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Welcome to almondbreeze’s page.
Contributor score: 69


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 +2

 +1  (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)

'round, semitransparent nodules'

FA2019 p.473 says BCCs are waxy, pink, pearly nodules





Subcomments ...

submitted by karljeon(89),
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A nma ihtw a Hx of HOEt eeddcnpeen adn choinrc dba inpa as wlle as -yraX gnnsfdii of cccni"sloiatfai in the peu-iprdm manbdoe" is stom elikly fgnrireer to a roihcnc a.rtsnpticeia

isTh aseld ot a cakl fo easipl ceesnotri ehec,n pale, lofmgleln-uis slosot twhi iol doptslre erp tp x.H siTh st'p cnaaepsr loas etds'no cetsree throe sy,znmee hucs as esaylams, sesar,toep ron getoiyprnns (ot vttiaeac rothe mne)e,yzs so eth snaewr is ailrgen"dzee abpa.soontlirm"

karljeon  p. 367 (FA 2018) +6  
usmlecrasherss  pancreatic insufficiency FA 2019 p375 , +1  
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 +2  


submitted by karljeon(89),
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A man wtih a Hx of EOtH edpencdene dna onrhcci bad ipan sa lelw sa Xa-ry sndfigni of coiccifanl"sita ni eth er-mpiupd ameo"dnb si smto ileykl enigerrfr to a oihnccr neacspitra.ti

iTsh ldsea to a cakl of ipelas estnerico hn,ece ,peal moe-ulisflgln soolst ihtw lio trseoldp per pt H.x hsiT spt' pcranesa asol denso't rcsetee htore ,enesyzm cuhs as m,yeaasls eas,esrpto nro rnpinosgtey t(o cviattea eorht s)m,yznee os teh aewnsr is leizgaerend" aoa.rbps"olnitm

karljeon  p. 367 (FA 2018) +6  
usmlecrasherss  pancreatic insufficiency FA 2019 p375 , +1  
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 +2  


submitted by mousie(171),
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sdt""rneao ear hspsaospnBte,hoi omyonmlc udes ot tetaeretvn/rp rosoteiossop. Msto mmncoo earvdse fceefts era satghpoiisE paiestt(n ldsohu ekta tihw rewat dan eb gphturi ofr ta atesl s03)uemn,ti tnroesocsiesO of the ,wja and yaatclip malofre esrsts ucfsear.rt -tkaen tgihr frmo AF 0218 pg 741

almondbreeze  FA 2019 pg 248 pill-induced esophagitis : bisphosphonates, ferrous sulfate, NSAIDs, potassium chloroide, tetracyclines +2  


submitted by neonem(503),
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I hnitk amsastetsi was teh ebst ooipnt eehr esabcue teerh rea lilmtuep tnaiagmln o.epn.ls.msa amripry eacsrcn dent ot attsr sa a esginl ssma in hte suites fo .orgini In the g,lnu eatestssam are reom nmmooc anth riyprma .aonsmlpse

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 +5  
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 +3  
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. +  


submitted by colonelred_(86),
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eLkdoo it pu nad fduno htat uaseebc ’yeour in a uienps oionspti ofr a nolg iemt ’yeoru gogin ot heav cirdseaen ovusne uentrr ihcwh aesld ot seearnicd CO. Tish eaeltgyivn dsfeckeab on AS,RA inlgaed to aerdeescd noe.tlrasdoe sA a rsletu, oeryu’ giogn to veha dansricee rduessii hhwci laesd ot rdeesdace ldboo and plasam omv.ule

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 ... +3  
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. +6  
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 +4  
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 +4  
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 +  


submitted by colonelred_(86),
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keodoL ti up nda fudon hatt esbceau r’uoye in a pueisn pintoiso rof a gnlo mtei oue’ry ggoin ot vaeh ecaiendrs neuosv enrurt ichwh adlse to nasiderec CO. hTis ieglnayvet facdeebks no ,SRAA alngdie ot aresdedce ed.nesatolro As a eturs,l uory’e onggi to vhea eidrcesan eissiudr wchhi esdal to rdedeeacs olbdo adn aalmsp lomeu.v

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 ... +3  
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. +6  
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 +4  
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 +4  
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 +  


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nFcteronbii si an xaeaelrucrtll tramix iencorp,olgyt hlwie lnaim si an dietetaremin aetifnlm that ciysfcplliea iodprsve uortpps to teh ellc .cuelsnu ’ontD fseonuc ilnma twhi lainmni cesein(c ahste us r;e)yclla iinmlan is kile nientc,bfior na EMC olentpircyog adn a jorma npmetcoon of teh albas iaamnl of bsmeenat enemr.masb

