17th July 2023

Anatomy and Physiology

Vasculature

The arterial supply of the stomach comes from branches of the coeliac trunk.

• Cardia – left gastric artery
• Fundus – short gastric arteries (arising from splenic artery)
• Lesser curvature – right gastric artery (inferiorly) and left gastric artery (superiorly)
• Greater curvature – left gastroepiploic artery (superiorly) and right gastroepiploic artery (inferiorly)

Blood supply to the stomach

Image Source: Wikimedia Commons (2017). Stomach blood supply, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Stomach_blood_supply.svg (Accessed on: 9 June 2022).

Stomach acid

The normal pH of the stomach ranges from 1.5 to 2.5. Gastric acid secretion increases dramatically during a meal and can be split into three phases:

1. Cephalic phase (20%) – activated by sight, smell and act of chewing food. Vagally mediated.
2. Gastric phase (50-60%) – activated by the presence of digestive products in the stomach and distention of the stomach by food. Mediated by the hormone gastrin.
3. Intestinal phase (5-10%) – activated by the presence of acidic chyme in the duodenum.

Gastrointestinal hormones

There are a large number of hormones in the normal functioning of the gastrointestinal tract. Some of these are tested in the MRCP examinations.

Table 7: Function of gastrointestinal hormones

Satiety is also mediated by gastrointestinal hormones:

• Appetite is increased by ghrelin
• Appetite is decreased by cholecystokinin (CCK), pancreatic polypeptide (PP), glucagon-like peptide-1 (GLP-1) and leptin

Gastric transit

In a normal functioning stomach, food transits in 4-6 hours. This process is controlled by the autonomic nervous system, smooth muscle, and pacemaker cells (interstitial cells of Cajal) within the stomach. Symptomatic slow gastric transit, in the absence of mechanical obstruction, is termed gastroparesis. Symptoms may include: nausea, vomiting, early satiety, bloating and abdominal pain.

Common aetiologies of gastroparesis include:

• Idiopathic – this is the most common form of gastroparesis (50% of cases)
• Neurogenic – seen postoperatively (especially after vagotomy), diabetic neuropathy, neurological problems such as stroke and MS, following viral infection (VZV and EBV) and Chagas disease.
• Myogenic – rheumatological (scleroderma, polymyositis, SLE), muscular dystrophies, amyloidosis.
• Drug-induced – listed below
• Other aetiologies – Zollinger-Ellison syndrome, peptic ulcer disease, anorexia, endocrine (hypothyroidism), radiation

Table 8: Drugs that impact gastric emptying time

Investigation of gastroparesis involves assessing gastric motility using gastric emptying scintigraphy, as well as excluding mechanical obstruction. The latter is often done by direct visualisation endoscopically but may also involve cross-sectional imaging or fluoroscopic assessment.

Management hinges on dietary modification, maintaining adequate nutrition and managing any precipitating factors (such as diabetes). Patients with ongoing symptoms despite this may be treated with oral prokinetics (e.g. dopamine antagonists). With patients presenting with acute dysmotility, it is important to manage their nutrition. In general, enteral feeding (of some form) is always the preferred option.