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Welcome to lilyo’s page.
Contributor score: 72


Comments ...

 +1  (nbme18#29)
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enynAo ehva an diea on how to croapaph tshi ?sotqneiu

gdupgrant  So the thing i think they tried to catch people on was that the SMV Joins with the splenic to become the portal vein and the IMV feeds into the splenic vein. And they want you to know that cecum is midgut, so drained by the SMV. so my approach was automatically eliminate any answer that included IMV or Splenic vein and that left me with only Ileocolic → superior mesenteric → portal → right hepatic branch of the portal +16

 +0  (nbme24#6)
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sssthiaoCle liwl stnrepe htiw eadetlev onajecgtdu birnuibl,i Aklnalei a,phthseapso GGT. dnDeigenp on eht scaeu fro ssaleiscoth ti acn retpnes thiw eapl sosotl dan drka ne.iru


 +2  (nbme20#10)
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sttciPoher evavls aer eon of het sceasu of artsexvulaacr lmhsseyoi os pcsseut tshi in a aiettpn atht sah ompstysm fo eimana uchs sa ufaegt,i p,lrola nejaidcu. hrtruFe rusptnipog idnveeec ni hsit ptteian si eth eeiasrcdn ircdenti nubb.irlii lA,os okol orf etevaedl ,LHD srddaecee otgbpnhi.alo

nephroguy  All of this is correct except its intravascular hemolysis, not extravascular. Also look for hemosiderinuria, hemoglobinuria and schistocytes on blood smear +3
dermgirl  Is not intravascular hemolysis, it is extrinsic hemolysis, specifically macroangiopathic hemolytic anemia. FA 2020 page 423. +
vishnu_c_singh  This is actually BOTH intravascular hemolysis & extrinsic hemolysis. Extrinsic = hemolysis that isn't caused by an internal defect of the RBCs, like an enzyme/membrane defect (in other words, it's hemolysis due to an external factor like a mechanical valve). Intravascular = hemolysis that occurs within the blood vessels (RBCs get damaged as they pass through the valve). This is in contrast to extravascular hemolysis which describes hemolysis that occurs outside of the blood vessels (e.g. inside the spleen) +4
sexymexican888  This is so dumb... but helpful I just realized -intrinsic hemolysis (something intrinsically wrong w/RBC i.e G6PD, PNH, sickle cell anemia, hereditary spherocytosis ) VS extrinsic hemolysis (something on the outside of RBC i.e. autoimmune hemolytic anemia, MAHA,mechanical destruction [aortic stenosis, infection) is NOT the same as -intravascular (in blood vessels i.e. complement) VS extravascular hemolysis (in the spleen) so prosthetic valve hemolysis is INTRAVASCULAR EXTRINSIC hemolysis. Hope this helps understand that better, theyre mostly classified by intrinsic/extrinsic (whats wrong with the RBC) vs intravascular/extravascular (where does it happen) +1

 +0  (nbme20#29)
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ysaecrTnetlic msot mnmcoo edearsv feseftc rea eienovms/aai/dhrataru nad veityiiohs.nsptto Cna ffctea seobn dan eetht of nnwroeb fi ginve ot teragnnp wo.nem lsAo thsi drgu sslac evosrc ,SGA ,BGS -+/ MR,AS ypreorisatr lfaor adn lrir.lntcalaeu

Wyh iCpro is ont eth sare:wn cdiorelaM vcseor GNR + Poseud, eetrofreh ton a naertmtet for aenc in(sk .ol)raf nAd ocmnom eeadrvs sffetce era .CiffD icen,fnoti QT ntrnlp,ogooia dnetno ru,trpue ttoaecrnegi .ctsefef



 +2  (nbme20#8)
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aTke a kloo at AF p3.6g2 for tnerna esgsta of asxleu nteme.lvpoed

baja_blast  (This is the right page for FA 2019) +1

 +0  (nbme20#16)
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I saw hgnitkni olang het slnei of fliaca iontnsesa hwich is itedamde yb het mgtliinear erevn nda the cfat taht the rgtniameil enrve is toalcde ni eht p.nos


