Gastritis, Peptic Ulcer Disease, Gastric Neoplasia Flashcards
UGI bleed potential causes
esophagus
- severe esophagitis
- Mallory-Weiss tear
- esophageal varices
stomach
- peptic ulcer disease (gastric ulcer)
- AV malformation
- gastric varices
- malignancy
duodenum
- peptic ulcer disease (duodenal ulcer)
- AV malformation
atrophic gastritis = risk factor for
- gastric intestinal metaplasia/dysplasia
- gastric cancer (adenocarcinoma)
How do NSAIDs promote acute gastritis?
block prostaglandins, inc H+, promote mucus/bicarb prod
causes of chronic gastritis
H. pylori
- non-atrophic
- atrophic
AI gastritis
H. pylori
microaerophilic, gram neg, spiral shape, multiple polar flagella
most protein products allow survival, colonization, virulence
UREASE
fecal-oral transmission
H. pylori infects which boundaries of the stomach
entire stomach (acute, 85% of chronic)
isolated antrum (15% of chronic, mostly CagA strains, ulcer disease assoc.)
Which type of H. pylori infection leads to inc gastric pH?
chronic atrophic gastritis
via damage to parietal cell and urease effects (urea –> NH3 +CO2)
Which type of H. pylori infection leads to dec gastric pH?
chronic non-atrophic gastritis
more duodenal and gastric ulcer disease
colonization of astral G cells
- hyperplasia of G cells
- inc gastrin –> inc acid
NSAIDs –> ulcers, major MOA
toxicity to GI mucosa due to COX 1** inhibition (RLS) in prostaglandin synthesis
(prostaglandins usu enhance mucosal BF, so if blocked, mucosa vulnerable)
H. pylori testing
non-invasive
- serology
- stool antigen
- urea breath test
invasive
-biopsy
+ urea breath test will show
CO2 in exhaled breath
suggests H. pylori infec
AI gastritis
inflamm @ body/fundus
Abs against parietal cells, IF, and block proton pump
–>B12 deficiency, megaloblastic anemia (inc MCV), hypOchlorhydria or achlorhydria
dx: serum parietal cell Abs
AI gastritis low/no acid levels lead to high ___ which is a risk factor for which 2 pathologies?
low/no acid –> inc gastrin
risk factor for
- type 1 gastric neuroendocrine tumors (carcinoid) via xs ECL stim
- intestinal metaplasia (precursor to gastric adenocarcinoma)
punched out pathology
peptic ulcer
NSAIDs –> ulcers, minor MOA
topical effect
- nonselective NSAIDs are weak acids, un-ionized in stomach, lipid soluble
- diffuse across gastric epithelial cell
- in cell - ionize in neutral pH
- high intracellular [NSAID] –> toxic
peptic ulcer sx
epigastric pain (gnawing) N/V poss improve w/ oral intake poss bleeding (hematemesis "coffee ground")
NSAID induced ulcers may cause no sx except ____
bleeding
ulcer obstruction usually occurs at
pylorus
tx of gastric and peptic ulcer disease
tx H. pylori
H2 receptor antagonists
PPIs
NSAID prophylaxis (misoprostal)
Zollinger-Ellison syndrome
- massive amounts of acid secretion
- neuroendocrine tumor secretes gastrin
- tumor arises in gastrinoma triangle, most from pancreas
- ulcers in somach, duodenum (outside of bulb), jejunum
- severe reflux esophagitis possible
- can be metastatic
dx: clinical history, gastrin level, CTscan or octreotide scan
gastrinoma triangle
defined by duodenal walls, bile ducts, pancreas
octreotide
somatostatin
splanchnic vasoconstrictor
inhibits gastrin, VIP, insulin, others
which gastric polyp has a high risk of malignancy?
adenomatous polyps
most comm in antrum
common location of fundus gland polyps
fundus and gastric body
