- Gastric anatomy
- Gastric physiology
- Acute gastritis
- Chronic gastritis
- Idiopathic gastritis
- Atrophic gastritis
- Hypertrophic gastritis
- Eosinophilic gastritis
- Gastric foreign bodies
- Gastric ulceration
- Gastric neoplasia
- Gastric motility disorders
- Reflux gastritis
- Pyloric stenosis
- Gastric dilation and torsion
The stomach is a direct continuation of the oesophagus lying caudal to the liver and deep under the costal arch. The fundus of the stomach lies on the left side of the abdomen while the pylorus lies to the right, continuing as the duodenum. The stomach is semi-lunar in shape with a convex greater-curvature and concave lesser-curvature, the latter being divided by a fold called the angular incisure. The cardiac zone is small and continuous with the oesophagus while the fundus forms the largest zone linked to the pylorus by the body. The pyloric zone is divided into the pyloric antrum which leads to the pyloric canal with its associated pyloric sphincter ().
The stomach wall has four layers; from the outside inwards, the serosa, muscle, submucosa and mucosa. The serosa is a transparent sheet of mesothelial cells attached to the underlying muscle by loose connective tissue. The muscle layer comprises of three layers of smooth muscle, the outer longitudinal muscle fibres are continuous with those of the oesophagus and duodenum and merge with the external oblique fibres at the greater- and lesser-curvature. The inner circular muscle fibres line all zones except for the fundus, and the fibres become especially thinkened at the pylorus where they form a true anatomical sphincter. Some internal oblique fibres exist, and fan out from the cardiac zone and form the weak cardiac sphincter. The submucosa contains elastic fibres and other connective tissue, blood vessels, nerves and lymphoid tissue (). Mast cells are commonly found in the mucosa and submucosa ().
The mucosa is thrown into folds called rugae formed by the muscularis mucosae. The surface mucosa is covered in mucus-secreting columnar epithelial cells which extend into numerous invaginations forming the gastric pits. The proliferative zone for epithelial renewal lies at the isthmus of the gastric pits from where cells migrate onto the mucosal surface. Epithelial cell turnover occurs every 3 days ().
Each zone in the stomach contains specific types of glandular cells. In the cardiac zone epithelial cells secrete mucus. In the fundus and body regions the parietal cells found in the mid-region of the gastric pits secrete hydrochloric acid while chief cells found near the base of the pits secrete pepsinogen which digests protein. Renewal of parietal and chief cells occurs from sites deep in the pits at the much slower rate, of approximately 25 days (). Argentaffin cells are found in the gastric pits of the fundus region secreting serotonin and the antrum where gastrin is produced from G cells (). These cells are part of the (amine precursor uptake and decarboxylation (APUD) cells). The lamina propria of the mucosa contains connective tissue and the muscularis mucosae.
The stomach has three main functions: (1) it acts as a reservoir for ingested food without any increase in intragastric pressure, (2) it mixes food with hydrochloric acid and pepsin to start the digestive process; and (3) it controls the flow of ingesta into the intestine.
When food is ingested, relaxation of the stomach allows filling to occur without increases in intragastric pressure. The capacity of the stomach is very variable and ranges between 0.5 and 8 litre depending on the size of the dog or cat (). The ability of the stomach to relax is centrally mediated so with each swallowing process there is relaxation of the fundus and body of the stomach. This is reinforced by a local reflex where distention of the stomach itself further induces relaxation.
Initial digestion occurs by addition of hydrochloric acid and pepsin from the fundus and body of the stomach, and following thorough mixing of the contents in the pyloric antrum there is slow release of chyme into the duodenum. Gastrin is produced by the G cells in the mucosa of the pyloric antrum and duodenum. In order for the parietal cells to produce hydrochloric acid it is necessary for receptor sites on these cells to be occupied by one or more of acetylcholine, histamine and gastrin (). Blocking one of these receptors seriously reduces the amount of hydrochloric acid produced by the cells. Natural inhibition of gastrin occurs by negative feedback mechanism from high acid levels in chyme reaching the antrum. Gastrin not only stimulates hydrochloric acid production, it also causes hypertrophy of the fundal mucosa, increases antral motility and increases the tone of the gastro-oesophageal sphincter. Gastrin is normally catabolized by cells in the kidney or liver among other tissues (). Hydrogen ion is produced from the breakdown of carbonic acid to bicarbonate and hydrogen ions, involving the enzyme carbonic anhydrase. Production of large amounts of hydrogen ion is an energy-dependent process involving active transport at membrane levels.
