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Welcome to gh889’s page.
Contributor score: 117


Comments ...

 +0  (step2ck_form7#1)

• Perivascular changes secondary to recurrent small PE → ↑ pulmonary vascular resistance → ↑ pressure in the pulmonary circuit → ↑ RV afterload → dilatation and/or hypertrophy of the right heart

• Will present as pure right sided HF (JVD, dyspnea, ascites, LE pitting edema, cardiomegaly but NO pulmonary edema (pulmonary edema is associated with left sided HF)


 +1  (step2ck_form7#41)

• Severe SBO presents with:

• ↓ bowel sounds when it is a complete block (hyperactive/high pitched when less than 100% b/c the body is trying to push pass it) • Distended and tympanic abdomen • Postprandial pain • Pain relieved with vomiting (relieves some intra-abdominal pressure)

• SBO initially has high pitched bowel sounds but a complete obstruction has ↓ or absent bowel sounds


 +4  (nbme23#14)
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Gater ieovd on S1 nad sit' !tsl!ip


 +4  (nbme23#47)
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opcsinromes of hte omocmn raelnpeo rvene as it rsapw drnaou eht neck fo eth ulfabi assceu edrseaecd sesatinon fmor hte lairiuescfp elnearop n,vere slrbesnopei for eth aerltleotnaar csatep dna udmsro of teh leg nda otfo

peDe arpeoeln evnre si ysoesnr to the ceewsbap ewtebne hte lulhxa nda dn2 dtiig

pci

maxillarythirdmolar  You might be able to damage the superficial peroneal nerve with damage to the lateral malleolus but the description in the stem has deficits in the end targets of both the deep and superficial peroneal nerves +1

 +6  (nbme23#34)
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rirRegfen to sRNTI adn sINTRN sa asiamtny fo etnerttma

aia:sMynt aienrzefv I)(NTNR, nfoveoitr (INT),R dna rnieibicteamt N(T)RI

ususmle  I guess he is asking about integrate,,,,, where his should be integrated into host dna to get replicated .. triple therapy includes. 2drugs NRTIs and other one is integrate +
whoissaad  @ususmle NRTIs would still inhibit DNA synthesis since they mess with the reverse transcriptase which is needed to make viral DNA. +2
thotcandy  @ususmle HIV triple therapy is 2 NRTIs/NNRTIs + 1 protease inhibitor. Plus, if her CD4+ cunt is already 60/mm, that shit is well integrated in her CD4 cells already, right? +1
brotherimodu  I was confused because isn't HIV an RNA virus? +1
focus  @brotherimodu yes and therefore it uses a reverse transcriptase +1

 -3  (nbme22#35)
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Fmro ySerdHueahkkonnoo no dderi:t

hatW hte ieuqsotn si gneitgt at si hte tmacepshyti achni wsa eadp.rs tI saw a ireelbtr ayw of odirnwg i.t

Yruo riearnto othspmauyahl is roeleibspns fro lgoicno tureeafs and si reund aypaschitptmrea rtnc.olo A lienos odlwu ecuas trr.yahmpihee

Yruo trorispeo pltsoaymuhah si ipbreenolss for hieatgn nehw yoru'e ocld dna to eagernte the evFre srnoseep nad is ednur smypitaecht cro.ntlo A oisnle lwdou uscae hpr.ahyiemot

In isht tnioqeus ti si yilspm isknga a neospr setg sck,i ouhhytaslmpa asw d,rsaep ahtw hepaps.n

ne:wsAr lhhsaauotmyp iwll llsit eb elab ot eeltave set ybdo rmeurpetate to ttelab tifonicen.

Hin:t FI tyeh iegv a nqseuoti lmasiri ot sith ubt rweedord to diulecn a neilso fo hte sytphmaceit rsbife ro fo eht uat,lpyaomhsh yuo lduow ni urtn TNO eb ebal ot eagrneet a revef oespersn to efc.nnitoi hTe patyalmhosuh ldouw eb tlnyiree eudrn ittehycamrapaps ootlnrc

hsTi ddas rmeo coextnt to eht acft eth Q aetsst that the ihctyaetsmps asw apdser

oslerweberrendu  So, this says sympathetic also spared and hypothalamus also spared. Then what was wrong with this clinical case?? +
adong  i think the sympathetic system is actually impaired b/c it's cut before it can "outflow"...at least it's the only way this makes sense +3
suckitnbme  I agree. I think the question stem is saying the sympathetics were lesioned. Not that they were spared. +3

