Diseases of the Stomach | Medibuddy
17th July 2023

Diseases of the Stomach

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)

MRCP Part 1 - Blood supply to the stomach

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.

Hormone Source Function
Gastrin G-cells of stomach Increases gastric acid secretion
Cholecystokinin (CCK) I-cells in duodenum Increases pancreatic enzyme secretion

Increases gallbladder contraction

Somatostatin Pancreatic delta cells Decreases secretion of many other hormones (e.g. gastrin and digestive enzymes)

Prolongs gastric emptying time

Vasoactive Intestinal Peptide (VIP) Parasympathetic ganglia Increases enzyme secretion

Reduces gastric acid secretion

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
Drugs that speed up gastric emptying Drugs that slow gastric emptying
Anticholinesterases – e.g. neostigmine

Dopamine antagonists – e.g. domperidone, metoclopramide

Macrolide antibiotics – e.g. erythromycin

Opioids

Ondansetron

Anticholinergics – including tricyclic antidepressants

Dopamine agonists – e.g. anti-Parkinsonian medication

Proton pump inhibitors

Alcohol

Calcium channel blockers

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.

Helicobacter Pylori Infection

H.pylori is a gram-negative bacterium that has been implicated in a number of gastrointestinal pathologies.

Pathology Details
Chronic gastritis H. pylori can predispose patients to other conditions, such as neoplasm
Peptic ulcer disease H. pylori has been implicated in:

  • 90% of Duodenal Ulcers (DU)
  • 70-80% of Gastric Ulcers (GU)
Gastric adenocarcinoma H. pylori associated with a 1-2% lifetime risk of gastric adenocarcinoma
B cell lymphoma of MALT tissue 75% of MALT lymphomas are successfully treated with H. pylori eradication therapy

Table 9: Sequelae of chronic Helicobacter pylori infection.

Investigations (BSG guidelines)

  • 1st line: Urea breath test/stool antigen testing
    • Requires a 2-week PPI washout period and 4 weeks for antibiotics
    • Urea breath test is the preferred investigation to test for eradication post treatment
  • 2nd line: Serology (does not differentiate between active and past infection, so cannot be used for retesting)

If a patient is undergoing OGD, the endoscopist can take biopsies to perform a rapid urease test (also known as the CLO test – Campylobacter-Like Organism) to test for H. pylori.

Treatment

7 days high-dose PPI + amoxicillin + metronidazole/clarithromycin

  • If the patient is penicillin allergic, use high-dose PPI + metronidazole + clarithromycin (7 days).

Antiulcer medication

Reduction/neutralisation of stomach acid:

  • Proton pump inhibitors (antisecretory)
  • Histamine-2 receptor antagonists (antisecretory)
  • Antacids (neutralising)

Other mechanisms:

  • Sucralfate (forms a protective barrier over the ulcer)

Bleeding Lesions in the Stomach

Bleeding gastric lesions, which are commonly tested in the MRCP examination, are listed in table 10.

Lesion Details
Peptic ulcer Breaks in the mucosal layer can penetrate down the muscularis mucosa of the stomach and duodenum.

They are associated with burning epigastric pain.

  • GUs are most often seen on the lesser curvature of the stomach. The arterial supply to this area is the left gastric artery.
Gastric varices Can occur secondary to portal hypertension. Causes:

  • Liver cirrhosis
  • Non-cirrhotic portal hypertension
    • Venous thrombosis (portal vein/splenic vein/hepatic vein = Budd-Chiari)
    • Cardiac (constrictive pericarditis, restrictive cardiomyopathy)
    • Schistosomiasis
    • Idiopathic non-cirrhotic portal hypertension
Erosive gastritis Multiple erosions seen in the gastric mucosa.

Causes: H. pylori, medication (steroids, NSAIDs), alcohol.

Gastric neoplasms Gastric adenocarcinoma – most often found in the cardia

Gastrointestinal stromal tumours (GISTs)

Neuroendocrine tumours

Gastric lymphomas

Dieulafoy’s lesion Vascular malformations where aberrant tortuous arterioles can erode through the submucosal layer and cause bleeding. They account for 5% of UGIB.
Gastric Antral Vascular Ectasia (GAVE) An uncommon cause of chronic gastric bleeding caused by fragile antral vessels.

Question clue: the classic ‘watermelon stomach’ appearance described on endoscopy.

Zollinger-Ellison Syndrome (ZES) Gastrin producing tumours (gastrinomas) secrete excess gastrin in the duodenum and pancreas. Suspicion for ZES should be raised in cases of multiple peptic ulcers, ulcers in the jejunum, ulcers that are non-responsive to PPI therapy. 20% of patients have MEN-1.

Investigation:

  •  x3 measurements of high fasting gastrin levels
  • Secretin stimulation test in patients with a non-diagnostic fasting gastrin level.

Question clue: diarrhoea + multiple peptic ulcers + not responding to PPIs

Angiodysplasia Small vascular malformations which can be found throughout the GI tract.

Table 10: Bleeding lesions in the stomach

Other Stomach Pathology 

Ménétrier’s Disease: a rare disorder characterised by giant gastric folds. Patients have decreased acid secretion and may develop a protein-losing gastropathy. This results in hypoalbuminaemia, which may manifest with oedema.

Autoimmune Gastritis: autoimmune destruction of the stomach results in atrophic gastritis evidenced by flattened rugal folds and visible subcutaneous vessels on endoscopy. Patients may have antibodies to parietal cells and/or intrinsic factor. Intrinsic factor is required for B12 absorption in the terminal ileum, so a lack of this can result in pernicious anaemia.

Cyclical vomiting syndrome (CVS): characterised by bouts of severe vomiting that may last several days, with intervening periods of good health. A similar condition, cannabis hyperemesis syndrome (CHS), is seen in people with heavy, often daily use of cannabis – it has a similar presentation to CVS. Symptoms often improve with abstinence from cannabis. Many patients with CVS and CHS find that their symptoms are relieved by hot showers or baths.

Bariatric Surgery

Bariatric procedures can be considered for the management of severe obesity and its complications. Surgery is reserved for those with:

  • A BMI of 40 kg/m2 or more, or
  • Between 35 kg/m2 and 40 kg/m2 with evidence of other significant disease (e.g. type 2 diabetes mellitus or obstructive sleep apnoea) which will improve with weight loss

In these patients, surgery is only considered when all appropriate non-surgical measures have been tried. There are two main surgeries to be aware of for the purposes of the MRCP:

  • Roux-en-Y gastric bypass – a small gastric pouch is created, which is anastomosed to the jejunum (restrictive and malabsorptive)
  • Sleeve gastrectomy – a partial gastrectomy reducing the volume of the stomach (restrictive)

Complications:

There are many complications for which the following could be tested in the MRCP examination:

  • Nutritional deficiencies – malabsorptive procedures are at increased risk of deficiencies. Risk of anaemia and metabolic bone disease.
  • Anatomical – Stricture formation, marginal ulcers, small capacity (early satiety)
  • Gallstones – because of distorted anatomy, ERCP can be difficult in these patients!
  • Short-bowel syndrome
  • Dumping syndrome
  • Change in bowel habits
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