Gastritis morphology, gross, types, etiology, clinical Symptoms, treatment

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Gastritis: Complete Overview

Definition

Gastritis is a mucosal inflammatory process of the stomach. When inflammatory cells are absent or rare despite mucosal damage, the preferred term is gastropathy.

Robbins, Cotran & Kumar Pathologic Basis of Disease, p. 720

Classification (Sydney System)

The most widely used classification (Updated Sydney System) categorizes chronic gastritis by topography, morphology, and etiology:

Type	Etiology	Synonyms
Nonatrophic chronic gastritis	H. pylori, other factors	Chronic superficial gastritis, Type B gastritis, Diffuse antral gastritis
Atrophic - Autoimmune	Autoimmunity (± H. pylori)	Type A gastritis, Diffuse corporal gastritis, Pernicious anemia-associated
Atrophic - Multifocal	H. pylori + environmental	Type AB gastritis, Atrophic pangastritis
Reactive gastropathy	NSAIDs, bile reflux, alcohol	Chemical gastropathy
Lymphocytic gastritis	? H. pylori, celiac disease	Varioliform gastritis
Granulomatous gastritis	Crohn disease, sarcoidosis, TB	-
Eosinophilic gastritis	Allergic, idiopathic	-

Yamada's Textbook of Gastroenterology, Table 51.1, p. 1081

A staging system called OLGA (Operative Link for Gastritis Assessment) adds detailed grading of glandular atrophy to predict gastric cancer risk.

Types of Gastritis

1. Acute Gastritis

A dense neutrophilic infiltration of the gastric mucosa. True acute neutrophilic gastritis is rare; most "active" gastritis is chronic inflammation with superimposed neutrophils (as in H. pylori infection).

Special severe forms:

Phlegmonous (suppurative) gastritis: infection of the gastric submucosa and muscularis propria; may spare mucosa. Organisms: gram-negative bacilli, anaerobes, group A streptococci, fungi (mucormycosis). Presents as a septic abdomen with peritonitis. Associated with alcohol binge, respiratory infections, AIDS, liver transplantation.
Emphysematous gastritis: caused by gas-producing organisms (Clostridium perfringens, E. coli, S. aureus); gas seen in stomach wall and portal venous system on CT. Risk factors include recent gastroduodenal surgery and ingestion of corrosives. May progress to gastric gas gangrene.
Sleisenger and Fordtran's GI and Liver Disease, p. 909

2. Chronic Gastritis - H. pylori (most common)

Produces diffuse antral gastritis initially (nonatrophic pattern)
With time can progress to multifocal atrophic gastritis (corpus + antrum)
Associated with 70-80% of peptic ulcer disease and risk of gastric adenocarcinoma and MALToma

3. Chronic Gastritis - Autoimmune (Type A)

Spares antrum; involves body and fundus
Causes pernicious anemia; less than 10% of chronic gastritis; prevalence ~2% in patients >60 years

4. Environmental Metaplastic Atrophic Gastritis (EMAG)

H. pylori + dietary/environmental factors (high-salt diet, smoking, carcinogens)
Patchy involvement beginning at incisura, spreading to antrum and corpus

5. Special/Distinctive Forms

Lymphocytic gastritis, Collagenous gastritis, Eosinophilic gastritis, Granulomatous gastritis (Crohn, sarcoid, TB), Infectious gastritis (CMV, fungal, parasitic)

Etiology

Category	Agents
Bacterial	H. pylori (most common), H. heilmannii, streptococcal (phlegmonous), Clostridium (emphysematous), TB, syphilis
Viral	CMV (especially immunocompromised), HSV, EBV
Fungal	Mucormycosis, Aspergillus, Cryptococcus (immunocompromised)
Parasitic	Strongyloides, Anisakis, Giardia, Cryptosporidiosis
Drugs/Chemicals	NSAIDs (most common after H. pylori), aspirin, alcohol, bile reflux
Autoimmune	Anti-parietal cell antibodies (anti-H+/K+-ATPase), anti-intrinsic factor antibodies
Systemic diseases	Crohn disease, sarcoidosis, amyloidosis, graft-versus-host disease
Physical	Radiation injury, nasogastric tube trauma, stress
Iatrogenic	Immune checkpoint inhibitors (nivolumab can cause autoimmune hemorrhagic gastritis)

