Diseases of the Stomach Flashcards
Where are the following cells located within the stomach and what products do the cells secrete:
- Mucous neck cells
- Parietal cells
- Chief cells
The mucous neck cells, parietal cells and chief cells are all located within the mucosa of body of the stomach.
- Mucous neck cells:
- Pepsinogen A
- Gastric lipase
- Parietal cells
- Gastric acid
- Pepsinogen A
- Intrinsic factor (gastric)
- Chief cells (deep within the gastric pit)
- Pepsinogen A
What neuroendocrine cells are located within the gastric glands?
- Enterochromaffin-like and somatostatin-producing cells are interspersed within the gastric glands of the fundus
- Somatostatin and gastrin producing cells are located within the antrum
What hormones do the gastric neuroendocrine cells release?
What is the primary role of each cell type / cell product?
- Enterochromaffin-like glands produce histamine.
- Histamine binds to the parietal cell and stimulates the production and release of gastric acid
- Stimulated by gastrin
- Somatostatin (gastric)
- Reduces gastric secretions
- Exerts a negative effect on the production of gastrin in the stomach and secretin in the duodenum
- Reduces gastric motility
- Gastrin
- Stimulated by peptides within the stomach lumen and luminal distension
- Binds to cholecystokinin B receptors on the enterochromaffin-like cells stimulating histamine release
Describe the basic mechanism and counter-regulation of gastric acid secretion
- Luminal peptides, gastric distension, acetylcholine and gastrin releasing peptide (released by the post-ganglionic fibres of the vagus nerve) stimulate the pathway to acid secretion
- The 4 stimulators above trigger gastrin release from the G cells in the pyloric glands of the gastric antrum
- Gastrin binds enterochromaffin-like cells stimulating release of histamine
- Histamine binds to the parietal cells
- Parietal cell binding of histamine stimulates upregulation of the H+/K+-ATPase incorporation into the canalicular membrane
- Acid produced within the parietal cell from the ionization of water is released via the “acid pump” into the gastric lumen
- Somatostatin is released in response to a gastric pH < 3
- Somatostatin decreases gastrin, histamine and acid production
Describe the components of the gastric mucosal barrier
- Tightly apposed epithelial cells
- Bicarbonate rich mucus
- Abundant mucosal blood supply
- delivers bicarbonate, oxygen and nutrients
- Local PGE2 regulates local blood supply, bicarbonate secretion and epithelial cell turnover
- Local production of epidermal growth factor helps ensure rapid repair and integrity of the epithelial layer when damaged
Describe the basic regulation and modulation of gastric motility and emptying
- Normal motility is the result of smooth muscle interaction with neural and hormonal stimuli
- Pressure differences between the stomach and duodenum and pyloric resistance controls release of secretions
- Intestinal osmoreceptors and chemoreceptors modulate gastric emptying
- Dietary amino acids and fatty acids simulate release of cholecystokinin in the duodenum
- Reduces gastric motility
- Dietary amino acids and fatty acids simulate release of cholecystokinin in the duodenum
- Large undigestible solids are expelled from the stomach during fasting by phase III contractions
- Controlled by motilin release in the duodenum
- High pH in the duodenum may stimulate release
- Motilin release is inhibited by glucose and luminal gastric contents
List the enzymes responsible for digestion of food in the stomach.
What is the major role of the gastric digestive enzymes?
- The stomach has a limited role for digestion of proteins, fats and micronutrients.
- Gastric acid helps to breakdown food particles
- Pepsin digests proteins
- Only active when the pH is < 3
- Limited effect once food leaves the stomach
- Gastric lipase
- ~30% of total lipase produced and starts to digest fats
- Gastric intrinsic factor - dogs only
- Binds cobalamin for absorption in the ileum
Gastric enzymes are not essential for dietary fat and protein assimilation. However, the presence of amino acids in the duodenum, released by this initial digestion process, helps to control gastric motility, emptying and release of the pancreatic enzymes
Note the relevant clinicopathological abnormalities that may be seen with primary gastric diseases
The presentation of primary gastric disease is highly variable from mild gastritis where no clinicopathological abnormalities would be expected, through the GDV where shock, dehydration and DIC may be present. No clinicopathological findings are pathognomonic for primary gastric disease
Clinicopathological tests are primarily used to help identify primary disease causing secondary gastric signs.
- CBC -
- Increased HCT/RCC seen with dehydration or shock
- GDV, AHDS
- Decreases with ulceration and haemorrhage
- Increased HCT/RCC seen with dehydration or shock
- Electolyte abnormalities
- Metabolic alkalosis or acidosis
- Alkalosis is most common with gastric outflow obstruction
- Acidosis is more common with more diffuse GI disease
- Variable decreases in Cl-, K+, and Na+
- Metabolic alkalosis or acidosis
- BUN - increased with GIT bleeding or pre-renal causes
- Creatinine - increased with pre-renal causes (or primary renal disease)
- Albumin - hypoalbuminaemia is occasionally seen
- Urinalysis:
- Paradoxical aciduria - due to preferential volume preservation over maintenance of pH status. Bicarbonate is preserved and Na+ is exchanged for H+ leading to aciduria
List the various tests utilised to investigate primary gastric disease.
- Routine CBC, biochemistry and urinalysis
- Abdominal radiography
- Contrast radiography
- Abdominal ultrasound
- Fluoroscopy
- Endoscopy
- Evaluation of gastric emptying
- Gastric secretory testing
Note the indications and utility of the various imaging modalities for investigating primary gastric disease
- Plain radiographs
- Survey test
- Diagnostic for GDV
- May be useful for identifying foreign bodies
- Contrast radiographs
- Primarily indicated for assessment of gastric emptying and motility
- Ultrasound
- Screening test to assess for gastric wall disease
- Sensitive for detection of obstructive disease and foreign bodies (especially intestinal)
- Good screening test for extra-gastric disease such as pancreatitis or for identification of metastatic disease in the case of gastric neoplasia
- Fluoroscopy
- Primarily used to identify cardia patency and motility disorders
- Endoscopy
- Test of choice for identification of mucosal disease including neoplasia and ulceration
- Allows the collection of mucosal samples
When is gastric secretory testing indicated?
When the following conditions are present and otherwise unexplained.
- Recurrent or severe oesophagitis
- Gastric ulceration
- Mucosal hypertrophy
- Copious amounts of gastric fluid with a suspicion of hypersecretion
Explain the process of assessing for gastric hypersecretion?
Note the relevant interpretation of the results
- Stop anti-secretory therapy for at least 48 hours prior to test
- Fasting gastric pH and serum gastrin are measured concurrently
- Renal and hepatic dysfunction can lead to increased gastrin levels
- Note: fasting gastric acid levels vary widely from pH 1 to pH 8
Interpretation:
- High gastrin and pH < 3
- Excludes mast cell tumour and achlorydia.
- Raises concern for a gastrinoma
- Low gastrin and pH > 3 is normal. pH can be variable and still normal if gastrin is low.
What is a gastrinoma?
What provocative testing can be performed to help identify a gastrinoma?
- A gastrinoma is a neuroendocrine tumour of the G cells
- G cells are located in the endocrine pancreas, duodenuma and to a lesser extent within the stomach.
- Excessive gastrin, produced by a gastrinoma, can cause excessive gastric acid production, gastritis and ulceration
- Blood is collected for basal gastrin levels
- Secretin, calcium or both are infused and levels are assessed again
- A 50% increase above baseline is expected in gastrinoma patients
