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submitted by nwinkelmann(257),
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oeDs yneano hvae a odog itnpaolneax fro yhw eedecrads lsveel fo nhibini is wgn?ro rFmo ym ,tnnunerasdgid hnniibi and ictnvai kwor roghtet,e ni htta iihbnni dinsb dan sbclok tcinvai lidngae to edrdacees dkbafeec no sluoytamhhap dna acvniti nsiereasc FSH adn RGHn opn.di.ctrou ,thus fi uyo sreeadec iinibhn enht ouy lowud vhae ceiresand ctaiivn iwhch dluow ldae to ciaseednr nGHR adn FS,H itgh?r I onudf noe laricte klgitna utoab it in ardgrse to pbyetru, tbu ti sseme ot be a h/shstipoetnoy cemnridof at thsi .i.o.tnp si that hyw? tBu l..tl.is how od I ruel it uot no a ?tset

yb_26  I also picked decreased inhibin. may be it was one of the "experimental questions", which are not even counted on the real exam +  
artist90  Inceased FSH will lead to spermatogenesis and spermiogenesis NOT Increase in Testosterone which is causing increased Height of this pt +4  
artist90  Inhibin B only has negative feeback on FSH not GnRH. see the diagram on the topic of semineferous tubules in FA. Testosterone has a negative feedback on BOTH LH and GnRH +1  
usmile1  Kind of like how nocturnal pulsatile GNRH release occurs during sleep to stimulate growth (FA page327), the same thing happens for puberty. Pg 325 in FA, "pulsatile GnRH leads to puberty and fertility." It doesn't explicitly state during sleep, but pulsatile release of GnRH leading to pulsatile release of LH and FSH will lead to puberty. Puberty starts in the brain, its onset really has nothing to do with decreased inhibin levels which happens in the testes. hope that makes sense! +2  
sars  From what I understand, inhibin is only released by granulosa cells when FSH levels are high. This is a boy. Next off, this question is about puberty, which is due to pulsatile GnRH leading to large amounts of LH and FSH, leading to large amounts of dihydrotestosterone (males) and estradiol (females), and eventually secondary characteristics of puberty. The increased pulse of estrogen and testosterone leads to GH release, which is metabolized into IGF-1 in the liver. This leads to long bone growth from what I understand, which is not much. +  
cassdawg  @sars inhibin B is also released by sertoli cells in males and will feedback to inhibit FSH release, its not just a female thing. Also, there is actually an inhibin B pubertal surge in both females and males that corresponds to maturation of the granulosa and sertoli cells, respectively. Hormones are wack. https://pubmed.ncbi.nlm.nih.gov/15319819/ +  


submitted by nwinkelmann(257),
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oesD ynaeon vhea a odgo ntaxapinelo rfo hwy cradsedee veesll of nihbiin si r?gnow oFmr ym engn,iadntsudr bininhi and iacvtin kwor rtht,geeo ni tath inhinbi sidnb nda obklcs niaivtc ilagnde ot eaeedcdrs cefabdek on hyatuhspmola nad iiavnct ceinaerss SHF dna HRGn c.nodpriu.to u,hst fi yuo draseece iibinnh ehtn ouy ulwod veha snaeicerd ticnavi which luwdo edal ot ceisraned HGnR dan S,HF r?hgti I fudon noe ircetal aktlgin aobtu it ni srgrade to ept,rybu but ti sesme to eb a osseytpo/ihthn efrcmodin at isht ...nptio si ttah yw?h But .ls.lit. how do I leru it out no a ?etst

yb_26  I also picked decreased inhibin. may be it was one of the "experimental questions", which are not even counted on the real exam +  
artist90  Inceased FSH will lead to spermatogenesis and spermiogenesis NOT Increase in Testosterone which is causing increased Height of this pt +4  
artist90  Inhibin B only has negative feeback on FSH not GnRH. see the diagram on the topic of semineferous tubules in FA. Testosterone has a negative feedback on BOTH LH and GnRH +1  
usmile1  Kind of like how nocturnal pulsatile GNRH release occurs during sleep to stimulate growth (FA page327), the same thing happens for puberty. Pg 325 in FA, "pulsatile GnRH leads to puberty and fertility." It doesn't explicitly state during sleep, but pulsatile release of GnRH leading to pulsatile release of LH and FSH will lead to puberty. Puberty starts in the brain, its onset really has nothing to do with decreased inhibin levels which happens in the testes. hope that makes sense! +2  
sars  From what I understand, inhibin is only released by granulosa cells when FSH levels are high. This is a boy. Next off, this question is about puberty, which is due to pulsatile GnRH leading to large amounts of LH and FSH, leading to large amounts of dihydrotestosterone (males) and estradiol (females), and eventually secondary characteristics of puberty. The increased pulse of estrogen and testosterone leads to GH release, which is metabolized into IGF-1 in the liver. This leads to long bone growth from what I understand, which is not much. +  
cassdawg  @sars inhibin B is also released by sertoli cells in males and will feedback to inhibit FSH release, its not just a female thing. Also, there is actually an inhibin B pubertal surge in both females and males that corresponds to maturation of the granulosa and sertoli cells, respectively. Hormones are wack. https://pubmed.ncbi.nlm.nih.gov/15319819/ +  