Robbins, Cotran & Kumar, p. 714-720; Sleisenger & Fordtran, p. 908-910

Gross Morphology

Acute Gastritis / Stress Ulcers

Mucosal hyperemia, edema, and congestion
Erosions (superficial) to frank ulcers; ulcers typically < 1 cm, rounded, base stained brown-black by acid digestion of blood
Lesions are multiple and distributed throughout the stomach (unlike peptic ulcers which are usually solitary/antral)
Phlegmonous gastritis: thick, edematous gastric wall, multiple perforations, granular/purulent mucosa, mucosal hemorrhage and necrosis

H. pylori Chronic Gastritis

Antral mucosa appears erythematous, coarse, or nodular (endoscopic "chicken-skin" appearance = nodular gastritis)
In dense colonization, rugal folds can appear thickened

Autoimmune Atrophic Gastritis

Fundus/body mucosa appears markedly thinned
Rugal folds are lost (flattening)
Residual islands of oxyntic mucosa may appear as small polyps or nodules endoscopically

Multifocal Atrophic Gastritis

Patchy mucosal atrophy beginning at incisura, extending to antrum and corpus
Grayish-white or pale mucosa where normal reddish glandular epithelium has been replaced by intestinal metaplasia
Sleisenger & Fordtran, pp. 908-914; Robbins, pp. 715-716

Microscopic Morphology (Histology)

H. pylori Gastritis

Fig. A: Warthin-Starry silver stain showing spiral H. pylori organisms in surface mucus. B: Intraepithelial and lamina propria neutrophils forming pit abscesses. C: Lymphoid aggregates with germinal centers (asterisk) and subepithelial plasma cells (arrows). - Robbins Pathology

Key features:

Neutrophils infiltrate gastric pits - "pit abscesses"
Plasma cells in clusters within superficial lamina propria
Lymphoid aggregates with germinal centers (MALT induction)
H. pylori organisms visible in superficial mucus on H&E; best seen with Warthin-Starry silver stain or immunostains
"Active" chronic gastritis: both neutrophils and chronic cells (lymphocytes, plasma cells) coexist

Autoimmune Atrophic Gastritis

Autoimmune gastritis histology - A: deep lymphocytic infiltrate with glandular atrophy. B: intestinal metaplasia with goblet cells (arrows)

Fig. A: Deep inflammatory infiltrate centered on gastric glands with atrophy. B: Intestinal metaplasia - goblet cells (arrows) within gastric foveolar epithelium. - Robbins Pathology

Key features:

Deep inflammation centered on gastric glands (not superficial lamina propria as in H. pylori)
Infiltrate: lymphocytes, macrophages, plasma cells - no prominent neutrophils
Loss of parietal and chief cells in body/fundus
Intestinal metaplasia: goblet cells, absorptive cells, Paneth cells
Enterochromaffin-like (ECL) cell hyperplasia and neuroendocrine hyperplasia
May progress to multicentric low-grade neuroendocrine tumors (gastric carcinoids)

Common to All Chronic Forms

Intestinal metaplasia (goblet cells in gastric epithelium) - risk factor for gastric adenocarcinoma
Dysplasia may develop as precancerous change
Robbins, pp. 715-717; Yamada's, pp. 1874-1887

Comparison: H. pylori vs. Autoimmune Gastritis

Feature	H. pylori-Associated	Autoimmune
Location	Antrum (initially)	Body/Fundus
Inflammatory infiltrate	Neutrophils + plasma cells	Lymphocytes, macrophages
Acid production	Increased to slightly decreased	Decreased (achlorhydria)
Gastrin secretion	Normal to increased	Markedly increased
Other lesions	Hyperplastic/inflammatory polyps	Neuroendocrine (ECL) hyperplasia
Serology	Anti-H. pylori antibodies	Anti-parietal cell (H+/K+-ATPase), anti-intrinsic factor antibodies
Sequelae	Peptic ulcer, adenocarcinoma, MALToma	Pernicious anemia, adenocarcinoma, gastric carcinoid
Associations	Low socioeconomic status, poverty, rural areas	Hashimoto thyroiditis, Type 1 DM, Addison disease, Graves disease

Robbins, Table 17.2, p. 716

Pathogenesis of H. pylori Gastritis

H. pylori is a gram-negative, helical/spiral-shaped, flagellated bacterium infecting >50% of the world's population (70-80% in developing nations).