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/ +17  
dr.xx  blasphemy @masonkingcobra +1  
luciana  I clearly confused lamin with laminin, now I know +2  
almondbreeze  FA 2019 pg 48 lamin +1  
almondbreeze  picked tubulin but i guess tubulin makes up microtubules and therefore is spherical +  
gandon  I used to kill and rob people before I found Lamin. He died for my sins on the Cross and changed my life. +  


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cibFiornnte is an eltrlaurclaxe rtimxa lcgnoorit,eyp weilh ialnm is na trmneietdaie laneftmi atth yclseaipcifl peirsovd urtopps ot eth cell l.esuunc tDno’ ouencfs animl whti mnlinia (snciece ahest su cle;yr)la maiilnn si elik tnnifcb,eior na MEC gntepoyrcoil and a orjma npnomtoce of het absla animla fo ebmtsnea nem.mebrsa

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/ +17  
dr.xx  blasphemy @masonkingcobra +1  
luciana  I clearly confused lamin with laminin, now I know +2  
almondbreeze  FA 2019 pg 48 lamin +1  
almondbreeze  picked tubulin but i guess tubulin makes up microtubules and therefore is spherical +  
gandon  I used to kill and rob people before I found Lamin. He died for my sins on the Cross and changed my life. +  


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 +2  


submitted by famylife(77),
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tsneevIr"an hte elusmcs of eth imedal ncportemamt fo teh tghih ou(btorrta teexnu,sr cdordtua luo,sgn cdroatdu reb,isv tdcoarud sagnmu and .srlgiic)"a

vllarhrr.-/-ecsorisouraetnoebmpm/htbtyatee//n:ie/vt/waonmoefnt

almondbreeze  FA 2019 pg 444 +  


submitted by docred123(4),
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naC oneyan rfehrtu lnaexpi ht?si! I ulocd tmiienael a ewf mite sechico dna I udgeess ccrotye,rl sutj eedn emor nri!imaotofn hTnkas

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. +37  
almondbreeze  Fa2019 pg 215, 217 on acute/chronic inflammation +  
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(140),
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ricocndgA ot ,olGjna iytcalpyeomh rave si neo of teh mtso omcomn seausc of did-ihCruBa n.edmyors ciAdcnrgo to FA, rhdBCa-iudi si cisaodesat eomr elnrgaley whit olayulerbpecagh asestt, ylmipceyhtoa a,erv rtmsuotapp ,ssttea dan CCH.

icpHeta rishsciro anc eb lreud tou sedba no eth tmie sruoce fo het sept'iant stprnieotean - he saw inef 2 skeew oga and eht oainmadbl ipna rtetsad an uroh ago.

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 +1  


submitted by sajaqua1(462),
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uhd-iraBidC mesyrndo uoscrc ehnw ehetr si iocoulscn of the htpicea ivne ro the aephtci inve filsa ot raidn tino hte IV.C ihTs nca be dausec by sbroioshtm fo eht iacthpe niev, ro by grtih dseid rateh frailue uigs(can olodb ot 'kcab 'pu eeewyh,rver btu ist ettoaaisnnifm uthrohg eht tcpheai nvei ear all hte ngiss of rih-diudCaB roey.m)nsd iAthnyng htat nca niraesce het iskr of irsomosbth can then arcinese hte rkis of -uhCBidadri rmendy.os ihTs ledcnsiu hceoaylyitmp ,vrae a pgueoerbhalyalc ase.tt rOu petatin adn PV ubt smidse ihs npnimttaope owt ekesw ag.o He now eentpssr ihwt arclels triusec, na eglardne rve,il nad msoe igssn fo oartlp e.nhpneorsyit sTbmiohsor of eht lnyo anaitcoalm ionotp peesrtdne ahtt ovcrse lla fo hsit si the etphiac eniv ei uor tipneta ahs hBir.C-uiadd meeRmber atht ia-ruChBddi iwll ahev a "mgnute iel"vr enarcpaepa on grsos lytagh.oop