Vagal fibres are stimulated by the sight, smell and taste of food, resulting in the release of gastrin and consequently hydrochloric acid and pepsinogen (). Distention of the stomach together with the presence of digested protein also stimulates gastric secretion. Finally the presence of amino acids and peptides in the duodenum leads to increased gastric secretion via gastrin and histamine release. Histamine output occurs mainly during the early phase of gastrin secretion.
Pepsinogen, the inactive precursor of pepsin, is produced by the chief cells found in the fundus of the stomach. Control of secretion is determined by the same mechanisms as those controlling acid production. Pepsinogen is converted to pepsin in the lumen of the stomach by the presence of hydrochloric acid. If the pH of gastric juice rises, pepsin is rapidly inactivated and this happens naturally when gastric chyme enters the duodenum where bicarbonate neutralizes the gastric acid and thus pepsin.
Mucus is composed of glycoproteins, protein and carbohydrate. It coats the gastric mucosa and protects it from acid and mechanical damage and also functions as a lubricant. Mucus secretion is stimulated by irritation of the mucosa and also by acetylcholine action. Mucus contains pepsin inhibitors and some buffering capacity against hydrochloric acid.
Gastric mucosal barrier
The gastric mucosal barrier is designed as a defence mechanism to protect the stomach from irritant ingested food, hydrochloric acid and excessive pepsin activity. It consists of two parts: a layer of mucus covering the gastric mucosa; and secondly columnar epithelial cells lining the surface of the mucosa. Although the mucus has some buffering capacity and can. inactivate pepsin, its role in barrier formation is minor. The major component of the barrier is provided by the epithelial cells and more specifically the lipoprotein layer on their apical surface. Damage to this barrier leads to disruption of the epithelial cells and breakdown of tight junctions between the cells. Such damage may follow use of various drugs, e.g. aspirin, phenylbutazone, interferences with gastric blood flow leading to ischaemia, reflux of bile or pancreatic enzymes into the stomach and the possible involvement of autoimmune mechanisms (). Damage to the barrier allows acid and pepsin to inflame the mucosa and underlying tissues with disruption of mast cells releasing histamine which stimulates further acid production and thus further damage ().
The fundus acts as a hopper and controls emptying of liquids while the antrum acts as a mixing chamber grinding solid foods. The pyloric sphincter has little control over emptying of liquids but may influence the particle size of solids emptied into the duodenum. In addition it prevents reflux of duodenal contents into the stomach ().
The stomach has an inbuilt electrical pacemaker located in the greater-curvature which produces five slow waves per minute which spread over the stomach and may initiate muscle contraction (). Contractions only occur if the slow wave triggers a spike potential and this does not always occur, as hormones and neural control mechanisms influence the initiation of spike potentials. Three types of gastric motility are recognized. The first, digestive motility, occurs after ingestion of a meal when there are slow continuous antral mixing contractions. Interdigestive motility occurs when the stomach is empty, and involves high amplitude contractions which cleanse the stomach, emptying any stomach contents into the duodenum. Lastly are the intermediate contractions which are a transition between the above types of motility ().
The stomach empties liquids faster than solids and carbohydrates faster than fats. Solids are retained for further antral mixing until they are reduced in size to 2 mm, suspended in liquid and then emptied into the duodenum. When large undigestible plastic spheres were fed as an experiment they remained in the stomach (). The greater the nutrient density of the diet, the slower the stomach empties (). Gastric emptying is controlled by other factors such as the presence of chyme of low pH, or chyme containing fats and products of protein digestion in the duodenum, all of which reduce gastric emptying ().
