Gastritis

Aamir Sharif,

BEMS 4th ProfessionalDepartment of Eastern Medicine & Surgery

Presented By:

3

Stomach

3 muscle layers Oblique Circular Longitudinal

Regions Cardiac sphincter Fundus Antrum (pylorus) Pyloric sphincter

Vascular Inner surface thrown into folds – Rugae Contains enzymes that work best at pH 1-2

Normal Stomach Anatomy

Stomach - Normal

Stomach - Normal

7

Stomach

Functions Mix food Reservoir Start digestion of

Protein Nucleic acids Fats

Activates some enzymes Destroy some bacteria Makes intrinsic factor – B 12 absorption Destroys some bacteria

AbsorbsAlcoholWaterLipophilic acidB 12

InflammatoryDisease of Stomach

GASTRITIS

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 pepsin

and defensive factors

mucus production bicarbonate and blood flow

Protective factors vs. hostile factors

Gastritis

Acute Chronic

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 aspirinexcessive alcohol consumptionheavy smokingsevere stress e.g. trauma, burns,

surgeryIschemiaSystemic 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 Action

Diet Dyspepsia, may pain - not believed to cause ulcer or assist healing

Physiologic stress

↓ mucosal blood flow, tissue hypoxia, mucosal lining degradation; e.g. ICU, sepsis, burn, trauma. Associated with multiple erosions & significant bleeding

Etiology of GastritisA) NormalB) Increased Attack *Hcl*Pepsin.*NSAIDs.

C) Weak defense *Helicobacter pylori

*Stress, drugs, smoking

Acute Gastritis - Pathogenesis

All above Factor Acid secretion+ back diffusion

+ Bicarbonatebuffer

+

Blood flow

Disruptionof

Mucus layer +

DirectMucosal

Injury

Acute Gastritis

Stages of Acute Gastritis

Acute superficial gastritis

Inflammation of superficial gastric

mucosa.

Acute erosive gastritis

Destruction of multiple small zones of

superficial mucosa.

Acute Gastric Ulceration

Destruction of full thickness of mucosa

Mucosal congestion ,edema inflammation & ulceration

ACUTE GASTRITIS - MORPHOLOGY

Acute Gastritis - MorphologyRanges from edema with neutrophil infiltration, vascular congestion,& an intact epithelium, to erosion (mucosal defect that does not cross the 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

AsymptomaticEpigastric pain, nausea & vomitingHemorrhage, 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

Complications:

Malignancy

Hemorrhage

Perforation

Obstruction

Chronic Gastritis

Definition

Chronic mucosal inflammatory changes leading to atrophy and metaplasia (usually without erosions)

Dysplasia and ultimate neoplasia are complications.

Chronic Gastritis

Type B

Antral Gastritis

Type A

Autoimmune 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

Web Path

H. pylori organisms along superficial mucus layer of antral biopsy

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 Features

Usually 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 elevatedAntibiotics are treatment of choice

Clinical Complications

H. pyloriH. 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 gastritisPossible autosomal dominant

inheritance

Morphology of chronic gastritis

Chronic inflammatory cell infiltration

Mucosal atrophy Intestinal (goblet cell)

metaplasia

Seen 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 -Morphology

PJ Goldblatt, MD

Diffuse mucosal damage of the body and fundic mucosa. Antrum less involved.

Clinical Features Usually only a few symptoms: nausea,

vomiting, upper abdominal discomfort

AutoimmuneHypo to achlorhydria (severe loss of

parietal glands)Hypergastrinemia10% have pernicious anemia

Chronic Gastritis

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 GastritisMorphology

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]

Hyperplastic gastropathies

proliferative, inflammatory, and infiltrative conditions are associated with large folds due to excessive number of mucosal epithelial cells

Ménétrier's disease Epithelial hyperplasia

involving the surface and foveolar mucous cells (i.e., foveolar hyperplasia); the oxyntic glands can be normal or atrophic.

Zollinger-Ellison syndrome

Increased numbers of parietal cells with no change in surface and foveolar mucous cells.

Hyperplastic gastropathies

mixed-type in which both mucous and oxyntic glandular cells show hyperplasia, may be seen in as lymphocytic and H. pylori gastritis.

Stomach Acute Gastritis= inflammation of gastric mucosa

acute – presence of neutrophils Chronic –lymphocytes and plasma cells

Caused by ingestion of strong acids or alkalies, NSAIDs, cancer chemotherapy, irradiation, alcohol, uremia, severe stress & shock states

Proposed mechanisms: ↑ acid production with ↓ surface bicarbonate buffer

Morphology: Mucosal edema, hyperemia, PML infiltration, erosions (not deeper than muscularis mucosa) & hemorrhages

Stomach Chronic Gastritis = Chronic mucosal inflammation Leading to mucosal atrophy, intestinal metaplasia &

dysplasia. Pathogenesis: Chronic infection by Helicobacter pylori (90%): MCC of

chronic gastritis, Elaboration of urease produces ammonia that buffers gastric acid, protecting organism from acid

Other diseases associated with H. pylori Infection Peptic ulcer disease Gastric carcinoma Gastric lymphoma

Autoimmunity (>10%): Antibodies to parietal cells cause parietal cell destruction (HCl & intrinsic factor)

Stomach Chronic Gastritis Morphology:

Autoimmune diffuse mucosal damage of the body-fundic mucosa H. pylori affect antral mucosa

Histology: Lymphocytic & plasma cell infiltrate of the lamina propria atrophy, regeneration, metaplasia (to intestinal type mucosa) &

dysplasia. H. pylori detected on the mucosal surface

Clinically: Mild abdominal discomfort, nausea, vomiting; hypochlorhydria,

hypergastrinemia & rarely Overt pernicious anemia (in autoimmune) gastritis).

Long-term risk of cancer is 2-4%