gastritis

GASTRITIS
Definition:
inflammation of the gastric or stomach mucosa with mucosal injury. Gastritis may be
*acute, lasting several hours to a few days,
*or chronic, resulting from repeated exposure to irritating agents
*or recurring episodes of acute gastritis
* male to female ratio 1/1
causes:
I- acute gastritis:
*drugs: aspirin, NSAIDs, iron preparation
*H. pylori
*alcohol
*stress: burns, CNS trauma.
*bile reflux
*viral infections: CMV, HS
*radiation
II- chronic non-specific gastritis:
*HP infection
*autoimmune (perniciuos an)
*post-gastrectomy
III-  chronic specific gastritis:
*infection, CMV, TB
*Crohn’s disease
*sarcoidosis, GVHD
*idiopathic, granulomatous G

Acute gastitis
definition: an acute mucosal inflammatory process, usually of a transient nature.
*pathophysiology: inflammatory mucosal changes, with neutrophils predomenant.
*symptoms:
1- asymptomatic.
2- dyspepsia, anorexia, nausea,vomiting & hematemesis or malena.

Diagnosis:
1- clinically, no need investigations
2- may need endoscopy & biopsy to exclude  PU or cancer.
*Treatment:
1- treat underlying cause
2- symptomatic therapy with antacids, PPIs & antiemetics (e.g. metoclopramide)

 
Chronic gastritis
Definition:
prolonged inflammation of the stomach.
*Pathophysiology: chararctrised by mononuclear cell infiltrate especially lymphocyte and maccrophages  of gastric mucosa

Some types of Ch Gastritis
1- ch g due to HP infection:
*is the most common cause.
*lymphocytes & plasma cells.
* poor correlation between clinical & endoscopic or pathological findings.
*most pt are asymptomatic   & managed by modifying patient’s diet& do not require treatment , but if pt develop dyspepsia may benefit from HP eradication.
2- autoimmune ch gastritis:
*it results from autoimmune activity againast parietal cells.
*involves the body of stomach & spares the antrum, characterized by diffuse chronic inflammation, atrophy & loss of fundic glands, intestinal metaplasia & some times hyperplasia of enterochromaffin like cells(ECL).
*Ab to parietal cell & intrinsic factor may be present.
*may be severe lead to pernicious anemia.
3- Menetrier’s disease:
*disease of middle & old age.
*the gastric pits are elongated & tortuous, with replacement of the parietal & chief cells by mucus-secreting cells.
* mostly involve the body & fundus.
*most pt are hypochlorhydric.
*ass with protein losing enteropathy.
*treated with antisecretry drugs or partial gastrectomy.

Peptic ulcer disease (PUD)
Definition:
break in the gastrointestinal mucosa exposed to gastric acid and  pepsin, which penetrate the muscularis mucosa, more than 5 mm  in diameter may be acute or chronic.
In the acute ulcer, there is no evidence of fibrosis. While in erosion, there is no penetration of muscularis mucosa & less than 5 mm.
*Site:
()lower oesophagus
() stomach ()duodenum
()Jejunum after surgical anastomosis to the stomach
()rarely  in the ileum adjacent to a Meckel’s diverticulum. 

Gastric & Duodenal ulcer
introduction:
* it’s more common in developing countries& Higher prevalence in low socioeconomic classes
*the lifetime risk for developing a peptic ulcer is approximately 10%
*family history: 3-4 increased risk .
*male/female ratio: DU (5:1 to 2:1) GU (2:1 or less)
*DU  usually occur in 30-50 years of age while
*GU usually occur in 50-70 years of age. 
* the MR : approximately 1 death per 100,000 cases.
*The hospitalization rate is approximately 30 patients per 100,000 cases.
*ch GU is usually single; 90% on the lesser curve within the antrum or at the junction bet body & antral mucosa.
*ch DU is more than one DU in 10-15% of cases, occur usually in the 1st part of duodenum, 50% on the ant wall .
* GU & DU may coexist in 10% of patients.
Causes
1-  H pylori infection
2- Nonsteroidal anti-inflammatory drugs : The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of cyclooxygenase 1 (cox-1), which is essential for the production of these prostaglandins
3-Smoking:  more with GU & less extent to DU.
4-Severe physiologic stress ,Burns , CNS trauma , Surgery
5-Severe medical illnessHypersecretory states (uncommon) , Gastrinoma (Zollinger-Ellison syndrome) or multiple endocrine neoplasia (MEN-I) Antral G cell hyperplasia
Systemic mastocytosis , Basophilic leukemias
6-Diseases associated with an increased risk of PUD include cirrhosis, chronic obstructive pulmonary disease, renal failure, and organ transplantation.
7- Additional rare, miscellaneous causes include radiation-induced or chemotherapy.

pathophysiology
H pylori:
*is G –ve & spiral,
*Has multiple flagella at one end
() make it motile
()allowing it to burrow to live deep Beneath the mucus layer
*has following antigens:
1- adhesin molecule (BabA) which Bind to Lewis b antigen on epith Cells to buffer acidity of stomach By urease enzyme to raise PH.
2- cytotoxin-associated gene (cag A):
Provoke a local inflammatory response in the underlying epithelium by cell replication & apoptosis.
3- vacuolating cytotoxin (vac A) :
*Increase cell permeability,
*efflux of micronutrients from epithelium
*induction of apoptosis
* suppression of local immune cell activity.
4- outer inflammatory protien A(oip A)
* in developed countries, HP infection raise with the age, 50% of people over the age of 50. While in developing countries, affect up to 90% of the adult population.
*HP infections are probably acquired in childhood, the vast majority of colonized people remain healthy & asymptomatic.
*HP responsible for 90% of DU & 70 % of GU
*HP spread by person to person via  gastric reflux ate or vomit.