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MUCOSAL

BARRIER &

PEPTIC ULCER

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GASTRIC MUOSAL BARRIER

The gastric mucosal barrier is the property

of the stomach that allows it to contain acid

If the barrier is broken, then the acid

diffuses back into the mucosa and damage the

stomach wall

The gastric mucosal barrier is made up of 3

components:

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GASTRIC MUCOSAL BARRIER

a) Compact epithelial cell lining

with tight junctions

b) Gastric mucus covering (gel like

coating)

c) Bicarbonate ions, secreted by the

surface epithelial cells. The

bicarbonate ions act to neutralize

harsh acids

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GASTRIC MUCOSAL BARRIER

• The gastric mucosal barrier is the

property of the stomach that allows it to

contain acid.

• The barrier consists of three protective

components. These provide the

additional resistance for the mucosal

surface of the stomach. to neutralize

harsh acids.

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THREE COMPONENTS

The three components include: • a) A compact epithelial cell lining. Cells in the

epithelium of the stomach are bound by tight junctions that repel harsh fluids that may injure the stomach lining.

• b) A special mucus covering, derived from mucus secreted by surface epithelial cells and Foveolar cells. This insoluble mucus forms a protective gel-like coating over the entire surface of the gastric mucosa. The mucus protects the gastric mucosa from auto digestion by e.g. pepsin and from erosion by acids and other caustic materials that are ingested.

• c) Bicarbonate ions, secreted by the surface epithelial cells. The bicarbonate ions act as buffers

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MUCUS

Mucus is secreted by mucus cells

Present allover the GIT

Acts as a protectant and lubricant of wall of gut

Mucus is a viscous gel which contains mucin,

phospholipids, electrolytes (mainly HCO3) and water

Separates the epithelial cells from acid of stomach

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CONT’D

This maintains the Ph of epithelial cells

alkaline despite gastric acid

Mucus is strongly resistant to digestion by

gastric enzymes

Has buffering properties (neutralize acid)

Helps in propulsive movement by lubrication

Easy slippage of food

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PEPTIC ULCER

Ulcer :- An Ulcer is a discontinuity or

break in a bodily membrane, or breach in

the epithelium

Ulcer may occur anywhere in the body

When it occurs in stomach its gastric

ulcer

In duodenum its duodenal ulcer

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CONT’D

Ulcer occurring in either of these two

sites is called peptic ulcer

Its also known as acid peptic disease

(APD)

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PATHO PHYSIOLOGY OF PEPTIC ULCER

Defect in the mucosal barrier

Hyper secretion of acid

Helicobacter bacterial infection

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DEFECT IN THE MUCOSAL BARRIER

If the secretion of mucus is impaired

Or bicarbonate production is

impaired

Such damage is caused by drugs like

asprin, NSAID

Chronic stress conditions (stress

ulcer)

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HYPER SECRETION OF ACID

Chronic anxiety

Common in people with busy life style (Type A

personality)

Hurry, worry, curry

Intake of spicy food – leads to hyper chlorhydria

Conditions with hyper chlorhydria

(Zollinger Ellison syndrome ) gastrin secreting

tumor

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H.PYLORI INFECTION

Major cause of peptic ulcer

This bacterial infection causes Damage

to the mucosal barrier

Increase in gastrin secretion from G

cells

Reduce somatostatin from D cells

Initially causes gastritis which later on

leads to peptic ulcer

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CONTD …..

Helicobacter pylori, previously Campylobacter

pylori, is a Gram-negative, micro aerophilic

bacterium found in the stomach, and may be

present in other parts of the body, such as the

eye.

It was identified in 1982 by Australian

scientists Barry Marshall and Robin

Warren, who found that it was present in a

person with chronic gastritis and gastric ulcers,

conditions not previously believed to have a

microbial cause.

It is also linked to the development of

duodenal ulcers and stomach cancer. However,

over 80% of individuals infected with the

bacterium are asymptomatic and it may play an

important role in the natural stomach ecology.

