Definition The term gastritis is used to denote inflammation associated with mucosal injury. Gastritis is mostly a histological term that needs biopsy to be confirmed. Gastritis is usually due to infectious agents (such as Helicobacter pylori) and autoimmune and hypersensitivity reactions.
Definition Epithelial cell damage and regeneration without associated inflammation is properly referred to as "gastropathy.― Gastropathy may be referred without histological evidence and just according to gross appearance in endoscopy or radiology Gastropathy is usually caused by irritants such as drugs (e.g., nonsteroidal anti-inflammatory agents and alcohol), bile reflux, hypovolemia, and chronic congestion.
Sex: Male-to-female ratio of gastritis is approximately1:1 Male-to-female ratio of PUD is approximately 2:1
Pathophysiology The mechanisms of mucosal injury in gastritis is thought to be an imbalance of aggressive factors acid production or pepsinand defensive factors mucus production bicarbonate and blood flow
Acute & Chronic Difference Acute refers to short term inflammation Acute refering to neurophilic infiltrate Chronic referring to long standing forms Chronic referring to mononuclear cell infiltrate especially lymphocyte and macrophages
Acute Gastritis Definition An acute mucosal inflammatory process, with neutrophilic infiltrate, that is usually transient. There may be hemorrhage into the mucosa or sloughing of the mucosa. Severe erosive form is an important cause of severe GI bleeding
Etiology Frequently associated with, among others: heavy use of NSAIDS, especially aspirin excessive alcohol consumption heavy smoking severe stress e.g. trauma, burns, surgery Ischemia Systemic infection Often, idiopathic
NSAIDs NSAIDs and aspirin also interfere with the protective mucus layer by inhibiting mucosal cyclooxygenase activity, reducing levels of mucosal prostaglandins
Smoking Promotes gastritis & ulcer occurrence Increases the likelihood of ulcer complications Mechanisms Stimulate gastric acid secretion Stimulate bile salt reflux Causes alteration in mucosal blood flow Decrease mucus secretion Reduces prostaglandin synthesis Decrease pancreatic bicarbonate secretion
Effects of Diet and Stress Diet and Stress ActionDiet Dyspepsia, may pain - not believed to cause ulcer or assist healingPhysiologic ↓ mucosal blood flow, tissue hypoxia,stress mucosal lining degradation; e.g. ICU, sepsis, burn, trauma. Associated with multiple erosions & significant bleeding
Acute Gastritis - Pathogenesis Acid secretion + BicarbonateAll above Factor + back diffusion buffer + Direct Disruption Mucosal + of Blood flow Injury Mucus layer Acute Gastritis
Stages of Acute Gastritis Acute superficial Acute erosive gastritis gastritis Inflammation of Destruction of multiple superficial gastric small zones of mucosa. superficial mucosa. Acute Gastric Ulceration Destruction of full thickness of mucosa
Acute Gastritis - MorphologyRanges from edema with neutrophil infiltration, vascular congestion,&an intact epithelium, to erosion (mucosal defect that does not crossthe muscularis mucosa) and hemorrhage.
Acute Gastritis Gastric mucosa demonstrates infiltration by Neutrophils
Acute Gastritis diffusely hyperemic gastric mucosa causes for acute gastritis alcoholism drugs infections, etc.
Acute Gastritis Clinical Features broad range of signs and symptoms that depend on the severity of the condition Asymptomatic Epigastric pain, nausea & vomiting Hemorrhage, massive hematemesis, melena, or fatal blood loss One of the major causes of massive hematemesis, particularly in alcoholics. ~25% patients taking aspirin for rheumatoid arthritis will develop acute gastritis, and some will bleed
Chronic Gastritis Definition Chronic mucosal inflammatory changes leading to atrophy and metaplasia (usually without erosions) Dysplasia and ultimate neoplasia are complications.