Key virulence factors:

Urease - hydrolyzes urea to NH3, neutralizing local acid; essential for colonization
Adhesins - facilitate mucosal adherence
CagA pathogenicity island - injected into epithelial cells; activates signaling, structural remodeling; present in 90% of isolates in high-gastric-cancer-risk populations; associated with body colonization, atrophy, and intestinal metaplasia
VacA (vacuolating cytotoxin A) - causes epithelial vacuolization and barrier disruption
HP-NAP (neutrophil activating protein)
LPS, Oip A, peptidoglycan - inflammatory mediators

Outcomes depend on interplay of:

Host genetic polymorphisms (IL-1, TNF, IL-10)
Bacterial virulence (CagA+, VacA s1m1 strains)
Environmental factors (smoking, high-salt diet, refrigeration access)
Robbins, p. 715; Sleisenger & Fordtran, p. 914

Clinical Symptoms

Acute Gastritis

Often asymptomatic
Epigastric pain or burning
Nausea and vomiting
Hematemesis (if erosions/stress ulcers)
Severe forms (phlegmonous/emphysematous): acute abdomen, sepsis, fever, hypotension, peritonitis, purulent ascitic fluid

Chronic Gastritis (General)

Typically less severe but more persistent than acute
Nausea and upper abdominal discomfort/pain (most common)
Vomiting (less frequent)
Hematemesis - uncommon
Bloating and belching
Significant weight loss (particularly if atrophic)

H. pylori Gastritis Specifically

Many patients are asymptomatic
May present only when complications arise (peptic ulcer, GI bleeding)

Autoimmune Atrophic Gastritis Specifically

Symptoms develop slowly over 2-3 decades
Pernicious anemia: fatigue, pallor, glossitis, neurological symptoms (subacute combined degeneration of the cord - due to B12 deficiency)
Achlorhydria symptoms: poor digestion
Increased risk of gastric carcinoid tumors
Robbins, pp. 715-720; Sleisenger & Fordtran, p. 909

Diagnosis

Test	Type	Notes
Urea breath test	Non-invasive, indirect	Detects urease activity; sensitive and specific
Stool antigen test	Non-invasive, direct	Good for post-treatment confirmation
Serology (IgG anti-H. pylori)	Non-invasive	Cannot distinguish active from past infection
Biopsy urease test (CLO test)	Endoscopic	Fast, inexpensive
Histology (H&E ± Warthin-Starry)	Endoscopic	Gold standard; shows morphology + organisms
Culture	Endoscopic	Allows sensitivity testing; low sensitivity
PCR	Endoscopic	High sensitivity; detects resistance genes

For autoimmune gastritis: serum anti-parietal cell antibodies (anti-H+/K+-ATPase), anti-intrinsic factor antibodies (present in up to 80%), reduced serum pepsinogen I.

Sleisenger & Fordtran, p. 913-914

Treatment

Acute Gastritis / Stress Ulcers

Remove/treat the underlying cause (most effective approach)
Proton pump inhibitors (PPIs) - prophylactic in critically ill ICU patients
Healing with complete re-epithelialization occurs within days to weeks after treatment
Supportive care: IV fluids, antiemetics

H. pylori Eradication (Chronic Gastritis / Peptic Ulcer Disease)

First-line regimens:

Triple therapy: PPI + Clarithromycin + Amoxicillin (or Metronidazole) for 14 days
Bismuth quadruple therapy: PPI + Bismuth + Tetracycline + Metronidazole (used in areas of high clarithromycin resistance)

Goals: eradication, mucosal healing, prevention of complications. After successful H. pylori eradication, peptic ulcer recurrence rate is less than 20%.

Autoimmune Atrophic Gastritis

No curative treatment (autoimmune process)
Vitamin B12 replacement (intramuscular injections monthly, or high-dose oral supplementation)
Iron supplementation as needed
Endoscopic surveillance for gastric carcinoid and adenocarcinoma
Treat any coexisting autoimmune conditions

NSAIDs / Reactive Gastropathy

Discontinue the offending NSAID (including selective COX-2 inhibitors)
PPI therapy for mucosal healing
If NSAIDs must continue: use lowest effective dose + PPI co-therapy

Granulomatous Gastritis (Sarcoidosis)

Glucocorticoid therapy (cornerstone)
Subtotal gastric resection reserved for obstruction or severe hemorrhage

