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Welcome to titanesxvi’s page.
Contributor score: 77


Comments ...

 +9  (nbme24#22)
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  • tAurdodc smulces nda iialrsgc rea tneearvnid by teh oautrrbto vnere
  • Exeantlr libuoeq si iredvntena yb eth oigihclrtisoayp erenv
  • roorabtut sinenrtu si vnareedint by het truobtroa ntnusrie erevn )(LS2–5
  • rosiirfimP is eetvdnarin yb eth isatcci nreev -53)S(L

 +2  (nbme24#20)
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hsTee srlcmeoeto lsecl idifeefrtnate tnoi sntdosclrobah tath fmro eht soiatguraicln oprrcrsues of hte lixaa lenoktse dna eosnb fo eth iancral ebas o(mfr tnetre miro)eb


 +0  (nbme23#28)
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reeH is a gdoo csoeerru

oytcnee.udessdkswpwmsImpo/smoee/cw_ndwocatbornonl_//_lssmtgaih/:.plr


 +0  (nbme23#28)
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wyh nto sedcraee AC itctvayi ni the mxpalrio eulu?bt tsih slao odlcu ldae to eliacotbm ssdico.ia

ergogenic22  carbonic anhydrase inhibitors can cause Type 2 RTA but it is not the cause here (cystinosis) +
doublethinker  Yeah, I said CA too. Problem is that CA deficiency wouldn't lead to lack of reabsorption of all the ions listed. +

 +2  (nbme22#4)
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Teh htoer ewsrasn rae ngorw ce:asbeu (fi I ma nowrg alesep ccroert em)

A) hsTi udowl eb etru ni a tpaetin hitw eivrl or hipenrcot ynmresdo

C) iTsh odlwu be rtrcoce if teh ew snraceei icyaallpr tyairlmbpeie pxl(meae ssp)sie

D) Thsi si tfel ehatr friulae

)E ishT lcduo be ADRS otn( seur u)otghh

)F cnlanaMigy


 +4  (nbme22#6)
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eohp thsi mgaei pelh to tarnuddesn ti, het pumsp d'otn rkow eeasucb klac fo TAP





Subcomments ...

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Jstu eueascb es’h nivgah rd(nuteopc)te sxe tdn’soe name eh stndoe’ veha sieplm icofsitnue ucse.snoooimnl Teh sxe mlpiies ’esh sloa ksisnig neesomo! Pynhrisiatg + lphym deson + ufategi = omon.

titanesxvi  The triad of classic symptoms for infectious mononucleosis is lymphadenopathy (swollen glands), splenomegaly (large spleen), and exudative pharyngitis accompanied by high fever, malaise, and often hepatosplenomegaly (large liver and spleen) +2  


submitted by fahmed14(28),
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nsmaiHtie ypsal a rjamo loer in the airclnda sgsni of nanitaomlif.m tI ehslp eitmade vsinolatodai and savuacrl traeieilmypb iav( olnhitelade lelc tn.ocnctaori) shTee wto isnfutcon era eadyalr rotynrca to A, ,B C, dan D. By nnsrgcieai ludif in hte testliniaitr a,ecps oyu cna sroaen atht teher lwil be adecrensi mlhyp .lofw

youssefa  If more transudates are leaking into the interstitium wont this dilute the interstitial proteins and cause a decrease in oncotic pressure and increase in interstitial hydrostatic pressure? +11  
titanesxvi  @youssefa I think because it is an exudate from increased permeability of venules, the oncotic pressure in the interstitium is not going to decrease +6  
thotcandy  @youssefa transudate is like pulmonary edema due to CHF, no proteins, just fluid congestion and leaking out. That would decrease interstitial oncotic pressure because it has very little protein. Exudate due to inflammation/histamine has a high amount of protein (due to inc permeability) so the IOP doesn't change. +5  


submitted by vshummy(152),
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oS the tseb i ocldu indf swa ni siFrt diA 2910 gp 436 enrdu Deabtici soitcao.iKsde hTe cmlyegryeahip and ihekapelmrya uecas na oimocts iuserdis so eht irteen ybdo tgse peeddetl fo ilsf.ud cneeH yhw rtap of eht artntetem orf AKD is IV usfidl. Yuo higtm enev ryle no ttha ecepi fo tiromainnof aoeln to eanrws itsh eti,qusno hatt DKA si tetarde ithw VI sd.ufil

