Pathology Of Benign Gastric Disease Flashcards
Congenital gastric disease
Pyloric stenosis
Pyloric stenosis
Idiopathic hypertrophy of circular pyloric muscle → outflow obstruction
Pyloric stenosis
Affect
M: F =
4 – 5:1
Familial /genetic basis
Pyloric stenosis
Symptoms
Projectile vomiting 2-3 weeks after birth
Pyloric stenosis
Treatment
surgical incision of hypertrophic muscle
Gastropathy
Epithelial cell damage and regeneration with minimal or no inflammation
Gastritis
inflammation associated with gastric mucosal injury
Gastropathy + gastritis
Symptoms
▪ asymptomatic or epigastric pain, nausea, and vomiting
▪ In severe cases: mucosal erosion, ulceration, hemorrhage, hematemesis, melena, or
massive blood loss
Gastropathy
Causes
- chemical (reactive) : alcohol, bile reflex, NSAIDs….
- vascular : portal hypertensive(congestive) gastropathy, gastric antral vascular ectasia
- ischemic gastropathy : cocaine, hypovolemia, sepsis,burns, trauma,..
Gastritis
Causes
- Infectious: h pylori…….
- autoimmune
- granulomatous disease: crohns, sarcoidosis
- other; ..
Gastropathy + gastritis
Pathogenesis
Imbalance
between defensive and
damaging forces
Chronic gastritis
Causes
▪ Helicobacter pylori – most common
▪ NSAIDs, Chemical-Bile reflux, radiation
▪ Autoimmune gastritis
▪ Lymphocytic
▪ eosinophilic – food allergy
▪ granulomatous – Crohn’s disease, sarcoidosis
H. pylori
Shape
Spiral-shaped or curved Gram-negative bacilli
H. pylori
associated with ———-status and
———-, acquired in———, prevalence rises with age
low socioeconomic
poor hygiene
childhood
H. pylori
Routes of infection:
Oral,
Fecal-oral,
Environmental spread
H. pylori
Present in
90% chronic antral gastritis,
100% in duodenal ulcer
H. pylori
Virulence due to:
▪ Flagella
▪ Urease
▪ Adhesins
▪ Toxins(encoded by cytotoxin-associated gene A (CagA) )
Chronic gastritis caused by h
h.pylori
Two types?
- Antral predominant gastritis
- Body predominant/pan-gastritis:
Antral predominant gastritis ( most common)
increased acid production resulting in
duodenal ulceration in 10–15%
Body predominant/pan-gastritis:
decreased acid secretion and gastric ulceration
Body predominant/pan-gastritis: decreased acid secretion and gastric ulceration (due to
reduction in parietal cell mass → low acid secretion → hypergastrinemia → intestinal
metaplasia → 3-6 fold increased risk of gastric adenocarcinoma)
——biopsies are preferred for evaluation of H. pylori gastritis ,
Why?
antral
H. pylori shows tropism for gastric foveolar epithelium (in antrum)
H.pylori chronic gastritis
Histology
▪ The organism is concentrated in
▪ Mucosa is
▪ Inflammatory cells:
▪ Lymphoid
-superficial mucus overlying epithelial cells (mostly
in antrum)
- erythematous, Thickened (initial stages) → Atrophic (later stages)
- intraepithelial neutrophils +subepithelial plasma cells
-Lymphoid aggregates with germinal centers – May progress to (MALT) lymphoma – type
of NHL
H.pylori chronic gastritis
Clinical features:
Nausea, Upper abdominal discomfort, Vomiting
H.pylori chronic gastritis
Diagnosis:
▪ Serologic tests for anti-H. pylori antibodies
▪ Fecal bacterial detection
▪ Urea breath test
▪ Biopsy Rapid urease test, Culture (stains: H&E, giemsa, silver stain,
immunohistochemical stain which stains organism brown), PCR
Urea breath test
high CO2 indicates presence of H. pylori
< 10% of cases of chronic gastritis
Autoimmune gastritis
H. pylori most common in——-whereas Autoimmune gastritis
antrum
Spares the antrum
Autoimmune gastritis
Pathogenesis:
Autoantibodies against parietal cell (specifically H+,K+ -ATPase) → Loss of parietal