 +4  (nbme22#26)
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ogicdcran ot aupodtet tdhisazie uceas a diml yeohclmvpio tsate uhst ruoy TPC lliw ese emro aN dan 2HO -;-g&t by pirlncpei that teh PCT walays srbarbeso 06% fo ahwt ti ,sees it liwl obesrrba more teawr adn N.a

almondbreeze  in sketchy as well +

 +4  (nbme22#24)
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tKloecora si a sblvreiree SNIDA gevin IV, all AsSDIN aehv a krsi fo itisateiltrn rtn,hiispe lnear i,esmchai garicts urec,sl and apcaislt aamen.i

het tseb sanrwe is alern afuerli cb/ ti si ngive IV nda sah slse of a hcncea of acgiuns tsaricg clsure

tiredofstudying  I would also take into account that this patient has had HTN and T2DM for 20 years. His kidneys are probably shot. +5
jackie_chan  @tiredofstudying 100%, thats probably why the mentioned it, if you didn't know wtf ketorolac was (I didnt) but i saw a long 20 year history of HTN, DM I assumed his kidney def could not be fully functional +
faus305  I just ordered sushi from Japan. +

 +5  (nbme22#42)
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aserwn si deilgna uoy ot sidnifaerte - rucata5s-ehapled iitnbhoir rof PBH nad amle eeartnptd easndlsb - ti soklbc the nicerosovn of otsetnteoesr onit HDT


 +5  (nbme22#9)
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eTh arae dbeaell C si the psto seomdsoems teweben wto yocemsty dna ewehr ntcia mtailefsn rtinse no eht momeaarlcs

NKLI


 +2  (nbme22#2)
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The esarnw is eud ot na necoitxpe ituoelnd here eehrw naiinc si uesd in spt /ow stdebeia how vaeh rcatyroerf rglermpiydchietariey at ihhg rkis ro ash a hx of a.isnreciaptt

I ergae that srfaiebt rae tsfir lein na(d so sedo htta ira)lcet tbu ENBM asw iognhn ni no a fisicpce poeenicxt hatt iaicnn nca lsoa be dseu csnei VLDL dan sGT rea hgih ni yliypgrcrati.mieedrhe

eTh "c"leu htey adh saw "uenrctrer taisi"nrpteca hwhci is ysuppesdlo a edal swadtor iacnin.

I also ptu ercanies ..DH..L

wutuwantbruv  Correct, you would not want to give fibrates to someone with recurrent pancreatitis since fibrates increase the risk of cholesterol gallstones due to inhibition of cholesterol 7α-hydroxylase. +
kernicterusthefrog  FYI @gh889 can't follow your link w/o an NYIT username and password, unless there's a more tech-savvy way around that.. I appreciate the info, though. Niacin rx for familial hypertriglyceridemia w/ recurrent pancreatitis. Now I know.. +2
impostersyndromel1000  Great points, very in depth knowledge taking place here. Also, familial hypertriglyceridemia (per FA 2019 pg 94) has hepatic overproduction of VLDL so picking this would have been the easiest answer (in retrospect) +2
hyperfukus  @impostersyndrome1000 literally that's the ONE thing i remembered and i went YOLO lol cuz i was staring for a while +
osler_weber_rendu  @gh889 I agree niacin is the answer, but even niacin causes increase in HDL. As if getting to the drug wasnt tough enough, NBME puts two of its actions in the options! What a shit question +1
mtkilimanjaro  I forget where I saw (maybe UWorld), but I always thought increasing HDL is never really a primary form of lipid control. You want to lower the bad cholesterol etc. since increasing good cholesterol wont change LDL VLDL etc. +

 +0  (nbme22#35)
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uloCd oesemon lpsaee aipnlxe hhwic sdrgu (if nay) rae ta D dna E?

usmleuser007  1) label D (VLDL -->ILD --> LDL) = anything that increased LPL = Fibrates which use PPAR-alpha (Rx) are good at reducing [VLDL]; therefore, less VLDL means more ILD. 2) VLDL --> fatty acid oxidation = using fats (TAGs) for energy production Here PPAR-gamma plays a role= which are Thiazolidinediones (also called glitazones) are a class of medicines that may be used for the treatment of type 2 diabetes. They are also good at reducing serum TAGs Note VLDL are very rich in TAGs +1




Subcomments ...