fulminant_life  I just dont understand how that is the cause of his altered state of consciousness. Why wouldnt altered affinity of oxygen from HbA1c be correct? A1C has a higher affinity for oxygen so wouldnt that be a better reason for him being unconscious? +6  
toupvote  HbA1c is more of a chronic process. It is a snapshot of three months. Also, people can have elevated A1c without much impact on their mental status. Other organs are affected sooner and to a greater degree than the brain. DKA is an acute issue. +5  
snafull  Can somebody please explain why 'Inability of neurons to perform glycolysis' is wrong? +3  
johnson  Probably because they're sustained on ketones. +3  
doodimoodi  @snafull glucose is very high in the blood, why would neurons not be able to use it? +1  
soph  @snafull maybe u are confusing bc DK tissues are unable to use the high glucose as it is unable to enter cells but I dont think thats the case in the neurons? +1  
drmomo  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2909073/ states its primarily due to acidosis along wth hyperosmolarity. so most relevant answer here would be dehydration +1  
drmohandes  I thought the high amount of glucose in the blood (osmotic pressure), sucks out the water from the cells. But you also pee out all that glucose and water goes with it. That's why you have to drink and pee a lot.. +7  
titanesxvi  Neurons are not dependent on insulin, so they are not affected by utilization of glucose (only GLUT4 receptors in the muscle and adipose tissue are insulin dependent) +24  
drpatinoire  @titanesxvi You really enlightened me! +  
mutteringly  I don't make the connection of what titanesxvi said to the question - can someone explain? +  
motherhen  @mutteringly it explains why the answer choice "inability of neurons to perform glycolysis" is wrong +1  


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yWh si ti atth eht uroplmyan ypicallar gdeew spussreeree si rdeinsae?c on .pg 730 of AF 1092 it ssya ti can eb esdareinc or edraeesdc /:

giggidy  Depends on where the infarct is I guess? Crackles in lung base means increased left sided pressure and therefore PCWP. At least that's how I thought of it. +9  
titanesxvi  Because think the circulation as a closed circuit, in this case the heart isn't pumping well and the pressure is going to backup. that is why the PCWP is increased +3  
mw126  It depends if the patient goes into heart failure because of the infarct or whatever the insult is. The crackles in the lungs gave it away. If crackles are present then there is blood backing up. the increased pressure in the pulmonary vasculature causes leaking into the alveoli which we hear as crackles when the lung expands. +  


submitted by krewfoo99(87),
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Cna eeomnos ipaxnle hwat teh utirpec is posdsepu ot s?who Is ti eppodssu ot eb sndtgmeee hnpiosut?ler

titanesxvi  yes do to B12 deficiency +  


submitted by wired-in(67),
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tenMnniacae sdeo rolmfau si ssC( × lC × uat) ÷ F

eewrh sCs si -tdsseytaaet getrta lapsam c.cno of dgr,u lC is cnl,caeaer uat si adogse iaerlntv ;&mpa F si baiovliy.alibtai

eeNitrh ogsaed ervanitl orn abllitoiivaiyab si gevin, so nnoiiggr hoste m;&pa lgpgnuig ni eht snemrbu cufl(are to rntovec ituns to )/d/m:akgyg

2( =1 Lg/mu × 1 m/000g1 gu) × 09.(0 hrg/Lk/ × 0100 m1L/ L × 24 /1rh ady)
= .9522 ygakd/m/g

.wih.hc. 'ntsi any fo eht wranse ceihsco esid.tl eTyh smut hvae udrndoe 009. grLkh// ot .10 Lk/gh,/r and oding os vgeis alytcex 8.28 ay/dg/mkg (ccehoi C)