Phlegmonous/Emphysematous Gastritis

Broad-spectrum IV antibiotics (covers gram-negative bacilli, anaerobes, gram-positive cocci)
Surgical resection/drainage may be necessary
Mucormycosis: resection of affected necrotic stomach; anti-fungal therapy (amphotericin B)
Robbins, p. 715, 720; Sleisenger & Fordtran, pp. 905-912; Harrison's Principles of Internal Medicine 22E

Complications of Chronic Gastritis

Peptic Ulcer Disease - usually H. pylori-induced hyperchlorhydria
Gastric Adenocarcinoma - via intestinal metaplasia → dysplasia → cancer (Correa cascade); risk greatest in autoimmune metaplastic atrophic gastritis
MALToma (MALT Lymphoma) - B-cell lymphoma arising from H. pylori-induced MALT; can regress with H. pylori eradication
Pernicious Anemia - autoimmune atrophic gastritis; megaloblastic anemia from B12 deficiency
Gastric Neuroendocrine Tumors (Carcinoids) - ECL cell hyperplasia driven by hypergastrinemia in autoimmune gastritis
Dysplasia - intermediate precancerous lesion

Robbins, pp. 720-722

Key Sources: Robbins, Cotran & Kumar Pathologic Basis of Disease (pp. 713-722) | Sleisenger and Fordtran's GI and Liver Disease (pp. 908-920) | Yamada's Textbook of Gastroenterology (pp. 1080-1087) | Harrison's Principles of Internal Medicine 22E

Give me the details about gastritis

The detailed overview I just provided covers all the key aspects of gastritis. Here is a structured summary of everything covered:

Gastritis - Complete Details

1. Definition

Gastritis is a mucosal inflammatory process of the stomach. When mucosal damage occurs without significant inflammation, the preferred term is gastropathy.

2. Classification (Updated Sydney System)

Based on topography, morphology, and etiology:

Type	Etiology	Old Name
Nonatrophic chronic gastritis	H. pylori	Type B gastritis
Autoimmune atrophic gastritis	Autoimmunity	Type A gastritis
Multifocal atrophic gastritis	H. pylori + environment	Type AB gastritis
Reactive gastropathy	NSAIDs, bile reflux	Chemical gastropathy
Lymphocytic gastritis	H. pylori, celiac	Varioliform gastritis
Granulomatous gastritis	Crohn, sarcoidosis, TB	-
Eosinophilic gastritis	Allergic, idiopathic	-

The OLGA staging system adds detailed atrophy grading to estimate gastric cancer risk.

3. Types

A. Acute Gastritis

Dense neutrophilic infiltration of mucosa
True acute gastritis is rare; "active" gastritis = neutrophils superimposed on chronic inflammation

Severe subtypes:

Subtype	Features
Phlegmonous gastritis	Infection of submucosa/muscularis propria; organisms: gram-negative bacilli, streptococci, anaerobes, fungi
Emphysematous gastritis	Gas-producing organisms (C. perfringens, E. coli, S. aureus); gas in stomach wall + portal venous gas on CT; may progress to gastric gangrene

B. Chronic Gastritis - H. pylori (Most Common)

Starts as diffuse antral gastritis
Progresses to multifocal atrophic gastritis
Risk of peptic ulcer, adenocarcinoma, MALToma

C. Autoimmune Atrophic Gastritis (Type A)

Body and fundus only (antrum spared)
Anti-parietal cell + anti-intrinsic factor antibodies
Leads to pernicious anemia, gastric carcinoids

D. Multifocal Atrophic Gastritis (EMAG)

H. pylori + environmental cofactors (salt, smoking)
Begins at incisura, spreads to antrum and corpus

E. Special/Distinctive Forms

Lymphocytic gastritis - thick folds, varioliform erosions; associated with celiac, H. pylori
Collagenous gastritis - subepithelial collagen band > 20 µm
Eosinophilic gastritis - eosinophil-dominant infiltrate; allergic or idiopathic
Granulomatous gastritis - non-caseating granulomas; Crohn, sarcoidosis, TB
CMV gastritis - immunocompromised patients; intranuclear "owl-eye" inclusions

