NBME Answers ↦
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.
"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."
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
"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.
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
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.
*idk if they're high yield
*any other kind of bug gosh dang it, lol, definitely in dedicated rn