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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 mna hiwt a Hx fo tHOE ecenpednde dna chonirc abd pani as ewll sa rX-ya isinfdgn fo sioctfi"clniaac in hte -iedruppm ond"bema si mtso eylkli rnregrife to a rcnicoh i.csptaaeirtn

shTi dsael ot a aclk of paiesl eecironts ec,hen lea,p oufemngislll- oostsl iwht oil opdsrtle per tp H.x Thsi spt' cpnaeasr aslo 'eondst esertec htoer ,eeszmyn husc as alyssaem, tsrae,pose onr oneptsngryi (ot taatecvi hoert )nzeems,y os the rensaw si e"ladgeznrei apatrbisolmo.n"

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 mna whit a xH of EtHO necpddeeen dan ionrhcc dba apin as lewl as yXar- idfngsni fo aolnfcii"iscatc in eth u-pedmirp o"emdabn si most elkyli rrngeerfi to a ohiccrn re.piaitctsna

iTsh edlsa to a ackl fo aspiel eeirtsnco ehnce, ap,el lgollnusmef-i oltsso twhi loi tslrodpe erp tp x.H Tihs st'p sancreap losa dseto'n seecter ehtor eenm,zsy hcsu sa eaasy,lms soatperes, onr esntipgoynr o(t taevciat ertoh szne)y,em os eth swarne si gnideezer"la inpbro.osamlt"a

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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"ntdorea"s rea o,nBoheappsshsit lmoymnoc sued to rterene/ptavt pio.osssooter Msot mocmon eedsavr tsefecf aer iosgEshtpia (aittnsep oudshl atek iwht teraw and eb igthrup orf at aelst tn3i)eu,s0m oorescsOtisne of hte ja,w and capiytal mefoarl estssr arusterfc. ne-kat htirg rfom AF 8210 pg 174

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 hknit smiastatse asw hte estb tioonp erhe uebesac rheet aer miultlep tmgniaanl nos.s.lp.mea rarimyp casrnce dtne to attrs as a nesilg sams in teh utesis of giron.i In hte ung,l saeetatmss ear meor mcomno thna ryampri seslpnoma.

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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edokLo ti up dna nfudo ttah baseecu yoeru’ in a enisup otiiosnp ofr a olng iemt ro’yeu inogg to aevh eireacsnd suenov retrun cihhw ldaes ot erscenida CO. shTi nevlegtyai eakesfcdb no RA,AS dlanegi to cedreased tlradeso.eon As a te,urls ou’yre gngoi ot hvea cdniesear riissued whhci aelds to rcedeades boodl dan lpmaas .lmouve

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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edkoLo it up dan fduno ttha ubascee ’royeu in a eiupns oistopin rof a ognl mtie eryuo’ ognig to vahe asreenicd vnosue rrteun chwhi dslae ot dencearis .OC iTsh evanyietgl febksedca on RSAA, eainldg ot radedcsee rtl.ndoeaeos As a ruelt,s ouyer’ oggin ot veha dcnreaeis esrisidu cwhih esdla ot eadeecrds blood adn aapsml o.meulv

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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nbocitnFeri si na eeraluctxallr ximtar tyocerlpnog,i hiwle nmlai is na mrtateedeiin enlmafit atth csilfypcleia sodrpive puotpsr ot het lcel nuelcu.s t’Dno euscfno linma ihtw liainnm ie(cecns taehs us alcry;l)e nimnial is like ,nitebofrcni an ECM ogoitcenylpr dna a mrajo etmonocpn fo eht abasl aialnm of tsembnea emrme.sanb

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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nFcrentbiio si an latrlauxrecel rtxmai y,toergcoipln liweh anmli is an meienerttadi iaftmlen that clfciyapeils pdvesrio sotuprp to het ellc c.eslunu nt’Do sufnoec liman thwi ininlma (iescecn etsah us car)le;yl nalinim is keli fertninbi,oc na CEM cgtpoinolyre dan a rjoam npmoeontc of the lsbaa inmaal fo msebeant mmnaeb.rse

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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"savnIreten the umscles of eht dleaim noreamtmptc fo eth hthig ot(rbtouar x,utsreen acdoutdr luo,gsn uctaoddr brev,is ddoacutr snamgu dna "iial)crg.s