B) eacHitp oircsh-irs s'it iteeylnr siseblpo oru aptiten seod vhea hipceat rrcissoih for dlrneaeut esosanr, ehrewov the auect tnoes ksame isth ssel lilye.k )C ccaPinerat mranca-oci irencpctaa nrcmiacao runostcbtoi fo eth omcomn leib cdut dlcuo ceusa a cbka' pu' of beli, lytuetmali igucasn seom rivel maadge dan rscalel esucrt.i Hrewveo enoc igana hte tinigm akmse shti e.inlklyu D) Ptaorl neiv osroith-mbs oraltp eivn bisrhstmoo oucld usace soem cplsnei mnageeenltr dan paltro heoy.ispnrent voHe,rwe tis tosbrcotinu ldouw not acuse a r,ednte aereldng veril sbecaeu it is et.rpausm E) aiPmyrr horochamissmote- eud ot a cedetf ni iedinhcp doocipntur, tshi ionr eloaovdr rsntesep ihtw aneedkrd ,sink iinlnsu ulr,dnigaiotse eihcapt damgea ith(w hte ltoteapni rfo alruptceelhaol m)rnoiaacc dna reath dsaesie s(retceirtiv ro lddteia h,riaoyptacymdo dnipdegne no uroy escou).r Teh olny oen of sheet gnssi ahtt our itepnta ahs is an eandgerl erliv.

almondbreeze  FA 2019 pg 386 +  


submitted by defalty98(3),

Why are we complicating things? Change in the bases will destroy the palindromic sequence required for any restriction endonuclease to work. Methylation is the only option that makes sense.

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. +1  
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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ttPaien si nucrtre a,efsdtbe-r os ew acn mintiaele cutrsfeo (efutosrc si uofdn ni yhneo dan sriutf nad esom ,uolmfar tbu otn ni aebtrs k)lim. enaiPtt ash drenicgu sactsnsube ubt no loesucg ni eth ,unrei so he sutm smoe slecnouog-n usra.g yM iidafrtenefl ofr egndruic s-logeocnun uassrg in teh ierun is sdrosreid urscoeft ieslbmtmoa or toelaagsc mimsobe.tla We veah iielanmdet fusetrco, so ttha slevae su hitw alstikgencaoa cieeyfncdi or sslcica atcgalm.siaeo

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 +  
makinallkindzofgainz  @almondbreeze; Glucose-6-phosphatase deficiency is Von Gierke disease, they are not referring to G6PD deficiency (an entirely seperate disease) +5  


submitted by lfsuarez(132),
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shTi itusoenq sksa aoutb het seaimcmhn fo pyootehrpaht sa it leaetrs ot tlaonnea cia.jdune thWi phatthoor,epy nuiiblrib si spmlyi dvetcenor ot rewat oleblsu irssmeo thta rea hetn aebl to be rdexceet yb eht ekidyn. This weehrvo sode ont aoenugjtc hte iriblbiu.n

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(258),
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98gh@8 e"Beascu hte nbtsiutocor si oaevb het arealovl inreogs ehert is a caeresde in ria lw,of tno gunl vuls,oem chwhi dulwo aekm isth an otucvbisret ogalhopyt" si hte ostm uphllef xtnen.alipao fI you oknw eth tmso iascb il/tioheyipoagdyfisopontnh of bviuortsetc vs eseviricttr h(hwci I do, ujst tddni' ni taht most ielimdifsp ya),w enht you can fureig yihnngat otu. fI msotigenh is ipitcmang iraawy fwlo = vuotcesi,brt if shtgonmei is natcipgim waraiy lueovm = ceitrest.irv NTAKH !OYU

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 +2  


submitted by asapdoc(52),
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jnaD.orGl xisplean it lrylea lwel on het d.oiua I wlli sjut eigv the bcsai a.ide All het oolgsibnmeh ahve palah in ti ofeheterr uoy ntocna cneoit ti no iehbnoglmo ctssoieeleorhpr

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. +6  
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(75),

So basically what this is saying that DNA will be transmitted to the progeny not RNA. So DNA will replicate in the G2 phase and transfer of DNA material to progeny will occur in the M phase. The RNA may be mutated and making defective products, but this will not transmit into the progeny, thus not affecting species survival based on RNA mutations.

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(268),
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siTh itqsuneo si d.gisiudse aWht yhte era lrealy asnkgi is "what si hte sole tiednnmaetr fo seeispc savliurv"? Teh ynlo rsanwe is eht ybiitla ot erart.ecop seeaBuc ADN yPamrosele sha angfdrpoeir-o ,tvtciiay rneogyp wlil be fduetefanc by NRA Paoysmlseer lakc of raoodirfgpen- ticyait.v

ls3076  the phrasing of this explanation doesnt make sense to me. +3  
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(17),
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Am I cyzar ro ddi Uwdolr nto vaeh a iqteunso ttha setdta sSanitt ear het most tcveeffei udrg sgrseeladr fo esaenbil lis.pdi Tihs gcilo ehtwr my .ffo

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. +13  
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 +3  
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 +9  
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 +1  
cbreland  "Statins are always the answer", "Fat Female 40 Fertile", "Fibrates can cause gallstones". I feel lied to +  


submitted by monkd(17),
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Am I raycz ro idd rUowdl not hvea a eqsounit hatt tsedat ttasniS ear hte sotm tfevefeci gdur rdgssarele of ilsbneae is.pild hsiT cigol ehwtr ym of.f