lispectedwumbologist  That's so infuriating I stared at this question for 20 minutes thinking I did something wrong +69  
hyoid  ^^^^^ +11  
seagull  lol..my math never worked either. I also just chose the closest number. also, screw this question author for doing that. +9  
praderwilli  Big mad +9  
ht3  this is why you never waste 7 minutes on a question.... because of shit like this +8  
yotsubato  Why the FUCK did they not just give us a clearance of 0.1 if they're going to fuckin round it anyways... +18  
bigjimbo  JOKES +1  
cr  in ur maths, why did u put 24h/1day and not 1day/24h? if the given Cl was 0.09L/hr/kg. I know it just is a math question, but i´d appreciate if someone could explain it. +1  
d_holles  LMAO games NBME plays +2  
hyperfukus  magic math!!!!! how TF r we supposed to know when they round and when they don't like wtf im so pissed someone please tell me step isn't like this...with such precise decimal answers and a calculator fxn you would assume they wanted an actual answer! +1  
jean_young2019  OMG, I've got the 25.92 mg/kg/day, which isn't any of the answer choices listed. So I chose the D 51.8, because 51.8 is double of 25.9......I thought I must have make a mistake during the calculation ...... +6  
atbangura  They purposely did that so if you made a mistake with your conversion like I did, you might end up with 2.5 which was one of the answer choices. SMH +3  
titanesxvi  I did well, but I thought that my mistake was something to do with the conversion and end up choosing 2.5 because it is similar to 25.92 +2  
makinallkindzofgainz  The fact that we pay these people 60 dollars a pop for poorly formatted and written exams boggles my mind, and yet here I am, about to buy Form 24 +15  
qball  Me after plugging in the right numbers and not rounding down : https://i.kym-cdn.com/entries/icons/original/000/028/539/DyqSKoaX4AATc2G.jpg +1  
frustratedllama  Not only do you feel like you're doing sth wrong but then that feeling stays for other questions. sucks so baad +  
fexx  'here.. take 50mg of vyvanse.. I just rounded it up from 30.. dw you'll be fine' (totally doing this with my patients 8-)) +1  
cbreland  I was so close to picking 2.5 because I thought I did a conversion error. 5 minutes later and still didn't feel comfortable picking 28.8😡 +  


submitted by hello(298),
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ihcwh teletr si CN IX ni sith igmard?a

titanesxvi  A think is D, but it is not very clear +1  
usmlecharserssss  A WHAT anatomical structure is this ???????? +  


submitted by lfsuarez(141),
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rsFit retah uonds S)(1 is gtaeeendr yb two arthe sael:vv het atlmri veavl nad ciptrsdui aevv.l ylearN ntaemussulio cosling fo hetes savlev arlmoyln engsarete a nsgile 1S dno.us iingtlptS fo teh 1S douns si edrha newh italrm nda cdrtuisip eslvva esloc at syilghlt refdtienf i,stem hiwt asululy eht trilma gnscoli freoeb psicdturi

yotsubato  Then why the fuck is it describing a mitral valve sound in the tricuspid area +22  
dr.xx  it's describing a splitting S1 — consisting of mitral and tricuspid valve closure — that is best heard at the tricuspid (left lower sternal border) and mitral (cardiac apex) listening posts. +30  
titanesxvi  tricky question, I though what sound it is in the left sternal border, so I chose tricuspid valve, but what they where asking was, what is the first component of the S1 sound +4  
titanesxvi  tricky question, I though what sound it is in the left sternal border, so I chose tricuspid valve, but what they where asking was, what is the first component of the S1 sound +1  
drzed  It shouldn't matter where you hear a split sound. For example, no matter where you auscultate on the heart, the second heart sound in a healthy individual will always be A2 then P2 (whether you are at the mitral listening post or the aortic listening post) The key is recognizing that the right sided valves in healthy individuals will always close later (e.g. the heart sounds are S1 S2, but more specifically M1 T1 A2 P2). The reason for this is simple: if you take a breath in, you will increase preload on the right side of the heart, and thus the greater volume will cause a delayed closure of the valve. This is physiologic splitting, and is better appreciated in the pulmonary and aortic valves because they are under greater pressure, and thus louder, but it can also be heard in the first heart sound. +9  
alexxxx30  yes agreed!! This question is mostly asking if you understand a few basic things regarding cardio physio. The left side of the heart is the higher pressure side so left sided valves will close first. The right side of the heart is the lower pressure side, which means right sided valves will open first. [Left closes first, Right opens first]...Secondly, it requires you to know what S1 and S2 sounds come from. S1 is the mitral/tricuspid valve closing and S2 is the Aortic/pulmonary valves closing. So really the question asks what is the first component of S1 (mitral or tricuspid closes first). And since we know that the left side will always close first, it must be mitral valve closure. Sorry if that was a long explanation. +10  
jesusisking  Thanks @alexxxx30, you the man! RIP Kobe +  


