunya, dengue, and zika +  
lovebug  FA2019, page 167 RNA virusesy. +  
lovebug  Found that Chikungunya also have Rash./// An erythematous macular or maculopapular rash usually appears in the first 2–3 days of the illness and subsides within 7–10 days. It can be patchy or diffuse on the face, trunk and limbs. It is typically asymptomatic but may be pruritic (Taubitz W, Cramer JP, Kapaun A, et al. Chikungunya fever in travelers: clinical presentation and course. Clin Infect Dis. 2007; 45: e1. ) +1  
beto  it is chikungunya->fever, polyarthralgia, diffuse macular rash, dengue has retro-orbital pain mostly +1  


submitted by fatboyslim(40),
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m(Fro UW 1518)2 eSom dmaoscnteii cdgnniuli iodispo, atrcorsndoita s,dye dan meos tiaoisbintc e(..g ma)ycinnvco acn cdineu nda DEEDT-NgPENNEII tams clle ngaoreutdnila by tnacaoitiv of ntipero ikesna A adn 3IP asniek, wichh tulsrse in learese of iai,tshnem riyadnb,nik adn etroh ccottamihce asocrtf g&;-t iesfudf iitgc,nh nai,p sbpanrs,ohcmo dna zolcedlia ilwsen=leg artac.r(ui)i

almondbreeze  just to add : more agents causing such reaction - beta-lactams, sulfonamide, aminoglycoside +  
drzed  Are those IgE dependent, or just allergic reactions (asking because the sketchy for beta-lactam penicillins mention acute interstitial nephritis as an allergic reaction)? +  


submitted by hayayah(1076),
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vsiySntiite sstte era dsue rfo cegrs.inne cicfeySipit sttse era udes orf fnoicomrinat retaf stvieoip nisng.serce

eyttiinviSs tstes ear eusd orf egiens how myna pelepo ryult ahve eth eaesisd. iccSipftiye setts aer rfo hoets hwo do nto aehv the essia.ed

A lgyhih envtissei tse,t ehwn te,vnagie ursle OTU s.idesea A hyhlig eicpscif ett,s hnwe eviopist, suelr IN ae.desis oS, a sett wthi ithw wol sitsvetiyni ctnano rlue tuo a ae.dsesi A etst ithw owl icpftieycsi cant' lreu in issea.de

eTh rcotod dan pnatiet watn to snrece ofr nlcoo ccrnae dan erlu ti .uto hTe ocotdr wdlou ntwa a sett wtih ighh yvtsnteiisi ot eb bela to od htta. eH nkwso thta igsntet reh lotos orf olobd wlil otn ulre out eth sitosbiiply fo loonc C.A

sympathetikey  SeN Out (Snout) --> sensitive test; - test rules out SPec In (Specin) --> specific test; + test rules in +23  
usmlecrasher  can anyone pls explain why it is not << potential false- positive results >> ??? +  
almondbreeze  correct me if I'm wrong, but 'high FP (choice C)=low specificity (choice B)'. Whereas high specificity is required to rule in dz +2  
almondbreeze  picked positive predictive value myself. can anyone explain why not PPV? +  
williamfreakingosler  The principle @hayayah is talking about (a negative test being relied upon to reliably rule out) is negative predictive value ("NPV"). I don't see why "uncertain NPV" isn't the correct answer, particularly because NPV is predicated on the disease having the same base rate in the person(s) being tested as in the population that was characterized for the test statistic. Given that the patient has a strong family history of colon cancer, the NPV of FOBT is uncertain. Said another way, the sensitivity of a test does not change with the population, but the NPV does. The whole reason the doctor is denying FOBT is because of bayesian thinking (a priori information related to family history), and from my point of view bayesian logic is more relevant to PPV/NPV than to sensitivity, hence my confusion over why NPV isn't the right answer. +2  
ibestalkinyo  I thought negative predictive value for the same reasoning +  
raga7  AFTER THE RESULT OF TEST WE CAN USED PPV OR PPN, BUT FOR TEH FIRST TIME LOOKING ANY DESEASE USE SENSITIVITY OR SPECIFICITY. +  