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CONTD…..

More than 50% of the world's population harbor

H. pylori in their upper gastrointestinal tract.

Infection is more prevalent in developing

countries, and incidence is decreasing in Western

countries.

H. pylori's helical shape (from which the genus

name is derived)(Screw like, spiral) is thought to

have evolved to penetrate the mucoid lining of the

stomach.

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SIGNS & SYMPTOMS OF H. PYLORI INFECTION

Up to 85% of people infected with H. pylori never

experience symptoms or complications.

Acute infection may appear as an

acute gastritis with abdominal pain (stomach ache)

or nausea.

Where this develops into chronic gastritis, the symptoms,

if present, are often those of non-ulcer dyspepsia: • stomach pains• Nausea• Bloating• Belching• sometimes vomiting or black stool.

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Individuals infected with H. pylori have a 10 to 20% lifetime

risk of developing peptic ulcers and a 1 to 2% risk of

acquiring stomach cancer.

Inflammation of the pyloric antrum is more likely to lead

to duodenal ulcers, while inflammation of the corpus (body of

the stomach) is more likely to lead to gastric ulcers and

gastric carcinoma.

H. pylori possibly plays a role only in the first stage that

leads to common chronic inflammation, but not in further

stages leading to carcinogenesis.

A meta-analysis conducted in 2009 concluded the eradication

of H. pylori reduces gastric cancer risk in previously infected

individuals, suggesting the continued presence of H.

pylori constitutes a relative risk factor of 65% for gastric

cancers; in terms of absolute risk, the increase was from 1.1%

to 1.7%.

H. pylori has also been associated with colorectal polyps

and colorectal cancer.

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ADAPTATION TO THE STOMACH’S ACIDIC ENVIRONMENT

To avoid the acidic environment of the interior of the

stomach (lumen), H. pylori uses its flagella to burrow into

the mucus lining of the stomach to reach the epithelial

cells underneath, where the pH is more neutral.

H. pylori is able to sense the pH gradient in the mucus and

move towards the less acidic region (chemotaxis).

This also keeps the bacteria from being swept away into the

lumen with the bacteria’s mucus environment, which is

constantly moving from its site of creation at the epithelium

to its dissolution at the lumen interface.

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CONTD…..H. pylori is found in the mucus, on the inner surface of the

epithelium, and occasionally inside the epithelial cells

themselves.

 It adheres to the epithelial cells by producing adhesions,

which bind to lipids and carbohydrates in the epithelial cell

membrane.

One such adhesion, BabA, binds to the Lewis b

antigen displayed on the surface of stomach epithelial cells. 

Another such adhesion, SabA, binds to increased levels

of sialyl-Lewis x antigen expressed on gastric mucosa.

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CONTD…..

In addition to using chemotaxis to avoid areas of low

pH, H. pylori also neutralizes the acid in its

environment by producing large amounts of urease,

which breaks down the urea present in the stomach

to carbon dioxide and ammonia.

The ammonia, which is basic, then neutralizes

stomach acid.

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SYMPTOMS OF PEPTIC ULCER

Upper abdominal pain

Pain usually by empty stomach

relieved by food or antacid

Vomiting

Blood vomiting and perforation in

severe cases

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FACTORS THAT STIMULATE ACID SECRETION

Acetylcholine

Gastrin

Histamine

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TREATMENT

Anti histamines

Anticholinergic drugs

Proton pump blockers

Sucralfate

Gastrin blockers

Antacids

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NON SPECIFIC TREATMENT

Avoid stress

Adequate sleep

Regulation of diet

Avoid spicy foods, alcohol

Withdrawal of drugs like aspirin,

NSAIDS

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SURGICAL TREATMENT

Vagotomy

Gastrectomy

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FACTORS THAT CAN DAMAGE THE BARRIER

Bacterial Infection by

Helicobacter pylori

-Alcohol

-Aspirin

-NSAID

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