Flashcards in Gastritis & PUD Deck (66):
What is gastsritis?
inflammation associated with mucosal injury
What is gastropathy?
epithelial cell damage and regeneration with minimal to no associated inflammation from irritants
What immune cell to you expect to see in acute and chronic gastritis respectively?
chronic-lymphocytes, plasma cells, macrophages
Key features of acute helicobacter pylori gastritis?
epigastric pain, nausea, vmoiting, NO fever
acute inflamatory changes
usually goes to chronic
Key features of chronic helicobacter pylori gastritis?
antrum and body
early-increased gastrin, decreased somatostatin-->increased acid sec
late-fall in acid secretion w/loss of G cells facilitates proximal migration
Common histological finding of chronic H. pylori?
What is helicobacter heilmannii gastritis?
treated like H pylori
What is metaplasic (chronic) atrophic gastritis? Types?
mucosal thinning, gland loss, change in epithelial cell types
autoimmune and environmental types
What is pseudopyloric metaplasia?
replacement of parietal and chief cells in oxyntic glands by mucus secreting cells found in the antrum
Waht is intestinal metaplasia?
replacement of suface, foveolar and glandular epithelium in oxyntic or antral mucosa by intestinal epithelium (goblet cells)
What are the main types of intestinal metaplasia?
Complete (type I)-fully formed SI epithelium
Incomplete (type II&III)-goblet cells interspersed among gastric-type mucin cells
Which type of intestinal metaplasia is associated with an increased risk of gastric adenocarcinoma?
Key features of AMAG?
inherited, associated w/immune response in the oxyntic mucosa against the parietal cells AND IF
more common in women
risk of pern. an. (vit B12 deficiency)
assoc. w/other autoimmune
body and fundus
AMAG increases the risk of what malignancies?
gastric carcinoid tumors
esophageal squamous cell carcinoma
Key features of EMAG?
environemental exposure to nitroso compouds or H. pylori
NO achloriydia, serum gastrin NOT elevated, NO abs against parietal cells/IF, NO pern. an.
increased risk of gastric ulcer
EMAG increases the risk for what type of cancer?
intestinal type gastric cancer
What is granulomatous gastritis?
organized aggregate of histiocytic, lymphocytic and plasma infiltrate
can be infectious, non infectious or idiopathic
can be non caseating, caseating or necrotizing
What is mucosal eosinophilic gastritis?
distral antrum, nonspecific symptoms
nodularity on EGD
30s, assoc w/allergies, tx w/prednisone
What is eosinophilic gastritis muscle layer disease?
tickened rigid gut, distal antrum
Waht is subserosal eosinophilic gastritis?
ascites, can occur w/ mucosal or muscle layer disease
What are the 3 main causes of lymphocytic gastritis?
What are the causes and symptoms of acute hemorrhagic erosive gastropathy?
damage to epithelium via agents or hypoxia
abdominal pain, nausea, vomiting, hematemesis
What are the causes and symptoms of chronic chemical gastropathy?
long-term exposure to substances that injure the gastric mucosa
foveolar hyperplasia, edema, inc sm muscle in lamina propria, vascular dilation and congestion
What is hyperplastic gastropathy (menetrier's disease)?
enlarged gastric folds/hyperplasia of gastric epithelial cells
caused by overproducition of TGFa which leads to proliferation of epithelials cells
CMV may cause in kids
Key features of CMV?
owl's eye inclusion bodies
What are the symptoms of menetrier's disease?
abdominal pain, protein losing enteropathy, wt loss, nausea, vomiting
Tx of menetriet's disease?
What malignancy does menetrier's disease increase the risk of?
What is Zollinger Ellison syndrome?
gastric acid hypersecretion due to hyperplasia of parietal cell
increase in histamine-secreting enterochromaffin-like cells
body and fundus
What is nonhyperplasic gastropathy? causes?
non oxyntic gland cells leading to gastric fold enlargement
infiltrative disease, malignancy (lymphoma, adenocarcinoma, carcinoid)
What is peptic ulcer disease?
defects in the gastrointestinal mucosa extending through the muscularis mucosa
What are the major risk factors for PUD?
