GASTRITIS

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ANATOMY AND PHYSIOLOGY OF THE STOMACH



The stomach is roughly J-shaped, although its size and shape vary considerably. It tends to be high and transverse in the obese short subject and to be elongated in the asthenic individual; even in the same person, its shape depends on whether it is full or empty, on the position of the body and on the phase of respiration. The stomach has two surfaces the anterior and posterior, two curvatures the greater and lesser: and two orifices- the cardiac and pylorus.

The stomach projects to the left, above the level of the cardiac, to form the dome-like gastric fundus. Between the cardiac and the pylorus lies the body of the stomach leading to a narrow portion, immediately preceding the pylorus, which is termed the pyloric antrum. The junction of the body with the pyloric antrum is marked by a distinct notch on the lesser curvature termed the incisura angularis. The junction of pylorus with duodenum is marked by a constriction externally and also by a constant vein (of Mayo) which crosses it at this level (Waugh & Grant, 2018).

The thickened pyloric sphincter is easily felt and surrounds the lumen of the pyloric canal. The pyloric sphincter is an anatomical structure as well as a physiological mechanism, The cardiac on the other hand, although competent (gastric contents do not flow out of your mouth ), is not demarcated by a distinct anatomical sphincter. The exact nature of the cardiac sphincter action is still not fully understood, but the following mechanisms have been suggested, each supported some experimental and clinical evidence (Waugh & Grant, 2018).


DEFINITION OF GASTRITIS


Gastritis is the inflammation of the stomach lining which can either be an acute or chronic condition. (Waugh & Grant. 2018).

 It can also Occur when there is either an excess of acid in the stomach or insufficient mucus to protect the surface epithelium of the stomach. (Waugh & Grant, 2018).


 INCIDENCE OF GASTRITIS 

The frequency of gastritis is decreasing in developed countries but increasing in developing countries. Gastritis occurs in all ages but there is a high incidence of infectious gastritis over the age of 60 (Coker et al, 2017).


ETIOLOGY OF GASTRITIS

Bacterial infection : Most cases of gastritis are caused by infestation of Helicobacter pylori that lives deep in the mucous layer of the stomach causing inflammatory responses.

Regurgitation of bile into the stomach. If the pyloric sphincter is weak and does not close properly, bile can flow back into the stomach leading ; to inflammation of the mucosal lining.

Regular use of analgesics: Drugs such as Non-steroidal Anti-inflammatory drugs(NSAIDs), aspirin and cortisone can cause stomach inflammation reducing the protective lining of the stomach.

Radiation and chemotherapy: large doses of radiation cause irreversible erosion of the stomach lining and destruction of acid producing glands.

Excessive intake of caffeine, alcohol and smoking: These irritate and erode the mucosal lining of the stomach making it vulnerable to caustic effects of normal stomach secretion.


TYPES OF GASTRITIS

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 (Hinkle & Cheever 20 18).


ACUTE GASTRITIS

Acute gastritis is often caused by dietary indiscretion. The person eats food that is contaminated with disease -causing microorganisms or that is irritating or too highly seasoned. Other causes of acute gastritis include overuse of aspirin and other non-steroidal anti-inflammatory drugs(NSAIDS), excessive alcohol intake, bile reflux, and radiation therapy. (Hinkle & Cheever 2018).


CHRONIC GASTRITIS

Chronic gastritis and prolonged inflammation of the stomach may be caused by either benign or malignant ulcers of the stomach or by the bacteria Helicobacter pylori. Chronic gastritis sometimes associated with autoimmune diseases such as pernicious anemia; dietary factors Such as caffeine; the use of medications, especially NSAIDs: alcohol; smoking; or reflux of intestinal contents into the stomach (Hinkle & Cheever 20 18).


 *PATHOPHYSIOLOGY* 

The pathophysiology can be discussed under acute and chronic stages.

ACUTE STAGE: The stomach becomes inflamed by either ingesting food infected with helicobacter pylori, excessive alcohol intake or after ingestion of an irritant. The inflammatory process begins 2-4 hours after taking in the irritating factor, while the clinical symptoms such as heart burns, epigastric pain, nausea and vomiting, feeling of fullness in the upper abdomen follows later. The mucosa becomes oedematous, hyperaemic and undergoes superficial erosion. The walls of the stomach may be perforated. The onset of the condition starts with hyperacidity which is followed by decreased gastric secretions.

CHRONIC STATE: Following repeated attacks of acute gastritis, a progressive form develops. A destructive inflammatory change that begins on the surface of the mucous membrane extends to affect the whole membrane including gastric glands. The mucosa of the stomach is thickened, and then the wall becomes thin resulting in lesser quality and quantity of secretions, eventually consisting of mucous and water only (Hinkle &Cheever 2018).


*CLINICAL MANIFESTATIONS*

  • Vomiting
  • Nausea
  • Burning abdominal pain
  • Anorexia
  • Abdominal bloating
  • Heart burns
  • Belching
  • Hiccough
  • Weight loss
  • Halitosis
  • Dehydration
  • Black, coffee or dark stool
  • Fever
  • Diarrhea
Body pains (malaise) and headache (Hinkle & Cheever 2018).


 COMPLICATIONS

  • Gastric obstruction
  • Stomach cancer
  • Intestinal perforation
  • Peritonitis
  • Peptic ulcer disease
  • Dehydration
  • Stomach haemorrhage
  • Nutritional disorders
  • Internal haemorrhage
  • Pernicious anaemia (Hinkle & Cheever 2018).


 Diagnostic Investigations

  1. Endoscopy
  2. Stool for routine examination
  3. Full blood count
  4. Physical examination
  5. Abdominal computed tomography
  6. Gastric analysis
  7. Culture and sensitivity test
  8. Blood for haemoglobin level
  9. Medical history of patient
  10. Histologic examination of a tissue specimen obtained by biopsy
  11. H. pylori antibodies test (Hinkle & Cheever 2018).

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