 +0  (nbme22#44)
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I dah het esma nitousqe agdnreigr .ihts I onkw hatt nlaxeetr mohroisrehd rlarye lebde and liertnan osrohmrheid tpnsree as lsepansi gnbdilee so in my ndmi I eknw I asw gbeni sdeka otabu nterailn oriemd.hhosr wveH,ore orupresi ar&lcgte;t-- efoirinr nmectirese t-vn&e;g-i rtpoal iv,ne anc oeynan etll me wyh het rawnse wsa prorsuie etarcl dna nto niiorrfe mcre?nieste

dubywow  Because the wording sucks. It's a confusing way to word the question. I too was confused what direct tributaries was referring to and chose Inferior mesenteric because I suck and also because this question sucks. Really its asking where are the hemorrhoids? They are on/from the superior rectals even though those veins feed to Inferior mesenteric. +3
drdoom  Defining tributary: https://i.imgur.com/2zDxPbW.png Nice images make the term easier to recall. Smaller streams "pay tribute" to larger rivers (by flowing into them). +5




Subcomments ...

submitted by sugaplum(376),
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eth reedep the oenmmaal egos teh owers het ssoniogrp

wishmewell  isn't the basement membrane the deepest? +  
wishmewell  nvm! lol +1  
lilyo  I also picked basement membrane but unlike you I haven't had a "nvm" moment. Help please. +2  
mcdumbass  @lilyo Basement membrane is between the epidermis and dermis; beneath the dermis is the subcutaneous tissue +5  
blah  I think some people might have picked basement membrane because we're taught once cancer goes through the BM it turns from in situ to invasive. This is correct, but subcutaneous as the others pointed out are deeper so the prognosis is worse (BM + deeper tissue). +3  


submitted by vshummy(162),
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I tnkhi mero lne,yrgael rteonpi nlfdoig ehsnpap at teh RRE dna het mest ysas eht rtinoep dtsoen’ odfl lr.oprpey ipliScf,lycea teh tsom oomnmc FC oitanumt si a lisdodemf oernipt adn het irnoetp si iadtreen ni het RER adn tno psernrtadot ot eht llec mbrnmaee - AF 1902 gp 0.6

uroosisyed5  Which makes sense if we think about the pathophys of elevated Cl- and Na intracellularly. Both of these ions go up inside the cells due to the retention of the misfolded proteins in the RER. +  
lilyo  I actually disagree with this reasoning. The pathophysiology in CFTR is not due to accumulation of misfolded proteins. It is due to decreased/absent ATP gated transmembrane Chloride channel. According to Uworld, the miscoded protein is detected by the Endoplasmic Reticulum. The abnormal protein is targeted for destruction by the proteasome and never reaches the cell surface. There is NO retention of misfolded protein, there is degradation of misfolded protein and therefore absence of chloride channels on the membrane. This is what leads to impaired removal of salt from the sweat as well as decreased NaCl in mucus. I dont think the answer should be ER. Can anyone tell me if I am missing something here that makes the answer ER as opposed to cytoplasm? Because the way I see if is misfolded proteins go form the ER into the cytoplasm to reach the proteasome and then be destructed. Uworld questions ID are 805, 802, 1514, and 1939. +15  
drdoom  @lilyo The CFTR is a transmembrane protein. Like all proteins, its translation begins in the cytosol; that said, CFTR contains an N-terminus “signal sequence”, which means as it is being translated, it (and the ribosome making it!) will be transported to the Endoplasmic Reticulum.^footnote! As it gets translated, its hydrophobic motifs will emerge, which embeds the CFTR protein within the phospholipid bilayer of the ER itself! That means the protein will never again be found “in the cytosol” because it gets threaded through the bilayer (which is, in fact, how all transmembrane proteins become transmembrane proteins at the cell surface -- they have to be made into transmembrane proteins in the ER first!). +8  
drdoom  @lilyo (continued) So, yes, ultimately, these misfolded proteins will be directed toward a proteasome for degradation/recycling, but that will happen as a little vesicle (or “liposome”); the misfolded protein, in this case, is not water-soluble (since, by definition, it has hydrophobic motifs which get “threaded through” a bilayer to create the transmembrane pattern), which means you won’t find it in the cytosol. +5  
drdoom  ^footnote! : The movement of active* ribosomes from the cytosol to the Endoplasmic Reticulum is why we call that area of ER “rough Endoplasmic Reticulum (rER)”; on electron microscopy, that section was bespeckled with little dots; later, we (humans) discovered that these dots were ribosomes! +1  
drdoom  * By “active ribosomes”, I just mean ribosomes in the process of converting mRNA to protein! (What we call “translation” ;) +1  
wrongcareer69  How many goddamn ways are they going to test us on CF. I'm so over this! +2  
furqanka  also in FA, under alpha 1 antitrypsin, its says 'Misfolded gene product protein aggregates in hepatocellular ER". might be the same concept. +4  
joanmanuel26  According to Kaplan; All proteins that are synthesized in the ER must fold correctly in order to be transported to the golgi aparatus and then to their final destinations. If the mutation cause a misfolded protein, the result will be the loss of the protein function and, in some cases, accumulation of the protein in the ER. +  
drdoom  @lilyo Thinking about this more. You will not find the (misfolded) protein in the cytosol. The misfolded protein may be inside a proteasome—and a proteasome may live in the cytosol—but the misfolded protein itself will never appear in the cytosol. The products of its degradation might (constituent amino acids or small peptides) but if you had an antibody for the misfolded protein and asked it “Where is the misfolded protein?”, the antibody would answer: “Most of what I could find appears to be in the rER.” +  
yesa  Check out the calnexin cycle, usually proteins that are made in the RER and misfolded get tagged and 'refolded' and then scanned again for proper folding...and if they really can't be refolded, they're degraded then and there! So the only place misfolded CFTR could accumulate if misfolded is....RER... (Link to calnexin cycle: https://www.google.com/search?q=uggt+in+rer&sxsrf=ALeKk02X8jH8eveQ2IVM9IsVOlO47Qjh5A:1597110732938&source=lnms&tbm=isch&sa=X&ved=2ahUKEwiI75yPhZLrAhUTZjUKHWxgCaIQ_AUoBHoECAwQBg&biw=886&bih=1045#imgrc=4UYRaaYQDDFbDM) +  