submitted by lfsuarez(141),
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Frist htrae sonud )1S( si ertdgneae yb owt aerht :svelva the ialrmt elvva adn tuirdcisp ve.avl Nryela umistnelusoa ogincls of stehe lavevs omaylnrl gsrteneae a egnils 1S duos.n nSilpigtt fo hte 1S nusdo si hrdea hnwe lmtira dan sicutprid slveav ocsel ta ilylhgts nedfirfte t,smie ihwt suaulyl het almrit ngoclis eerfbo pcuidrtsi

yotsubato  Then why the fuck is it describing a mitral valve sound in the tricuspid area +22  
dr.xx  it's describing a splitting S1 — consisting of mitral and tricuspid valve closure — that is best heard at the tricuspid (left lower sternal border) and mitral (cardiac apex) listening posts. +30  
titanesxvi  tricky question, I though what sound it is in the left sternal border, so I chose tricuspid valve, but what they where asking was, what is the first component of the S1 sound +4  
titanesxvi  tricky question, I though what sound it is in the left sternal border, so I chose tricuspid valve, but what they where asking was, what is the first component of the S1 sound +1  
drzed  It shouldn't matter where you hear a split sound. For example, no matter where you auscultate on the heart, the second heart sound in a healthy individual will always be A2 then P2 (whether you are at the mitral listening post or the aortic listening post) The key is recognizing that the right sided valves in healthy individuals will always close later (e.g. the heart sounds are S1 S2, but more specifically M1 T1 A2 P2). The reason for this is simple: if you take a breath in, you will increase preload on the right side of the heart, and thus the greater volume will cause a delayed closure of the valve. This is physiologic splitting, and is better appreciated in the pulmonary and aortic valves because they are under greater pressure, and thus louder, but it can also be heard in the first heart sound. +9  
alexxxx30  yes agreed!! This question is mostly asking if you understand a few basic things regarding cardio physio. The left side of the heart is the higher pressure side so left sided valves will close first. The right side of the heart is the lower pressure side, which means right sided valves will open first. [Left closes first, Right opens first]...Secondly, it requires you to know what S1 and S2 sounds come from. S1 is the mitral/tricuspid valve closing and S2 is the Aortic/pulmonary valves closing. So really the question asks what is the first component of S1 (mitral or tricuspid closes first). And since we know that the left side will always close first, it must be mitral valve closure. Sorry if that was a long explanation. +10  
jesusisking  Thanks @alexxxx30, you the man! RIP Kobe +  


submitted by keycompany(294),
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Teyp I sbeetDai si erdrhaicezact as eht rosdettucni of iapaeccntr estsli ccsif(eilpayl teba cll)es yb ce-Tl.ls heT otms leylik ucase for yogaypmceihl nwoflloig niusiln ntaoimnrtiaids, he,roftree is teh rscntuioted fo aahpl elslc htta rnudruso the bate e.lcls ihTs luodw aeusc ecsredead elelsv of catrngiiluc ouggclan.

titanesxvi  I think rather that high insulin is going to block the release of glucagon +6  
mdmikek89  No, his answer is more correct. Obviously insulin will decrease glucagon release, but it says PROLONGED. So if I give a rapid acting insulin, serum glucose decreases, the insulin degrades...no rise in glucagon. The alpha cells are destroyed as well. This is the how I came to the answer and the best explanation. +1  
melanoma  the answer is not correct +1  
melanoma  his answer +1  
prolific_pygophilic  I actually think this has some merit. I believe there is a U world question that talks about how very long history of T1DM (20 years in this patient) can progress to destruction of alpha cells and hence impaired release of glucagon and episodes of hypoglycemia. Thats how I reasoned it. The first answer is also possible. +  


submitted by yotsubato(961),
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5p3 is edtuatm nad tcan indb eht AATT ,bxo os twha spnpeah to iponicntrtsra fo roiihibynt strnop?ie

