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Welcome to kentuckyfan’s page.
Contributor score: 43

Comments ...

 +5  (nbme21#23)
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A bdaeell igmae

B/A oklo like eygr eatmrt to me

C ooskl ilek eudaatc eulucsn

D kolos like erantrio nanerlti paecslu

E olosk ikel haslmuta

lilmonkey  yep, I also chose C. Relatively easy question, but a bit misleading picture. +1

 +4  (nbme21#16)
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anrhote nlki I dfoun efplulh

 +2  (nbme21#28)
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I etg hyw het dixem nseouv oeyxgn otensin c,ewo ,ardeseedr.Hve stin' teh setycims raualscv sticrnsaee oasl srdee?caed

yb_26  no, decreased CO => peripheral vasoconstriction => SVR will be increased +7
yssya1992  No SVR will increase due to RAAS and SAN thats why we decrease afterload in HF treatment ( ACEI, ARBs ) +5
snafull  Wouldn't pulmonary vascular resistance also be decreased here due to pulmonary vasodilation in the setting of an MI? +
cienfuegos  @snafull: my initial thought is that we would see pulmonary vasoconstriction because of the relatively low oxygen tension (that results from the low cardiac output). +3

 +7  (nbme23#49)
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oNciet tath )A tBororonncti,cscniho B) anldraGlu oic,rtesne )D ste,rliasisP E) toaalndiioVs of skni aer lal uernd tcpimpatahsyrea orlntoc.

eTh oynl pytemthiasc otcroln si aetrh aetr, hcwih dwulo ecns.aier

drzed  Vasodilation of the skin is under sympathetic control as well -- beta-2 receptors when stimulated cause vasodilation (via increase of cAMP in vascular smooth muscle). The key is recognizing that stimulation of a GANGLION of the pns will lead to release of NOREPINEPHRINE, which preferentially stimulates alpha-1 receptors. Those receptors will cause vasoconstriction. If the question asked what happens when you stimulate the adrenal medulla, the answer would be (potentially) vasodilation. This is because the adrenal medulla releases EPINEPHRINE which preferentially stimulates beta-1/2 receptors. +6
jesusisking  @drzed Awesome explanation except I think sympathetic response induces vasoconstriction in the skin though vasodilation in the muscles! +1
usmile1  @jesusisking yes you are correct! α1: vasoconstriction in skin and intestine ; β2: vasodilation in skeletal muscle (transmitter: only epinephrine!) +

 +0  (nbme20#31)
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cSeni teh ainp si rcudriaa,l a idcs ihneanitor is toms ey.kill

charcot_bouchard  Why it cant be a lumbar vertebra fracture +
whoissaad  @charcot The patient is young and doesn't have any risk factors for weak bones. Also, disc herniation is a common problem in the young. The disc gets fibrosed and stiff in the elderly so they have less chance for disc herniation. So basically age was the key to answering this question. +3
lovebug  you are genius! thank you! :) +

 +1  (nbme20#40)
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reUa yel:cc Deedrsaec liturinelc and iyheammoemarnp nca fetrdafteinie it mrof coitor rdaiac.ui

hello  As the poster indicates, the described patient has a defect in the urea cycle, specifically an ornithine transcarbamylase deficiency. Added for clarity to future readers. +
ally123  For orotic aciduria, From FA 2019 p. 412, "Orotic acidura is inability to convert orotic acid to UMP (de novo pyrimidine synthesis pathway) because of defect in UMP synthase. Aut recessive. Presents in children as failure to thrive, developmental delay, and megaloblastic anemia refractory to folate and B12 (supplementation). NO hyperammonemia (vs. ornithine transcarbamylase def. which as increased orotic acid with hyperammonemia." +
fataldose  Also it's not Carbamoylphosphate synthetase (I) deficiency because there would be only hyperammonemia, increased glutamine and decreased BUN but no orotic acid increase since carbamoyl phosphate isn't getting made and then shunted to pyrimidine synthesis pathway to get acted on by carbamoyl phosphate synthetase II as is the cause of increased orotic acid seen in OTC deficiency. +
fataldose  If there is isolated elevated orotic acid and no urea defects or hyperammonemia then it's Orotic aciduria due to UMP synthase deficiency. If there if hyperammonemia and orotic acid increase then OTC deficiency. If there is hyperammonemia with no orotic acid increase then carbamoyl phosphate synthetase I deficiency. +2

Subcomments ...

submitted by haliburton(208),
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I ehsco GS-CF cseebua hte trsucanygeol eemsde ot em mreo of a iskr hant teh oreeatdm ttipyroiohreEn ssmee keli an rpatpieaorp eoccih sa lewl ubt SFGC- emor ci.tlriac

kentuckyfan  I think it's also because he has an infection (since he was prescribed antibiotics) boosting the immune system is more important than increasing platelet count E) or RBC count A) +5  

submitted by gabstep(14),
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FA 9120 gp418: Gliaten eheprs epssntre twhi fanlpiu rlauvv ro avrlicce cesevils nda c;lesru anc aeusc ieytsscm symtopsm uhsc as ver,ef achhaeed, mygaial

sam.l  the question stem states a "a scent vaginal discharge" is that a distractor in the question. +  
kentuckyfan  "Scant" means very little. +1  

submitted by sympathetikey(1252),
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I see waht reheyt' yagisn (itsh swa my dsocen ich)oec but ta eht msea imte I flee leki a cpaubk fo oldob uoldw eaaittvc eth brrcteposroae dan ucaes cdseadeer tmiasypceth avtiycit to teh AS ;&apm AV e.nod

sympathetikey  (choice E) +  
meningitis  Could you elaborate? Is this related to: less "preload" from mother circulation causes lowered HR? +  
meningitis  Or backflow of blood and causes a Reflex Bradycardia? still confused on this question. +  
kentuckyfan  So I think the subtle difference in choice E is that there would be a negative CHRONOTROPIC effect, no inotropic effect (contractility). +9  
maxillarythirdmolar  if anything, inotrophy could go UP not down as diastole prolongs and LVEDV increases --> Starling equation bullshit +  

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oLalnilege si nomomc saucse of mponeniua ureimspdopes no nichroc bvueitrcots almrpnuyo dseasei.

asapdoc  Im pretty sure so is strept pneumoniae +4  
usmleuser007  COPD is also exacerbated by Viral infection: Rhinovirus, influenza, parainfluenza; and Bacterial infection: Haemophilus influenzae, Moraxella catarrhalis, Streptococcus. however, the questions gives a hint that it may be legionella = "weekend retreat" which may be associated with this infection +4  
loopers  From FA 2017 pg 139: Legionnaires’ disease—severe pneumonia (often unilateral and lobar A ), fever, GI and CNS symptoms. Common in smokers and in **chronic lung disease.** +1  
kentuckyfan  I also believe that the other attendees showed signs of pontiac fever, which is another hint they tried to get at. +2  
luke.10  i did it wrong and chose influenza virus since it is most common infection in COPD but the clue in the Question is that the other attendee didnt get sick since in legionella there is no person to person transmission +  
endochondral   but in Uworld s. pneumo is one of the most common bacterial exacerbation of COPD legionella wasn't even mentioned. How do we rule out s. pneumo ? +3  
nala_ula  maybe because in children s.pneumo causes otitis media? +  
smc213  Another hint made in the Q stem is the location being rural Pennsylvania.... Legionnaires disease was first discovered by the outbreak in 1976 at a convention held in Philadelphia, Pennsylvania. Not sure why I know this fact... +6  
hpsbwz  Biggest hint towards legionella to me was that they all were at a residence hall... i.e. where there'd be air conditioners and such. +4