How is this due to decreased renal blood flow when the BUN/Cr is <20 ?

gh889  ischemia of the kidneys can cause intrinsic renal failure - w/ a BUN/Cr <15 +  
step_prep5  for more, see comment: https://nbmeanswers.com/exam/step2ck_form7/1977#5900 +  


submitted by gabeb71(44),
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hTe elristocpuba lms,uec wchih si one fo het esscmul atht psmreoci eht velicp olfro and asypl an npamoirtt oerl in boht lecaf ocnnenceit adn acoendfeti, is incyloalt rocdetanct nad nanmsatii eth ctaaenlor lgaen ta te.sr

erhe is a ir:tcpue cs/te-wt-rrnuhlhts-orw.mgd-lh-s--hels.n:apmemrt-2hs-pttitvawcopusvok70-ae4trahlo/eaw-uutou-5cneo-c-dosarh3ecoofio-_otfr.hti-mb-cf9et8l-teoo4petrtncf/n1-6-_

gh889  How do you differentiate this from hypertonicity of the internal anal sphincter? +1  
gh889  nvm. im dumb lol +  
qball  Uworld Q ID 17004 +  
focus  @gh889 I made the same mistake... fecal INCONTINENCE meaning she CAN pass stool-- in fact, way too well... more than we want. Hypertonicity of the internal anal sphincter would cause constipation-like symptoms. +2  


submitted by gabeb71(44),
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The erbliotcupsa cmusl,e hhciw si neo of het esslmcu that cpsroeim eht levcpi lrofo dna ylsap an tarptomin roel in both calfe otnecnecni dan oeiftecnda, si lyltcniao cdaonerttc and antiimnsa teh taarcenlo nagle ta etr.s

erhe is a cutir:pe bcrso4otlokio-9scroemulu7t:-rmch-rptdrtt--op5--h-ewtuf--8l--.2ef6awerh-t.ne-eowrmr-/mlca_ittts3socovaothth40w/eoe-poc-ig-att-au/svepndhthfcnhfse_a1n.uslon-

gh889  How do you differentiate this from hypertonicity of the internal anal sphincter? +1  
gh889  nvm. im dumb lol +  
qball  Uworld Q ID 17004 +  
focus  @gh889 I made the same mistake... fecal INCONTINENCE meaning she CAN pass stool-- in fact, way too well... more than we want. Hypertonicity of the internal anal sphincter would cause constipation-like symptoms. +2  


submitted by docred123(6),
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iH ugsy cna onmseoe lsapee abreltaoe on seeth idfng.sin I enndturdas hes sah gnul cnrace sth'ta igpeidmn erh hrecaat. uBt how is ihst epvnttieraerse of na eusctboivtr sodr?idre tA'nre ungl ncsecar ritretviecs fi ?tnanihyg Taks hn

nlkrueger  I agree that it's confusing but I looked at it as a physical *obstruction* since it's impinging on the airway.... but yeah idk this is weird +  
ferrero  Doesn't the trachea have cartilage rings so it wouldn't collapse which makes it seem less like a typical obstructive disorder? I'm really not sure why FVC would change because I don't see how total lung capacity or residual volume would change because those are static conditions where there is no airflow at all. I understand FEV1, peak expiratory flow, peak inspiratory flow etc. +2  
mousie  Agree this is a really tough Q but I also think I really over thought it... I eliminated all with a normal Ratio bc something obstructing would obviously produce an obstructive pattern although I don't know why FVC would be decreased. I wasn't sure about both peak expiratory and inspiration flow being decreased can someone help me with this or tell me I'm totally overthinking again.. are they both decreased simply bc theres an obstruction ..? +3  
mimi21  Yea I got confused on this question. But I guess they wanted us to look at it as a obstructive disease . If this were the case all of those function tests would dec. ( See FA ) +  
gh889  Because the obstruction is above the alveolar regions there is a decrease in air flow, not lung volumes, which would make this an obstructive pathology. +3  
charcot_bouchard  FVC here dec same way it dec in Obstructive lung disease. Read the concept of Equal pressure point of BnB. There he says in bronchitis we have onstructive pattern because inflammed airways gen more resistance. so EPP comes early. I guess here due to tracheal narrowing pressure inc downstream. which collapses smaller airway. result in air trapping. +1  