submitted by lsmarshall(347),
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ehT mtso itercd ,phta and most ieyllk hpta, ofr rsateb ecncar ot estiszameta ot the vabrreet aer hte aoilrnsttec .vines iThs asw no an reialer MEBN ttes sa ewl.l rtsaBe ncearc wlil esauc exi,dm yltic nad bactsli nsesilo ceon in eob.n

On an rtaneludae ;onet I inaflyl emac pu whit a ceedtn way ot mreebemr ltciy s.v sitbacl enrccsa ni oeb!n

deInkY dan YIdtorh eascu ltYIc

etapstor gt&; aaltbset t;&g tialbcs

wTo ssabret ;g&t tow ptsey of isolnes > B trase escaus B oth

Tow unlgs ;gt& otw syept of lesison gnneie(pdd no yetp fo ulng reac)cn

ca-esmllll ulng ;> m"asll ltbass"

olslamn-n elcl t;g& lytic

artist90  VEINS: 1-Intercostal veins drain into Azygous vein which drains into SVC BUT some blood from this Azygous vein is also draining into BATSONS VERTEBRAL VENOUS PLEXUS how the breast cancer metastasizes to vertebral column. 2-Internal thoracic(mammary) vein drains directly into Brachiocephalic vein. 3-Lateral thoracic vein drains into Axillary vein which drains into Subclavian vein which drains into Brachiocephalic vein. ARTERIES ARE DIFFERENT: Subclavian artery----branches into---Internal thoracic(mammary) artery---Intercostal arteries. Internal thoracic artey is used for CABG if there is 1 vessel block. +10  


submitted by lsmarshall(347),
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areU ylceC ersDdiosr &tg; lsaedtIo veseer memmrniyoaepah &;(gt 00;10 i.e,. no reoht veeser amteilboc itenudsracsb

rOenihint maasysnatrbaelcr ncfeydceii ;g&t ms(to nmcomo reau lccye .di)s citroo reiacuacaiimd/dia, mieaenrympoham

ngriacO caAisdmie gt;& nrHmoyiemaeamp, onin-gapa dos,siaic kitoess ofrm( eyhag)liycmpo

i-encuMiahdm lyAa-Cco oghdyesneared feiiycdenc ;t&g mpmaanryHmei,eo oehotycpikt gcheymolypai e(nes ni tidβaxno-io os,redidsr CEXETP pryoderonyeosdaku)htl

evirL oudcnitnfsy ;t&g eipo,nmaHeamyrm sTFL edesms u,p rodle .tp

lsmarshall  Summary of metabolic issues relating to hyperammonemia +5  
seagull  i'm leaning towards Ornithine transcarbamylase deficiency. +2  
notadoctor  Not sure why this isn't considered a mitochondrial disorder since the issue is Ornithine transcarbamylase deficiency in the mitochondria? +2  
charcot_bouchard  if it was mitochondrial disorder no one would escape +2  
wowo  figure in OTC deficiency, they might have to explicitly mention the orotic aciduria AND typically presents earlier, around 24-48hrs of life after they've fed (at least per BB) + also per BB, propionic acidemia and MM acidemia have an onset of weeks to months and lead to build up of organic acids --> acidemia in addition to hyperammonemia (not sure why, but several aa enter the TCA cycle via propionyl CoA --> methylmalonyl CoA --> succinyl CoA, but now this is defunct d/t enzyme deficiencies...?). Anywho, propionic acidemia described on FA2019 p85, but doesn't list hyperammonemia +2  
artist90  i think it cannot be Ornithine transcarbamylase deficiency bc it is XR disease. this pt has a healthy 2yr old brother which rules out X-linked recessive disease correct me if i m wrong +3  
artist90  it is 100% Propionic acidemia Uworld Q-id: 1340. it is an exact copy question of uworld. i got it wrong bc i forgot these are organic acids. But i am still confused on 2 things 1-how does acidosis cause Hypoglycemia and Ketosis. 2-why is Ammonia elevated in these pts bc urea cycle will be fine? +  
yb_26  1) hyperammonemia is seen in all urea cycle disorders except arginase deficiency 2) organic acids directly inhibit urea cycle => hyperammonemia (from UWorld) +1  
yex  According to UW, there is another question # 1341. This one refers to methylmalonic acidemia (ORGANIC ACIDEMIA). HYPOGLYCEMIA results from overall increased metabolic rate leading to increased glucose utilization and direct toxic (-) of gluconeogenesis by organic acids. The presence of hypoglycemia leads to increased free fatty acid metabolism that produces KETONES, resulting in a further anion gap met acidocis. Finally, organic acids also directly (-) the urea cycle, leading to HYPERAMMONEMIA. +7  