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Teh ssdiaee heer si ucersoft ahptsspshaiboe ednf.eciciy In ti, VI lrlgyceo ro rsefotuc nsod’et help seeabuc hobt tneer the olosgniensgeecu pwhaayt lwboe esfotruc hobsiastppea.h lcGsaeaot no eht oerht dnah rsneet ebaov ti. I dont’ nkiht yuo ylealr need to wkno sthi ot eschoo hte tocrcre weasrn enisc the lcicianl ieuctpr of nagsift oamcyhlpygie tath is ecoerdtrc /w osem orts fo augrs that cna erten eht oeisngscougeeln apawyht shudol clue ouy noti teh ighrt rn.sawe

neonem  I don't think you could have *totally* ruled out the other answers - I picked glycogen breakdown because it sounded kind of like Von Gierke disease (glucose-6-phosphatase) to me: characterized by fasting hypoglycemia, lactic acidosis, and hepatomegaly since you're not able to get that final step of exporting glucose into the blood. However, I guess in this case you wouldn't see that problem of glycerol/fructose infusion not increasing blood glucose. Nice catch. +25  
vshummy  I think you were super smart to catch Von Gierke! Just to refine your answer b/c I had to look this up after reading your explanation, von gierke has a problem with gluconeogenesis as well as glycogenolysis. So they’d have a problem with glycerol and fructose but also galactose since they all feed into gluconeogenesis before glucose-6-phosphatase. Great thought process! +22  
drmomo  glycerol and fructose both enter the pathway thru DHAP and glyceraldehyde-3-ph. Galactose enters thru Gal-1-ph to glu-1-ph conversion +2  
linwanrun1357  In this cause (fructose bisphosphatase deficiency.,),fructose should help to increase serum glucose, bcz it can become into glucose-6-P by hexokinase. Therefore, this question makes me confused.... +  
krewfoo99  According to uworld, fructose infusion will not increase blood glucose levels in Von Gierkes Disease as well +  
atbangura  I believe Von Gierke is not a plausible answer choice because a galactose infusion would still not see an elevation in glucose levels. Remember, galactose could be converted to galactose 6 phosphate, but in order to complete gluconeogenesis and allow glucose to leave the Liver for an increase of its concentration in the blood, the patient would still need glucose 6 phosphatase which is eliminated in Von Gierke. +1  
lilyo  So what disease is this??? I mean couldnt we have just answered the question based on the fact that the patient responds to galactose being infused and we know that galactose feeds into gluconeogenesis?? I am so confused. +1  
djtallahassee  Its Hereditary Fructose intolerance right? gets sick after fructose and I guess glycerol can jump in via aldolase B on this pathway via page 74 of FA2019. It looked like a fructose thing to me so I just marked out the other ones and moved on. +1  
paperbackwriter  @djtallahassee I was wondering same, but hereditary fructose intolerance also results in inhibition of glycogenolysis :/ confusing question. +  
amt12d  A much simpler way to think about this, without trying to figure out a diagnosis, I looked at the time frame for when the child was presenting. He has eaten poorly for 3 days, by now, his glycogen breakdown is gone. His body would be trying to make glucose, therefore, gluconeogenesis is impaired, not glycogen breakdown. +4  