submitted by hayayah(1076),
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eiiitstnSyv sttes ear ueds rfo .engicresn eiipiScfyct ttess are usde rfo cioarmtnfnoi faret ptoeviis c.neissgenr

ntytsivSiei tsset ear edus ofr iesneg who namy epeopl ytulr heav hte sdaesie. Scitfiipecy tetss rae rfo toshe owh do otn ahev eht sea.eisd

A ighhly vsseineti s,tte hnew gieaevn,t eurls OTU ise.desa A lhghyi ccepsfii tte,s enwh ovtip,sie lseru IN a.sieesd ,oS a tets tiwh with low tiivnytises aconnt uelr tou a ea.sdies A sett iwht olw tyceiicsfip tcan' relu in .ieessda

The rtcood adn eiatptn twan to ceesrn fro onolc nracce nda eurl it uto. eTh toorcd wuold twna a tset twhi hhgi yensstivtii ot be leba ot od hat.t eH snwko hatt tsgtien hre toosl for olodb ilwl ton reul otu het bpiystoliis fo onolc .CA

sympathetikey  SeN Out (Snout) --> sensitive test; - test rules out SPec In (Specin) --> specific test; + test rules in +23  
usmlecrasher  can anyone pls explain why it is not << potential false- positive results >> ??? +  
almondbreeze  correct me if I'm wrong, but 'high FP (choice C)=low specificity (choice B)'. Whereas high specificity is required to rule in dz +2  
almondbreeze  picked positive predictive value myself. can anyone explain why not PPV? +  
williamfreakingosler  The principle @hayayah is talking about (a negative test being relied upon to reliably rule out) is negative predictive value ("NPV"). I don't see why "uncertain NPV" isn't the correct answer, particularly because NPV is predicated on the disease having the same base rate in the person(s) being tested as in the population that was characterized for the test statistic. Given that the patient has a strong family history of colon cancer, the NPV of FOBT is uncertain. Said another way, the sensitivity of a test does not change with the population, but the NPV does. The whole reason the doctor is denying FOBT is because of bayesian thinking (a priori information related to family history), and from my point of view bayesian logic is more relevant to PPV/NPV than to sensitivity, hence my confusion over why NPV isn't the right answer. +2  
ibestalkinyo  I thought negative predictive value for the same reasoning +  
raga7  AFTER THE RESULT OF TEST WE CAN USED PPV OR PPN, BUT FOR TEH FIRST TIME LOOKING ANY DESEASE USE SENSITIVITY OR SPECIFICITY. +  


submitted by laminin(15),
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eynTelisaccrt hvea a hghi fyiftian to omfr selcahte thwi aneptylolv cllieamt notcisa hscu as e+,F++ F,e++ +l+,A+ +Mg+ nad a+C+. nMay of eehst mtnleteey-tiacracl lmpcoxsee are hetrie lulsiebon or retisewho orpoly boaselrabb mfro eth tnnostaasrgte-lii at.trc kiMl dan eroth rdiya td,urocsp ncaitsad nnitoacnig ylonvptale aciso,nt sa ewll sa sauvoir onri talss deeigsnt ayulusiestnmol thwi cytntlceraie ia,divserevt mhgit rrntefiee htwi itrhe tasrnobiop by 50 ot 9%0 or veen re.mo eouc: sr ib.nmml6i8uvw9wsh/:b.o5ptn./n4d/wc.e9t/phg