.mptretmea/v/e:mtecebotlab/ar-/een/rivnhtsnht-iouoofwo/lnrsyra

almondbreeze  FA 2019 pg 444 +  


submitted by docred123(4),
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nCa aneoyn teurrhf ilnaxpe ht!s?i I lcudo tamenleii a ewf tmei scochie nad I dgseues lytoec,rrc tusj ende rmeo frominio!atn kThsan

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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gcdonircA to loa,nGj thoypmlacyie vaer si eno fo eth stom mocnmo saeucs of uarB-hiddCi .srdemyon Aoccnidrg ot AF, BidCarhi-du is oedaiatssc mroe erleaynlg tiwh eaabgcrhelupylo sts,aet oyathyclpime vear, sutatrppmo ,stsaet and HCC.

ctpHaei rcishriso anc be urlde tuo bsdae on teh etmi uorsec fo the antep'tis rtaisenenpto - he saw nief 2 kswee oga and eht biaodlanm pani asdertt an rohu .gao

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(461),
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-ddrCBiiahu ndmoysre ccuors newh reeht si uocnsloci fo hte eithacp eivn or teh pitceha eniv sialf to andir nito the IV.C iTsh cna be caduse yb soitmobsrh fo hte ihtacpe e,niv or yb grhti esidd areht irelfua nscgi(au bolod ot bck'a p'u rhe,weeevyr tub ist aniietoatfmns ruhgtoh het iatpehc vein rae lla eht sngsi fo iu-hadCiBdr .yomensdr) iAgntynh htat can ncsreaei the ksir fo stirosmbho nac nthe easciren eht sikr fo Cia-Bhudrdi syonre.dm hTis lduceins ctmlyeypoaih eva,r a lbelrpuhacoeyag esat.t uOr petnait dan PV utb desims shi npapietntom wto ekwes .ago He nwo tesenspr tiwh lcerasl tecruis, na rgandlee i,lver nda eosm sgsni fo lrotap n.ehosnetpiyr imossTobhr fo hte nylo aanalmotic noitop ensetdepr ttha ovecrs lla fo htsi is hte ecaihtp veni ei our pitetan sah Buia-dCi.dhr rbmeReem ahtt Bddhrii-uaC liwl vhae a gnutm"e re"vli rcnaapepea no osrgs oglaohp.ty

B) eHitacp i-risrcsoh ts'i tryenile belispso oru eatitpn dsoe eavh atiephc roihrcssi for naruleetd onarsse, ewevorh eth tceua ensto aesmk htis lsse ie.lkly )C tnccaiaPer mcanca-ori cecnatairp aaormicnc otirsntoubc fo eth nmmooc ileb ctdu olucd secau a ckba' u'p fo ei,lb eltlutmiay siangcu eoms eivrl gaamde dan lserlac u.iecrst weHvoer eocn gania eth mtigni ekmas isht klln.iuey )D Parotl eivn ibssr-toohm aptolr vnie tismrbohos lcdou sceau omse snpleic alegertnmen dna alport ryeonntp.sehi eeHwvro, its oisbnotruct lwuod ton casue a dern,et agnederl rilev usabece it si m.tspuera )E ryiraPm soisoarmhetco-mh ude to a edfcte ni hcnpiied ,durtnoiopc tsih inro ooavlrde nresetps tihw deekanrd i,nks siuinnl uoitlsr,nadegi tihacep aedgma (ihtw the tnpleatoi rfo leplleaarhuotc a)acnriocm nda ahtre aesside rieis(tvtrce ro edadlit ,orahpmcyaioytd idednepgn no yruo reoc).su ehT oynl noe fo heets nisgs ttah rou iteptan sah si na egrnldea irle.v

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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Paitten is uerrcnt ebf-dt,aesr so ew cna litameien fseutcor tfures(oc is nfodu ni nyeho nad srftiu dna osem or,maulf ubt nto in ebrsat mil)k. Pttiena ahs curngdei esutscbasn utb no ugoecsl in hte r,uein os eh tmus oems no-gncsloue .augrs yM iaeredlfnitf orf euncdrgi lsoocnge-nu suasgr in the euinr is dsirosedr torcuefs aeslbitmom ro stocaelag oms.ietlamb We ehva emlenaitid uosrtc,fe so thta vsaeel us wtih gtaneakiaslco dcinyieefc ro csicasl s.lcgiataomea

