VANO-FRANKIVSK NATIONAL MEDICAL UNIVERSITY DEPARTMENT OF INTERNAL MEDICINE 1

Chronic gastritis
Associate professor Vira Vyshyvanyuk

natomy

and

histology

Normal fundic mucosa

Normal antral mucosa

Gastric Mucosal Barriers

Protective mechanisms of the gastric mucosa against mucosal injury 1. Mucus secretion 2. Bicarbonate secretion 3. Epithelial regenerative capacity 4. Mucosal blood flow 5. Prostaglandin synthesis

GASTRITIS
Inflammation of gastric mucosa Types : - Acute gastritis - Chronic gastritis Affect the fundus or antrum or both

Ethiology of Gastritis
Multifactorial etiology. Combined etiological factors are frequent in single patients. The following are known causes and factors related to gastritis: Bacterial infection (most often by Helicobacter pylori) Fungal infection (most often in people with immunodeficiency) Parasitic infection Bile reflux NSAIDs (nonsteroidal anti-inflammatory drugs) Cigarette smoke Autoimmune disorders Excessive alcohol consumption Excessive caffeine consumption Certain types of radiation Stress Allergic (osinophilic gastritis) Non-infectious granulomatous (Crohn, sarcoidosis, vasculitides)

ICD-10 (2003) Classification Gastritis and duodenitis (K29)

K29.0 Acute haemorrhagic gastritis K29.1 Other acute gastritis K29.2 Alcoholic gastritis K29.3 Chronic superficial gastritis K29.4 Chronic atrophic gastritis K29.5 Chronic gastritis, unspecified K29.6 Other gastritis K29.7 Gastritis, unspecified K29.8 Duodenitis

K29.9 Gastroduodenitis

Classification of Gastritis
Autoimmune gastritis chronic gastritis type A (fundal gastritis) Antral gastritis chronic gastritis type B (associated with H.pylori) Chemical gastritis chronic gastritis type C (reflux-gastritis) Mixed gastritis chronic gastritis type A+B Particular forms of chronic gastritis (eosinophilic, lymphocytic, granulomatous, hyperplastic)

Idiopathic chronic gastritis

Topography of Gastritis

Antral gastritis Corpus gastritis Pangastritis

Specific (Distinctive) Gastritis

Infections Bacterial
Tuberculosis Syphilis Eosinophilic gastroenteritis

Gastrointestinal tract disease

Crohns disease

Viral
Cytomegalovirus

Systemic disease
Sarcoid Graft - vs - host disease

Herpesviruses

Fungal
Candidiasis Cryptococcosis Aspergillosis Chronic granulomatous disease

Miscellaneous (unknown association)

Mntriers disease Focal lymphoid hyperplasia

Parasites and Nematodes

Strongyloidiasis Amebiasis Toxoplasmosis

Pathophysiology
The mechanisms of mucosal injury in gastritis are thought to be an imbalance of aggressive factors, such as acid production or pepsin, and defensive factors, such as mucus production, bicarbonate, and blood flow. Erosive gastritis usually is associated with serious illness or with various drugs. Stress, ethanol, bile, and nonsteroidal anti-inflammatory drugs (NSAIDs) disrupt the gastric mucosal barrier, making it vulnerable to normal gastric secretions. Infection with Helicobacter pylori, a short, spiral-shaped, microaerophilic gramnegative bacillus, is the leading cause of PUD and is associated with virtually all ulcers not induced by NSAIDs. H pylori colonize the deep layers of the mucosal gel that coats the gastric mucosa and presumably disrupts its protective properties. H pylori is thought to infect virtually all patients with chronic active gastritis. NSAIDs and aspirin also interfere with the protective mucus layer by inhibiting mucosal cyclooxygenase activity, reducing levels of mucosal prostaglandins.

Pathogenesis
Increased acid secretion with back diffusion
decreased HCO3 buffer reduced blood flow disruption of mucosal barrier direct injury to mucosal epithelial cells = gastritis

Autoimmune Gastritis (CAG) Type A

A severe form of chronic gastritis affects the body and fundus autoimmune etiology 10 % of chronic gastritis Assoc with other autoimmune disorders : Hashimotos thyroiditis and Addison ds

Autoimmune Gastritis
Pathogenesis: presence of autoAb against parietal cells & intrinsic factor and H+,K+-ATPase (an acid producing enzyme ) gland destruction, mucosal atrophy decrease acid production (hypo- or achlorhydria) and IF Pernicious Anemia

Autoimmune gastritis morphology

1. Diffuse mucosal atrophy 2. Intestinal metaplasia 3. Destruction of the parietal and chief cells 4. Inflammatory cell infiltrates (lymphos, macrophages, plasma cells ) 5. Nuclear enlargement of the epithelial cells 6. absence of H. pylori