4. Etiology

Category	Agents
Bacterial	H. pylori (#1), TB, syphilis, streptococcal, Clostridium
Viral	CMV, HSV, EBV
Fungal	Mucormycosis, Aspergillus, Cryptococcus
Parasitic	Strongyloides, Anisakis, Giardia
Drugs	NSAIDs, aspirin, alcohol, corticosteroids
Autoimmune	Anti-H+/K+-ATPase, anti-intrinsic factor Ab
Physical	Radiation, NG tube trauma, stress (Curling/Cushing ulcers)
Systemic	Crohn disease, sarcoidosis, amyloidosis, GVHD
Iatrogenic	Immune checkpoint inhibitors (nivolumab)
Bile reflux	Post-gastrectomy, pyloric dysfunction

5. Gross Morphology

Acute Gastritis

Mucosal hyperemia, edema, congestion
Superficial erosions to frank ulcers
Ulcers < 1 cm, rounded, base stained brown-black by acid digestion of blood
Multiple throughout stomach (vs. peptic ulcers - usually solitary/antral)
Phlegmonous: thick, edematous wall with granular/purulent mucosa and necrosis

H. pylori Chronic Gastritis

Antrum appears erythematous, coarse, or nodular endoscopically
"Chicken-skin" (nodular gastritis) - visible on endoscopy

Autoimmune Atrophic Gastritis

Fundus/body mucosa thinned, rugal folds lost
Residual oxyntic islands may look like small polyps/nodules endoscopically
Pale, atrophic appearance

Multifocal Atrophic Gastritis

Patchy pale/white mucosa at incisura spreading outward
Areas of intestinal metaplasia appear grayish-white

6. Microscopic Morphology (Histology)

H. pylori Gastritis

Feature	Detail
H. pylori location	Superficial mucus layer, gastric pit lumens
Best stain	Warthin-Starry silver stain or immunostain
Neutrophils	Infiltrate gastric pits - "pit abscesses"
Lamina propria	Plasma cells in clusters, lymphocytes, macrophages
Lymphoid tissue	Lymphoid aggregates with germinal centers = MALT
Active gastritis	Neutrophils + chronic cells simultaneously

Autoimmune Atrophic Gastritis

Autoimmune gastritis - deep glandular lymphocytic infiltrate (A) and intestinal metaplasia with goblet cells (B)

Feature	Detail
Inflammation location	Deep - centered on gastric glands (not superficial)
Cell types	Lymphocytes, macrophages, plasma cells - no neutrophils
Glandular changes	Loss of parietal and chief cells
Metaplasia	Intestinal metaplasia - goblet cells, absorptive cells, Paneth cells
Endocrine changes	ECL cell hyperplasia; may form multicentric carcinoid tumors
Megaloblastic change	Nuclear enlargement in epithelial cells if severe B12 deficiency

Common to All Chronic Gastritis

Intestinal metaplasia - goblet cells in gastric epithelium; risk factor for adenocarcinoma
Dysplasia - nuclear pleomorphism, loss of polarity; precancerous

7. H. pylori vs. Autoimmune Gastritis - Comparison

Feature	H. pylori	Autoimmune
Location	Antrum (initially)	Body/Fundus
Inflammatory cells	Neutrophils + plasma cells	Lymphocytes + macrophages
Acid production	Increased to slightly decreased	Decreased (achlorhydria)
Gastrin	Normal to increased	Markedly increased (hypergastrinemia)
Serology	Anti-H. pylori Ab	Anti-H+/K+-ATPase, anti-IF Ab
Other lesions	Hyperplastic polyps	ECL hyperplasia, carcinoids
Complications	Peptic ulcer, adenocarcinoma, MALToma	Pernicious anemia, adenocarcinoma, carcinoid
Associations	Low socioeconomic status, poverty, rural	Hashimoto thyroiditis, Type 1 DM, Addison, Graves

8. Pathogenesis of H. pylori

H. pylori is a gram-negative, helical, flagellated bacterium infecting >50% of the world's population.

Key virulence factors:

Factor	Function
Urease	Splits urea → NH3; neutralizes local acid; essential for survival
Adhesins	Mucosal attachment
CagA (pathogenicity island)	Injected into epithelial cells; activates oncogenic signaling; present in 90% of isolates in high-cancer-risk populations
VacA	Epithelial vacuolization, barrier disruption
HP-NAP	Neutrophil activation, oxidative burst
LPS	Weak immunostimulant; Lewis Ag mimicry causes molecular mimicry with gastric epithelium

