LECTURE 10 – INFECTION: PEPTIC ULCERS

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ESSAY 5 – INFECTION: PEPTIC ULCERSESSAY 5 –

INFECTION: PEPTIC ULCERS

Disease in the gastric tract are place an enormous

burden on the global health care systems. With nearly 50% of the population

affection a closer examination on conditions of gastric alimentary tract is a

must. The most common illnesses involving ulcers are chronic gastritis, gastric

lymphoma, gastric adenocarnemoma and so forth.

A ulcer is a breach in the mucosa of the

alimentary tract which extends through the muscularis mucosa into the submucosa

or deeper. Patients with ulcers often

complain of a burning aching pain or an epigastric gnawing. Until recently it

was postulated that the hostile acidic environment of the stomach was

responsible for the ulcers and consequently the use of alkylating medication was

quite popular. However this paradigm was rejected in favour for helicobacter

pylori being the aetiology for peptic ulcers.

There are several lines of evidence

implicating H. Pylori in the development of gastric and duodenal ulcers. . H.

Pylori is found in most patients who have peptic ulcers in absence of NSAID use.

Presence of H. Pylori is a risk factor for the development of ulcer. 3. Eradication

of H. Pylori significantly reduces the recurrence of gastric and duodenal

ulcers. 4. Treatment of H. Pylori infection leads to more rapid and reliable

ulcer healing than does treatment with anti-secretory therapy alone.

It is believed that Pylori are acquired

via oral ingestion in early childhood. For the bacteria to cause disease is

hugely dependent on the virulence of the strain, the type of immune repose. The

modulating cofactors including the hosts genetics and environment. The stomach

is incredibly acidic as such the bacteria that inhibits this environment be

highly specialised. Pylori is a non-sporing curvier gram negative OD that has

been adapted to the environment due to two key factors. Motility and acid

resistance. The bacteria has flagella that allow for corkscrew motility. It

also has urease which breaks down urea into ammonia and carbon dioxide. The peri plasm of the bacteria can also sense

neutral pH and move towards it such as the mcosal layer

Alongwith this thy have a huge genetic drift,

high mutation rate and ability to transform. The BabA gene which facilitate

adhesion to gastric epithelial cell, the cagA gene associated with ulcer formation

and cytotoxicity and Vac a gene which form a voltage gated channel can all be

passed on from one bacteria to another.

Father more the bacteria is relatively immune

to the host response as it can change its LPOS to reduce recognition, in bit NO

production in host macrophages and have enzymes which combat bactericidal oxidative

stress.

When the bacteria is orally ingested it initiates

the recruitment of PMN and the release of cytokines. This imitates chronic

infection which allows for the innate and adaptive immune response to be ensued.

Epithelial cells die and the altered mucus layer causes increased release of

gastrin. Th1 and TH2 are differentiated. If a TH1 pathway is taken chronic

gastritis is ensued. If the inflammation is pursued in the corpus it becomes a gastric

ulcer however inflammation in the antrum results in ulcers in duodenum. This

poses risks to patients as duodenal ulcers are metaplastic. Gastric lymphomas

are a result of MALT acquisition. Oxidative damage and antigen stimulation nares

responsible for lymphoma

It is important to establish that certain

individual genetics as contribute to adenocarcinoma. IL-1 gene cluster, TLR

polyprpohism and HLA polymorphism also contribute to peptic ulcer disease. Life

style chaises cuss has alcohol, tobacco and no steroidal anti-inflammatory

drugs do contribute to this lines

The

current goal is to eradicate Pylori. At the moment a pop ton pump inhibitor along

with antbioictcs is used. Antibiotic efficacy in the acid environment along

with vaccine development for the condition are the current challenges in play