Gastroenterological disease

Gastroenterological disease

'Gastroenterological disease' is a catch-all term that covers a host of conditions that affect tissues and organs from the mouth to the anus. It includes digestive disorders, GI tract motility issues, cancers of GI tract tissues, gastroenteritis, dyspepsia, gastro-oesophageal reflux disease, peptic ulcers, infections, haemorrhoids, diverticular disease, polyps, and inflammatory bowel diseases amongst many others.

Treatment depends on whether the disease is caused by structural defects and/or dysfunction of physiological processes.

A wide range of different drug classes are used in this branch of medicine. We will summarise the pharmacological treatments for some of the most common GI disorders in this module.

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Constipation (chronic)

Chronic constipation can be idiopathic (with an unknown cause or mechanism) or can be caused by aetiologies that include systemic disorders and drug-induced constipation (a very common side-effect of long-term opiate use). Idiopathic Chronic constipation is often associated with normal or slow colonic transit and/or defecatory dysfunction.

The choice of treatment depends on the cause of the condition. Effective management will normally include a range of interventions, not drug treatments alone.

Pharmaceutical treatments include stimulant laxatives such as bisacodyl, sodium picosulphate, anthroquinines (e.g., senna), and parasympathomimetics such as bethanechol chloride (a muscarinic cholinergic receptor agonist), neostigmine and pyridostigmine bromide (both acetylcholinesterase inhibitors) increase intestinal motility. Over-use can cause diarrhoea and hypokalaemia.

A short video overview of laxatives and cathartics can be found here. More details about different types of laxative drugs is included in the Drugs/Gastrointestinal system module.

UpToDate is a clinical decision support resource for healthcare professionals that is maintained by Wolters Kluwer. This page was last updated in June 2022. It summarises the management pathways for idiopathic chronic constipation.

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Peptic ulcer disease

Gastric and duodenal ulcers are subtypes of peptic ulcers. They are characterised by erosion of the epithelial layer of the gastric or duodenal mucosa, which causes upper abdominal pain. Less frequent symptoms include dyspepsia and nausea. Gastro-intestinal perforation and haemorrhage are serious (possibly life-threatening) complications of peptic ulcer disease.

Two very common causes of peptic ulcer disease, which can occur independently or together, are Helicobacter pylori (H. pylori) infection and use of non-steroidal anti-inflammatory drugs (NSAIDs).

Treatment for all patients with peptic ulcers includes a proton pump inhibitor (PPI: omeprazole, esomeprazole, lansoprazolerabeprazole or pantoprazole). An H2-receptor antagonist (H2RA: cimetidine or famotidine) has antisecretory activity in patients with peptic ulcers as well, but PPIs result in faster control of disease symptoms and higher healing rates due to strong suppression of acid secretion.

If H. pylori infection is confirmed, a PPI is administered together with an antibiotic regimen to treat the infection. Eradication of H. pylori in patients with peptic ulcer disease results in higher healing rates and lower ulcer recurrence rates in patients with duodenal and gastric ulcers. The selection of antibiotic regimen depends on the patient's potential for antibiotic resistance (and any potential hypersensitivity). In patients without risk of resistance to macrolide antibiotics, triple therapy with clarithromycin, amoxicillin and a PPI is used. In penicillin-allergic patients, metronidazole can be used instead of amoxicillin. In patients with macrolide resistance, quadruple therapy with bismuth subsalicylate, metronidazole, tetracycline and a PPI can be used.

Patients with NSAID-induced ulcer can be treated with a PPI as maintenance therapy if the patient needs to remain on an NSAID or aspirin therapy.

In addition to the antisecretory agents, other drugs with antiulcer activity include antacids (e.g., aluminum hydroxide, calcium carbonate), sucralfate, bismuth, misoprostol, and potassium-competitive acid inhibitors (e.g., vonoprazan).

Rare complications of peptic ulcer disease include bleeding (at the site of the ulcer), gastric perforation, and gastric obstruction.

Further details of PPIs, H2-receptor antagonists and agents used to treat other forms of dyspepsia are included in the Antisecretory drugs topic within the Drugs/Gastrointestinal system module.

This webpage from the Wolters Kluwer UpToDate series summarises the epidemiology, etiology, and pathogenesis of peptic ulcer disease. It was last updated in July 2022.

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Gastric and duodenal ulcers are subtypes of peptic ulcers. They are characterised by erosion of the epithelial layer of the gastric or duodenal mucosa, which causes upper abdominal pain. Less frequent symptoms include dyspepsia and nausea. Gastro-intestinal perforation and haemorrhage are serious (possibly life-threatening) complications of peptic ulcer disease.