(possibly tylenol at high dose)
increased acid production
decreased duodenal bicarb secretion
What leads to duodenal ulcers in h pylori infection?
increased gastric acid secretion
downregularion of mucosal defense mechanisms
What leads to gastric ulcers?
proximal to distal antrum
normal to low acid
How does dueodenal PUD ulcer present?
burning or hunger-like epigastric pain 2-5hr after meals or at night
relief w/food, antacids or antisecretory meds
How does gastric PUD ulcer present?
burning or hunger like epigastric pain
less freq relief w/food/antacids
pain soon after meals
What are the general clinical presentations of PUD?
dyspepsia (food provoked or relflux-like)
w/constipation or IBS sx
Presentation of penetratin PUD?
localized intense pain that radiates to the back, not relieved with food or antacids
Presentation of perforated PUD?
severe, diffuse abd pain
other complicated presentations of PUD?
GI bleeding (IDA)
Tx of PUD?
acid suppression--helps stabilize blood clots
somatostatin/octreotide (decreased blood flow, inhibit gastric acid sec.)
angiography w/transarterial embolization
What symptoms comprise dyspepsia
epigstric pain or burning
Definition of functional dyspepsia?
dyspepsia+no evidence of structural disease
sx 3 of the last 6 months
Types of functional dyspepsia?
postprandial distress syndrome
epigastric pain syndrome
Why does functinoal dyspepsia occur?
h. pylori infection
altered gut microbiome (post infec.)
Tx of functional dyspepsia?
antidepressants (tricyclics, trazodone)
buspirone (fundic relaxant)
antinociceptive agents (carbamazepine, tramadol, pregablin)
What enzymes are distinctive for H pylori?
catalase, oxidase, urease positive
What type of epithelium does H pylori infect?
gastric type only
s noninvasive, but stimulates an imflamm resonse (IL-8 activates PMNs, recruits other cell types)
What is VacA?
passive urea transporter that can create a favorable environment for infectivity
What are the most commonly associated conditions with H Pylori?
IDA w/o bleeding
Functional dyspepsia (?)
Vit B12 def.
H pyrlori associated Acid reflux causes what two types of gastritis?
H Pylori assoc corpus-predominant gastritis features
decreased acid secretion due to local inflammation and increased cytokines, mild worsening with treatment
H pyrlori assoc antrum predominant gastritis features
associated w/increased gastrin level
improvement with treatment
What endoscopic testing is done for H pylori?
histology +/- special stains
What can cause false positives for H pylori?
What noninvasive testing is done for Hpylori?
Urea breath test (for initial dx and confirmation of eradication)
IgG serology (only way to prove complete cure)
13C-urea blood test
Tx for H pylori gastritis
Acid suppression w/PPIs
10-14 day regiment
How do NSAIDs cause gastroduodenal toxicity?
inhibits constitutively active COX1, which makes prostaglandins--have cytoprotective effects (ie/ mucin, bicarb and phospholipid secretion)
blocks cytoprotective effects of nitric oxide through NO synthase
What are the 2 main repair mechanisms of gastroduodenal toxicity?
restitution-rapid migration of new epithelial cells from progenitor cells
proliferation-less rapid regeneration of new epithelial cells from progenitor cells
(prostaglandins and NO important in both)
What are risk factors for development of PUD w/NSAID use?
duration of therapy (comp usually first 3 mo)
history of GI tox w/nsaids
history of PUD
Are dyspepsia and GI toxicity from NSAIDs related?
How do NSAIDs cause toxicity in stomahc?
block cox1 mediated prostaglandin production
interfere w/resitution and proliferation
How do NSAIDs cause toxicity in the duodenum?
dependent on stomach acid
(H2 blockers/PPIs to prevent)
How do NSAIDs cause toxicity in the small intestine and colon?
high local concentration necessary
localized injury->inflammation and ulceration->fibrosis and stricture
via inhibition of prostaglandins, alterations of blood flow and increased SI permeability
How does NSAID GI toxicity present?
stomach/duodenum: edema, erythema, subepithelial hemorrhage, erosions, ulcers
distal SI and colon-IDA, bleeding, hypoalbuminemia, malabsorption, bow obstruction form strictures, diarrhea, acute abdomen from perforation