tyrionwill  if fructose kinase is not available (fructose intolerence), then some fructose may go to F-6-P by hexokinase, then goes to G6P if gluconeogenesis is needed. however this patient's fructose kinase was intact, so no fructose would have go to F6P, so there would be no blood glucose increment after injection of fructose. +  
shayokay  You had to know that fructose and glycerol enter glycolysis at DHAP/G3P, and galactose enters glycolysis at G6P (gal-> gal-1-p -> glu-1-p -> glu-6-p). This means that one of the 3 enzymes between G6P and DHAP/G3P is not functioning properly. Most likely this would be fructose-1,6-bisphosphatase because there does not appear to be anything wrong with glycolysis. "Fructose-1,6-bisphosphatase (FBP1) deficiency is characterized by episodic acute crises of lactic acidosis and ketotic hypoglycemia, manifesting as hyperventilation, apneic spells, seizures, and/or coma. Acute crises are most common in early childhood; nearly half of affected children have hypoglycemia in the neonatal period (especially the first 4 days) resulting from deficient glycogen stores. Factors known to trigger episodes include fever, fasting, decreased oral intake, vomiting, infections, and ingestion of large amounts of fructose." https://www.ncbi.nlm.nih.gov/books/NBK550349/ +1  
shayokay  Also, even though Von Gierke is categorized as a glycogen storage disease it is really a problem with gluconeogenesis not glycogen breakdown. So even if you thought this was VG, you still could have gotten the right answer. In VG, any monosaccharide other than glucose (fructose, galactose, glycerol, etc.) will not raise the plasma glucose level because they all require gluconeogenesis to be converted into glucose and this cannot happen because there is no glucose-6-phosphatase. This is why the treatment for VG is frequent oral glucose in the form of cornstarch and avoidance of fructose and galactose. +  


submitted by lm4(9),
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ni eth coxernei nrespa,ca badgdll,rlea dna iervl htoolygap noeitsc of ,hatpamo aatrts mstonine that eht euihteipml nnigil ayrilbi rtcat sah ialaknel sshhoppatae so hnwe hety era deadgma ti rssleeea sit,h nigeaicrsn rmesu alk sh.op

lilyo  Cholestasis will present with elevated conjugated bilirubin, Alkaline phosphatase, GGT. Depending on the cause for cholestasis it can present with pale stools and dark urine. This patient has cholestasis due to choledocolithiasis. Look at FA 2019 page 390. +  
sars  From what I understand, this could be acute cholangitis (inflammation of the bile duct-charcot triad-hypotension, RUQ pain, jaundice). Biggest risk factor for this is choledocholithiasis. Damage to bile ducts releases ALP and GGT. Thanks +1  


submitted by urachus(16),
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ont PEO cb s'it akisng ht'wsa aedm rofm eth oenb waorrm. POE si ofmr ikndey

lilyo  Thanks, I was wondering why EPO was not correct. So EPO synthesis would be stimulated in case of blood loss? its just wrong becase they ask specifically what is going to be produced in the bone marrow? +2  
suckitnbme  @lilyo yes because it's specifically asking what the bone marrow is synthesizing. EPO would also be upregulated but this happens in the kidneys. +3  