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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ishT uoneqtsi ksas btuao hte shnaemicm fo tphaterohpoy as it tleeasr to leontaan acnduij.e hWti ptohtparehyo, brubiinli si plimys edevortcn to treaw soelubl meoisrs hatt rae nteh aleb ot eb dexeerct yb hte nid.eky Thsi ehoervw esod ton aogjnutec eth uiilb.nbri

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(257),
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h988g@ "useeBca hte ntiuscborto si oveab eth arlloave sioegrn reeht is a eeeadrsc ni rai f,owl nto guln umeols,v hcihw wdlou keam hits an oeistcbtruv "tpoayhgol is eth sotm lphfleu etonp.xanail fI you kwon het toms biacs onhdooiyy/apstionihpgetlfi fo eocvutstrbi sv cstiveteirr (iwhhc I ,od tjsu dntdi' in taht msto semlfdipii y)aw, neht you can uerfig nhinytga tou. fI hongtiesm si tmipcanig ywiraa olwf = ueitrvstcb,o fi netogihsm is imntciapg aariyw luovem = iettcvrsire. TAKNH 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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lrn.jaGDo spnaielx it alyelr llwe on the daou.i I llwi tjsu evgi eth bcasi eadi. llA hte mhnsoelogbi heva lpaha ni it tehrrofee uyo nacton itnoec it no lghobmioen csptolsrreeieho

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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Tish qniestou si .sgdeusdii hWat thye rea leyalr nikasg is "hwta si teh oels etanmrditne fo epescis vliavrsu?" eTh noyl enrswa is hte aibtily to rt.aeopcer scueaBe AND roePaylmes ash dio-gnorperaf tivac,tyi noepygr will eb dceaeuftfn by ARN molearssPye klca fo peoangoifd-rr iict.avty

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 ryazc or did rwlodU otn eahv a oqiestun tath aettds sntatSi aer hte tosm fveicetfe drug slregdesar fo lbanesie s.piidl hTsi olcgi wreth ym off.

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 czyra ro ddi loUdwr not hvea a qtueions htat ttedsa naStits rea eht otsm eefceftiv gurd gadslerers fo slbenaie ilsd.pi Tihs iolgc rthwe my .off

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 ignog ot ays ist’ X ikelnd amuamgemlgniaaolbi trhear atnh DSI,C tbu eth ecneferdif wbeenet ehset wto are ityn utb htsi si hwy I hiktn ’tis het :refrmo

  • oBy aeincsr(ed rkis tub btho AB and CDIS are x len)dik
  • Rrcetenur aritacble coetisnnif tbu ’notd inenotm rhidarae ro thrshu chwih si ni ICDS
  • miieTlne si rtaef 6 mtsoh,n so teh meoshrt’ iiosnbtaed erow ffo.

CDIS luhdso eb imdmaeyeitl cbauees teyh utjs to’nd vahe het 2IL r.eerostcp DVIC swsoh up hwen t’yhree 4020- reyas ldo. uoY gte nsabet gelrnima cenrest ni .thob oN menoitn of abestn tciymh dhsowa which si in SIDC.

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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ahzhiolyrioodtdrceho si DCO orf eeogprniNch ebsDeita snsupdiii ecseabu ti ydrlaxaaclopi aussce an ascerien ni BP by nernagsiic oumsid otiranpsbo nad hust wetra a,rbnpsooit tmPaoah exalisnp iths n.iceyl

Dnesproiemss is enoccritr ebseuca npuo gtisafn idlu(f rnes)oitrcit HDA is dscearnei genmani DHA si ingbe eaerelds yrnaetlCl but si otn nwirgok ni hte eiydksn at eht 2V rsoetecpr fo teh etalhielip neral lcesl at itoCglceln u.cdt

nO hatt toe,n dAieomlri si dsue orf imuitLh unceidd ercopinnhge DI.

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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cngaridoc to ttoaupde ztidsaihe usace a mild pmloyoecivh etsat tshu uory TCP wlli ese mroe aN nda 2HO ->- yb rcppenlii ttah the CTP lwaysa sorsrbeab %06 fo hawt ti es,es ti llwi bbarerso mroe raewt dan Na.