submitted by lsmarshall(347),
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erUa yClce sDdieosrr &g;t odltesIa esever ineomremypaahm g(&;t 0010; ..e,i no teorh eesevr lecbatmio cenaidsbtsru

inOrnihte rmeatarsaacsybln cyfeincied g;t& ots(m mnmcoo aure ylcce i)d.s rticoo idaemadi/araicuci, nmaaiohymperme

aiOncrg mdsceAiia &;tg ,eonHmirpamamye ngipn-oaa idais,sco koetssi m(ofr hpcyelmagioy)

ecn-hauMmiid Coyc-Aal hoagenrydseed cideecifyn &;tg nHmey,aompamire htitooypkce cghpyiyleoma sne(e ni xdiatooni-β rdosie,drs CEETXP odlshrduyretaepokn)yo

Lvier cyndntuifos &g;t maaHyemnmioper, TsLF eessmd ,pu oreld p.t

lsmarshall  Summary of metabolic issues relating to hyperammonemia +5  
seagull  i'm leaning towards Ornithine transcarbamylase deficiency. +2  
notadoctor  Not sure why this isn't considered a mitochondrial disorder since the issue is Ornithine transcarbamylase deficiency in the mitochondria? +2  
charcot_bouchard  if it was mitochondrial disorder no one would escape +2  
wowo  figure in OTC deficiency, they might have to explicitly mention the orotic aciduria AND typically presents earlier, around 24-48hrs of life after they've fed (at least per BB) + also per BB, propionic acidemia and MM acidemia have an onset of weeks to months and lead to build up of organic acids --> acidemia in addition to hyperammonemia (not sure why, but several aa enter the TCA cycle via propionyl CoA --> methylmalonyl CoA --> succinyl CoA, but now this is defunct d/t enzyme deficiencies...?). Anywho, propionic acidemia described on FA2019 p85, but doesn't list hyperammonemia +2  
artist90  i think it cannot be Ornithine transcarbamylase deficiency bc it is XR disease. this pt has a healthy 2yr old brother which rules out X-linked recessive disease correct me if i m wrong +3  
artist90  it is 100% Propionic acidemia Uworld Q-id: 1340. it is an exact copy question of uworld. i got it wrong bc i forgot these are organic acids. But i am still confused on 2 things 1-how does acidosis cause Hypoglycemia and Ketosis. 2-why is Ammonia elevated in these pts bc urea cycle will be fine? +  
yb_26  1) hyperammonemia is seen in all urea cycle disorders except arginase deficiency 2) organic acids directly inhibit urea cycle => hyperammonemia (from UWorld) +1  
yex  According to UW, there is another question # 1341. This one refers to methylmalonic acidemia (ORGANIC ACIDEMIA). HYPOGLYCEMIA results from overall increased metabolic rate leading to increased glucose utilization and direct toxic (-) of gluconeogenesis by organic acids. The presence of hypoglycemia leads to increased free fatty acid metabolism that produces KETONES, resulting in a further anion gap met acidocis. Finally, organic acids also directly (-) the urea cycle, leading to HYPERAMMONEMIA. +7  


mousie  http://www.sparknotes.com/biology/cellreproduction/cellcycle/section3/page/2/ +3  
fahmed14  Cyclins help regulate cell cycle phases. They help with checkpoints before progression to the next phase of a cell cycle. Therefore the checkpoint before mitosis would be in G2 and probably where mitotic specific cyclins are synthesized +9  
artist90  https://en.wikipedia.org/wiki/Cyclin . 4 types of Cyclins and when they rise and fall. +2  


submitted by lsmarshall(347),
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laaeMaspit - A eerirbvels etviadpa snersoep in hihcw ehret si gaemgiorpn"Rmr fo etms lpelscmtelcaenreŽ of noe cell pety yb rtaonhe thta anc ptaad ot a ewn tes.r"ss tBho rea lanmro l.ecsl aRretypriso eetr osduhl not veha omuuqsas sclle uintl yraprrteosi ihlscerobno ereob(f hta;t blducaio in rte.m b.nor &;gt ncramulo ni rhnb.co t&;g ofdsiedrutptseai clmnraou in rga.el oh.b.rcn)

shayan  if its a metaplasia, then how it be normal ? I mean Metaplasia is not normal? +1  
artist90  i got it confused bc the question stated that there was a mass in one lobe of lung and i didn't knew that squamous metaplasia also presents as a mass in lung. i missed that on biopsy they were clearly stating squamous metaplasia. +4  
suckitnbme  @shayan The term "normal" in the answer is used to indicate that the cells appear normal (meaning appropriate size/architecture/appearance). Remember that metaplasia is a normal response to stress. +4