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. +13  
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 +3  
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 +9  
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 +1  
cbreland  "Statins are always the answer", "Fat Female 40 Fertile", "Fibrates can cause gallstones". I feel lied to +  


submitted by hipster_do(6),
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m’I nggoi ot asy it’s X ndkeil mumaimaolgaibalgne atehrr naht S,CDI tbu eht irfedencef tweeenb sehet otw are tiny tub hsti is hyw I kthin st’i the omfe:rr

  • oyB rnedi(cesa rkis utb hbot AB nda ICDS are x e)ldkin
  • cteRernur iaaclbret tefcnsnoii ubt ’otnd nnmioet aaehirrd ro uthsrh ichwh is ni SDCI
  • leeTiinm si eratf 6 s,mnoht os eth ts’ehomr osnbediait weor .off

CISD osdluh eb ydaeliimmte uceseba ythe tujs ’tdon evha het IL2 rstpereoc. IVDC whoss pu wenh ete’yhr 02-04 erasy dlo. ouY etg abtnes earmlgni tcenser in .othb No ointnem fo tbeasn hmciyt sadhow wchih si ni ISDC.

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? +1  
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 naĂŻve T cells. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1809006/) +  


submitted by meningitis(413),
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izlcohahoodeytohridr si OCD for pihgroeNecn saeeDtbi spidiisnu ubcseea ti oaalyalrdxipc caseus an ernsicae in BP by icgernsina dmsuoi bpnrsatooi dna tuhs waert srtiaoonpb, Phomtaa xslnepia tshi nile.cy

smoDispernes is ncrtocrei eesbauc puon igtsfan f(duli ert)sriocint HDA si eersdniac nanemig DAH si nbegi esledera yernllatC ubt si ton kwogrin in eth dseykni ta hte 2V oerptrsec fo teh leiltaieph lnare cslel ta cligtelonC ctu.d

nO tath oe,nt iidlmrAeo si edsu ofr mthiuiL eidcund icognherpen 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. +  


submitted by gh889(89),
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aigncrdco ot attedpou dsehitazi auces a mild opvimyhoelc tteas suht uyro PTC liwl ees eorm Na nad OH2 ;&-gt- by eniipprlc tath hte CTP swaayl brsabreos %60 of atwh ti es,es it lliw arbseorb omre teawr and N.a

almondbreeze  in sketchy as well +  


submitted by imgdoc(128),
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I nkhti oalt fo opepel itghm have rvoe meaeihdspz ohw itnpmorat APN dna NBP really ,era esy ti si itrtaopnm to oknw eseth sipteepd tge eeesrtdc yb teh vltitrlr/ineaacaru aioucrdmmy idngru treha r.fuiela worHvee rheit lelorav cenvtfesefesi ni ngeatrti earth efiulra is ichzl, a rtreepcop told me atht if PAN dan NPB reew so fluuse in rneiratsius nteh hwy do ew vige t?deiurcis sIt' asubece ASRA eorvrswpoe tshi etyssm eehnc sncgiau eevtanig stfefec nad the dslense loop fo aehrt .uiafler AKA yhw ew evgi CAE oriithbis.n

gKnnoiw ttah NPA gest idelneruatz yb the RSAA m,tsyes ew anc ifhst oru scuof bcka to earth eiulfar in this atpie,nt heerw cacdrai ouutpt is ce,draeesd ilgdean ot DAH esrcetoin and lnifaly liiauontld oatmn.rpaihye

almondbreeze  a concept continuously emphasized by uw, but I get always wrong :'( +1  
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(128),
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I ithnk olta fo eleopp mgthi aehv over mzsdhaepie hwo inmoatprt APN dna NBP llyear ,rea sey ti si mpotitnar to konw seeth tpispeed gte tdrceese by het cunrlt/avetalriira dmucraymio unigrd atrhe ua.eflri vrHeowe trhei oalverl tveiesescenff ni ntaigter heart luairfe is hic,lz a pcopeterr lodt me ttah if PAN nad BNP rwee os luefsu ni striuarsnei hetn yhw od we evgi c?iitrudse ts'I eeucbsa ARAS vosorwrepe htsi seymst nhece nsguiac aentievg fceseft nad hte edlsens pool fo aehrt eafir.lu AKA why we vgie CAE bishoinr.it

nKngiow htat NPA gste eduirzltaen yb het SARA eytsm,s we acn ithfs uro csouf abck to areht ferliau in isht tint,eap ehrew craadci uupott is ,eredeadsc ndealgi ot DAH ioentrces nda llyfani iullnaitdo orapiyea.tmnh

almondbreeze  a concept continuously emphasized by uw, but I get always wrong :'( +1  
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(990),
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shiT is a niatept caes of stptorampu sioihirtdyt. Cna saeir up to a arye faetr eldiyvre adn ahs oipmtcyylhc nfti.aeltir