almondbreeze  FA 2019 pg. 192: Do not take tetracyclines with milk (Ca2+), antacids (eg. Ca2+ or Mg2+), or iron-containing preparations b/c divalent cations inhibit drugs' absorption in the gut +1  
fatboyslim  This is also why tetracyclines are teratogenic and should not be given to children because tetracyclines chelate with the calcium in the teeth and cause tooth discoloration and inhibit bone growth in the fetus/growing child (Source: SketchyPharm) +  
kevin  just remember fluoroquinolones also are prone to chelation. you know it's gonna pop up on the real one +  


submitted by hayayah(1076),
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iAiomnrtisndta of cilienliPn rof ispSylih aym adel ot het -rriaHehimxehecrJs ioencrta huors ratfe rmtatntee. ucrscO eud to yssli fo sthceropise (os ti nca orucc thwi rBiaorel nda siLrtpopseosi sa l.)elw ehT eiortanc is hactczreaedir by erevf nad lsilh.c

heT cllsaisac ontaixepaln of het erxreehimH eotiarcn is ttah tnetmaret slustre in het udnsde dathe dan trsteinodcu fo lrgae renbums fo toeesm,penr hwit eht trbeiliona of ipoetnr usdtporc adn sixont.

almondbreeze  FA pg.148 +5  


submitted by hayayah(1076),
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aeptiCta dna eutaln ear ni the entecr fo hte .mlpa tCaietpa si nto an toip,on os utnela is teh nw.saer

Dcsliainoto fo etlanu aym sueca eacut plueratanln c edsmnroy.

yotsubato  Lunate is the only carpal bone that is frequently dislocated. Scaphoid is frequently fractured. Hook of hamate is also frequently fractured. +3  
redvelvet  and also point tenderness in the anatomical snuffbox may indicate a scaphoid fracture. +3  
chandlerbas  yes lunate is the most common dislunated carpal bone ;) +4  
almondbreeze  FA 2019 pg. 439 : dislocation of lunate may cause acute carpal tunnel syndrome +  


submitted by monoloco(136),
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hTsi si hte olyn cehoci ttah escmo eclos ot kgiicnn teh athciocr ud,tc pliflcyaiesc at sti ine,tl eht tfle asvnlb.uaic

kpjk  why not midsternal thoracotomy? +3  
wuagbe  because the thoracic duct ascends the thorax posteriorly, and enters venous circulation from behind. link to image: https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/thoracic-duct +5  


submitted by johnthurtjr(144),
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hieWl I nac etg on odabr hwti Amtsdujten rrsdi,eoD I dnot' ees who hist nawrse si ayn ebettr tnah aocitSm ympmoSt id.oerrDs Fmro FA:

ytrVaei of iodylb mcptsaloin agsnlti ntshmo to erasy casotiades htiw se,vxseeic sniepttser htuhsgot dan enatiyx touab yssomptm. yMa aaocrpep- iwht lnssil.e

DSS gensblo in a ugpro of reodrdssi ardcietehacrz by shyalicp tyopmsms isancgu asignfcniti sesdsitr dna itnmam.eirp

savdaddy  I think part of it stems from the fact that this patients symptoms are occurring within the time-frame for adjustment disorder while SSD seems to have a longer timeline. Aside from that I find it difficult to see why SSD wasn't a possible answer. +4  
chillqd  To add to that, I inferred that the obsession with checking temp and with the tingling sensation were signs provided to him by the physicians of recurrence. He is anxious over his cancer recurring, and they are more specific than a variety of body complaints +1  
hello  In somatic symptom disorder, the motivation is unconscious. I think for the patient in this Q-stem, his motivation is conscious -- he wants to make sure that recurrence of cancer is not going "undetected". +14  
cienfuegos  I also had issues differentiating these two and ultimately went with SSD, but upon further review it seems that a key differentiating feature was the timeline. His somatic symptoms would have had to have been present for at least 6 months per the DSM criteria https://www.ncbi.nlm.nih.gov/books/NBK519704/table/ch3.t31/ +3  
almondbreeze  @chillqd Same! Why not OCD? He's fearful that something bad might happen (=cancer relapse; obsession) and calling his doc (=compulsion) +  
kevin  great reasoning @hello, this was confusing me but that makes perfect sense +  


submitted by sympathetikey(1354),
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cioChe .A ldwuo ahev eenb rtcocre if sith tntpiea asw dmm.nmeoisirpcomuo erP riFts A,id If" DC4 1&0lt0,; adie.s.nl.gotraBFlin:n Nrthpeiolcui .Ifnmmoatalni