Autoimmune Gastritis
Clinical Features :
1. Achlorhydria / hypochlorhydria 2. Decrease of serum pepsinogen 1 3. Hypergastrinemia 4. Pernicious Anemia 5. atrophic glossitis 6. peripheral neuropathy

Gastritis due to H. pylori infection: Type B

Barry Marshall and Warren (1984)
Characteristics of H. pylori curvilinear gram negative bacillus resident bacteria of gastric and duodenal mucosa Humans are the only known host Infection probably acquired via faecal-oral route

H. Pylori organisms

Found in the antrum

Gastritis due to H. pylori infection:

Characteristics of H. pylori motile with flagella elaboration of urease acts on urea NH3 production buffering gastric acid elaboration of adhesin binding of H. pylori to gastric epithelial cells Toxins (cagA, vacA, iceA) Ability to initiate and perpetuate chronic gastric mucosal injury

Type B gastritis
Associated with low socioeconomic status, poverty, residence in rural areas Site: Antrum PATHOGENESIS : Imbalance between gastroduodenal mucosal defences and damaging forces (inc. acid production & digestive enzymes)

Type B gastritis
Bacterial (non-atrophic): Helicobacter pylori 3 phenotypes Antrum-predominant gastritis: hyperchlorhydria with inc. risk of duodenal ulcers development Corpus-predominant gastritis: hypochlorhydria, atrophy, intestinal metaplasia associated with gastric ulcers and cancer Pangastritis

Type B gastritis
Morphology: 1. Hyperemia, edema appearance 2.demonstration of H. pylori 3. inflammatory cell infiltrates; neutrophils & plasma cells 4. mucosal atrophy 5. Intestinal metaplasia 5. Lymphoid aggregates

Diagnosis: 1. gastric biopsy 2. serologic test for H. pylori AB 3. urea breath test

Diseases associated with H pylori

Chronic gastritis PUD Gastric carcinoma Gastric MALT lymphoma

Symptoms
The following symptoms can be a result of gastritis or can be related to the underlying cause: Upper abdominal pain or discomfort

- Epigastric to left upper quadrant

- Frequently described as burning - Usually occurs after meals Hyper- or hypochlorhydria Appetite loss Belching Nausea

Vomiting
Lethargy Anemia (eg, fatigue, dyspnea)

Diagnosis

Diagnosis
Complaints, anamnesis

Gastroscopy

Roentgenoscopy (a barium meal test)

Endoscopic biopsy and histologic evaluation pH-metry of stomach

Tests for Helicobacter infection

Endoscopic Signs Associated with Gastritis

Edema

Erythema
Hemorrhagic mucosa Friability Erosions Hyperplasia Atrophy Intestinal metaplasia

dema

rythema

Hemorrhagic Gastritis

Linear erosions

Endoscopic erosive gastritis

NSAID gastropathy

Gastric mucosa on electron microscope

Normal mucosa Mucosa in gastritis

The destruction of mucosa architectonics, atrophy of epithelial cells are marked

-metry of stomach

Hyperacidity

Hypoacidity

Microphotograph of H.pylori (first preparation made by R.Worren)

B.Marshall and R.Worren openers of H.pylori (July 1984)

Helicobacter pylori

H. p y l o r i i n i t i a t i o n o f m u c o s a l i n f l a m m a t i o n

Evasion of the host chronic inflammatory reaction by H. pylori leads to chronic active gastritis

Antibodies

Monocytes and lymphocytes

Two major patterns of H. pylori gastritis

Pattern of gastritis Antrumpredominant Gastric pathology Acid output Duodenal pathology

Peptic ulce risk

Chronic inflammation Polymorph activity

Gastric
Increased metaplasia

Active chronic
inflammation

Duodenal ulcer

Pan-gastritis

Chronic inflammation Polymorph activity Atrophy Intestinal metaplasia

Reduced

Normal

Gastric ulcer

R e l a t i o n s h i p o f H. p y l o r i t o g a s t r i c c a n c e r

Stages in the development of Gastric Cancer

Normal Gastric Mucosa Superficial Gastritis
Pre-cancerous

H. pylori

Atrophic gastritis Intestina l Metaplasia

Dysplasia

Carcinoma

Treatment
Treatment goals are the relief of discomfort and protection of the gastric mucosal barrier to promote healing.

Cessation of the causative agent and antacids may be sufficient outpatient

therapy in mild cases. Most patients require an H2-receptor antagonist or a proton pump inhibitor,

which has been proven to provide faster and more reliable healing than
antacids. Either an H2-receptor blocker or a proton pump inhibitor can be used as a first-line agent. With continued symptoms, they may be used together. In refractory cases, sucralfate also may be indicated.