submitted by m-ice(340),
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ishT rlig ahs noMo ducsae yb EtrnisBr-epa s.ruVi eTh soymptsm are elaetryilv ,evgua tub poaahnylydtphem eikl tihs odwlu eb omonmc fro noM.o heT CBC hwsos eevldtea yleysmotc,ph pinylimg siht si not a tclreaaib lsle,sin os rilva si leyl.ik mCnboide wtih eth h,tdpyyoehpaalnm hist amkes su rrowy tobua .oMon hTe MonoStp-o tste ofr BEV is hwta het oqsutien is riregenrf to enhw ncebrsidig het peseh rchyeeostrty iggataltnniug. oFmr ,reteh tshi tsqounei eqrruise htta yuo wokn thta in EVB niftcnie,o EBV nfteics B e,scll tub edos otn ceasu tehm to cbeeom orlmna.ab d,tenIas 8DC cesl,l iwhch rea eatvcyli ynirgt to klli eht B lslec, beecmo n.aloambr

medskool123  NBME does trick now and then.. when they zig you zag. then when you think they are going to zag, they zig just to destroy yourself confidence. +17  
kylemax  The abnormal T-cells are known as Downey type II cells (Sketchy) +3  
haliburton  I was recognized EBV, then knew EBV infects Bc, and the atypical lymphocytes are Tc. Then I said CD8 are MHC1 for virii, and bingo bango, boom. +6  
trichotillomaniac  congrats you played yourself +3  
lilyo  Soooooooo EBV infested B- cells is not considered atypical WTFF?? +  
med4fun  They are atypical b/c usually you do not see a super high amount of CD8+ in peripheral blood. Now there are a ton to try to stop the infected cells. +1  
aneurysmclip  oh and primary CNS lymphoma caused by EBV has T cells NOT B cells. I just try to remember the peripheral blood has atypical lymphocytes which are CD8+ T cells, and the CNS lymphoma is the opposite, ie; B cells +  


submitted by hayayah(1079),
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ntiatsS cna heva a edsi cffeet fo syoisyhdblaorm.

lilyo  Statins have an increased risk of myopathy, specially when combined with other medications like Fibrates. This patient presents with muscle pain along with an elevated CK and + myoglobin test in urine. Consistent with myopathy. +2  


submitted by xxabi(260),
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sihT si a yghtoosrslla cdut scy.t ehT agolylsrsto tduc may espirst dna lruste ni a ssyaoglolhtr ctdu sytc cgiurc(orn in iidelnm nera dioyh enbo or ta hte esba of eth )o,getnu htus ilwl alllisyccsa omve up whit nawgoiwlls or uoetng rtp.osniruo

eTh oenrmaf eucmc (of teh oetn)gu si eht laonmr mnenart of eth ohyoltslagrs udct

lilyo  I got it wrong though because the question clearly asks what does this structure (thyroglossal duct) DEVELOP from, not this structure eventually develops to form which structure. If it asked that then I would have picked option A but because it didnt that was the first option I crossed out. +16  
misterdoctor69  It was a poorly worded question no doubt. But when they say "endoderm of foramen cecum" they're referring to the endoderm which is a primitive structure. The "foramen cecum" part is just a modifier that is added to describe what that endoderm would eventually become. +  
lovebug  FA 2019, page 322page! +  


submitted by hello(315),
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s'netatiP mmtypsso bnage 03 imn tfaer nmogiw nlaw .i(e. tfrea iondg lshpiyca t)itavyci. eH hsa reeesv cesth pian dan is oc,lo m,aclym eoda.phirict eH ash edcsniaer yourlnmpa rrteay reusepsr nda acreinsde tlfe liaart ruspse.er naekT erlgat,theo hsti si dgiiceranoc ohks.c

gdiiCrcaneo kosch is a earht pmup mboeplr -- eth VL stn'i n.iowrgk

hWne hte LV, 'tsin krnwo,ig ti uescas a ackb up in het einocrdit tspipeoo ot ohw odlob aolnmylr swo.fl f,oreeeTrh ldoob llwi kbac up ni hte sngu.l

hTis sueasc arencisde allcipray dryshoictat useprser -t&-;g siht devsri roem fudli tnoi hte sttitmnreiui &-t;-g sthi scseau denaicsre iittnselriat hryoctidtsa peserusr g&;-t- erthe si now omre lufdi atnh raolmn ni hte iitsntertium &g-t;- sthi safcetf eht toprnei aoirt ihiwtn eth umirttentis tg&--; ihts cauess rsdeceaed tainetslirit cnootci sprerseu.