Heoewr,v as shit niptaet sah a tpoenmcte nemmiu m,etyss ubzz dosrw era aseltlte ztecinngroi aomsagrunl.

yotsubato  Everyones choice A is different. +  
sugaplum  they mean- Diffuse neutrophil infiltration +1  
macrohphage95  what does stellate necrotizng granuloma means ? +1  
krisgsxr600  always with the details! losing dumb points :( +1  
futuredoc12345  @sympathetikey Doesn't the biopsy finding vary with the biopsy location: Lymph nodes have stellate granulomas and Bacillary Angiomatosis (skin lesion) has neutrophilic inflammation. What do you think? +  
chextra  @sympathetikey Pathoma chapter 2 says cat scratch disease forms non-caseating granulomas +1  
almondbreeze  @ chextra Same with FA 2019 pg. 218 +2  
almondbreeze  Sketchy micro: Immunocompetent: regional LN in axilla in one arm (like our pt here) Immunocompromised: bacillary angiomatsis is transmitted by cat scratches +  


submitted by sympathetikey(1354),
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iCcohe A. olwud veha been crtoecr if this atinept swa .onsmmroiempcumdio rPe tsrFi Ad,i "fI DC4 00;l,1t& BFlnrn..ota:lgdnias.ei lrtiecNpouhi toiaf.lIanmmn

rovw,Hee as hist ntetpia sah a oeecnptmt eumnim seystm, bzzu osdrw aer stlteeal cgzotennrii gausralnom.

yotsubato  Everyones choice A is different. +  
sugaplum  they mean- Diffuse neutrophil infiltration +1  
macrohphage95  what does stellate necrotizng granuloma means ? +1  
krisgsxr600  always with the details! losing dumb points :( +1  
futuredoc12345  @sympathetikey Doesn't the biopsy finding vary with the biopsy location: Lymph nodes have stellate granulomas and Bacillary Angiomatosis (skin lesion) has neutrophilic inflammation. What do you think? +  
chextra  @sympathetikey Pathoma chapter 2 says cat scratch disease forms non-caseating granulomas +1  
almondbreeze  @ chextra Same with FA 2019 pg. 218 +2  
almondbreeze  Sketchy micro: Immunocompetent: regional LN in axilla in one arm (like our pt here) Immunocompromised: bacillary angiomatsis is transmitted by cat scratches +  


submitted by sugaplum(373),
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B Hes-eeln taC ctSarhc in emoumtmnoctniop- - mtsctn:cmycahwltsmh.lsetwpt/rcih.aytoodhocoa/hwtolpi/ntpolgpue./lanero Ba tl senlhaee ni duemImo-pmmoio-csnr rlcBaaiiy aiaottmsngosi oLoks elki oksipa oraacms ef"fus Di pniurihotlec "attilfrnei F A 2190 717

almondbreeze  FA 177 says Kaposi has lymphocytic inflammation whereas Bartonella spp has neutrophilic inflammation. I guess this does not apply when immunocompromised? But doesn't Bartonella usually affect the immunocompromised ppl? +  
almondbreeze  Got it after seeing that she's immunocompetent +  


submitted by sugaplum(373),
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B eeenlHs- aCt tcachSr in meoonn-toimmptcu - cg.scptwpnhlpymhim//ieaosoah/.chttlpo.lreonysw:towttautctlo/cdmhaerltnBl o a naelsehe in m--umomoisdpcroIenm aiariyBlc osaaitigtnoms oo Lsk ikle paksoi aamcsor sif"efD u hiuoceintlpr ttnalfe"iri AF 9012 771