Diet with gastritis

Foods to Avoid

Alcohol, black and red pepper, chilies, chili powder, and hot peppers often irritate the stomach lining. Foods with caffeine can increase the amount of stomach acid. These foods include coffee (regular and decaf), teas, colas, cocoa, chocolate. Avoid or limit these items if they cause you pain.

Limit your intake of tomatoes, tomato juice, peppermint, fatty foods, and citrus juices, if they cause heartburn or pain in your esophagus. You may need to limit seasonings such as onions, garlic, cinnamon, and cloves if they upset your stomach.

Drug Category: Antacids - Aluminum-containing and magnesium-containing antacids can be helpful in relieving symptoms of gastritis by neutralizing gastric acids. These agents are inexpensive and safe.

Drug Name

Aluminum and magnesium hydroxide (Maalox, Mylanta) -- Neutralizes gastric acidity, resulting in increase in stomach and duodenal bulb pH. Aluminum ions inhibit smooth muscle contraction, thus inhibiting gastric emptying. Magnesium and aluminum antacid mixtures are used to avoid bowel function changes. 2-4 tsp PO qid prn

Adult Dose

Drug Category: H2-receptor antagonists - Inhibit the action of histamine on the parietal cell, which inhibits acid secretion. The 4 drugs in this class are all equally effective and are available over the counter in half prescription strength for heartburn treatment. Although the IV administration of H2 blockers may be used to treat acute complications (eg, GI bleeding), the benefits are yet to be proven.

Drug Name

Ranitidine (Zantac) -- Competitively inhibits histamine at the H2 receptors of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and reduced hydrogen concentrations.

Adult Dose

150 mg PO bid or 300 mg PO qhs; not to exceed 300 mg/d 50 mg/dose IM/IV q6-8h
Famotidine (Pepcid) -- Competitively inhibits histamine at the H2 receptor of the gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and reduced hydrogen concentrations. 40 mg PO qhs 20 mg/dose IV q12h; not to exceed 40 mg/d Nizatidine (Axid) -- Competitively inhibits histamine at H2 receptors of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and reduced hydrogen concentrations. 300 mg PO hs or 150 mg PO bid

Drug Name

Adult Dose

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Adult Dose

Drug Category: Proton pump inhibitors -- Bind to the proton pump of parietal cell, inhibiting secretion of hydrogen ions
into gastric lumen. Proton pump inhibitors relieve pain and heal peptic ulcers more rapidly than H2 antagonists do. Drugs in this class are equally effective. They all decrease serum concentrations of drugs that require gastric acidity for absorption, such as ketoconazole or itraconazole. Omeprazole (Prilosec) -- Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump. Used for up to 4 wk to treat and relieve symptoms of active duodenal ulcers. Physicians may prescribe for up to 8 wk to treat all grades of erosive esophagitis. 20 mg PO qd for 4-8 wk Lansoprazole (Prevacid) -- Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump. Used for up to 4 wk to treat and relieve symptoms of active duodenal ulcers. Physicians may prescribe for up to 8 wk to treat all grades of erosive esophagitis. 30 mg PO qd for 4-8 wk Rabeprazole (Aciphex) -- Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump. For short-term (4-8 wk) treatment and symptomatic relief of gastritis. Used for up to 4 wk to treat and relieve symptoms of active duodenal ulcers. Physicians may prescribe for up to 8 wk to treat all grades of erosive esophagitis. 20 mg tab PO qd 4-8 wk Pantoprazole (Protonix) -- Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump. For short-term (4-8 wk) treatment and symptomatic relief of gastritis. Used for up to 4 wk to treat and relieve symptoms of active duodenal ulcers. Physicians may prescribe for up to 8 wk to treat all grades of erosive esophagitis. 40 mg PO qd Esomeprazole (Nexium) -- S-isomer of omeprazole. Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump. Used for up to 4 wk to treat and relieve symptoms of active duodenal ulcers. Physicians may prescribe for up to 8 wk to treat all grades of erosive esophagitis. 20-40 mg PO qd

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Drug Category: Gastrointestinal agents - Are effective in the treatment of peptic ulcers and in preventing relapse. Their mechanism of action is not clear. Multiple doses are required, and they are not as effective as the other options.
Sucralfate (Carafate) -- Binds with positively charged proteins in exudates and forms a viscous adhesive substance that protects the GI lining against pepsin, peptic acid, and bile salts. Used for short-term management of ulcers. 1 g PO qid

Drug Name

Adult Dose

Drug Category: Prostaglandins - Can prevent peptic ulcers in patients taking NSAIDs and may be used with NSAIDs in patients at a high risk of complications.
Drug Name Misoprostol (Cytotec) -- A prostaglandin analog that protects the lining of the GI tract by replacing depleted prostaglandin E1 in prostaglandin inhibiting therapies. 200 mcg PO qid with food; if not tolerated, decrease to 100 mcg qid or 200 mcg bid with food

Adult Dose

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