Is caiallbys whta htis soqitenu is gritny to .s..ak

So on AATT box ortmpoer tg;=& Deesarced idinbgn of NRA rlyeampose

link981  You said it, they are "trying" to ask. Should use better grammar. +3  
titanesxvi  This is on first aid, and says that the promoter region is where RNApolymerase binds +  
nootnootpenguinn  Hakuna NO-TATA box... thank you for this explanation! +  


submitted by enbeemee(13),
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ekhcsty yass taht o'isapsk ash ltngniiatfri hy,scmplyeto so ywh olduw aeglr tgrggseaae of iytaplca ysmeholtpcy eb irontcecr?

titanesxvi  Bcz I think vascular is the key thing here, whereas atypical lynphocytes would be more of EBV +2  
d10s  the lymphocytes seen in kaposi sarcoma are not atypical. +3  


submitted by g8427(0),
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If emos eno nac hlep me usatnedrnd cb im a bti .osuefdcn I nradsdenut teh oghttuh opssrec nda I lrdezeai atth tihs saw na RA adseesi dna I oals otg hte 41/ ,fedfecat /12 arrrcei nad 4/1 eetncfua.fd tBu I oshce 0% bc I idfureg if it asw na RA esdseia het 1 dilch rldyaae esddiase asw ohyszomugo faetfecd /1(4 fadef)etc. hciWh laed em to ktinh htta het hetor irsest asw rethei a iecarrr or nto dcftfeea at .lal Am I sujt ovre gtkinihn tshi or ma I nto fuyll rsnaitdudenng aswth gongi n?o

rush  you have to think about each child individually, doesn't matter what the siblings have. The question states what are the odds of the child getting the disease. So regardless of the other siblings it still is Mom (1/2) dad (1/2) which makes it 1/4 AR +  
titanesxvi  But how do we know that the parents are heterozygous for the mutation +  
need_answers  we know that the parents have to be heterozygous Aa X Aa because on a 2x2 table, the only way the daughter could be homozygous for an AR is by having both parents be carriers (Aa) so the question was asking what are the chances the sister has the same alleles (aa) and there is only a 25% of having the same alleles. +  


submitted by usmleuser007(370),
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tsuJ neot yhw roeth wrenass are not octe:rrc

  1. bsgEopys;nionhp& na dsieacren esnonaecr fo ocevi ssdnou edrha hewn anttgaucilsu the gusl,n neotf seaudc yb gnlu ndtolcosiaoni nda .sbfisiro

    • a. tI is deu ot ehacnend ssnitmsoianr fo ucfhqhe-yrneig sduon srsoca dui,lf suhc sa in larobmna gnlu is,tseu wiht elwor urqefeinces ieltrefd o.tu
  2. rhpWesedi rreorsec&po;bestlypiqfun to na acdeensir udosnsle obo;etnnnpgpwhsde&frspb;ins&i nurdgi tlsauitcunoa hwti a pceetsthoso on hte nulg esdilf no a sat’nepti ortos.

    • .a lsyulaU esnkop snouds fo earhvsnep;spn;o&eupiwsmdbbl& by eth epanitt olwdu nto eb ahred by eht icincainl tiuaalngtcus a ulgn field itwh a s.ocpetetsho

    • b. roeeH,vw ni esaar of teh lugn ewehr rteeh nignsbpus;l& ntlcnosioa,dio ethes idsweherp skeonp sdousn yb the tpeitan hsu(c sa iygasn nie‘’ietnn)-yn illw be ryallce adrhe troughh teh se.tcosphtoe

    • .c Tshi csienaer ni dosun isestx aseuceb sndou rvaelts rfatse nda sthu htiw lwore slso of entnystii hgrtouh idliqu or osldi if“(lud a”sms ro “dilso ,sa”ms ,epercsityvle ni hte nul)g rsvsue essaoug iar( in het )ngul .idmae