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(198),
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tI asw a iernrguFsuo -b;s-etg&ido sots.ebsasi gniuerrouFs dbosie are eedbleiv ot eb dfoerm by asrpeaomhcg ahtt veah dochoypeatsg nad eptttedma to edstgi hte ribs.fe

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 +6  


submitted by rogeliogs(8),
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yM aorcppah to this snuotqei aws rmeo ujts iufgcnos in eth fion yhet rae gign.vi Nneo fo hte erhto oitpon maesk seens eueacbs eehrt is tno edveeinc to lakt utoab ht.em I saw rvey pmteedt ot ckip hte ceersae"d lpniet "dntpooruic btu I edmmbeerre rD jGoanl asinyg hT"nik ilp,sme htnki ,ecahp hety rea nto gyrnit ot itkcr u.y"o ,oS bucybh nratspe = cbbyhu sd.ik

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(25),
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ailo:obaeRstntm

The ycpsinhai idas eth oyb is lkniylue to plvdeoe yan horte a,lmospnse os eh ednts'o evah teh tedehinri bR .nutiatom

nI sthi seac, he sah eth odrcsipa .ariomsnltatobe rodSacpi oislrntmabatoe eruiserq wot siotcma nustmiota fo bR in eth msae taelrin .lecl

Jstu sa a ides noe:t neidtreIh airoomesttblasn nedt to be tib.ralale cporiSad ear ulrlaeant.i

carls14  aren't retinal cells a type of somatic cell? Why not is the mutation not considered in the somatic cell of the child? +8  
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. +11  
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. +6  
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 +  


submitted by jooceman739(25),
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alomttsnaob:eRi

The iyihsnapc sdai teh boy is iylklenu ot evleodp ayn roeht ,aolemsnps os eh td'nseo evah eht eienhtrid Rb tnta.ouim

nI this cesa, he ahs eht casodrpi ro.tasimelnoabt croidaSp tmlaoontersiba eeqriurs two tamcosi iatnomtsu of Rb in hte smae iealrnt cl.el

tsuJ sa a sedi no:et neIhietrd sbanemoialrtost dten ot be biell.aart rdacSopi are leil.uratna

carls14  aren't retinal cells a type of somatic cell? Why not is the mutation not considered in the somatic cell of the child? +8  
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. +11  
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. +6  
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 +  


submitted by armymed88(48),
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udWno aighnle mailamn ortfy rfo pu lti 3 yasd t(so,cl P,NMs vrootleaaPc )imfserir 3ysda tli se-wek lnigtaaunor eusti,s new evssel,s wne i,upielthme ironcacntot ia(repr dna aieger)nenort e Relodm w1k tli m6- crapeel loegcnal III wiht I, scineera gtsernht p(u to 0-%607 igolianr ghersntt lsp)eisob

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(48),
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oWdnu aiehgnl ltniaromy maf rof up ilt 3 yasd ,lt(ocs ,MsPN railv taseomrfro)eicP sd3ya ilt -kewes ugrlaaitnno is,setu enw se,levss ewn elit,muhpei nicoatrotcn pre(iar adn gr)enroienaet m eRoedl w1k itl 6m- epcrlae celagonl III wtih I, ceeainsr hettnsrg pu( ot 006-%7 roigalni retngsht b)ioelsps

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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mntdqie-tbiudaUeii opyeotlsirs is tno esrbevirly actffede yb lniuni.s eTh tnsqioeu sksa for beversilre wsya htat niisnul cesfaft it, nda unibiqttouaini owdul laed to dotnraadegi vai pessora,te hhwci si tno .rlebevrsie acNopmlurt/yislccae hunsintg ekasm seens bcseaue OOXF si a oicsantrtnirp toa,frc os it t’anc do sti ojb if it si ni teh oysmatp!cl

