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Peptic ulcer diease pathophysiology

# Overview
- The overview section should include the disease name in the first sentence.
- The goal is to summarize the pathophysiology page in several sentences. This section can be the same as the pathophysiology segment on the overview page.
- To see an example of an overview section on a symptoms page, click here.

## Template
- The overview is highly dependent on the individual disease pathophysiology. There is no specific template preference for the first sentence.
Template Sentences:
Examples:

# Pathogenesis
Pathogenesis is the mechanism by which a certain factor causes disease (pathos = disease, genesis = development). The term can also be used to describe the development of the disease, whether it is acute, chronic, or recurrent. It can also be used to describe whether the disease causes inflammation, malignancy, necrosis etc.

### Template Sentences
- It is found that peptic ulcer disease is the result of self-digestion which occurs due to  an excess of auto-peptic power in gastric juice over the defensive power of gastric mucosa  and is mediated by two major factors  which disrupt mucosal resistance to injury: Helicobacter pylori (formerly Campylobacter pylori) infection in 75% cases and nonsteroidal anti-inflammatory drugs (NSAIDs)
- Helicobacter pylori-gram negative bacteria,spiral-shaped, urease positive and highly motile through flagella .Upon entry ,it display urea- and bicarbonate-mediated chemotactic motility toward the mucus layer . The spiral morphology and flagellar motility then assist in penetration into the viscous mucus layer, where the more pH-neutral conditions allow growth of the gastric Helicobacter species.
It secrete cytotoxins and produce virulence factors like Cag A, VacA, and OipA.Cytotoxin-associated gene pathogenicity encodes protein CagA and vacuolating cytotoxin VacA aids in the colonization of gastric mucosa and it modulates host's immune system.It causes local production of a range of proinflammatory and immunoregulatory cytokines, neutrophil infiltration, specific T- and B- cell responses and the development of gastric lymphoid follicles.Bacterial factors and complement activation leads to neutrophilic activation including reactive oxygen me*It is found that peptic ulcer disease is the result of self-digestion which occurs due to  an excess of auto-peptic power in gastric juice over the defensive power of gastric mucosa  and is mediated by two major factors  which disrupt mucosal resistance to injury: Helicobacter pylori (formerly Campylobacter pylori) infection in 75% cases and nonsteroidal anti-inflammatory drugs (NSAIDs)
- It secrete cytotoxins and produce virulence factors like Cag A, VacA, and OipA.Cytotoxin-associated gene pathogenicity encodes protein CagA and vacuolating cytotoxin VacA aids in the colonization of gastric mucosa and it modulates host's immune system.It causes local production of a range of proinflammatory and immunoregulatory cytokines, neutrophil infiltration, specific T- and B- cell responses and the development of gastric lymphoid follicles.Bacterial factors and complement activation leads to neutrophilic activation including reactive oxygen me*It is found that peptic ulcer disease is the result of self-digestion which occurs due to  an excess of auto-peptic power in gastric juice over the defensive power of gastric mucosa  and is mediated by two major factors  which disrupt mucosal resistance to injury: Helicobacter pylori (formerly Campylobacter pylori) infection in 75% cases and nonsteroidal anti-inflammatory drugs (NSAIDs)
- Helicobacter pylori-gram negative bacteria,spiral-shaped, urease positive and highly motile through flagella .Upon entry ,it display urea- and bicarbonate-mediated chemotactic motabolite.Following injury to astric mucosa it secretes interleukns and chemokines ,which further leads to neutrophilic migration to  the site of infection.Cag A and Vac A leads to activation of IL-8 which leads to inflammation of gastric mucosa 
It secretes various enzyme :Urease,Phospholipases,Alcohol dehydrogenase and Catalases- causes damage the host gastric muscosa by generating toxic metabolities
- It secretes various enzyme :Urease,Phospholipases,Alcohol dehydrogenase and Catalases- causes damage the host gastric muscosa by generating toxic metabolities
- NSAIDs-
it inhibits  systemic prostaglandins production and cause ulcers
more common in the stomach than the duodenum
- it inhibits  systemic prostaglandins production and cause ulcers
- more common in the stomach than the duodenum
- Other factors responsible for peptic ulcer disease:
Smoking
It decreases the production of prostaglandins in fundic and antral part of stomach
It causes reflux of bile acids
It causes alteration of blood flow and lead to ischaemia
- Smoking
It decreases the production of prostaglandins in fundic and antral part of stomach
It causes reflux of bile acids
It causes alteration of blood flow and lead to ischaemia
- It decreases the production of prostaglandins in fundic and antral part of stomach
- It causes reflux of bile acids
- It causes alteration of blood flow and lead to ischaemia
- Duodenal ulcer:
Abnormalities of acid secretion:
Increase in basal acid output.
Increase in acid response to GRP
Increased maximal acid response to exogenous gastrin
Increased ratio of basal acid output to maximal gastrin-stimulated output
Increased ratio of maximal GRP-stimulated acid output to maximal gastrin-stimulated output.
Decreased in bicarbonate secretion and low ph leads to gastric metaplasia induced duodenitis which further increases the risk of acid damage and leads to ulcer .
- Abnormalities of acid secretion:
Increase in basal acid output.
Increase in acid response to GRP
Increased maximal acid response to exogenous gastrin
Increased ratio of basal acid output to maximal gastrin-stimulated output
Increased ratio of maximal GRP-stimulated acid output to maximal gastrin-stimulated output.
- Increase in basal acid output.
- Increase in acid response to GRP
- Increased maximal acid response to exogenous gastrin
- Increased ratio of basal acid output to maximal gastrin-stimulated output
- Increased ratio of maximal GRP-stimulated acid output to maximal gastrin-stimulated output.
- Decreased in bicarbonate secretion and low ph leads to gastric metaplasia induced duodenitis which further increases the risk of acid damage and leads to ulcer .
- Gastric ulcer
There is decrease in acid and decrease in parietal cell volume which further predisposes to development to ulcer formation.