almondbreeze  FA 177 says Kaposi has lymphocytic inflammation whereas Bartonella spp has neutrophilic inflammation. I guess this does not apply when immunocompromised? But doesn't Bartonella usually affect the immunocompromised ppl? +  
almondbreeze  Got it after seeing that she's immunocompetent +  


submitted by xxabi(258),
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sra’ocB sipaaah: ressivpexe o(ortm hai)apas hwti smmitaamgar ps(t wraea tath yhet odtn’ meak sene)s - raea Wc’iskA eern hapa:ias ceiprteve (o)ysrsen aaaisph tiwh rdaeimip nrniceoopshme sp(t lakc hn)sgtii

breis  Why would B be incorrect? I realize Broca is "technically lower" but A seems too low to be causing weakness of the lower 2/3 of the face? Am I missing something? +  
shaeking  @breis B is incorrect because of the lower 2/3 of the face weakness. B isn't located on the motor cortex but in the premotor cortex, plus it isn't low enough for the lower two thirds of the face. https://thebrain.mcgill.ca/flash/a/a_06/a_06_cr/a_06_cr_mou/a_06_cr_mou.html https://www.sciencenews.org/blog/science-ticker/homunculus-reimagined +1  
cienfuegos  @breis, per UW: "a/w r. hemiparesis (face & UE) bc close to primary motor cortex" +  
almondbreeze  B is close to premotor cortex which is involved in learned or patterned skills & in planning movements. (i.e. two-hand coordination) slide 25/37 :https://www.slideserve.com/hal/the-motor-system-and-its-disorders +  
almondbreeze  B is also close to frontal eye field; eyes look toward the lesion FA pg. 499 +  
frijoles  I incorrectly picked C. When answering this, Broca's "broken speech" was my first thought, but I figured a lesion causing a facial droop would have to involve the motor strip so I prioritized that and chalked up the speech issue to dysarthria (I understand this is more of a "slurred speech" than broken, abrupt speech, but again, I simply misprioritized concepts.). So for the record, Broca area is part of the motor cortex? +1  


submitted by xxabi(258),
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oa’rBsc spai:aah reisespvex om(otr aia)hasp wtih amtmaarsmig st(p reaaw taht yhte nd’to keam ene)ss - reaa W’eiAc eknrs spahaa:i tciepevre )sres(oyn pisaaah whti ipraedmi prchoensmnioe ts(p alkc i)sihgtn

breis  Why would B be incorrect? I realize Broca is "technically lower" but A seems too low to be causing weakness of the lower 2/3 of the face? Am I missing something? +  
shaeking  @breis B is incorrect because of the lower 2/3 of the face weakness. B isn't located on the motor cortex but in the premotor cortex, plus it isn't low enough for the lower two thirds of the face. https://thebrain.mcgill.ca/flash/a/a_06/a_06_cr/a_06_cr_mou/a_06_cr_mou.html https://www.sciencenews.org/blog/science-ticker/homunculus-reimagined +1  
cienfuegos  @breis, per UW: "a/w r. hemiparesis (face & UE) bc close to primary motor cortex" +  
almondbreeze  B is close to premotor cortex which is involved in learned or patterned skills & in planning movements. (i.e. two-hand coordination) slide 25/37 :https://www.slideserve.com/hal/the-motor-system-and-its-disorders +  
almondbreeze  B is also close to frontal eye field; eyes look toward the lesion FA pg. 499 +  
frijoles  I incorrectly picked C. When answering this, Broca's "broken speech" was my first thought, but I figured a lesion causing a facial droop would have to involve the motor strip so I prioritized that and chalked up the speech issue to dysarthria (I understand this is more of a "slurred speech" than broken, abrupt speech, but again, I simply misprioritized concepts.). So for the record, Broca area is part of the motor cortex? +1