Two very common causes of peptic ulcer disease, which can occur independently or together, are Helicobacter pylori (H. pylori) infection and use of non-steroidal anti-inflammatory drugs (NSAIDs).

Treatment for all patients with peptic ulcers includes a proton pump inhibitor (PPI: omeprazole, esomeprazole, lansoprazolerabeprazole or pantoprazole). An H2-receptor antagonist (H2RA: cimetidine or famotidine) has antisecretory activity in patients with peptic ulcers as well, but PPIs result in faster control of disease symptoms and higher healing rates due to strong suppression of acid secretion.

If H. pylori infection is confirmed, a PPI is administered together with an antibiotic regimen to treat the infection. Eradication of H. pylori in patients with peptic ulcer disease results in higher healing rates and lower ulcer recurrence rates in patients with duodenal and gastric ulcers. The selection of antibiotic regimen depends on the patient's potential for antibiotic resistance (and any potential hypersensitivity). In patients without risk of resistance to macrolide antibiotics, triple therapy with clarithromycin, amoxicillin and a PPI is used. In penicillin-allergic patients, metronidazole can be used instead of amoxicillin. In patients with macrolide resistance, quadruple therapy with bismuth subsalicylate, metronidazole, tetracycline and a PPI can be used.

Patients with NSAID-induced ulcer can be treated with a PPI as maintenance therapy if the patient needs to remain on an NSAID or aspirin therapy.

In addition to the antisecretory agents, other drugs with antiulcer activity include antacids (e.g., aluminum hydroxide, calcium carbonate), sucralfate, bismuth, misoprostol, and potassium-competitive acid inhibitors (e.g., vonoprazan).

Rare complications of peptic ulcer disease include bleeding (at the site of the ulcer), gastric perforation, and gastric obstruction.

Further details of PPIs, H2-receptor antagonists and agents used to treat other forms of dyspepsia are included in the Antisecretory drugs topic within the Drugs/Gastrointestinal system module.

This webpage from the Wolters Kluwer UpToDate series summarises the treatments that are appropriate for peptic ulcer disease. It also addresses secondary prevention. The page was last updated in August 2022.

Average: 4 (1 vote)

Gastro-oesophageal reflux disease (GORD)

Gastro-oesophageal reflux disease (GORD; also known as GERD Gastro-esophageal reflux disease)

GORD is a common cause of dyspepsia. It is caused by leakage of stomach contents back into the oesophagus through the lower esophageal sphincter (acid reflux), and this induces corrosive damage to the oesophageal mucosa. GORD is characterised by an extended period (>4 weeks) of upper abdominal pain/discomfort, heartburn, regurgitation and nausea and/or vomiting. It can become a chronic condition. Factors that favour acid reflux include stress and anxiety, smoking and alcohol, trigger foods (e.g., coffee, chocolate, fatty foods which delay gastric emptying), obesity (increases intra-abdominal pressure), prescription drugs that relax the lower oesophageal sphincter (e.g., alpha-blockers, anticholinergics, benzodiazepines, beta-blockers, bisphosphonates, calcium-channel blockers, corticosteroids, non-steroidal anti-inflammatory drugs (NSAIDs), nitrates, theophyllines, tricyclic antidepressants), pregnancy and the presence of a hiatus hernia.

Initial treatment will include a review of any existing medications that are known to exacerbate symptoms and prescription of a proton-pump inhibitor (PPI) drug such as omeprazole, esomeprazole, lansoprazolerabeprazole or pantoprazole for a period of 4–8 weeks. These drugs reduce gastric acid production, and allow the healing process to begin. Other antacids (simeticone, sodium bicarbonate, and alginates) may also be included to relieve symptoms. Any lifestyle factors (e.g. smoking, high alcohol intake, excess body mass) should be addressed, eating within 3 hours of bedtime should be discouraged and occasionally raising the head of the bed may reduce nocturnal symptoms.

For patients who experience refractory or recurrent disease despite adhering to PPI therapy, an extension of PPI treatment (including at an increased dose) can be initiated. This can be complemented with prescription of a histamine (H2)-receptor antagonist (e.g. ranitidine, cimetidine or famotidine) if oesophagitis has been confirmed. Long-tern PPI maintenance treatment may be required, and if this is the case patients should be screened annually to assess their symptoms, and to determine if stopping treatment might be appropriate.

Complications arising from long-term GORD include the development of oesophageal ulcers and oesophageal scarring and narrowing, that can make swallowing difficult. In rare cases surgery may be considered to correct any structural defect that's contributing to, or caused by chronic acid reflux. Barrett's oesophagus is a condition that can be precipitated after repeated episodes of GORD over many years. It is characterised by changes in the cells of the oesophageal epithelium. This should be monitored (usually by endoscopy every few years) as there's a small risk of the cellular changes transforming into oesophageal cancer.