almondbreeze  in sketchy as well +  


submitted by imgdoc(128),
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I thnki olat of leoppe gimht hvea revo zshdapmeie owh ttoinapmr ANP nda PBN lelary a,re sye it is pmtinotra to nowk hstee ippesetd get creesetd yb teh rcrauevt/arlaiitln mocrudyami ngrdiu htare elifu.ar oHvreew etihr lrlaove sevtneiscffee in niegttar ehrat lieafru si zci,hl a pctererop ltdo me ahtt if NAP dan BPN reew os fuslue in sartseiiurn hetn hwy od ew gvei idtrs?euci t'sI cbaeues SARA oropwsreve sthi mtyess ecneh iuasgnc vatnegie stffece nda eth sensdle lopo of ertah ri.ufela AAK why we ivge AEC .intsiorbih

gnwoiKn tath NPA gtse izteneurdal yb eth ASAR syte,ms we acn fihts our cufso abkc ot haret ureilaf ni htis ,ittenpa hwere cacdiar tptuuo is cseedard,e agednli to AHD oesretinc nda iyllfna iundilotla ranp.meyoaiht

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 nikht tloa of ppoele might aevh evor edsaipmzhe owh nitpatrmo PAN nda PNB yarlel ,aer yes it si attpnimor to nwko esthe epstpdei egt eesdctre by hte tai/ncaetralilvrru imauyocmdr gunird reath aferil.u ovHerwe ither verolal efsenevsfiect in artetnig arhet lraiefu is izc,hl a rprtcpoee otld em taht fi ANP nad PBN were os sefluu ni rtniuraises ehnt wyh do we egvi ciuiresd?t 'tIs sbceaue AARS rerposweov stih ssteym hecne angusic tgaeinve sfectef and het eednsls olpo fo rahet rieual.f AAK hwy ew vegi CAE .riibsontih

ngnoiKw htat ANP esgt neizradleut by teh ARAS ssm,yte we nac fsthi ruo suocf bcak to haret fleuira ni tish ,naettpi herwe adcarci uputot si es,ecdader dleagin ot HDA ceeortisn nad nflaiyl oadulltnii rioeyth.amnpa

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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hsTi is a antepit csae fo ptsmtoarpu dtrt.yiioshi nCa erias pu to a eary arfte iyeevdrl dna sah lyocmhtpyic irli.fttnea

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 saw a roueugsinFr edbg--ot&si; ssiabtoss.e ienFrsorguu sidebo rae blivedee to eb dfrmoe by gmreasoachp ahtt have daystoghcpeo and tpaettdem to segtid eth sir.bef

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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My caphopar ot htsi oeqtnusi saw more utsj ficogsun in the nofi heyt are igngv.i Nnoe fo eht ethro itopon kmaes nssee auecbse eehtr is nto veciened ot latk tboua et.hm I aws vyre mpetetd to cipk the "eesdecra enptil c"tropiundo utb I ebdrmemree Dr jlaoGn sayngi i"hnTk mise,lp ntikh h,aepc eyth rae tno igrnyt ot ritck y"o.u o,S hbcyub searnpt = bcyubh ikds.

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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aabstRotnilmo:e

eTh anyhcpsii isad the byo si yueinkll to lpeevdo any roeht eoasmlp,ns os he od'sent ahev eht tdeienrih Rb tot.unaim

In ihts ,csea he hsa eht ordscaip bterminoa.ltsao pSoardci orioeatatlbnms iqeseurr wto stamcio ttnoamusi fo Rb in eht same anieltr lec.l

sJut as a edis :eton rntIidehe talaontrbemsiso netd to eb aba.rlteli apiorSdc ear lirutaela.n

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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atns:ibmRetlaoo

The yichpaisn dsia eht oyb is inlelkuy ot olvedep ayn rtoeh ,lsnmsopea os eh eotsdn' haev the nereiidht bR t.muntoia

In hsit asec, eh ahs het rcdiaops steaablo.ormtni Sioradcp mtoneiaotblras srquieer wto asioctm otutnasim of bR ni hte aems arletin .lecl

suJt sa a ieds ento: itnehrIde osbesitolnratma tnde to be lat.rielba pcrSdiao era .renaluitla

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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uoWnd lehniag tariflmny amo rfo up itl 3 ayds ostlc,( N,PsM rP)asirt lrvmiafceooe y3sad ilt ke-wes ognartanliu tu,ssei wen vess,sle nwe ihulemit,pe ciotntonacr e(rrpai nad )rioeatgreenn oRm eeld kw1 til -m6 ecarlpe enlcaglo III thwi I, ensceria sgntreht u(p to 6700-% lgiraoni nrsegtth )ilpbeoss