Chronic gastritis may be described as a condition where there is chronic vomiting of variable frequency and character. It clinically describes any patient with chronic vomiting for which there is no diagnosis. Pathologists generally describe chronic gastritis by the changes observed on histopathology. Unfortunately it is possible to have histopathological changes but no clinical signs and clinical signs but no pathological changes. Any definition therefore has to be confined to those conditions where there are clinical signs and positive histopathology. Two forms occur: ulcerative and non-ulcerative. The non-ulcerative conditions may be further divided into idiopathic, atrophic, hypertrophic and eosinophilic gastritis. Ulcerative gastritis is associated with advanced forms of the above or other more serious conditions such as neoplasia. Non-ulcerative idiopathic gastritis is the type most commonly observed clinically, but the cause is rarely determined ().
The aetiology of chronic gastritis is complex and varied and will be discussed in more detail when describing the specific conditions in the following sections. However it includes dietary factors, interference with microcirculation leading to mucosal ischaemia, excess hydrochloric acid production, reflux of bile and enzyme into stomach, autoimmune disease and release of gastric antigen following physical damage ().
Idiopathic gastritis is a reversible condition which occurs following repeated exposure to a specific agent. It may be an early phase of a more serious form of gastritis when ulceration may develop and before changes have become irreversible.
The dog is often in good physical condition, with the exception of intermittent vomiting. There are rarely any changes in blood picture or radiographs, and endoscopy reveals very little, except that on histopathological examination of biopsy tissue, there is infiltration of the mucosa by plasma cells and lymphocytes with some degree of fibrosis in the lamina propria ().
Treatment may require correction of dehydration but this is only likely in advanced cases. The use of metaclopramide (Emequell; SmithKline Beecham Pharmaceuticals) 0.5 to l.0mg/kg every 8h is frequently helpful and dietary correction or modification using a low fat diet may also be beneficial. Any underlying cause should always be sought, although this is rarely found.
A rare condition of older dogs in which there is atrophy of the gastric mucosa and loss of secretory power which is thought to be immune-mediated (). There is a reduction in the thickness of the mucosa, and histopathologically in the size and depth of gastric pits. Parietal cells are replaced by mucus-secreting cells and there is cellular infiltration similar to that observed in idiopathic gastritis. Although the cause has not been determined, it may be the end-stage of idiopathic gastritis occurring over many months. A model has been produced where a dog was experimentally immunized with its own gastric juice resulting in changes similar to those produced in naturally occurring disease, indicating a possible autoimmune aetiology ().
In this condition there is a reduction in the volume of hydrochloric acid produced and this can lead to small intestinal bacterial overgrowth, malabsorption and chronic diarrhoea. Plasma gastrin is elevated in affected dogs because the normal negative feedback mechanism is inhibited by low gastric acid levels.
Chronic intermittent vomiting is the feature of this condition often occurring over several months. The vomitus may contain mucus, bile or food and there is rarely a direct association with feeding. Eructation and anorexia may also occur and occasionally there is evidence of abdominal pain, manifest by the dog assuming a praying position. Chronic diarrhoea and weight loss have occurred when bacterial overgrowth develops.
The clinical signs are non-specific and radiographs rarely provide additional diagnostic information. To obtain a diagnosis, endoscopy and biopsy of the gastric mucosa is required. Macroscopically there may be flattened rugal folds. The mucosa may bleed easily when touched by the endoscope and submucosal blood vessels may be easily observed. Microscopically there is loss of glandular tissue, plasma cell infiltration of the lamina propria and varying amounts of fibrosis.
Atrophic gastritis: Treatment
Prognosis is generally good in the majority of cases but treatment may be required for life. A meat and not a cereal-based diet should be fed and ideally a hypoallergen diet should be offered in frequent small meals each day. Azathioprine (Imuran; Calmic Medicals Division) has been suggested where autoimmune disease is suspected. Corticosteroids although anti-inflammatory, stimulate parietal cells to produce hydrochloric acid. However prcdnisolone may be of value when given at 1 mg/kg daily for 1 week to reduce the immune response (). Antibiotic in the form of tylosin at 20 mg/kg bid (Tylan; Elanco Products) may be required to control bacterial overgrowth and chronic diarrhoea.