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heT tnetapi hsa ANT socanyrde to aenlr i.ischame Deu to autlrub sres,ncoi the aietpnt lwil vaeh an edevteal aeNF. eTh tesapn'it reiun will oals eb ,uedilt ubt htsi lwil be rtcfeeeld by teh low iuern oytllm,isao otn teh NFea

mousie  Hypotension can also cause pre renal azotemia with a FENa <1%.... How do you know this is ischemic ATN and not hypotension induced Prerenal Azotemia? +11  
sympathetikey  I had the same thought as you @mousie, but I think "azotemia" and low urine output push it more towards ATN (looking back; I got it wrong too). Plus, the initially MVC / muscle damage probably caused some tubule injury by itself. +2  
ajo  This might help clarify why the pt. has ATN rather than pre renal azotemia. The question did mention, though subtly, that the bleeding was controlled. That most likely indicates that his hypovolemia has been corrected. Developing azotemia 24 hrs after correction of hypovolemia is more suggestive of ATN (since he doesn't have hypovolemia anymore). I hope that helps and feel free to correct me, if I am wrong. +39  
ajo  In addition to my earlier comment, I just noticed the question also explicitly mentioned that he was fully volume restored. Which is consistent with my earlier assumption! +14  
gh889  Although initially, hypotension causes prerenal azotemia, the volume correction pushes you away from prerenal azotemia. but they want you to remember that in hypovolemia, the kidneys are also becoming ischemic, and so development of azotemia 24 hours later is more indicative of intrarenal azotemia due to ATN +  
sugaplum  for anyone who wants to see it: FA 2019 pg591 +1  
divya  i'm confused about one thing. if the tubules aren't working like they should, the bun:cr ratio falls right? doesn't that essentially mean azotemia reduces too? +  
osler_weber_rendu  Lets all take a moment to admire how shit this question is "Bp 90/60.""Repeated episodes of hypotension in the OR" and still the answer is ATN +4  
donttrustmyanswers  @osler_wever_rendu ATN can be caused by ischemia. +2  


submitted by sakbarh(5),
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eSh has nmay arluvcsraaicod krsi ctrfosa and lielky sreufedf a esktor fo hte sbialra terary gauncis lkcoed in or.yemnds ngrcAocid ot FA isht anc asuce a isnoel ta hte ,pson auldl,mre ro orwle nbimdari -- ovheerw oinmlaaaylct teh biarlas reraty rnus hgtri no otp fo het osnp os yopritixm tsom lyekil kesma it the ghtir ea.nrsw

mousie  The Boards and Beyond video of SC strokes was really helpful at explaining this if you are a video kind of person! +1  
yotsubato  What pushed me away from pons was "dysarthric speech" which implied she still could speak to some degree.... which made me pick medulla. +3  
mimi21  I think FA may be misleading. Primarily it will effect the Pons because that is where the majority of the Basilar Artery is located. and I guess it could effect the other locations? but everywhere I have looked Locked-in syndrome is an issue with the Pons. But someone please continue to clarify, cause I was a bit tripped up at first with this question +  
cbrodo  Although FA says it can be pons, medulla, or lower midbrain, "locked-in" syndrome generally arises from BL pons lesions. Another way you can rule out medulla and midbrain in this question is the ocular movement findings. Since the patient has impaired horizontal gaze BL, you can conclude that the Abducens nuclei are involved on both sides. The abducens nuclei are located in the pons. +40  
gh889  USMLE secrets also states that it is most commonly in the pons Bates states that locked-in syndrome preserves consciousness but these patients have limited speaking ability +  


submitted by joha961(43),
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itnMaaencen dsoe = ssC( * LC * t) / F

... erhew t is elepdsa mtie weenebt sodes n(to varletne heer scnei st’i tcionsnouu nsoni)ufi and F si iytalaaiioilvbb (chihw si 010% ro 1.0 here seaubec i’ts nigve I)V.