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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oudWn ehilnga anftyammirol rof up ilt 3 ysad cot(,sl NM,Ps oiac)terlorsr eaPvfmi ay3ds ilt eswek- tarinoguanl tu,isse enw evslsse, wne eetpmuil,hi atccortinon p(irera dan eti)angnoeerr Rd eemlo wk1 tli 6-m ercpela algloenc III with ,I inceaesr tgnhtres pu( ot %-0760 igirolan gsrnthte pso)belsi

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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dUdttminiiiuqea-be oipsoeysrlt si otn slbereyvri efdcefat by ininslu. heT eoutnqis kass rfo ibrevrlese yasw htat nilinus cfeastf ti, nda uointaitubniiq oudlw lead ot rdgotdaiean via reopta,ess hcwhi si nto irlvb.eeesr rmaltysicu/ecpolaNc thnsnigu amesk ssnee asbeecu OXOF si a sipnrotanitcr afrt,co os ti n’act do tsi jbo if ti si in the amcsop!tly

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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taFs rea getinkoec te(expc odd cainh )F,A os etyh ueopcdr snetkeo for egryen octnoudpir C)(-toeyclAA rtaerh hant eocu.lsg fI het nqoiuest asked athw teh pmriyar srucoe of enrgey drtiupnoco ,wsa it dlwou tslli be olygcegn d(an tno nkot),ese cueeasb ihst is winith 24 ruo.hs eHeorvw rftea 24 sruoh the rasewn codlu eb eoketn sbeiod. deglRssa,re eht tnoqeius lcpiycaelisf idsa eht pt hda a uresm sucgole fo 1,00 iacintgdni ttha ew rea glkonoi ofr oimegthns taht iorsvped a tsbrutsea for egisneolc.ugsnoe

rugniD isoperd of tvast,rnaio reasstsubt rof oiesceeluonngsg come form two es:rcsou )1( rdbanoewk fo xgsietni c,msleu or (2) aiv i-ndahdoc AF uhtrhgo onpoloCA.-rpiy V(n*ieal osal efdse ntio rpniooply ,ACo tub si not enovdvli grudni orsiaavttn &-g-t; see bel)ow

()1 ehT aveylnnpaeaiu-rt cclye rsdiovpe isht ailteu(mgn ni csuelm + ypatruve g&-;-t lneniaa &;-t-g esog to relvi -g-t;& anmsoinaatrtin ot tplheotkg-taouaealr ;&--gt ertauvpy si spadeerta rmof igaelnumt -gt-;& ulmtenaig egos to earu cecy,l eaupvtyr oegs on ot ecieslunog.ognes) tLctaae can saol be uesd (hsti oudcl ahev eben a ihgrt easrwn if it reew )stedl.i

(2) Odd hainc sAF are aosl eccoguigl,n tub craeist caid (odipderv in hte swarne ichce)o ints’ odd ahn,ci os it si lony ctenkeigo adn cna eb ulrde o.tu

hugtohlA eainvl nd(a oreth ebhcnadr a)..a edfe onti ylnoApo-,PiorC hyte rea ton ueds in otrtivansa saeeubc vtsaintaor ctstlryi lseeir no itheapc ogseoigeeusnnc.l eshTe aa.. aer otn oedibmlezta in eth relvi beescau the vrlei lckas eacnhncrb-dahi .aa. rassetfrane z.neeym In stiFr ,Aid eBciomh eto,csni rdune oFtsaanSi,i/nttravg ni hotb the tiafngs“ a”etts (ihwhc is hwinti het mtie mafer of htis stino)uqe, ro het sart“vtanoi tsa,t”e thbo eutizli piathce esnegnoo.eslcgui My imuntsaosp si hatt nalevi is dseu drgniu rulgera mltoam,seib and not dugrni psordei of tns.oaaivrt

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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seeityenstcy-ieCn ionkehcem reorcpet 5 R5()CC is a oprniet unfod on het saerucf of C4D .elcls

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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-tnessyneiiceeCty iehceonkm cetporre 5 C(C)5R is a petrino unodf on the arfesuc of DC4 cs.lel

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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eosintuQ sdkae fro rmga ipvieots cocci in NAI.CSH S. uaeurs mrfso ,tsscelur einintalmgi ti. Thsi vseeal rutcoEsenocc sielfaca nda ourpG A step.r E. aisecafl is sedcisaato ihtw ITUs.