targetusmle  awesomely explained :) +  
lilyo  This was amazingly explained Thank you @Hello! +  
pseudopseudopth  For edema to occur shouldn't interstitial oncotic pressure be increased?(when proteins are there, they can pull the fluid) +1  
pseudopseudopth  And when increased interstitial hydrostatic pressure is pressure, shouldn't it oppose the edema by pushing against it? +1  
pseudopseudopth  *when interstitial hydrostatic pressure is increased +2  
pmofmalasia  You don't necessarily need to have increased oncotic pressure, you're correct in that decreased oncotic pressure would act against causing edema but as long as the net change in forces still acts "for" edema it will still occur. For example in this scenario, if the capillary hydrostatic pressure is greater than the change in interstitial hydrostatic and oncotic pressures. Also, the change in interstital hydrostatic and oncotic pressures is a direct result of the edema in this scenario, so it's more like they're responsible for setting the new equilibrium - if they didn't counteract it, you'd never come to a point where the leakage of fluid stops. +  


submitted by chandlerbas(100),
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eLgned:

BO = taobtlsesoci

CO = ito/eolstaeciocsstlytco

sote=atpPr, rbatsB=e, keiK=n,dy =odrhyTi,t =Llnug

my m:om nicneu Laed Kteetl

-------T--B------------------------------------P--L-K---

----OO--/O----BO/B---C--C--B----------OC-OC--O---

lilyo  @chandlerbas is this pneumonic in order of most common to least common, as in is prostate cancer the most common cause of metastasis to the bone regardless of wether the patient presents with osteoclastic or osteoblastic lesions? +  
hello_planet  One addition: Breast cancer causes mixed metastases, whereas lung cancer causes either lytic or blastic depending on the cancer type. Small Cell Lung Cancer causes blastic lesions and Non-Small Cell Lung Cancer causes lytic lesions. First Aid 2019: pg. 224 +3  
doublethinker  Uworld has a great Venn diagram on all the bone mets. +1  


submitted by cyrus_em(2),
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I ndto' nwok wyh I efel eht oectrrc reswna si 0%.10 Teh seuq ss,teat ahwt" is eth ncceha htat srsopgfnif wlli LNAETUVLEY oedevlp cnar,ce? tno heinitr the ttiua"nom

Pyocchlraitp mtlccyoeo or esel %010 EVELYLTAUN srrgesop ot C.CR

lilyo  I also chose 100% with that same reasoning!!! +  
lilyo  @usmlecrasher, Yes it does so which is why if they inherited they have 100% chance of developing colon cancer later in life and the question was confusing because it didnt ask what is the percentage that this patient will have children with this mutation? It might be my language barrier but I don't know. +  
diegolc26  Its a little tricky bk they want you to think the probability of developing cancer IF the offspring HAS the mutation, which is 50%. I mean, he has 50% chances of inheriting the cancer developing mutation. Thats how I think they want to trick us. +2  
mbourne  @cryus_em, you're putting way too much emphasis on the word "eventually". Either way the question and answer makes sense. It's an AD disease, so the chance of the offspring inheriting it would be 50% (and if they inherit it, they WILL develop adenocarcinoma of the colon, so the answer is still 50%). +1  


submitted by cyrus_em(2),
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I nod't oknw ywh I leef hte crrecto reasnw is .001% eTh sqeu esats,t wah"t si teh ncaehc htta fsgosrfinp lilw ELAYVEULNT pveedol c?eran,c tno iihtern the iontmu"ta