Host factors: IL-1, TNF-α polymorphisms → increased pro-inflammatory cytokines → pangastritis, atrophy, cancer progression

Environmental modifiers: High-salt diet, smoking, lack of refrigeration accelerate progression

9. Clinical Symptoms

Acute Gastritis

Often asymptomatic
Epigastric burning or pain
Nausea and vomiting
Hematemesis (with erosions/ulcers)
Severe forms: acute abdomen, sepsis, fever, hypotension, peritonitis

Chronic Gastritis

Symptoms less severe but persistent
Nausea, upper abdominal discomfort/pain
Vomiting (less common)
Bloating, belching
Significant weight loss in atrophic forms
Hematemesis - uncommon

Autoimmune Gastritis Specifically

Slow progression over decades
Pernicious anemia: fatigue, pallor, glossitis, neurological deficits (subacute combined degeneration due to B12 deficiency)
Achlorhydria: impaired digestion
Signs of associated autoimmune diseases

10. Diagnosis

Test	Method	Notes
Urea breath test	Non-invasive	Detects active urease; gold standard non-invasive test
Stool antigen test	Non-invasive	Best for post-treatment confirmation
Serology (IgG)	Non-invasive	Cannot confirm active vs. past infection
Biopsy urease (CLO test)	Endoscopic	Fast, inexpensive, accurate
Histology (H&E + Warthin-Starry)	Endoscopic	Definitive; shows organisms + morphology
Culture + sensitivity	Endoscopic	Guides antibiotic choice in resistant cases
PCR	Endoscopic	High sensitivity; detects antibiotic resistance genes
Anti-parietal cell Ab	Blood test	For autoimmune gastritis; positive in up to 80%
Serum pepsinogen I	Blood test	Reduced in atrophic gastritis

Sydney system requires 5-site biopsy protocol: antrum (greater + lesser curvature), corpus (greater + lesser curvature), and incisura.

11. Treatment

Acute Gastritis / Stress Ulcers

Treat the underlying cause (most effective)
PPI prophylaxis in critically ill ICU patients
IV fluids, antiemetics, supportive care
Healing in days to weeks after removing offending agent

H. pylori Eradication

Regimen	Drugs	Duration
Triple therapy (1st line)	PPI + Clarithromycin + Amoxicillin	14 days
Alternative triple	PPI + Clarithromycin + Metronidazole	14 days
Bismuth quadruple (resistance areas)	PPI + Bismuth + Tetracycline + Metronidazole	10-14 days

After successful eradication: peptic ulcer recurrence < 20% (previously notoriously difficult)

Autoimmune Atrophic Gastritis

No cure (autoimmune)
Vitamin B12 replacement - IM injections monthly or high-dose oral (1000 µg/day)
Iron supplementation
Endoscopic surveillance for carcinoid tumors and adenocarcinoma

NSAIDs/Chemical Gastropathy

Discontinue NSAIDs (including COX-2 inhibitors)
PPI for healing
If NSAIDs unavoidable: lowest dose + PPI co-therapy

Granulomatous Gastritis (Sarcoidosis)

Glucocorticoids (cornerstone)
Surgery only for obstruction or severe hemorrhage

Phlegmonous/Emphysematous Gastritis

Broad-spectrum IV antibiotics (gram-negative, anaerobic, gram-positive coverage)
Surgical resection/drainage for severe cases
Mucormycosis: resection + amphotericin B

12. Complications

Complication	Mechanism	Notes
Peptic Ulcer Disease	H. pylori-induced hyperchlorhydria	Stomach or duodenum
Gastric Adenocarcinoma	Intestinal metaplasia → dysplasia → cancer (Correa cascade)	Risk greatest in AMAG
MALToma	H. pylori-induced MALT → B-cell lymphoma	Can regress with H. pylori eradication alone
Pernicious Anemia	Autoimmune loss of intrinsic factor → B12 deficiency → megaloblastic anemia	AMAG-specific
Gastric Carcinoid Tumors	ECL hyperplasia from hypergastrinemia	AMAG-specific; usually low-grade
Dysplasia	Inflammation-driven genetic alterations	Precancerous; requires surveillance

Sources: Robbins, Cotran & Kumar Pathologic Basis of Disease | Sleisenger and Fordtran's GI and Liver Disease | Yamada's Textbook of Gastroenterology, 7th Ed. | Harrison's Principles of Internal Medicine 22E

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