This is a rare condition in which there is eosinophilic infiltration and diffuse fibrosis of all layers of the stomach wall. Occasionally there is focal granuloma formation which may resemble gastric neoplasia. The cause is not known but it has been suggested that immunological mediation involving allergens or parasites may be involved (). In particular Toxocara canis has been implicated (). An eosinophilic lymphadenitis and vasculitis may be seen.
The history may reveal chronic intermittent vomiting over a long period of time. There may be an association with dietary changes or increased levels of parasitism. Vomitus may contain blood and may or may not be associated with feeding. Signs of ascites and subcutaneous oedema may also develop in advanced cases, where hypoproteinaemia has occurred through protein loss across the gastric mucosa.
Routine haematology often reveals a persistent circulating eosinophilia and some degree of hypoproteinaemia. Barium studies may reveal filling defects, narrowing or thickening of the mucosa. The mucosa may bleed easily and ulceration has also been observed on endoscopy. The diagnosis is confirmed by histopathology of biopsy tissue which shows eosinophil infiltrates in mucosa, submucosa and muscle layers. The infiltration may be diffuse or focal and vasculitis often with thrombosis occurs.
Hayden & Fleischmann () described a scirrhous eosinophilic gastritis of three female dogs between the ages of 3 and 5 years, where there was weight loss, lethargy and recurrent vomiting with peripheral eosinophilia. These dogs had a palpably thickened stomach and sometimes pendulous abdomen.
Eosinophilic gastritis: Treatment
The use of a hypoallergen diets frequently results in a fall in the circulating eosinophil count without need for other treatment. Any evidence of endoparasites such as Toxocara canis should also be treated using a suitable anthelmintic. In addition prednisone at 0.5mg/kg daily for 2 weeks, tailing off to alternate day therapy should be provided. However in some cases longer-term therapy, in the order of several weeks is required.
Gastric foreign bodies
A wide range of foreign bodies have been found in the stomachs of dogs. They range from stones and balls to spoons, razor blades and fish hooks. On the other hand cats are fastidious eaters and foreign bodies are rare in this species. The exception is the fur or hairball which does occur but is grossly overdiagnosed. This occurs following excessive self-grooming especially in long haired breeds of cat.
Very often foreign bodies are detected by accident as they are asymptomatic unless they cause valve-like obstructions in the pylorus. However they can also account for acute episodes of vomiting. If the objects are sharp or abrasive then physical damage to the mucosa occurs and leads to chronic gastritis which gives more persistent symptoms. Earth or sand are good examples of abrasive foreign material ingested by puppies. In the authors’ experience depraved appetite and polydipsia in dogs with gastric foreign bodies may be seen.
There may be no clinical signs at all, or there may be episodes of acute vomiting with periods of complete remission. This occurs when the foreign body obstructs the pylorus and then moves back into the fundus relieving the obstruction. Occasionally vomiting occurs with blood present but this is not typical. Vomiting may or may not occur associated with feeding. The foreign body may in rare cases cause perforation of the stomach with resultant peritonitis. If this occurs the signs change to include marked abdominal pain and guarding on palpation. There will be pyrexia together with depression and dehydration. An exudative asciies may be detected on paracentesis of the abdomen.
Diagnosis of foreign bodies is usually simple following X-ray of the abdomen to reveal a radiodense mass in the stomach (). Occasionally however the object will be radiolucent and barium studies will be required to make a diagnosis. Evidence of peritonitis may be detected from radiographs as may ascites, giving a ground glass appearance to the abdomen and a lack of contrast ().
Gastric foreign bodies: Treatment
Foreign bodies are usually successfully removed following laparotomy and gastrotomy. Where perforation has occurred and peritonitis has developed it is essential to obtain ascitic fluid for culture and sensitivity, followed by high doses of a suitable antibiotic. Once the patient has been rehydrated and the infection brought under control laparotomy should be carried out to repair the defect and remove the foreign body.
Gastric motility disorders
There are three types of normal gastric motility. The digestive, intermediate and interdigestive patterns. When any of these motility patterns become disturbed the animal is described as having a gastric motility disorder. Such motility disorders may include situations where there is chronic vomiting of undigested food many hours after eating, gastric atony, reflux of bile into the stomach, reflux oesophagitis and even gastric dilation/torsion.