nt​aCotsr tiwh nadlgio esdo:

sCs( * dV) / F

... rehwe Vd is velomu fo tsii.dionrbut

yotsubato  So do we just have to memorize this... +9  
gh889  yep +12  
drschmoctor  @yotsubato Not necessarily. I can't remember a formula to save my life. The Css is the amount you want in the blood. The clearance is the fraction removed per unit time. Since we want to maintain a steady state, we only need to replace what is removed. Thus, maintenance dose = amount present * fraction removed. +8  
mambaforstep  https://www.youtube.com/watch?v=gnqOUmNhmdg good & short explanation +1  
castlblack  I remember CLoCk Time as in check the clock time to give the next dose Cl = clearance, C = concentration and T = half life. I have never had to use F. +21  
baja_blast  This is on p. 233 in FA 2019. +  


submitted by lnsetick(90),
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woH aer oyu aelb to letl atth eth CT lesci is nto ta eth lelve of dodme?nuu

zelderonmorningstar  I think the small intestine narrows as you go along, so jejunum would most likely intuss into the duodenum. +  
yotsubato  Duodenum is fixed to the retroperitoneal wall, and also has lots of named vessels attached to it, along with the pancreaticobiliary duct and ampulla. It cant really intussuscept. +  
gh889  You should also know that the duodenum is almost purely on the right side of the body +26  


submitted by meningitis(511),
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yAcullat, I ctecorr m:lfeys I koleod slorce nda teh iGneto amrlefo sha an trneealx Smaretcip cabhrn dna a auuiboniLmlng rh.acbn I ohttugh ti swa hte eoaneofGlrmti reven uaecesb hte ltineag hnacbr spessa htrghuo eth pdee iagnnuli ignr, etrens teh lgaiiunn nalac, gose to mspaeticr rocd dan psipsule het aetecmsrr nda otracls n.sik

eHser teh :aegim a2rtpinmegoapol/roy/se8uadisk.eidmiep/nomawd:it/.ig4/h/k/Gc.p4w

roretcC me fi I ma wogrn sa.lpee

gh889  I think you're right, FA2019 pp444 even states that sensory to the scrotum is via the Genitofemoral nerve +4  


submitted by dr.xx(143),
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As artp fo eoircbnmy epevot,endlm teh pasreanc fsrom sa otw bdus rfmo teh reut,ogf an eomrncybi bute thta is a pusrecror to hte rstilsagttenonia ac.trt It si efhrteoer of mldnerodea giniro.

ie:nnatrvneriph/kseaogmiwt/leD#/wkpc.siedap/tiPeo.

gh889  nice! I reasoned it as that most of the GI system is of endodermal origin +9  
taediggity  FA 2020 pg 613 +1  
mutteringly  FA 2019 pg 599 +  


submitted by meningitis(511),
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Tenrna esgats tarst ta TEN esayr lod

aeStg : I

  • I is fla,t sa in ltaf hs;ect
  • I si a,enlo sa in no exalus a.sihr

aSteg II ):2( aegst II ssrtta ta 11 y/o II( olok kiel 11)

  • 2 lasbl aetlit(srcu rtnnlge)meae
  • 2 ihars ibc(pu ihrsa now )aenapgpir
  • 2 aebtsr dusb rofm

gtaeS III )(3: stsrta ta 13 o y/

  • If yuo tetora 3, it koslo keil malsl earstsb tBrse(a smundo )orm;f
  • If oyu lsgieugq the III tyhe kloo keil clroycure+as pbicu hari
  • deIacsrne inpes nltgeh and isez can be dseeeepnrrt b:y II g-t&;- III
    r(ouy psnie was thni II ubt won tsi ikchret III)

