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free120/Block 2/Question#30 (reveal difficulty score)
An otherwise healthy 45-year-old man comes to ...
Elaboration of proteases and urease with local tissue destruction ๐Ÿ” / ๐Ÿ“บ / ๐ŸŒณ
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 +22 
submitted by โˆ—benwhite_dotcom(653),
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As awsyal, โ€™tis mtaols tbtree ot girneo eht spurtcie wneh ssoebp.il hsiT megtelnna has a ppetic ,lruec hciwh ew nokw si cuedas eryaeidnplomt yb H. lrpyio cnetioifn. H. yrlipo edusprco atsoepers nad uliyaptlarrc esre,ua hciwh wlaol it to ecaesrni teh pH of ist olcal tnoenemivrn yb laicegvn erau onti oimn,aam hcihw is xoitc ot ctsagri .uaomsc heT triuecp eestdmosratn H ,roypil chwhi era tedniev ihwt vesilr itasn.ign

joonam  Hey bro, thank you so much for your contributions on these free 120 questions. Your advice on test taking strategies for step 1 have been very helpful. +23  
luciana  "Elaborated enzymes by H. pylori may also contribute directly to epithelial cell injury. Ammonia produced through urease activity may be toxic to gastric epithelial cells. H. pylori protease and lipase degrade gastric mucus and disrupt the phospholipid-rich layer at the apical epithelial cell surface, allowing for cell injury from back diffusion of gastric acid." https://www.ncbi.nlm.nih.gov/pubmed/9394757 +4  
luciana  I got tricked :( Thought the damage was due to destruction of local somatostatin cells with increased gastrin and acid production... but this is actually the mechanism of duodenal ulcers development related to H. pylori But makes sense, so thats how the somatostatin producing cells are destroyed lol +6  
drpee  "Hyperacidity and gastric ulcer development" is also sort of true, but this is hinting at the mechanism for DUODENAL ulcer development from H Pylori. Irritation in the stomach leads to G Cell hyperplasia, increasing acid secrection which causes downstream ulceration. +7  
itsalwayslupus  Did anyone else pick the hyperacidity answer just because the correct answer had "local tissue destruction" in it? I figured that H. Pylori was non-invasive, so would not directly damage the tissue it is localized too +8  
cbreland  @itsalwayslupus exact same thoughts over here +1  



 +2 
submitted by houseppary(16),
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tub awht is gwonr htwi re"Sotpeihc nniovasi of gscriat l"ls?ec tI esems klei H yilpro is esoimsetm edcirsbde sa crudev nda emtmssioe as a chiteeors.p dAn ri"stgca lcsl"e si eranleg uoeghn tath I o'ndt see wyh it anc be .gnrwo reTeh si H rylipo ni het cirstga llcs.e

em_goldman  H pylori is sometimes described as helical but more often as curved, but is (confusingly) not a spirochete. Spirochete refers to a particular family, Spirochaete, and are markedly corkscrew. The three important spirochete bugs for Step 1 are Leptospira, Borrelia spp., and Treponema pallidum; Brachyspira spp. get an honorable mention but idk they're high yield for Step 1. Anything other kind of bug is not going to be a spirochete. Additionally, H. pylori is not invasive, and instead resides on the surface of the gastric mucosa. The picture showed some bacteria inside the lumen of glands, not intracellulary. +8  
em_goldman  *idk if they're high yield +1  
em_goldman  *any other kind of bug gosh dang it, lol, definitely in dedicated rn +1  
dang90  I also think spirochetes dont "invade" either. They colonize in the gastrum antrum releasing urease to thrive but don't invade. +1  



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