GI Intro, Esophagitis, Gastritis, H. pylori Flashcards
describe GI tract colonization after birth
immediately after birth = E. coli and Streptococci
describe GI tract colonization after breast feeding starts
breast fed =
E. coli, Streptococci, Bacteroides & Clostridium #s decline; Bifidobacterium #s remain high
describe GI tract colonization if babies are formula fed
formula fed = Lactobacilli present
describe GI tract composition at the begninng of weaning
beginning of weaning:
E.coli, Streptococci & Clostridium #s return to high levels
flora now similar to formula fed infants
describe oesophagitis and name cases where it can occur
- oesophagitis = inflammation of the esophagus
- odynophagia & dysphagia
- predominantly non-infectious (gastroesophageal reflux disease)
- infection: cancer chemotherapy, transplantation, HIV
- prominent: Candida albicans, CMV, HSV
describe esophagitis caused by Candida sp.
- diagnosis:
- endoscopy; whitish plaques
- double contrast oesophagram: discrete linear plaque-like lesions, upper-mid esophagus
describe what is seen in the image
esophagitis caused by Candida spp.
____ is the 2nd most common cause of esophagitis
HSV-1 is the 2nd most common cause of esophagitis
describe the diagnosis of esophgitis caused by HSV-1
- diagnosis:
- endoscopy/double contrast esophogram: multiple, small discrete, superficial ulcers (punctate, linear, stellate, or “volcano-like”)
describe what is seen in the image
esophagitis caused by HSV-1
esophagitis caused by ____ is increased in patients who had solid organ transplants
esophagitis caused by CMV is increased in patients who had solid organ transplants
describe the diagnosis of esophagitis caused by CMV
- diagnosis:
- endoscopy/double contrast esophagram: 1 or more giant (>10 cm), flat (ovoid, elongated or diamond shape) ulcers (sometimes with small satellite ulcers)
describe what is seen in the image
esophagitis caused by CMV
describe gastritis and name the causes
- gastritis = inflammation of stomach tissue with epigastric (sharp/burning) pain
describe peptic ulcer disease (PUD)
- gastric & duodenal: lesions in mucosa in the stomach (gastric ulcers) or uppermost portion of small intestine (duodenal ulcers), presents with epigastric sharp/burning pain after eating
- gastric ulcer = pain briefly after eating
- duodenal ulcers = pain a few hours after eating
- an endoscopy needed to differentiate
compare gastric vs. duodenal ulcers
describe the progression of gastric cancer
- progression:
- chronic non-atrophic gastritis → atrophic gastritis → intestinal metaplasia → dysplasia
- causes = multifactorial, H. pylori
describe Helicobacter pylori (H. pylori)
- G-ve
- non spore-forming
- curved to spiral
- motile (5-6 polar flagella)
- catalase +ve, urease +ve
H. pylori contains the enzyme urease which allows it to ____
H. pylori contains the enzyme urease which allows it to neutralize gastric acid and induce gastric mucosal injury by ammonia
_____ allows H. pylori to adhere to host cells and causes inflammation
LPS allows H. pylori to adhere to host cells and causes inflammation
describe the function of effectors in the pathogenicity of H. pylori
- effectors
- actin remodeling
- IL-8 induction, host cell growth, apoptosis inhibition
the exotoxin produced by H. pylori is ____ which causes gastric mucosal injury
the exotoxin produced by H. pylori is vacuolating toxin (vacA) which causes gastric mucosal injury
describe the most sensitive (non-invasive) test for diagnosing an H. pylori infection
-
serology = most sensitive (non-invasive)
- IgG antibodies
- not useful for response to treatment
describe a test to determine current infection (non-invasive)
-
fecal antigen = determines current infxn (non-invasive)
- specific, sensitive
- used to check response to treatment
describe the most specific test for diagnosing H. pylori infection
-
gastric biopsy: most specific, requires endoscopy
- look for presence of ulcers, cancer
- histological changes, presence of H. pylori
