Disorders of gastric secretion and motility, post-gastrectomy syndromes, postprandial syndromes

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Stomach is a muscular organ in the upper abdomen that is an essential part of digestive system (connecting esophagus to duodenum), using acid and enzymes to break down into chyme. Gastric motility depends on coordinated contraction of smooth muscle under the control of the enteric nervous system, vagal input, hormones and the interstitial cells of Cajal. [1]

Disorders of gastric motility[edit | edit source]

The muscular external is composed of smooth muscle cells orientated in 3 different directions (oblique, circular, longitudinal layer). These help to break the food bolus into smaller components by pushing the food forcefully back and forth in a churning movement. Only particles that are small enough will be able to move to duodenum.

Disorders of gastric motility are best divided into delayed gastric emptying and rapid gastric emptying. Important mechanisms include abnormal gastrointestinal motor function, a complex sequence of events involving the parasympathetic and sympathetic nervous systems, gastric smooth muscle cells, pacemaker cells within the stomach and intestine and the pyloric sphincter. Etiology includes idiopathic (50% of cases), diabetes mellitus, post surgical, viral infection, rheumatological diseases, Autoimmune, Medication and neurological conditions. Patients typically present with nausea, vomiting, early satiety, postprandial fullness, bloating, and sometimes weight loss. [2]

Increase motility[edit | edit source]

  • Dumping syndrome[3] (rapid gastric emptying often post surgery)
    • Esophagectomy
    • Gastrectomy
    • Vagotomy

Reduce motility[edit | edit source]

  • Hypothyroidism[4]
  • Idiopathic gastroparesis
  • Viral infections
  • Neuromuscular dysfunction

Disorders of gastric secretion[edit | edit source]

Disorders of gastric secretion involves the imbalance of substances including HCl, pepsin, bicarbonate and mucus leading to hypersecretion or hyposecretion of gastric acid.

Hypersecretion[edit | edit source]

Hypersecretion refers to an abnormal increase gastric acid production. This is important because it can damage oesophagus, stomach and duodenum causing peptic ulcer disease, gastroesophageal reflux, bleeding, perforation and malabsorption.

Example of causes includes

  • Zollinger-Ellison syndrome (Gastroma)
  • Idiopathic
  • Helicobacter pylori infection
  • Gastric Outlet Obstruction[5]

Hyposecretion[edit | edit source]

Hyposecretion refers to an abnormal decrease gastric acid production (pH > 3), often due to not releasing enough HCl. This will then lead to malabsorption, as well as making the stomach more prone to infections. [6]

Example of causes includes

  • Age (common in people over 65)
  • Atrophic gastritis
  • Helicobacter pylori infection
  • Proton pump inhibitors[7]

Post-Gastrectomy Syndromes[edit | edit source]

Postgastrectomy syndromes are a group of gastrointestinal disorders occurring after gastric surgery. Patients often have reduced appetite or early satiety easier due to the reduced capacity if they have underwent partial or total gastrectomy.

Dumping syndrome[3][edit | edit source]

  • due to increase motility of stomach, causing undigested food to reach the small intestine too quickly

Malabsorption[8][edit | edit source]

  • decrease absorption of iron, vitamin B12, vitamin C and calcium
  • Iron - Gastric acid helps to convert Fe3+ into Fe2+, if this doesn't occur -> iron bypass duodenum and decreases absorption
  • Vitamin B12 can't be released from food and less intrinsic factor (produced by parietal cells) will be produced
  • Vitamin C - ascorbic acid will be converted into a less active form
  • Calcium - gastric acid normally helps to dissolve calcium salts into soluble forms

Post-Prandial Syndrome[edit | edit source]

Dumping syndrome[3][edit | edit source]

  • due to increase motility of stomach, causing undigested food to reach the small intestine too quickly
  • Early dumping (within the 1h postprandial due to rapid fluid shifts into intestine under hyperosmolar conditions and increase GI hormone release
    • Symptoms include diarrhea, bloating, nausea, pain in abdomen
  • Late Dumping (1 - 3h after postprandial due to rapid carbohydrate delivery, hyperglycaemia and then hyperinsulinemic response with reactive hypoglycaemia
    • Symptoms include feeling tired, have irregular heartbeat, trouble concentrating, sweating, weakness

Reference[edit | edit source]

  1. ↑ Hsu, M., Safadi, A. O., & Lui, F. (2023, July 17). Physiology, stomach. In StatPearls. StatPearls Publishing. National Center for Biotechnology Information.
  2. ↑ Reddivari, A. K. R., & Mehta, P. (2024, February 28). Gastroparesis. In StatPearls. StatPearls Publishing. NCBI Bookshelf.
  3. ↑ a b c National Institute of Diabetes and Digestive and Kidney Diseases. (2019, January). Symptoms & causes of dumping syndrome. NIDDK.
  4. ↑ National Institute of Diabetes and Digestive and Kidney Diseases. (2018, January). Symptoms & causes of gastroparesis. NIDDK.
  5. ↑ Phan, J., Benhammou, J. N., & Pisegna, J. R. (2015). Gastric hypersecretory states: Investigation and management. Current Treatment Options in Gastroenterology, 13(4), 386–397.
  6. ↑ WebMD Editorial Contributors. (2024, February 20). Hypochlorhydria: Causes, symptoms, treatment, and more. WebMD.
  7. ↑ Cleveland Clinic. (2022, June 27). Hypochlorhydria (low stomach acid): Symptoms, tests, treatment. Cleveland Clinic.
  8. ↑ Kim, C.-Y. (2022). Postgastrectomy syndrome. Foregut Surgery, 2(1), 17–28. https://doi.org/10.51666/fs.2022.2.e4
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