plPyohcitrac tclcoomey ro lees 1%00 YALLTVUENE erssprgo to CR.C

lilyo  I also chose 100% with that same reasoning!!! +  
lilyo  @usmlecrasher, Yes it does so which is why if they inherited they have 100% chance of developing colon cancer later in life and the question was confusing because it didnt ask what is the percentage that this patient will have children with this mutation? It might be my language barrier but I don't know. +  
diegolc26  Its a little tricky bk they want you to think the probability of developing cancer IF the offspring HAS the mutation, which is 50%. I mean, he has 50% chances of inheriting the cancer developing mutation. Thats how I think they want to trick us. +2  
mbourne  @cryus_em, you're putting way too much emphasis on the word "eventually". Either way the question and answer makes sense. It's an AD disease, so the chance of the offspring inheriting it would be 50% (and if they inherit it, they WILL develop adenocarcinoma of the colon, so the answer is still 50%). +1  


submitted by monoloco(136),
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sA a relu of ,uhbmt fi ouy igve nesemoo an CEA toihnbiri and ythe teg a rebmpo,l eyth had nelar etarry sntoeiss aylulu(s tbaralyiel,l or os ew eerw tahtgu at our dem soloh)c. bloaPybr sha to od iwht cdeareesd RGF askhtn to radsdceee inntonAegis IveIielt–sce tootonnviascscri fo het nerffete rroeeilta =;g&t desaeecrd oduism yelvedir to amaluc aensd &=g;t arincedes inner l.aeseer

lilyo  Vasoconstriction of the EFFERENT arteriole actually leads to increased GFR. It selective VASODILATION of the efferent arteriole effect of ACE inhibitors since they undo Angiotensin II actions. This patient already has rescued renal blood flow due to bilateral renal artery stenosis, the addition of an ACE inhibitor further decrease GFR prompting an increase in renin due to loss of negative feedback. +2  
drpee  We should always expect GFR to drop a little after adding an ACE-inhibitor due to efferent arterial vasodilation. For this reason we should also expect Renin levels to rise via tubuloglomerular feedback. So it's not really the reaction to the ACE inhibitor that gives this away as RAS (which is why I got it wrong). I think what we are expected to be looking at it are lab values: Hypokalemia, and secondary hyperaldosteronism. https://www.aafp.org/afp/2017/1001/hi-res/afp20171001p453-t5.gif +  
stepwarrior  ACE inhibitors would actually have the opposite effect of AT-II, and result in efferent dilation. But the actual mechanism of increased renin activity per UWorld is lack of systemic vasoconstriction by AT-II leading to blood shunting away from the kidney. +  


submitted by xxabi(260),
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erlanimT tmoCeepnlm C(59-)C ceincDeifsie cseneiar uliciespsbttyi ot rncretuer erNsaesii at.eecabrim eiastnPt mtso ftoen etspern htwi uercrtren isn.imitneg

lilyo  FA 2019 P. 107 Early and Terminal complement deficiencies. +1  


submitted by strugglebus(165),
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oS yuo wonk atth 65% fo the atad illw lfal twihin S1D fo eth a.nme oS fi you ctbastur 15006- uoy lwil tge 5.3 Whhci sname atth uoatb %16 wlil alfl avobe nad 1%6 will llfa owleb 1 .DS heTy rae inagsk orf woh amny lilw fall vabeo 1 SD. I'm resu reteh si a eetbtr wya of nidog ,shit btu httas woh I tgo it lol.

sympathetikey  Same! +6  
sympathetikey  Except according to FA, it's 68% within 1 SD, so 34%, which split in half is 17%. +2  
amirmullick3  Sympathetikey check your math :D 100-68 is 32 not 34, and half of 32 is 16 :) +8  
lilyo  Can anyone explain why we subtract 68 from 100? This makes me think that we are saying its 35% of the data that falls within 1SD as opposed to 65. HELLLLLLP +  
sallz  @Lilyo If you consider 1 SD, that includes 68% of the population (in this case, you're saying that 68% of the people are between 296 and 196 (1SD above and 1 below). This leaves how many people? 32% outside of that range (100-68=32); half of those would be above 296 and the other half below 296, so 16% +5  


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lancartIezoo qursieer het iidcac nnmtoneivre fo teh atchoms to eb .abesrbod lOeamrpzoe niithibs hte H+/+K mupp of eht otm,ahsc ebtrhye aerigsndce het iyditac fo eht tacs.moh So wnhe hte eipttan ksaet emezOolapr and rtolIaocnzea ,eoterhgt retIaazoocnl n'otw be ebsrabdo inot the bydo. Tah'ts wyh ti hsa no ftfeec.