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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itetaPn aym ahve ayedrierht negoedm,iaa chwih is staaodisce thiw nuetr"rcre cksatta fo ienetn,s s,misaev idelcozal bncuteossauu eaemd vnnlgiiov hte teseiet,xrmi i,ignatale acf,e or rkun,t or lcbssouaum emdea fo prupe rayiwa ro e.swlo"b eTh ecliatr gose no ot say e"er1-tsaeCs nbhioitir rskwo cdtireyl on the tnpmelcmeo and ottcanc alpams cssdaeca to uderec kiybnnardi slearee" whchi si also oabyrbpl dogo ot n.kow

e6noni./ipvta.s31p/Mmt./ibc/lncr6/Phc8l3g.smthwCw/6:w

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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Mrjoa srik faocrt for rcaoti iiecnotdss si tsyehrpoe,inn dan ni tihs case tihgm be deu to cceoain e,us icwhh cuessa dmerka spi.eyrehnnot isnesictDos ecusa a arte in eth tuacin intima -- dbloo nca owlf swrbakdac noti eth eaprduimcri dna ecuas .emtoadnpa hisT efntmisas sa cceksalr ni hte unlg edu ot poor flet nvtrreluaci ufonctni ncllsigi(f/oliatdi elmrpbo deu to spsooreni.)mc

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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arjMo krsi aftrco rof roaitc odiistsenc si perethnisnyo, dan in shti csae hmtig be deu to aicecon es,u ihwch esuasc damerk nsterpo.ihney siseonDcsit suace a taer in teh uancit aiimnt -- oolbd can flwo wcskdarab ntoi eht mcidieurpar nda uecas md.eanatpo Tish atsnsfiem sa carkslce ni teh gnlu due ot rpoo ltef aelrruvticn uinfontc ltglianco(ii/fdils peborml ude ot nmo.epssorci)

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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oohtAprdr ofr ers,u tbu orf hte rderoc 'Im prttey eurs htsi saw uCyhkiangun is.Vur yOln otg stih frmo a lUoWrd seoitnqu sa I dan'th snee it uinlt enht, but altpeayrpn the lrtgrahaai si lealry adb, wihch is wtah wder me to eht wrnse.a

ni.hc:wk/c.gxs/hune/hwgtodnp.dya/uvltwmcti

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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tvSieiinsty stets ear sued for secinern.g iSpcictiefy ettss era euds rof rnamoioicnft aerft otievips gecnries.sn

tsiSytneivi tsest rae sdue ofr esngie who aymn peolep uytlr veah eth di.sesea ipiSfceiytc stets rea fro hoste ohw do otn vahe teh iae.essd

A glihhy isivetsne sett, ehnw n,geeiavt rsule TUO eaediss. A lhiygh icesfipc ,ttse ewhn osvpiiet, rlsue NI ssdi.aee ,oS a ttes thiw twih olw ytisstviine taonnc uelr otu a .esdasie A stte twih owl fcesiicipty tc'an ruel ni dese.asi

eTh codort dna pinaett want ot nrecse rof olonc ncarce nda reul ti ot.u Teh rtocod wuodl wtan a tets hiwt hgih vitiyesnsti to eb eabl ot od ath.t eH kwnso ttha ttiengs hre otols orf boldo iwll tno leru uto eht yobplssitii fo loonc CA.

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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sivnttyiSie sestt rae sdeu for egceri.snn cipySiitcfe tsets ear eusd ofr ntricnfoaiom rtaef veisoipt iges.sennrc

tvisyiteinS ettss rae sedu rfo seenig woh aymn pploee tyurl heva eth esiesa.d iptSeccyiif stset ear rfo ethos owh do nto ahev the d.eseasi

A yhhlig evsseinit se,tt nhwe enag,tvie ulser TUO essiead. A ihglhy cipfisec et,ts henw e,iitopvs lesur NI eeasis.d o,S a stte htwi hwti olw ntyveissiti ntaocn luer uto a idesae.s A tset hitw owl ipetficyics ct'an uler in seeds.ai

hTe drcoot dna eaipntt tnwa to secner rfo oocln earncc adn leur it tuo. heT rtoocd uldow wtna a sett tihw hhig istestvniyi ot eb ebal to do .that eH ksown htat tgtisne her tolso fro oobld iwll tno uerl tou het lsiboiptiys of onolc 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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Tyensceitrcal vahe a ihgh iyifantf to fmro ltaechse ihwt tnvaypoell ltaclemi atcison such sa +,Fe++ +e+,F +,Al++ M+g+ dan C++a. yaMn fo sheet ateaertmny-tceclli oexclepms rae teireh iubelsnlo or iwsohteer oyrpol sbbloaeabr rmfo eth lsosi-tgtatinnrae act.tr lkMi nad rhoet yidra cpudots,r iacnatds agonncitni lyeontpvla scanit,o sa wlle as aurovis roni altss gedetsni yalseusomltniu ihwt nteteilcarcy irvvisead,te gmhti rereinetf ihwt hriet irsotponba by 05 to 9%0 or veen mo.er :uosrce .mt/45ilpwi/hn:n89/./btcwgw6sopbuh.vd.me9n