Motility disorders may occur secondarily to underlying gastric pathology. Gastric atony and retention may be associated with gastric ulceration, neoplasia or pyloric stenosis. Other conditions such as pylorospasm, bilious vomiting and reflux oesophagitis may be primary motility disorders. Stress, excitement and flight or fight reactions can account for physiological gastric atony, but primary disorders of organized gastric motility do seem to occur (Table Gastric motility disorders).
Table Gastric motility disorders
|Bilious vomiting syndrome|
|Secondary||Fight or flight reactions|
|Gastric foreign bodies|
Diagnosis of primary motility disorders is made on the grounds that no evidence of other gastric disease can be found following an extensive investigation. There are very few methods of diagnosing motility disorders, although our recognition of the normal physiology of gastric motility is much improved. Blood chemistry, routine radiographs, barium studies and endoscopy are of little value. The only effective method of diagnosis is through the use of fluoroscopy and observing gastric motility.
Gastric emptying time is governed by the ingesta present and not on time itself. There is hormonal and neural control as well as that of the ingesta. Liquids empty faster than solids and carbohydrates faster than fats or protein. Retention of non-digestible substances such as hair or grass may be due to failure of ‘housekeeper’ contractions or ‘interdigestive’ contractions to occur.
This has also been termed bilious vomiting syndrome (). Reflux of bile and enzymes from the duodenum into the stomach is thought to be a normal event in fasted dogs. However if there is excess bile secretion, defective pyloric function, or reduced gastric motility, then bile is exposed to the gastric mucosa for long periods. Its detergent action damages the gastric mucosal barrier. This allows hydrochloric acid and pepsin to act on the mucosa causing further inflammation and, in severe cases, erosion and ulceration. Although the true cause is not known, it is most likely to occur where there is a failure of housekeeper contractions during periods of fasting and rest, allowing bile to pool and damage the gastric mucosal barrier.
Chronic vomiting of bile-stained fluid after a prolonged fast and when the animal is resting, usually occurs as an early morning event in dogs fed once daily in the afternoon. Those affected are described as having ‘bad days’ with total return to normal the following day. Owners describe the dog as restless early in the morning and if not fed quickly they will vomit a bile-stained fluid and remain anorexic for the remainder of the day. They rarely vomit throughout the day. Anorexia, depression, diarrhoea and borborygmi have also been reported by some owners.
Plain and contrast radiographs are of little value. Endoscopy reveals bile pooling in the stomach and biopsy confirms mild gastritis in most cases. The pylorus may be patent when examined endoscopically but this is variable. A diagnosis is made on the grounds of finding no other cause for the vomiting such as gastric or intestinal disease, in a dog exhibiting a typical history which is unresponsive to treatment.
Reflux gastritis: Treatment
If an underlying cause has been found, this should be treated. The prognosis is usually good but the condition can only be controlled at present, as there is no cure, so treatment may be required for life. Dogs should be fed three times daily, by giving an early morning meal, the main meal in the afternoon and a late-night meal. Cimetidine (Tagamet; SmithKline Beecham) 4mg/kg bid may be helpful but metaclopramide (Emequell; SmithKline Beecham) 0.5mg/kg given in the early morning and late at night is very effective in most cases ().
It is not clear whether this is a true clinical entity as documented cases are rare in the veterinary literature. The antrum and pylorus should act together as a single unit and peristalsis of the antrum rather than pyloric closure controls emptying (). In pylorospasm it is therefore likely that abnormal motility or peristalsis is the cause rather than true spasm of the pyloric sphincter. In the studies of Prove & Ehrlein () there is outflow obstruction with radiographic evidence of retention and failure of barium to enter the duodenum. Confirmation of the diagnosis may be possible by carrying out barium studies after the administration of 0.5mg/kg metaclopramide (Emequell; SmithKline Beecham) which causes relaxation of the pyloric sphincter. If there is no relief of gastric retention then pyloric stenosis is the most likely cause.
Selections from the book: “Digestive Disease in the Dog and Cat” (1991)
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