    • .d Wsdrpehei looeryuiqctp is a cnaciill tets ailtypcly orredmfep nidugr a ilacmde hapcslyi aaeiioxnmtn ot vaetaeul ofr hte ernceesp ognnu&bl;fsp oaoo,sicnldint cihhw cudlo eb adusec yb cncrea dosli( smsa) or paeouinmn lifd(u ss.am)

titanesxvi  why not wheezing? +  
miriamp3  @titanesxvi because the dx is CHF +  
leaf_house  I get why crackles are more likely in CHF, but wouldn't it also cause whispered pectoriloquy, if fluid allows better transmission of sound? +  


submitted by marbledoc(0),
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Wyh wduol oyu aks het tniepta to eytidifn the rops and oc?sn I no’td tge eth aroacpph !rhee

someduck3  There was a question about this in Uworld. for *stubborn* patients who are "not ready to quit" just yet you use the motivational approach. The technique acronym is OARS: Open ended questions, Affirmation, Reflect, Summarize. +6  
yotsubato  Additionally the guy himself says "I know smoking is bad for me" Like he knows its bad, he doesnt care, but give him nicotine replacement and maybe he'll quit... +5  
usmleuser007  I didn't think nicotine replacement was a good answer choice b/c if he isn't ready to quit then why would he agree to use alternatives. +  
usmleuser007  People who smoke and are addicted like the feel of the cigs and environmental ques. Using replacements would be more challenging. The second best answer choice would have been Rx. +  
titanesxvi  why not detail the long-therm health effects of smoking? +  
seracen  @ titanesxvi: I assume because they always like the most "open ended" response. If you start detailing the long term effects, the patient might interpret that as attempting to convince, and might resist or feel pressured. By having the patient elucidate what they consider pros and cons, you allow it to be an open discussion. +  
suckitnbme  Also because the patient states he already knows smoking hurts him in the long run so it may come off as lecturing on something he already knows. I view this as what is the least-judgmental way to facilitate the patient moving on to the next step of the stages of change model largely of their own volition. +2  
usmlehulk  i choose the option c which is initiate a pulmunary function test. why is that a wrong choice? +2  
makinallkindzofgainz  @usmlehulk - he's asymptomatic, knows it is not good for him in the long run, but is not quite ready to make a change. It is best to talk with him about the pros/cons of cessation so that maybe he will make the decision to quit smoking soon. Ordering a pulmonary function test is not going to be useful. Let's say it's decreased. Ok, so what? It doesn't change management in this patient right now. +1  
rainlad  Think of it as motivational interviewing +1  
tulsigabbard  Still don't like the answer given that the patient already stated that he knows that it can do him harm in the long run. It seems like overkill. +3  


submitted by bobson150(11),
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eTh gwrdoni of hsti suoeqtin oncdseuf em. hisT si asnikg h"ihcw of teehs elsesvs is teh ihgh ueessrpr "emstys trh?gi So hte hhig esepursr sperirou leartc is aucisng ersndeaic sspureer inot eth iifrneor earc?lt

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)" +  


submitted by sklawpirt(28),
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I khint het eida ehre is ylmsip that oen ludsho hitnk tuoab hwere ieecslsv rae ginmoc ormf no herti yaw to the goilg lecmo.px

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hayayah  pg. 47 on FA got the good visuals! +5  
notadoctor  COPII* proteins are needed to coat vesicles from the RER to Golgi. "Two(COPII) steps forward; one(COPI) step back." Anterograde goes RER -> Golgi -> Lysosomes/Secretory Vesicles -> Plasma membrane +22  
titanesxvi  why not small lysosomes? +3  
varunmehru  and I thought large lysosomes due to lack of enzymes to degrade +  
samsam3711  The size of the lysosome is not affected by the presence or absence of protein, but its function is compromised (eg. protein is getting stuck in the RER) +  
fattyacid  I hope this helps to whomever was lost like me Null mutation: A mutation (a change) in a gene that leads to its not being transcribed into RNA and/or translated into a functional protein product. For example, a null mutation in a gene that usually encodes a specific enzyme leads to the production of a nonfunctional enzyme or no enzyme at all. +2  
pingra  I think you made a typo: COPII (RER -> cis-Golgi); COPI (trans-golgi -> cis-golgi and cis-golgi -> RER), clathrin (endocytosis and trans-golgi -> lysosome) +  
kevin  So my thought process was if there is no COP signal then instead of going to Golgi it would be sent astray into cytoplasm, akin to how in I-cell Dx the enzymes get sent out of the cell since there is no trafficking signal (therefore I presumed large lysosome due to eating the aggregated protein). Are we saying without COP or Clathrin that the vesicle will simply stay put where it is? If I can get a reply before my exam (2 weeks) that'd be much appreciated +