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Comments ...

 +0  (nbme20#28)

I have a hard time understanding how annular pancreas can cause bilious vomiting when I'm seeing many sources say it is either bilious or non-bilious.

draykid  Ok, so after doing a little research. It can cause both, but if the annular pancreas wraps around the duodenum distal to the ampulla of Vater then you get bilious obstruction. +5




Subcomments ...

submitted by johnthurtjr(142),
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12F09A p 357 no toasGtalentrnsii dlboo pupysl and ciyatetrpapsamh ennriinotva:

  • uoFtgre gt-&;- alecic a,reryt gvusa rnnnaveioit
  • gMuitd t-;g&- M,SA ugavs
  • udgHtin --;&tg IMA, plvcei nvorinenait
neovanilla  Don't force it out, you gotta relax and it'll come out naturally ;) +  
mysteriousmantyping  Why couldn't the answer be Inferior rectal nerve since that controls the external anal sphincter? +1  
draykid  @mysteriousmantyping I think this question is looking at complications of T2DM, more specifically diabetic autonomic neuropathy. Patient more than likely has diabetic gastroparesis which may explain his constipation and abdominal distension. +1  
cuthbertallg0od  Pudendal nerve controls external anal sphincter (per FA), and gastroparesis wouldn't have anything to do w pelvic splanchnics but instead vagus nerve... Don't know why pudendal nerve couldn't be right if he was just clogged up from not being able to relax his sphincter anymore ---- is parasympathetic just more likely to be the issue statistically or something? +1  
cuthbertallg0od  Or would losing pudendal nerve result in incontinence... Its never been clear to me if activation/inactivation opens/closes sphincters... +1  
cuthbertallg0od  Just realized that says perineal... whoops +2  
vivijujubebe  External sphincter is innervated by pudendal nerve, more often damaged during labor. DM patients have autonomic neuropathy with parasympathetic/sympathetic nerves more likely damaged +  


submitted by draykid(26),

I have a hard time understanding how annular pancreas can cause bilious vomiting when I'm seeing many sources say it is either bilious or non-bilious.

draykid  Ok, so after doing a little research. It can cause both, but if the annular pancreas wraps around the duodenum distal to the ampulla of Vater then you get bilious obstruction. +5  


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p + q = 1 2 p^ + p2q + ^2q = 1 f i q^2 = 1006/1 = 000.063 enth q = (srtqq2^) = 00.52 s ovle fro p ot tge p = 1 - r = 1 - 025.0 = .9075 t eh reysheztogou earcrrsi = pq2 = 1 - p2^ = 1 - 0.95 = .05 q2^ anc eb edroppd b/c t'is mchu mlalrse anth p^.2 Te h dieotnel is nbrelsoepsi rfo 0%8 of teh antus.tiom 0.8 x 0.5 = 400. = 041/0 = 15/2

reThe tmgih eb an sreiae yaw to od ,isth ubt ti ewdkor fro .me

thechillhill  So apparently I don't know how to format very well. Sorry! +1  
pakimd  So because i couldnt spend more than a minute on this question and honestly didnt recall the Hardy-Weinberg equation this is how i solved it under a minute: so you know in a given population half of them will be carriers since its an autosomal recessive disease Aa Aa= AA aa Aa Aa so of that half 80% are due to deletion mutations and 20% are due point mutations by that logic 80% of half into 20% of half will give you 1/25 +1  
draykid  0.8 x 0.5 is 0.4 +  
topgunber  hate this whole scramble thing: In one line: 2 * q * 80%. This is for diseased individuals (two q alleles).I = 1/1600 = q^2 The frequency of q = 1/40 Now carriers is 2 p q. P is close to one assuming HW eqm (p+q=1). There's an additional step in this question due to the two different mutations. so 2(q) = 1/20. 80% of these carriers are deletions so multiply 1/20 * 0.8 = 1/25 +  


submitted by nala_ula(110),
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Teh ogoiylhst is of eesprschtoy (lmsla licrsepah lcesl o/w etnlrac ll)orap. eHdeayrrti scoisohpryets si eud to feetdc ni niestopr ntiicneragt wtih BCR emnmareb snkoetel dan msapla rebneamm ia(nkryn, dnab ,3 ptoiner ,4.2 epncrt)s.i tyoMls saltuomao mitoadnn ectehnirain (so sretoogyzueh mouttnai sinec oyu noly eedn eno nuttam aeelll to egt hte ea.ss)ied

wuagbe  To add to this: homozygous HS presents with hemolysis even in absence of stressors. this patient is only presenting with pale skin, and there are no schistocytes on the peripheral smear, so it's a heterozygous ankyrin mutation. +8  
pg32  I wanted to pick hereditary spherocytosis but the mean corpuscular concentration was normal and I thought it was supposed to be elevated? Also, why are there so many RBCs that are way bigger than the spherocytes? +6  
nephroguy  I'm assuming that the MCC is normal because the patient is heterozygous for HS. Not sure if this is correct, but that was my thought process +1  
draykid  Are there any papers that explain the difference in expression of homozygous vs heterozygous HS? +20  
waterloo  I don't know if that matters as much, like the phenotype difference of homozygous or heterozygous for this question. Since you only need one allele to show this, play odds. Is he more likely to have AA or Aa. That was my thought process. Also if you see spherocytes you'd be going for ankyrin right, not B-globin bc that should be target cells - regardless of MCHC. +1  
alimd  as I remember AD are always heterzygous. Because homozygous are always lethal. +4