Further details of PPIs, H2-receptor antagonist and agents used to treat other forms of dyspepsia are included in the Antisecretory drugs topic within the Drugs/Gastrointestinal system module.

 

This is a very short and simple animation with textual descriptions of where and how GORD takes effect.

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Gastro-oesophageal reflux disease (GORD; also known as GERD Gastro-esophageal reflux disease)

GORD is a common cause of dyspepsia. It is caused by leakage of stomach contents back into the oesophagus through the lower esophageal sphincter (acid reflux), and this induces corrosive damage to the oesophageal mucosa. GORD is characterised by an extended period (>4 weeks) of upper abdominal pain/discomfort, heartburn, regurgitation and nausea and/or vomiting. It can become a chronic condition. Factors that favour acid reflux include stress and anxiety, smoking and alcohol, trigger foods (e.g., coffee, chocolate, fatty foods which delay gastric emptying), obesity (increases intra-abdominal pressure), prescription drugs that relax the lower oesophageal sphincter (e.g., alpha-blockers, anticholinergics, benzodiazepines, beta-blockers, bisphosphonates, calcium-channel blockers, corticosteroids, non-steroidal anti-inflammatory drugs (NSAIDs), nitrates, theophyllines, tricyclic antidepressants), pregnancy and the presence of a hiatus hernia.

Initial treatment will include a review of any existing medications that are known to exacerbate symptoms and prescription of a proton-pump inhibitor (PPI) drug such as omeprazole, esomeprazole, lansoprazolerabeprazole or pantoprazole for a period of 4–8 weeks. These drugs reduce gastric acid production, and allow the healing process to begin. Other antacids (simeticone, sodium bicarbonate, and alginates) may also be included to relieve symptoms. Any lifestyle factors (e.g. smoking, high alcohol intake, excess body mass) should be addressed, eating within 3 hours of bedtime should be discouraged and occasionally raising the head of the bed may reduce nocturnal symptoms.

For patients who experience refractory or recurrent disease despite adhering to PPI therapy, an extension of PPI treatment (including at an increased dose) can be initiated. This can be complemented with prescription of a histamine (H2)-receptor antagonist (e.g. ranitidine, cimetidine or famotidine) if oesophagitis has been confirmed. Long-tern PPI maintenance treatment may be required, and if this is the case patients should be screened annually to assess their symptoms, and to determine if stopping treatment might be appropriate.

Complications arising from long-term GORD include the development of oesophageal ulcers and oesophageal scarring and narrowing, that can make swallowing difficult. In rare cases surgery may be considered to correct any structural defect that's contributing to, or caused by chronic acid reflux. Barrett's oesophagus is a condition that can be precipitated after repeated episodes of GORD over many years. It is characterised by changes in the cells of the oesophageal epithelium. This should be monitored (usually by endoscopy every few years) as there's a small risk of the cellular changes transforming into oesophageal cancer.

Further details of PPIs, H2-receptor antagonist and agents used to treat other forms of dyspepsia are included in the Antisecretory drugs topic within the Drugs/Gastrointestinal system module.

 

This is a 12 minute summary of GERD. It discusses terminology, etiology, diagnosis and treatments with a clinical focus.

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Gastro-oesophageal reflux disease (GORD; also known as GERD Gastro-esophageal reflux disease)

GORD is a common cause of dyspepsia. It is caused by leakage of stomach contents back into the oesophagus through the lower esophageal sphincter (acid reflux), and this induces corrosive damage to the oesophageal mucosa. GORD is characterised by an extended period (>4 weeks) of upper abdominal pain/discomfort, heartburn, regurgitation and nausea and/or vomiting. It can become a chronic condition. Factors that favour acid reflux include stress and anxiety, smoking and alcohol, trigger foods (e.g., coffee, chocolate, fatty foods which delay gastric emptying), obesity (increases intra-abdominal pressure), prescription drugs that relax the lower oesophageal sphincter (e.g., alpha-blockers, anticholinergics, benzodiazepines, beta-blockers, bisphosphonates, calcium-channel blockers, corticosteroids, non-steroidal anti-inflammatory drugs (NSAIDs), nitrates, theophyllines, tricyclic antidepressants), pregnancy and the presence of a hiatus hernia.