Saegt IV 4):( ttsras ta 14 y /o

  • sFrit :imaineg eTh I in IV nerptssere teh t,ighh nad the V in IV ooksl klei the osmn pbuis bweente yuro g:esl
    :INGENM A yuo ehav rahi ni nsmo iupsb V() ubt you vhae a drbreo nntigeida teh ahir fmor iwonrgg oitn hg.this
  • ehT V is oyptn,i as in own eth bsrtaes rae tyoinp isedra( eorlaa ro dnumo no duom)n

aetSg V 5:() 15 oy/

  • V ahs on orrbdse nneidgiat ihra rofm irowggn niot hgtish bupi(c airh + hghit h)air
  • 5 fesin(gars in nahd)s itfntnlaeg eht earasol nehw brgganbi meth a(oaler ltntfae at hits satge and on ermo udmon" on n"m)uod

meningitis  Sorry about the format, it came out wrong but I hope his helps. +1  
drdoom  looks good to me! +17  
gh889  According to FA2019, stage 2 ends at 11, stage 3 starts 11.5-13, and stage 4 starts at 13-15, where did you get your info from? +  
meningitis  You can change it to ENDS at 11, ENDS at 13, ENDS at 14... I simply have it as a range just like you stated in a couple of them. The importance is in how the kid presents because he/she will have some things mature but others not, the age will vary in questions. +  
endochondral1  stage 3 breast mound is for females not males btw +2  
endochondral1  see pg. 635 in FA it just pubertal. Idk if that correlates to the same stage as females +  
angelaq11  this is just too funny, I LOVE it! xD +2  
snripper  While this is impressive, this doesn't help with answering the question. +1  
yng  Pseudogynecomastia (False gynecomastia): this has nothing to do with puberty or hormones. Simple d/t the fast some guys have extra fat in chest area, making it look like they have breasts. The boy weight at 60 percentile while height at 50 percentile. +  


submitted by taway(30),
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stuJ sa a eton orf oybnayd lese ohw aws WTF at owh 09(330/02/3(2)) = ./a115.. lot of uisntqoe nkbsa rodnu 2039/ r(o nya rlsaymili eargl c)iatfnor uto to 1

gh889  I think you meant 2(29/30)(1/30) just to clarify! +7  
niboonsh  i am confusion +2  
arkmoses  You have to use the hardy weinberg formula (1=p^2+2qp+q^2)and p + q = 1 they basically tell you that q^2=1/900 which makes q=1/30 now you can figure out (p=1-q) so p=1-(1/30), p=29/30 then to figure out carrier you solve for 2qp, 2(29/30)(1/30)=1/15 I got it wrong cuz I forgot how to figure out p but hopefully wont happen on the real deal. +5  
garibay92  2pq= 2(29/30)(1/30).... Transform this to 2 1 1 2 1 x x = _ = ____ 1 1 30 30 15 +  
garibay92  Nevermind :/ It didn't come out as planned :( +  
garibay92  /Users/carlosgutierrez/Desktop/IMG_2423.jpg +  
pg32  How do we know this disease is autosomal recessive? I assumed it was just because they love these carrier frequency questions with AR diseases, but how do we know it's AR? +  
turtlepenlight  Sounds like Gaucher (ish?) if i'm remembering correctly +5  


submitted by egghead(1),
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Tsih is eon of hteso sioqesutn I was rveen ignog ot t.ge Its' ont in FA, I ntdo' khnti 'Iev esen it in .cslas

hungrybox  same :( +  
masonkingcobra  My issue was the stem said no skin damage (I would think pulling out your hair damages your scalp) [Turns out it does not](http://onlinelibrary.wiley.com/doi/full/10.1111/j.1529-8019.2008.00165.x) +  
gh889  FA 2019, pg 551 +8  
meningitis  Compulsively pulling out one’s own hair. Causes significant distress and persists despite attempts to stop. Presents with areas of thinning hair or baldness on any area of the body, most commonly the scalp. Incidence highest in childhood but spans all ages. Treatment: psychotherapy is first line; medications (eg, clomipramine) may be considered. +13  
step1soon  FA 2019 pg 551 +1  
teepot123  damn its in FA and Ive never ocne read it XO +  


submitted by mcl(586),
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toeMhineni is na tseneisla oaimn .daic lAl hrtose lstied rae to.n

scalpelofthenorth  Pg 81 Tyrosine is listed as an essential AA. Should be tryptophan for those who got this wrong like me. +  
neonem  But tyrosine can come from phenylalanine, so it's not really essential right? +  
gh889  in FA2019, it is listed as Tryptophan, not Tyrosine. That was corrected. +15  
usmleuser007  Note: Tyrosine is ONLY essential with PKU in children +  
niboonsh  bro FA2018 lists tyrosine as an essential AA. They played us. +1