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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mAdsinonattiir of iPelnlnici rof ihypSsil amy adel to eth iJearcershm-hixHer tocirena hrsuo rftae enttamt.er csOucr due to slysi fo retesoihpcs os( it acn rocuc wthi aeiorrlB nda teosprpLisois sa ).ewll heT recation is tarridcheaezc yb verfe nda .sllhic

ehT slcsalcia enlataxonip of hte rxiHemehre ronietac si taht mtratnete urlsset in eth dudsen hatde dan rotinecdtsu fo rlgea rusnbme fo emonts,eerp twhi teh laoibinter fo toerpni upcrtsod nad n.xtosi

almondbreeze  FA pg.148 +2  


submitted by hayayah(990),
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ipaCttea adn atleun era in het ncrete of teh m.pla paetaCit is otn na ipnoto, os autnle si teh n.sewra

otincoilaDs of anlteu mya scaeu catue lnaelpauc tnr rmdnyoe.s

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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Thsi si eht olyn ecicoh atht emsco lseoc to nckgnii teh iactroch uctd, pecalliyfcis at tsi einl,t eht etfl auivbns.acl

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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lWieh I nac gte on daorb wtih smntAdutej sDrrd,ieo I don't ees who hsit rewnas is ayn rttebe tahn oSctima typmSmo rrDesido. Fmor :FA

riatVye of yoldbi cintosplma gnailst ostmnh to esyra esoaastdic hiwt xvies,esce enisttrsep tuhothsg dna itanexy baotu motsy.psm yaM ao-ceaprp tihw s.nlslie

SDS lbgosen ni a ourgp of sdredosir dihetcarrceaz yb ichslpya osmystmp ignascu sitgciifnna sridtses and traenipimm.

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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coehiC A. uwdlo ahev bene ortecrc fi siht ntaptei wsa mmue.niprmsocimodo Pre irtFs di,A f"I C4D ;1t&l00, nllang:..teoF.siBdarin loNhtireucip tano.iImnfmla

Hw,reoev sa tish tpentai ahs a etmtpnoec mnmeiu yms,tes ubzz dorsw rae llsettae ciezinrtogn oasglarmun.

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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Cchieo A. dwlou vahe neeb ceotrrc fi hsit etpnait was oericosmnpudom.imm reP iFtsr diA, f"I C4D 0;,0t1l& .laai.lnB:sngodnrtFe.i iNruciepthlo oatImnalfin.m

ov,weerH as hist tientpa ahs a tptmcenoe eimmnu smste,y zzbu drsow ear lettelas gtiocnnzeir sglnruoama.

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 es-Hlene atC htracSc in opn-ecmmimnttuoo - ..i/nohltpeuswhgnem/dcmya.pohttpwhhotctocmclsay:lotao/l/cwtstirploa Brale tn lenaeseh in -opm-sieuoromIncmmd alcaiyBir istgtnaooamsi o sLko leik sikpao smaraco "Dus fefi tuenpoihircl itlarnfite" AF 1920 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(235),
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B l-seeneH aCt archtSc ni mtconiotepomm-un - ahhycsc./ltewo.ttsen/lhchdnto/tawpogpctiymaspp:hiowoc/luot.mltrmarntle o lBa eelheasn ni mrmcpmnosdumi-Ioe-o lyaiicBar tagosatoiisnm Looks liek spokia acrsamo "feusDf i ilrucnpietoh enrf"ttiail AF 9102 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 xxabi(224),
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osr’cBa :iaapahs eevxspsrie toorm( a)hpaasi iwth rmmasaagmit t(sp rewaa ahtt etyh t’dno meak ense)s - aare sn’eeiW kArc h:iaasap tcireevpe ensoy)r(s spaahai wthi peamirid pseoncemonhri s(pt lack )hsitnig

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  


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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