Gastrointestinal disorders

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Chapter 35 Gastrointestinal disorders

Chapter contents

Anatomy of the gastrointestinal tract 273

Microflora of the gastrointestinal tract 274

Gastrointestinal disorders 274

Anatomy of the Gastrointestinal Tract

There are five layers in the gastrointestinal wall (Figure 35.1):

• Longitudinal muscle layer: the outer layer of muscle. Combined with the inner circular muscle layer, its coordinated contraction creates peristalsis, which propels food through the gut.

• Circular muscle layer.

• Submucosa: a layer of dense irregular connective tissue with large blood vessels, an extensive lymph system and nerves branching into the external muscle and mucosal layer. This supply and drainage system becomes an important factor in the spread of secondary cancers.

• Mucosa: the innermost layer, which is in direct exposure to the lumen (i.e. the space within the tube of the tract). The composition of the mucosa varies depending on the area of the gastrointestinal tract. For example, in the stomach it has qualities that make it resistant to the effects of a low pH; in the small intestine it contains villi, which maximize absorption.

Figure 35.1 Cross-section of small intestine.

The blood flow from the small intestine is significant because it passes directly to the liver via the hepatic portal vein. Most of the water-soluble nutrients absorbed from the gut are transported to the liver in this way. Fat-soluble substances are absorbed by the intestinal lymphatic system and distributed to the blood by the thoracic duct, thus bypassing the liver.

The stomach mucosa contains many mucus-secreting cells; the mucus creates a protective layer over the lining of the stomach wall. The lining of the stomach is highly glandular and consists of four types of gland:

• Parietal cells: secrete hydrochloric acid (HCl) and intrinsic factor (see Chapter 13 ‘Vitamins and minerals’, p. 105).

• Mucous cells: secrete an alkaline mucus that protects the epithelium against damage due to shearing of the membranes and the acid environment of the stomach.

• Chief cells: secrete pepsin, a proteolytic enzyme. Its activity is low at a low pH (see Chapter 8 ‘Acids and bases’, p. 54) and the enzyme is therefore not fully active until it reaches the more basic medium of the small intestine (pH approximately 7.8).

• G cells: secrete the hormone gastrin.

Different areas of the stomach vary in their secretions.

Microflora of the Gastrointestinal Tract

The gastrointestinal tract is a complex and self-contained ecosystem of over 400 bacterial species. Anaerobic bacteria (bacteria that live in an environment where there is little or no oxygen) outnumber aerobic bacteria (those that require the presence of oxygen to function). Fungi are also present but, due to the population of the normal commensals, tend not exceed limits, except for a problem such as that caused by an overgrowth of, for example, Candida albicans.

Due to the existence of the commensals, a situation exists where host, bacteria and fungi live together without any adverse effects on one another. In many cases in the gastrointestinal tract, bacteria provide a very useful service, producing vitamins that are vital for health or taking part in chemical reactions necessary to activate compounds (see Chapter 13 ‘Vitamins and minerals’, p. 108). These bacteria are usually non-pathogenic. Most of the gut flora is found in the colon and lives in the lumen of the bowel; it does not normally penetrate the gut wall.

Ingestion of certain substances, e.g. antibiotics, can disturb the normal balance of these commensals, which is why carefully consideration of gut health after a course of antibiotics is important.

Gastrointestinal Disorders

Dyspepsia

This is a general term for a group of signs and symptoms:

• pain or discomfort in the upper abdomen

• bloating and feeling ‘full’ after eating

• nausea or vomiting.

All these symptoms are intermittent.

• Causes of Dyspepsia

• Acid reflux, oesophagitis or gastro-oesophageal reflux disease (GORD).

• Hiatus hernia.

• Functional dyspepsia: does not involve ulcer formation.

• Duodenitis: can be a precursor to an ulcer; a possible cause is NSAIDs.

• Gastritis: can be a precursor to an ulcer; a possible cause is NSAIDs.

• Duodenal and gastric ulcers.

• Conservative Treatment

• Check patient’s medication: patients who are taking NSAIDs or some other medications (e.g. some antibiotics, steroids) are required to stop medication.

• Patients must try to abstain from foods and drinks such as chocolate, coffee, alcohol, spicy foods and peppermint.

• Patients should try to stop smoking: chemicals inhaled from cigarettes are thought to relax the oesophageal sphincter.

• Patients might have to change posture if they habitually bend over during the day, and might have to avoid sleeping horizontally.

• At night, patients are discouraged from drinking or eating at least 2 hours before bedtime.

• Patients who are overweight should be encouraged to lose weight: the extra pressure on the stomach encourages reflux.

• Orthodox Medication

Antacids

• Attempt to neutralize the available stomach acid: they are weak alkalis.

• Are thought to stimulate the mucosal repair mechanisms around ulcers: possibly by stimulating local prostaglandin release.

