Gastric Mucosal Lesions Flashcards
H. Pylori: Microbiology traits
Where does it colonize?
How is it pathogenic?
What are the hallmark cellular findings?
What is the role of virulence factors?
Spiral shaped microaerophilic, gram negative bacteria
Exclusively colonizes gastric type epithelium
Noninvasive, but stimulates inflammatory and immune responses
Hallmark: Neutrophilic infiltration, along with lymphocytes, plasma cells, macrophages (chronic active gastritis)
Specific strains contain, increasing inflammation, damage, complications
Cytotoxin-associated gene A (CagA)
Where is H. pylori in early stages of chronic infection?
What secretory effects does it have?
Where does ulceration occur?
Confined to antrum
Inhibited D Cell somatostatin
Acid secretion increases
Duodenal ulcers
What is the location of chronic late stage infection?
What are the cellular/secretory effects?
Where does ulceration occur?
Colonization and inflammation expand to corpus/fundus
Destruction of parietal cells
Acid decreases, gastrin increases
Gastric ulceration
What are the immunologic responses after eradicatoin of H. pylori?
Neutrophilic infiltration resolves
Lymphocytic infiltration may persist
What is the epidemiology of H. pylori?
When is it acquired typically and how?
½ world population
Increased in developing countries, crowding, poverty, age
Declining in developed world
Transmission like fecal/oral or oral/oral
Acquisition 1%/year after childhood
What means of diagnosis of H. pylori are there?
What can result in false negatives or positives?
Endoscopic gastric mucosa biopsy
Urea breath testing
Stool antigen testing
False negative with recent antibiotics or PPI therapy
Serology: Persists even after eradication (false positive)
What adverse effects result from H. pylori?
Peptic ulcer
Enteric infections
Malnutrition/iron and B12 deficiency
Gastric neoplasias (Adenocarcinoma, MALT lymphoma, Carcinoid)
What are the evolutionary considerations of H. pylori?
What possible adverse consequences of eradication are there?
Coexisted with HP for millennia
Most infected persons have no adverse effects in reproductive years
GERD/adenocarcinoma of esophagus
Weight gain?
Atopic diseases?
What is autoimmune gastritis?
What is the gener association?
What is the mechanism?
What is it associated with?
Inherited form associated with immune response in the oxyntic mucosa against parietal cells and IF
Three times more common in women
Lymphocytic inflammation with destruction of parietal cells
Associated with other autoimmune (Thyroid, celic, T1DM)
What is atrophic metaplastic gastritis?
What are the two types, causes, locations?
What are the consequences?
Inflammatory destruction of normal mucosa with replacement by metaplastic elements (intestinal type with goblet cells)
Type A: Body and fundus, Autoimmune
Type B: Antrum (can extend proximally), H. pylori (may be absent)
Achlorhydria - Increased gastrin
Reduced/absent IF
Similar to reduced acid secretion
Pernicious anemia
Gastric cancer
Carcinoid
What is the difference between gastritis and gastropathy?
Gastritis: Inflammation associated mucosal injury
Infectious, autoimmune
Gastropathy: Epithelial cell damage and regeneration with minimal or no associated inflammation
Bile, alcohol, aspirin, NSAIDs, ischemia
What are the direct effects of NSAID gastric toxicity?
Trapped in epithelial cells
Uncoupling of ox-phos
Reduced energy production
Increased cell permeability
Rapid cell death and superficial mucosal injury
What ar ethe systemic effects of NSAID gastric toxicity?
Due to inhibition of COX-1:
Mucosal blood flow and oxygen delivery
Mucin, bicarbonate, and phospholipid secretion
Epithelial cell proliferation and migration
What is an ulcer vs erosion?
Ulcer: Destructive breach of mucosa that extends below muscularis mucosa
Erosion: Superficial to MM
What is the epidemiology of Peptic Ulcer Disease (PUD)?
What are major risk factors?
How is the association with H. pylori changing?
2% Prevalence
Risk with age and smoking
H. pylori associated decreasing
What percent of NSAID/Asiprin users have erosions?
What percent of chronic users have PUD?
What is the complication rate of these and resulting hospitalizations?
50% develop erosions
25% of chronic users have PUD
2-4% have complications, resulting in 100,000 hospitalizations each year in US
What are the major causes (90%) of PUD?
Aspirin/NSAIDs
H. pylori
Surreptitious/unaware NSAID use
What are lesser causes of PUD?
Gastric malignancy- Adenocarcinoma, Lymphoma
Viral (Herpes/CMV)
Bisphosphonates
Anastomotic ulceration (gastric bypass)
Stress ulceration
What are the rare causes of PUD?
ZE
Hypersecretory states
Crohn’s
Mesenteric ischemia (incl. cocaine)
Radiation therapy
Treponema pallidum
Hepatic artery infusion of 5-FU
What are the major risk factors of PUD?
Which drugs are associated?
Age > 65
Dose and duration of therapy
Prior PUD/complication
Concurrent use of:
NSAID
Glucocorticoids
Anticoagulants (Clopidogrel)
SSRIs
What are the complications of PUD?
Acute GI hemorrhage
Chronic GI blood loss/IDA
Perforation/peritonitis/pancreatitis
Gastric outlet obstruction
Gastrointestinal fistula
Malabsorption/malnutrition/weight loss
Iatrogenic complications
What are the symptoms of PUD?
Chronic dyspeptic epigastric pain
DU: 2-3 hours after meals/night
GU: Worse with meals
Waxes/wanes over weeks
Acute severe pain: perforation
Nausea
Anorexia/weight loss
Hematemesis (25% of TBV)
Melena, red blood per rectum (33% of BV)
Recurrent post-prandial vomiting (obstruction)
Diarrhea (fistula)
No symptoms