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. +9  
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 +1  
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(87),
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Ftsa aer tnkiecgeo txcpe(e dod icanh F,A) so ehyt orcdpue okesetn for rnyege pitocnodru (eyl-coAtCA) rathre hant leo.gucs If teh tiueqons aksde awht eth pirarmy eorucs fo eynrge douncoiptr sa,w it uwldo istll be elyggcno nd(a ont kse,on)et cesabeu iths is nithwi 42 .uohsr weveroH tfrea 42 urosh the wrsnea ducol eb tkeneo i.sdeob gseRsrdla,e eht nsoqiteu seayfiilccpl aids het pt ahd a erums oguclse fo ,010 innidaticg hatt we rae ikngool for eohgsmnti ahtt sivporde a ratutsesb orf gnueoogsilcn.ees

urginD odesipr of ai,sttornav sstbaresut orf coslnnusgieeoge eocm mfor otw :roseusc 1)( bknwoerda fo siigtexn mc,esul or 2)( iav cdniohd-a FA ohrutgh .-riAppyoonoCl el(*inaV aslo eesfd otin pyiporoln ,CAo btu si nto dnoleivv grindu iaostnavrt ;-gt&- see wb)oel

()1 Teh av-eptruinlyeaan ycelc oevdiprs stih (minlagetu ni eslucm + utpvraye g--;t& aaeilnn ;-t&g- egos ot reivl ;g&t-- nntroaatainims ot lhklteotpaa-uagrtoe t&g--; rtvayeup is estaaeprd form numeagtli g-;&t- eilgmtnau sego to uaer ccl,ey uveyrtpa gseo on ot nine.golcu)eosseg Lettcaa nac losa eb usde (hsti coldu veha nbee a hgtir aewnrs fi it ewre s)edi.lt

2() dOd icahn sFA are asol lngcogi,ceu utb icastre cdia doevpdri( in teh aswern hci)eoc ’snti odd incha, so ti is ynlo kceioegnt dna anc eb ureld to.u

Athuhogl eivlna dn(a roeth nadcbhre ).a.a feed toin oiP,nrCoAy-opl eyth rea nto edus in sortvatnia uebecsa rntistvaoa sryicttl eerlsi no htaecpi cnesil.oueengosg Tsehe .aa. rea not ozteebdimal ni eht evirl cbseuae the ilerv sklca nbrhdacni-caeh aa.. sernratseaf ezyn.me In rtisF id,A oeimhBc ieocns,t enrud tsia,rtngFvtiSnaa/o in boht the s“ingfat ”estta (hwihc si tihinw teh mite arfem of tsih ,i)noutqse or het irttovasn“a st,t”ae btoh uizteli tipeach leoisecsgeuognn. My nsoipsumat is atth ivlaen si used driung rregual masebl,otmi adn otn ndirgu resodpi of iv.tnaoarts

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. +4  
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 +4  
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 +  


submitted by hayayah(990),
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isCtineeyencesy-t nmheeicko reotcrep 5 5CC(R) si a pneirot nofud no eth ecusarf fo DC4 lelc.s

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


submitted by hayayah(990),
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yettsyCeesincne-i ekohmncie ecterpor 5 )CRC(5 si a ernpoti nudfo no het efurcas fo D4C slel.c

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


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ioustneQ kesda rof garm ivtseipo ccioc in SIC.NHA S. rueaus omrsf rlucss,et tlimiannige t.i Tihs velase onrctcsEceuo fsicaael and Gopur A petr.s E. cfaesial si osdsctaeai ithw TsUI.

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(517),
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ntiPeta yma hvae dahieterry eemaia,odng hihcw is adotsiscea hwit etrune"crr kattcas of t,nsinee ,saevism dcliloeaz oscsnbuatueu emade nvvolnigi the ,exiimesettr giietn,aal eac,f or kt,nur or umslcbasou emead of perpu ywaari or .elwsob" Teh caltier eogs on ot say esers1C-"tea ithnbriio swkor irtlyedc on teh omlcenmetp and ccatotn apsaml aaccsdes ot redcue yrnaindikb lseeera" wcihh is sola loybaprb oodg ot kon.w

awo.hss/tmw36i:Pbv3./hn/min/6cpMtC86rtcelc1w..lp/ng/i

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? +21  
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 +1  
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(11),

Why is is not pseudo aneurysm?

"Aortic pseudoaneurysms typically occur as a result of trauma +/- intervention, a considered subset of traumatic aortic injury in the majority of cases. They can be acute or chronic."

https://radiopaedia.org/articles/aortic-pseudoaneurysm?lang=us

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(503),
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aMjor ksri caofrt for rcoait onsdiiscte si rph,yoetsnnei dan in thsi scae thmig eb eud to naicoce seu, ihwch scause akemrd shrnoytnei.ep tsisesciDno uecas a etar ni het nacitu niiamt -- obold anc owlf cadkarwbs toni eth iuiarmcrdep nad ecasu peamdtoan. sThi mafssneit as rlekccsa ni teh ugln edu ot ropo felt nteaucrrvil tuicfnon i(nitflgs/lilcdaio operblm ued to smnicprs.o)eo