Chronic GastritisType B Type A Antral AutoimmuneGastritis gastritis
Type B (Antral Gastritis) 90% of patients with antral chronic gastritis: Helicobacter pylori infected Motile, gram negative curvilinear rods that elaborate urease (buffers gastric acid) & toxins and have adhesins to bind to the epithelium. Pathogenesis H. pylori (urease NH4+ + toxins) + Host (acid + peptic enzymes) Chronic Inflammation Antibodies Gland destruction + Mucosal atrophy acid intrinsic factor (which can lead to pernicious anemia)
Helicobacter gastritis 2 patterns of infection Diffuse involvement of body and antrum (―pan gastritis‖ associated with diminishing acid output) Infection confined to antrum (antral gastritis, associate with increased acid output)
Helicobacter pylori Adapted to live in association with surface epithelium beneath mucus barrier Causes cell damage and inflammatory cell infiltration In most countries the majority of adults are infected
H. pylori Gastritis - Morphology H. pylori organisms along superficial mucus layer of antral biopsy Web Path
Bile reflux gastropathy Bile reflux gastropathy typically results from the regurgitation of bile into the stomach because of an operative stomach, an incompetent pyloric sphincter, or abnormal duodenal motility. The effect of bile salts on gastric mucosa is comparable to that seen after chronic NSAID use
Chemical gastritis Commonly seen with bile reflux (toxic to cells) Prominent hyperplastic response (inflammatory cells scanty) With time – intestinal metaplasia
Clinical FeaturesUsually only a few symptoms: nausea, vomiting, upper abdominal discomfort Most infected person have gastritis, but are asymptomatic Hypochlorhydria, but NOT achlorhydria and pernicious anemia (parietal cells never completely destroyed) Gastrin normal to slightly elevated Antibiotics are treatment of choice
Clinical Complications H. pylori H. pylori predisposes to peptic ulcers in duodenum and stomach—Most patients with a peptic ulcer are infected. Risk of gastric carcinoma and lymphoma
Type A (Auto immune) Etiology Autoimmune - antibodies to parietal cells, gastrin receptor, intrinsic factor, and H+,K+ ATPase <10% of cases of chronic gastritis Possible autosomal dominant inheritance
Morphology of chronic gastritis Chronic inflammatory cell infiltration Mucosal atrophy Intestinal (goblet cell) metaplasiaSeen in Helicobacter and autoimmune gastritis (not chemical)
Autoimmune gastritis Autoimmune gastritis - pernicious anemia Chronic atrophic gastritis is associated with Ab’s - intrinsic factor - patietal cell bright green IF- in the parietal cells of the gastric mucosa.
Autoimmune Gastritis -MorphologyDiffuse mucosal damage of the body and fundicmucosa. Antrum less involved. PJ Goldblatt, MD
Chronic Gastritis Clinical Features Usually only a few symptoms: nausea, vomiting, upper abdominal discomfort Autoimmune Hypo to achlorhydria (severe loss of parietal glands) Hypergastrinemia 10% have pernicious anemia
Clinical Complications Autoimmune: Often seen in association with other autoimmune disorders (Hashimoto thyroiditis, Addison disease, and type I diabetes) Significant risk for the development of gastric carcinoma (2-4%) and endocrine tumors (carcinoid tumor)
Chronic Gastritis Morphology Varying degrees of mucosal damage possible Mucosal lesions are reddened, with thickened rugae Atrophied rugae in long-standing cases Lymphocytes and plasma cell infiltrate; neutrophils indicate ―active‖ inflammation (may or may not be present)
Regeneration - constant feature Metaplasia - mucosa of antral and body-fundic regions converts to columnar absorptive cells and goblet cells (intestinal metaplasia) Atrophy - marked loss of glands Dysplasia – precursor lesion to gastric cancer in atrophic gastritis
Hypertrophic gastritis Three variants are recognized Menetrier’s disease Hypersecretory gastropathy Gastric gland hyperplasia [the Zollinger-Ellison syndrome]