Initial treatment will include a review of any existing medications that are known to exacerbate symptoms and prescription of a proton-pump inhibitor (PPI) drug such as omeprazole, esomeprazole, lansoprazolerabeprazole or pantoprazole for a period of 4–8 weeks. These drugs reduce gastric acid production, and allow the healing process to begin. Other antacids (simeticone, sodium bicarbonate, and alginates) may also be included to relieve symptoms. Any lifestyle factors (e.g. smoking, high alcohol intake, excess body mass) should be addressed, eating within 3 hours of bedtime should be discouraged and occasionally raising the head of the bed may reduce nocturnal symptoms.

For patients who experience refractory or recurrent disease despite adhering to PPI therapy, an extension of PPI treatment (including at an increased dose) can be initiated. This can be complemented with prescription of a histamine (H2)-receptor antagonist (e.g. ranitidine, cimetidine or famotidine) if oesophagitis has been confirmed. Long-tern PPI maintenance treatment may be required, and if this is the case patients should be screened annually to assess their symptoms, and to determine if stopping treatment might be appropriate.

Complications arising from long-term GORD include the development of oesophageal ulcers and oesophageal scarring and narrowing, that can make swallowing difficult. In rare cases surgery may be considered to correct any structural defect that's contributing to, or caused by chronic acid reflux. Barrett's oesophagus is a condition that can be precipitated after repeated episodes of GORD over many years. It is characterised by changes in the cells of the oesophageal epithelium. This should be monitored (usually by endoscopy every few years) as there's a small risk of the cellular changes transforming into oesophageal cancer.

Further details of PPIs, H2-receptor antagonist and agents used to treat other forms of dyspepsia are included in the Antisecretory drugs topic within the Drugs/Gastrointestinal system module.

 

This 10 minute animated video by Armando Hasudungan is a brief and informative review of GORD (GERD) that covers pathophysiology, diagnostics, drug treaments and other interventions. Suitable for intermediate level learners, with an understanding of human physiology and biology.

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Diarrhoea

Diarrhoea is the abnormal passing of loose or liquid stools, with increased frequency, increased volume, or both. It can be classified based on its duration into:

  • Acute diarrhoea ≤14 days in duration, improving within 2-4 days
  • Persistent diarrhoea >14 days and ≤30 days
  • Chronic diarrhoea >30 days
  • Invasive diarrhoea (dysentery) is characterised by visible blood in the stool, fever and abdominal pain

Acute diarrhoea is typically the result of an infection (e.g., Campylobacter enteritis), a side-effect of a drug (e.g. antibiotic), or as an acute symptom of a chronic gastro-intestinal disorder (e.g. Crohn's disease, irritable bowel syndrome, ulcerative colitis). It may also result from the presence of non-absorbed osmotically active solutes in the bowel lumen because of malabsorption of a meal (e.g., lactase deficiency, chronic pancreatitis) or motility disorders of the bowel wall. All acute episodes of diarrhoea should lead to consideration of ingestion of potentially infected food, recent starting of a new drug or foreign travel. Consideration should also be given as to whether it might be a manifestation of another illness and the assessment should also include questions about any 'red flag' symptoms such as unexplained weight loss, rectal bleeding, previous episodes of diarrhoea, or systemic illness.

Most incidences of acute diarrhoea will resolve spontaneously, so the principal aim of treatment is to prevent dehydration and support electrolyte balance. Where there is a risk of severe dehydration urgent action to replace fluid and electrolytes may be necessary. Antimotility drugs such as loperamide can be used to provide rapid control of symptoms. Other drugs used for diarrhoea: codeine phosphate and co-phenotrope (diphenoxylate) are opioid-type drugs that inhibit gut motility; methylcellulose (absorbs water from the bowel, thus reducing dehydration and solidifying loose stool); rifaximin.(a rifamycin antibacterial drug that can be used to treat what's commonly referred to as travelers' diarrhoea; the major causes of which are exposure to unusual food- or water-borne contaminants in foreign destinations).

Long-term or chronic diarrhoea (i.e., lasting for >30 days), is often associated with chronic medical conditions including irritable bowel syndrome (IBS), inflammatory bowel diseases (Crohn's disease and ulcerative colitis), malabsorption syndromes (e.g., celiac disease), and sometimes long-standing infections. There are effective treatments for almost all cases of chronic diarrhoea. The best approach is to treat the underlying cause of chronic diarrhoea. Where this does not achieve resolution, the goal is to achieve control over symptoms, and again antimotility drugs (loperamide, diphenoxylate/atropine) and antispasmodic drugs (mebeverine, sold as Colofac® in the UK, and scopolamine butylbromide sold under the trade name Buscopan®) are widely used medications in this setting. 

Further information about additional classes of antidiarrhoeal drugs has been curated in the Drugs/Gastrointestinal system module

This page from the Wolters Klower UpToDate resource was last updated in January 2023.

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