s'It emdeeorcmnd to kate idscneamoti ta lesta 2 srouh opirr ot gnkita an .tacndai

necrotizingfasciitis  Just adding support to the above explanation: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3671798/ +3  
pakimd  do all azoles or just itraconazole only requires an acidic environment to be absorbed? +2  
chandlerbas  just itraconazole and posaconazole +5  
lilyo  @chandlerbas, where did you find this information? I was looking over this on FA but they do not mention it and I would like a bit more information. Thanks! +5  
chandlerbas  haha no stress! the article above submitted by @necrotizingfasciitis does a descent job explaining it, however its not good enough, I looked into a bit more on uptodate but wasn't fruitful in my endeavours. goodluck! +  
haozhier  How are we supposed to know this!! It is not in UWORLD or FA right? +10  
kevin  Someone said it on here, since there was no CYP inducer of the answer choices, the only way to even think about an answer to this question was to just go with a less acidic environment from the PPI affecting absorption. It was simply the only reasonable answer choice, I don't think there's any way we were expected to know of this exact interaction prior +1  
aoa05  Golan pharm book states the exact same thing. Cannot be given to patients with acholrhydria. +  


submitted by hayayah(1079),
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eH has cfeal itnceoicennn os hsi rlneaxte ceptrnshi is daamged, wchhi si tedneiarnv by eth aleundpd n. SS(2).-4 eTh plveic hnisccapnl ,srvnee hwhic aietdme teh cirteneo re,scpos era lsoa S4.2-S

thomasburton  Why could this not be dysuria? +3  
lilyo  I think that you are thinking about urinary incontinence. If we damage the pudendal nerve S2-S4, you can exhibit urinary and fecal incontinence since this nerve innervates both the urethral and the external anal sphincters. However since the pelvic splanchnic nerves also have roots that originate in S2-S4 a patient with pudendal nerve damage will also have impotence since these control the erection reflex. He wouldn't have dysuria which is painful urination. Most likely caused by a urethral infection or a blockade of the urinary tract. He would have urinary incontinence. I hope this helps. +16  
alexxxx30  dysuria is painful urination...if it said urinary incontinence then you'd be right. But decreased innervation wouldn't cause pain (that would mores be associated with UTI) +3  
peqmd  Another approach is fecal incontinence => parasympathetic nerve dysfunction => no boner +  
dul071  ahhhhh fucked up with terminology again thinking dysuria was urinary incontinence +  


submitted by bobson150(14),
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hTe grwdoin fo htis ntiousqe eosfdcnu .em hisT si asgikn hhciw" of teesh svslese si eht hihg sureersp eytmss" right? oS het hghi esesrpur puorries trleca si sanguci eanicedsr sreeuprs nito hte ireornfi tcea?lr

welpdedelp  Superior rectal comes from the inferior mesenteric vein which comes from the splenic vein --> portal veins Thus, this dude had cirrhosis so it would "back-up" into the superior rectal vein. FA 2018: p360 +13  
nc1992  Superior rectal not superior mesenteric. Took me a minute +  
hyperfukus  ugh am i ever gonna get these right EVER +5  
titanesxvi  why not the inferior mesenteric, since the superior rectal drains there +2  
thomasburton  @titanesxvi think it is because question says direct which is why superior rectal +2  
lilyo  thomasburton, so are they asking what vessels do internal hemorrhoids directly drain into? The order is Superior rectal vein--> Inferior mesenteric vein--> portal vein. +  
thomasburton  Yes exactly, so they do eventually reach IMV but not 'directly' +  
pg32  Also worded poorly because the varicosities are connections between the superior rectal and the middle/inferior rectal veins of the systemic circulation. So the blood could be in both the superior rectal vein and the middle/inferior rectal vein as that is what a varicosity is. +2  
snripper  You just gotta know indirect vs. direct hemorrhoids. In this case, it's an indirect hemorrhoid (superior rectal vein) because of the rectal bleeding. +  
jesusisking  @titanesxvi DrDoom explained it pretty well below: "Defining tributary: https://i.imgur.com/2zDxPbW.png Nice images make the term easier to recall. Smaller streams "pay tribute" to larger rivers (by flowing into them)" +