# Genetics
- Genes involved in the pathogenesis of peptic ulcer disease is CagA is a gene that codes for an immunodominant antigen, is present only in Helicobacter pylori strains that are associated with peptic ulcer disease
- Duodenal ulcer:HLA-DQA1 genotype related in Helicobacter pylori positive in Duodenal ulcer.  Allele frequency DQA1*0301 more common in H. pylori-positive and DQA1*0102 allele are significantly more common in H. pylori-negative

# Associated Conditions
- The most important conditions associated with peptic ulcer disease include:
Gastric cancer-Helicobacter pylori infection in duodenal ulcer leads to gastric metaplasia and gastric atrophy which increases the risk of gastric cancer
Gastric mucosa-associated lymphoid tissue (MALT) lymphoma-helicobacter pylori infection is associated with increased the risk of develeopment of MALT Lymphoma.
Idiopathic thrombocytopenic purpura-The ASH also recommended that eradication therapy for Helicobacter pylori be administered to adults with ITP who were found to have H. pylori based on a test of active infection.the patient who has a peptic ulcer disease is increased the risk of developing idiopathic thrombocytopenic purpura.
- Gastric cancer-Helicobacter pylori infection in duodenal ulcer leads to gastric metaplasia and gastric atrophy which increases the risk of gastric cancer
- Gastric mucosa-associated lymphoid tissue (MALT) lymphoma-helicobacter pylori infection is associated with increased the risk of develeopment of MALT Lymphoma.
- Idiopathic thrombocytopenic purpura-The ASH also recommended that eradication therapy for Helicobacter pylori be administered to adults with ITP who were found to have H. pylori based on a test of active infection.the patient who has a peptic ulcer disease is increased the risk of developing idiopathic thrombocytopenic purpura.

# Gross Pathology
- Gross pathology refers to macroscopic or larger scale manifestations of disease in organs, tissues and body cavities. The term is commonly used by pathologist to refer to diagnostically useful findings made during the gross examination portion of surgical specimen processing or an autopsy.
- Template Sentences 1: On gross pathology, Ulcers, , and  are characteristic findings of .
- Template Sentence 2: The most important characteristics of  on gross pathology are:
Organ 1: List of characteristics +
Organ 2: List of characteristics + image
Organ 3: List of characteristics + image
- Organ 1: List of characteristics +
- Organ 2: List of characteristics + image
- Organ 3: List of characteristics + image
- This section is a good place to include pictures. Search for copyleft images on The Pathology Wiki  and Ask Dr. Wiki .
- For an example of this section, click here

# Microscopic Pathology
- Microscopic pathology is the disease process as it occurs at the microscopic level.
- Template Sentence 1: On microscopic histopathological analysis, , , and  are characteristic findings of .
- Template Sentence 2: The most important histopathological characteristics of  are summarized in the table below:
- This section is a good place to include pictures. Search for copyleft images on The Pathology Wiki  and Ask Dr. Wiki .
- For an example of this section, click here.