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. +  


submitted by neonem(503),
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jMaor iskr orcaft for orciat iitcnesods is yenheisnoprt, nda in tsih seac gmith eb ued ot caceoin ,eus wichh eucssa kmared ospetrihnn.ye snitsDesico cesau a trea ni the cnatui matiin -- dlboo nac flow wsadkrbca iont teh diceuaimprr nad asecu tnepdm.aoa shTi iaensfmts as clsakcre in hte gunl deu to opro tfle itrvcuenrla ontfnuci iin/lotflgcd(siail mproelb eud ot p.crismoonse)

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. +  


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phordrAot ofr sr,eu btu fro eht rrodce 'mI rptyet usre iths aws unyCingaukh .sViur Only ogt itsh fmro a dUorWl enouiqts as I htnda' esne it ulnit tenh, utb paptelyanr eth glarrhtaia is ylrlae bad, chiwh si waht werd em to teh sanre.w

vhyecisw/thn/:p.unhw/aiouc./dgdlx.twgknmct

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. +10  
nala_ula  I'm shocked that I found a fellow puerto rican on this site! Good luck on your test! +1  
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/ +20  
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. +1  
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. ) +  


submitted by fatboyslim(25),

(From UW 11852) Some medications including opioids, radiocontrast dyes, and some antibiotics (e.g. vancomycin) can induce and IgE-INDEPENDENT mast cell degranulation by activation of protein kinase A and PI3 kinase, which results in release of histamine, bradykinin, and other chemotactic factors -> diffuse itching, pain, bronchospasm, and localized swee=lling (urticaria).

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(990),
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visnSitetiy etsst era eusd rof gnien.rsec iteifpycicS stste ear euds rfo niaoctoinmfr eatrf viisotpe essgiernc.n

tyinsSteiiv sttse era usde orf eniseg who namy peeolp ltryu eavh teh essid.ea ifticpieySc ettss ear ofr toehs ohw od not veha het e.dsasei

A ghiyhl nsestevii ttse, hewn evine,agt erslu UTO .esadsie A hhliyg ifscciep sett, ehnw ispvtoi,e ulres IN desisae. So, a stte hwit ihwt lwo iintvetissy otacnn uerl tuo a deeass.i A ttes with lwo fctyieispci ca'nt lure ni eised.as

hTe odroct and enittap tnwa to enresc rof cooln nracce adn ulre ti .out heT rodcto uwodl natw a etst ihwt gihh ityistsvien ot be elab to od .thta eH snokw ttah instegt rhe sootl for loobd liwl ton uelr otu teh pssilbitoiy of lncoo .AC

sympathetikey  SeN Out (Snout) --> sensitive test; - test rules out SPec In (Specin) --> specific test; + test rules in +10  
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(990),
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yniitetSisv stest are edus ofr c.nnegsire cciyfpStiie tsset rae esdu ofr motcniraoinf retfa tipoisev rcg.ineenss

iStvitnyise setts rea sued rfo einegs hwo yman elppeo luryt aevh teh issa.eed itcycSfiipe setst aer ofr tseoh hwo do otn ehav the esiaed.s

A hghyil sinievest ,tset nhew t,genviea esrlu OUT desieas. A ylighh spicifec ,ttse hnew eovpt,sii uelrs IN se.esida ,oS a sett hwit hwti wol vesiistitny nontac ruel uot a iaeeds.s A etst iwht low tyecscipifi tcna' uelr in .iseased

Teh odcort adn iatepnt wnta ot ecsnre orf olcon recnac adn eurl ti .uto Teh otodrc dowlu twan a tste wtih gihh yievtinitss ot be bale to od a.tht He ksnow that ntgtsie reh otsol orf obold wlil not urel otu hte potiysslbii of lcnoo A.C

sympathetikey  SeN Out (Snout) --> sensitive test; - test rules out SPec In (Specin) --> specific test; + test rules in +10  
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(14),
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eaylrccenTsti have a high inffyiat ot fomr hstcaeel whit ytevnallpo clamltie inatcos shuc sa +e+F,+ +e+,F A+l,++ M++g nad +aC.+ yaMn fo htsee realniecatt-mtycel sxecmepol aer ietrhe losebuiln ro ohtsweier oplroy blesobaabr mfro teh tsngtrit-iaaesonl rtatc. likM dna treho airyd rps,oudct isacatdn itncanogin yvonepltla inscat,o sa lewl sa raiosvu oirn salts dsnieetg latsuyiuonlsem hwit eyetincrlcat saevev,iridt tgihm treifnere tiwh ierth noatsribpo yb 05 ot %90 or enve .mroe uec: osr o69.4wp:bnpsh9mlg./dwtetvi/5n8.bn/cwmih/.u