• Medications include: magnesium hydroxide, magnesium trisilicate, aluminium hydroxide gel.

• Magnesium is a more effective antacid than aluminium but has a tendency to create diarrhoea.

• As small amounts of magnesium can be absorbed, any antacid preparation containing magnesium should be used with caution.

H2-Receptor Antagonists

These compete with histamine at the H2-receptor level. They are more effective when the stomach is empty, e.g. at night or when fasting, and less effective when food is present.

Adverse Reactions

• Diarrhoea and other digestive disturbances.

• Ranitidine (Figure 35.2): can be associated with darkening of the tongue and black stools.

• Cimetidine: has been associated with hair loss.

Figure 35.2 Chemical structure of histamine and various H2-receptor antagonists for comparison.

Drug Interactions

Cimetidine affects one of the liver detoxification pathways and thus can increase the time of metabolism of drugs removed by this pathway, leading to a build-up that can be toxic in some cases. Theophylline (a bronchodilator) and warfarin are two drugs that can be affected.

Proton Pump Inhibitors

These bind irreversibly to the proton pump mechanism on the parietal cell membranes. The proton pump is really an enzyme that actively secretes hydrogen ions into the gastric cavity. The medication is enteric coated to allow it to reach the small intestine, where it can be properly absorbed.

Omeprazole (Figure 35.3) interferes with the liver detoxification system and prolongs the presence of diazepam, phenytoin (an anticonvulsant; see Chapter 33 ‘Neurological disease’, p. 256) and possibly warfarin.

Figure 35.3 Chemical structures of proton pump inhibitors.

Proton pump inhibitors are used only in the short-term management of duodenal and gastric ulcers, particularly those caused by NSAIDs. They can also be used in combination with antibiotics when treating for Helicobacter pylori.

Adverse Effects

Treatment of Helicobacter pylori

The patient is given a non-radioactive isotope of carbon to drink. Helicobacter pylori breaks this down to ammonia and carbon dioxide. The labelled carbon dioxide is then tested. H. pylori is treated with antibiotics such as clarithromycin, tetracycline, amoxicillin and metronidazole (see Chapter 29 ‘Antimicrobials’, p. 218) and a proton pump inhibitor for 2 weeks.

Peptic Ulcer

• Aetiology

• NSAIDs can damage the lining of the gut. NSAIDs work by blocking the cyclo-oxygenase (COX) enzymes involved in producing prostaglandins (see Chapter 30 ‘Inflammation and the immune system’, p. 229). COX-1 helps to maintain the gut lining; COX-2 is less involved in this process. COX-2 inhibitors are supposed to help gastrointestinal effects because they allow the COX-1 pathway to carry on working while blocking the COX-2 pathway. The overall result is an anti-inflammatory effect and less gastrointestinal disturbance.

• Helicobacter pylori.

• Stress: originally thought to have an effect on the blood flow to the stomach; the damage by NSAIDs and H. pylori are now accepted as prime causal factors but stress might exacerbate the condition in some way.

• Diet: poor nutrition creates changes in the function of the gastrointestinal tract and secretions.

The entire gastrointestinal tract is covered by a protective mucus layer. Any reduction in the effectiveness of this layer renders the lining accessible and prone to attack by acid and enzymes, eventually creating an ulcer.

• Treatment

As above for dyspepsia.

Irritable Bowel

Reasons for this should be investigated if the condition does not quickly resolve with conservative treatment or other signs are present, such as blood in stools.

Coeliac Disease

Inherited condition in which exposure to gluten atrophies the gastrointestinal villi in the small intestine.

• Investigations

• IgA anti-tissue transglutaminase (tTG): now favoured.

• Treatment

Patients refrain from eating foods containing gluten.

Crohn’s Disease

A chronic, inflammatory bowel disease that can affect any part of the gut, but in particular the distal end of the ileum and the proximal colon.

• Signs and Symptoms

The following might or might not occur:

• possible diarrhoea for more than 6 weeks

• abdominal pain

• weight loss

• general feeling of being unwell

These can well occur in a fairly young patient.

• Investigations

• Blood tests: erythrocyte sedimentation rate (ESR) and C-reactive protein (see Chapter 41 ‘Scientific tests’, p. 331).

• Biopsy of relevant tissue.

• Treatment

Depends on particular pattern of condition. Will include:

• Aminosalicylates.

• Sulfasalazine: this drug combines sulfapyridine and an aminosalicylate. Both are poorly absorbed as systemic anti-inflammatories but as this combination is being used to reduce the inflammation of the gut lining the treatment can be very effective.

• Corticosteroids: see Chapter 30 ‘Inflammation and the immune system’ (p. 230).

• Immunomodulators: see Chapter 30 ‘Inflammation and the immune system’ (p. 232).

• Chronic Crohn’s Disease

If the pharmacological intervention is unsuccessful then surgery is necessary.

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