and chief cells → Deficient acid secretion stimulates gastrin release → hypergastrinemia and hyperplasia of antral G cells → if prolonged can develop NET (neuroendocrine tumor)
Autoimmune gastritis
due to destruction of parietal cells)
Antibodies to parietal cells and intrinsic factor
-Vitamin B12 deficiency leading to pernicious anemia and neurologic changes (due to loss
of intrinsic factor)
-Achlorhydria ( absence of Hcl)
Autoimmune gastritis
due to loss of chief cells
Reduced serum pepsinogen I levels
Antral endocrine cell (G cells) hyperplasia → hypergastrinemia
Autoimmune gastritis
Gross morphology:
Diffuse atrophy of gastric mucosa resulting in loss of HCl secretion
(hypochlorhydria) → acid producing mucosa in body and fundus markedly thinned,
and
rugal folds are lost
Autoimmune gastritis
➢ Histology:
▪ Infiltrated by lymphocytes, plasma cells, Inflammation extends deep into mucosa
▪ Loss of parietal and chief cells
▪ Fibrosis of the lamina propria
▪ Intestinal metaplasia (goblet cells) in body mucosa
▪ Antral endocrine cell (foveolar cells / G cells) hyperplasia → carcinoid (NET) tumors
Autoimmune gastritis
▪ Slow onset, Median age 60 yrs ▪ May be associated with other autoimmune diseases
Other
Clinical Features:
▪ Atrophic glossitis (beefy red tongue)
▪ Peripheral neuropathy → paresthesia and numbness ▪ Spinal cord lesions → loss of vibration and position sense
▪ Cerebral manifestations → personality changes and memory loss to psychosis
Autoimmune gastritis
Diagnosis
antibodies to intrinsic factor or parietal cells,
elevated fasting serum gastrin level,
staining with anti-chromogranin antibodies can show endocrine cell hyperplasia →endocrine
cells stain brown
Chemical gastritis aka
reactive gastritis,
bile reflux gastritis or
type C gastritis)
Chemical gastritis
Causes
-reflux of alkaline duodenal contents after partial distal gastrectomy,
-secondary motility
disturbances in patients with gallstones and after cholecystectomy,
-long-term use of NSAIDs, corticosteroids or chemoradiotherapy
Chemical gastritis
ommon denominator being repeated chemical injury
Presentation
bilious vomiting or less severe dyspeptic symptoms, Repeated damage to mucosa
may cause a gastric ulcer
Eosinophilic gastritis (rare) ➢ characterized by
oedema and increased eosinophils in absence of intestinal parasites (which
also cause eosinophilia)
Eosinophilic gastritis association w/
history of atopy or
connective tissue disease (scleroderma, SLE)
Lymphocytic gastritis
presence of numerous lymphocytes within surface epithelium
Lymphocytic gastritis Seen in 45% of pts with——-), 10% with H. pylori
infection, also patients with Crohn’s disease and allergies
gluten sensitive enteropathy (coeliac disease)
Granulomatous gastritis Histology
epithelioid cell granulomas
Granulomatous gastritis related to
infectious agents (TB, histoplasmosis, parasites), systemic granulomatous diseases (sarcoidosis, Crohn’s disease), presence of foreign bodies
Compilations of chronic gastritis:
PUD,
mucosal atrophy,
intestinal metaplasia and dysplasia
Peptic ulcers are
solitary lesion that can occur in any part of the GIT which is exposed to acid-peptic juices [Acid & Pepsin are required for peptic ulceration]
Peptic ulcers can occur in:
stomach (gastric ulcers)
duodenum (duodenal ulcers)
stomach (gastric ulcers) commonly located in
lesser curvature of stomach near the
interface of the body and antrum
duodenum (duodenal ulcers) → commonly
within a few centimeters of the pyloric
valve,
duodenal ulcers
more common than stomach ulcers, duodenitis with Brunner cell hyperplasia and
gastric mucin cell metaplasia
Ulcer sites: mostly at mucosal junctions