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) +  


submitted by hayayah(990),
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donniAstrtaimi of nlPiciilne ofr lyiisphS mya elda to het semerxJrire-Hihhca neoirtca shruo retfa enaetmrtt. rcuOsc deu ot sysli fo schereotisp (so ti anc rccuo tihw Baloreir nad ipspissooLert as .e)llw heT encorati is ciazcahrteder by veref adn s.hlicl

eTh csacaslli atnpaelinox fo teh iemxrHrhee itnocera is thta retetamnt lrestsu ni teh sndued tadhe nda reucidtnsto of arleg ubmnser of tp,enomsere htiw eht liaritonbe of otnirpe pdrtcosu dan otnsi.x

almondbreeze  FA pg.148 +2  


submitted by hayayah(990),
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epCitata adn luanet rea in eht enterc fo the lamp. taCpetia si nto an ,otoipn so ueantl is the rnwe.as

olacisintDo of tlnaue aym cuesa auect ealntr lpuacn rsdyo.emn

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(125),
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Tish si teh lyon ieochc ttha eoscm soecl to giinckn eht icohtcar ,cudt aiflpclyisce ta tis n,lite hte eflt c.isnuablva

kpjk  why not midsternal thoracotomy? +1  
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(127),
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hlWei I can gte on rdaob iwth tdstujnemA ,sdDrorei I o'ndt ese hwo isht snewra is any tetreb tnah cioStam toymSmp Dero.srdi omFr AF:

yVrtiae fo dobyil sapnmciotl tliasgn omshtn ot aersy tsdseiaaco twhi csxsvie,ee sinetseprt ghhoutts dan ayxietn tbauo .ptmymsos aMy a-oprceap wiht .slilens

SSD lnosegb in a urgpo of rssderdoi acrziechdraet by ahpslicy msmosypt nsgiuac giiacnstinf sessdirt nad rimn.miteap

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. +2  
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". +10  
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/ +2  
almondbreeze  @chillqd Same! Why not OCD? He's fearful that something bad might happen (=cancer relapse; obsession) and calling his doc (=compulsion) +  


submitted by sympathetikey(980),
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Cohice .A oldwu ehva been crorcte fi tihs neatipt asw cmmimruoipdeoo.msn Pre Ftirs dAi, If" C4D &;tl00,1 alF.nasBdirilng:n.t.oe lioephtcrNiu nlaotm.imIafn

wHoever, as tish aitpetn hsa a pneemtcto mmienu sysme,t uzzb roswd are teletsal iocteginnrz aagslnmruo.

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 +1  
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(980),
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iCcheo .A uldow hvae ebne ecrtocr if stih atpnite saw mmdmsioc.mpeonoiru Per sitrF id,A fI" CD4 ,;tl0&01 .nis.d:aB.lirtalonengF puielohrtcNi omnf.alatnImi

ewv,eorH as iths titpnae ash a pecntmteo menmiu etssmy, zubz worsd rae letaltes tgrneoicniz gsuolmrnaa.

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 +1  
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(235),
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B e-eslHen aCt actcrhS ni -oinuttpmoncmmeo - ghldm/iyou//tpcostpccl.tnmttcelo/thwoapeohyhmitcwshpa:swao.n.rltnrl oltBaae senheela in io-soomnrumdmcepIm- Bicaarliy gamiottsnsioa ksoL o ikle sipaok aamcrso fDfe ius" rphoneuiilct ltrifa"ntie FA 9120 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 sugaplum(235),
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B eesn-elH aCt crStcha in ooiconmtnmpte-mu - /lh.wawm:cmsthln.ipatostel/ctopochwyntosd/occtueahrmilo/.ppttyghlt elBonraa eaheslne ni mmosordI--cnpiouemm Bayriialc osniotagtaims sooLk leki kiasop scoamar "fDfuies prhicieulont eftrntil"ia AF 2190 177

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(224),
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cBro’sa ipha:asa iepxsvsree (omtro )siaahpa itwh migamtaamrs p(st waare atht heyt ontd’ maek se)sen - raea e c’ineAkrWs pisaaa:h trecpivee essyro(n) aapsiah twhi midaepir rohenpoceinms (stp aclk ngih)sti

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(224),
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oar’csB ahsai:ap vesxreipes trmoo( apia)hsa ithw gmiaatmmasr sp(t arewa htat teyh ’notd kmae ese)sn - aare nckiAse e’rW saaiah:p reeivecpt (eyrs)ons aaiapsh thiw pedmiira ennpomsrciheo (pts kalc itsngih)

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