▪ antral-proximal duodenum (>95%)
▪ other sites: Stomach, GE junction, Gastrojejunostomy site, Jejunum in ZE-syndrome
Peptic ulcer disease (PUD)
pathogenesis:
Imbalance between mucosal defenses and damagin forces → hyperacidity,
factors that cause hyperacidity:
H. pylori,
parietal cell hyperplasia,
excessive secretory responses,
Insufficient inhibition of stimulatory mechanisms such as gastrin release e.g. Zollinger-Ellison syndrome
Risk of peptic ulcer
H. pylori, chronic NSAIDs use (decrease PGs), smoking (impairs BF),
acidic drinks, stress, caffeine, corticosteroids (suppress PGs and impair healing)
▪ Age:
▪ Gender:
▪ Genetic:
-Duodenal 30-50, Gastric over 60
-Duodenal → increasing in older women
-family history, blood groups (blood group O are at increased risk of peptic
ulcers due to enhanced binding of H. pylori to their epithelial cells)
Acute vs chronic peptic ulcers:
Acute: acute gastritis, mucosal ischemia, extreme hyperacidity e.g. Zollinger-Ellison
Syndrome
Chronic: occurs where acid and pepsin first come in contact with susceptible mucosa
e.g. antral and proximal duodenum, associated with HP or chemical gastritis
Gross of peptic ulcer
Shape: Round to oval, Margins: Punched out, Edge: Overhanging, Floor: clean, Base:
Firm
Scarring -> puckering -> radiating mucosal folds (in spoke wheel pattern)
Microscopy
4 zones
▪ Zone of exudation (thin layer of fibrinoid necrosis)
▪ Zone of inflammatory cell infiltration
▪ Zone of granulation tissue
▪ Zone of scarring (only in chronic lesions)
Symptoms of peptic ulcer
▪ Epigastric tenderness (Gastric: left of midline, Duodenal: mid to right of epigastrium)
▪ Sharp, burning, aching, gnawing pain
▪ Dyspepsia (indigestion), Nausea/vomiting, Belching
Gastric vs duodenal ulcers:
Gastric: Pain occurs 1-2 hours after meals & usually does not wake patient &
accentuated by ingestion of food, has risk for malignancy, ulcer is deep and penetrating
Duodenal: Pain occurs 2-4 hours after meals & wakes up patient & relieved by food,
very little risk for malignancy
Diagnosis of peptic ulcer
▪ Esophagogastroduodenoscopy (EGD):
▪ Upper gastrointestinal series (UGI):
▪ Urea Breath Testing:
Urea Breath Testing: to
detect H. pylori
Esophagogastroduodenoscopy (EGD):
Endoscopic procedure → visualizes ulcer, take
tissue biopsy to R/O cancer and diagnose H. pylori
Upper gastrointestinal series (UGI):
Barium swallow → X-ray that visualizes structures of
the upper GI tract
Complications of peptic ulcers:
Hemorrhage
Perforation
Narrowing and obstruction (pyloric):
Anemia
Hemorrhage: if ulcer erodes into muscles of stomach or duodenal wall and damages
underlying BVs → Coffee ground vomitus or bloody tarry stools
▪ Perforation: if an ulcer erodes even further through the entire wall and reaches
peritoneum → Bacteria and partially digested fool spill into peritoneum (usually sterile)
→ peritonitis
▪ Narrowing and obstruction (pyloric): Swelling and scarring (especially in duodenal
ulcers near pyloric sphincter) → obstruction of food leaving stomach → repeated
vomiting and crampy abdominal pain
▪ Anemia: due to hemorrhage and blood loss → iron deficiency anemia
T
Mucosal atrophy and intestinal metaplasia
➢ Associated w/
long-standing chronic gastritis & increases risk for gastric adenocarcinoma
achlorhydria of gastric mucosal atrophy
achlorhydria permits
overgrowth of bacteria that produce carcinogenic nitrosamines
• Dysplasia
➢ Chronic gastritis over time → accumulation of genetic alterations that result in adenocarcinoma ➢ Preinvasive lesion: variations in epithelial size, shape, coarse chromatin, hyperchromasia
