Gastrointestinal disease

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6 Gastrointestinal disease

Questions

Please explain the role of the sympathetic nervous system in the gastrointestinal tract.

What is the difference between a submandibular salivary gland swelling and swelling of a salivary lymph node?

How does Barrett’s oesophagus develop?

Is it recommended to treat asymptomatic endoscopically diagnosed reflux oesophagitis with acid suppression and/or antireflux measures?

Is it recommended to give a young patient, diagnosed endoscopically to have mild reflux oesophagitis, life-long proton pump inhibitors (PPIs) to prevent the development of Barrett’s oesophagitis?

Is it safe to give a patient with reflux oesophagitis who is on proton pump inhibitors (PPIs) for treatment of acid suppression, aspirin in antiplatelet doses (75–325 mg per day)?

Does a combination of magnesium and aluminium hydroxide salts, taken as antacid for reflux oesophagitis, have serious long-term adverse effects?

In the treatment of reflux oesophagitis with a proton pump inhibitor (PPI), should the PPI be life long or given for 4–8 weeks, as mentioned by the drug manufacturers?

Would a patient who suffers with reflux oesophagitis as a result of a hiatus hernia, and who is not responsive to proton pump inhibitors (PPIs), benefit from a highly selective vagotomy?

1. What are the causes of belching and what appropriate drug can be used?

2. What are the effects of smoking on the gastrointestinal tract and what is its role in peptic ulcer disease?

Dear authors, why are gastric ulcers more common along the lesser curve, near the pylorus of the stomach?

What is the best time of day to administer omeprazole, and why?

Is it safe to use the drugs omeprazole and ranitidine during pregnancy?

Are non-steroidal anti-inflammatory drugs harmful to the stomach when taken parenterally, for example by intravenous or intramuscular routes?

Is it safe to give a patient with a past history of bleeding peptic ulcer aspirin in an antiplatelet dose of 75–325 mg?

Is sulpiride effective in the treatment of a peptic ulcer or gastro-oesophageal reflux disease (GORD)?

Is clopidogrel gentle on the stomach?

Is there a drug interaction between non-steroidal anti-inflammatory drugs (NSAIDs) and proton pump inhibitors (PPIs)?

Do antacids enhance mucosal resistance in the gastric mucosa? If so, please indicate the mechanism.

Is there a drug interaction between antacids and H₂-receptor blockers?

Does the combination of aluminium and magnesium hydroxide, given as an antacid, decrease the absorption of omeprazole if these are co-administered to help relieve heartburn quickly?

Should proton pump inhibitors be used with caution in patients with renal impairment?

Has cisapride been withdrawn from the market because of the danger of ventricular fibrillation?

In peptic ulcer disease:

1. What are the indications for an upper gastrointestinal endoscopy?

2. As this is an invasive procedure, is an oesophagogastroduodenoscopy (OGD) or barium meal X-ray preferable?

Is telithromycin as, or more, effective than clarithromycin in the treatment of Helicobacter pylori? If so, what is the recommended dosage and how long should treatment be continued?

Currently favoured regimens for eradication of Helicobacter pylori are triple therapy with a proton pump inhibitor along with two antibiotics for 1 week. For example:

• Omeprazole 20mg + metronidazole 400mg and clarithromycin 500mg (all twice daily).

• Omeprazole 20mg + clarithromycin 500mg and amoxicillin 1g (all twice daily).

Resistance to amoxicillin has not yet been demonstrated.

Previously, regimens such as omeprazole, metronidazole, amoxicillin and clarithromycin were recommended; are these regimens no longer used? The reason behind this question is the ‘sky-high’ cost of clarithromycin in Pakistan, which is inversely proportional to patient compliance (that is, low-cost regimens tend to have a higher rate of compliance).

What is the difference between the management of a gastric and of a duodenal ulcer?

How does omeprazole suppress Helicobacter pylori?

Does omeprazole cause rebound hyperacidity? Does this also apply to H₂-blockers?

On (K&C 7e, p. 249), you state that the postsynaptic neurotransmitter that inhibits the relaxation of lower oesophageal sphincter (LOS) is nitric oxide (NO). I have understood NO to promote relaxation of LOS by acting on the non-adrenergic, non-cholinergic (NANC) inhibitory neurones, which inhibits the action of cholinergic excitatory neurones. Could you please explain this paradox?

It is stated that nitric oxide (NO) inhibits the relaxation of the lower oesophageal sphincter (LOS) and that sildenafil is given for treating achalasia. As far as I know, sildenafil acts to increase the guanine monophosphate (GMP), just as NO uses the same mechanism to relax the LOS. Could you explain this paradox?

In Kumar and Clark Clinical Medicine you mention that auscultation is not important in cases of gastrointestinal disorders, but Harrison’s Principles of Internal Medicine gives this as being of equal importance because succussion splash and bowel sounds can help in presumptive diagnosis. Succussion splash indicates gastric obstruction (e.g. gastroparesis) and likewise bowel sounds can help determine the status of developing ileus. Would you agree that this is therefore a diagnostic tool?

Is it hazardous to give aspirin in the antiplatelet doses (75–325 mg/day) to a patient with a past history of haematemesis proved to be from a peptic ulcer?

How can upper gastrointestinal (GI) bleeding be distinguished from lower GI bleeding by using faecal analysis?

In upper gastrointestinal bleeding, without knowing the cause or source of bleeding, why do we give proton pump inhibitors (PPIs, e.g. omeprazole)? What is the role of these, if the source of bleeding is not peptic or duodenal ulcer?

Why is the incidence of coeliac disease increasing in many countries?

Are small amounts of gluten harmful to a patient with coeliac disease?

I refer to the treatment of complications related to diverticular disease. Under ‘bleeding’ you mention that ‘Persistent bleeding can often be arrested by undertaking an “instant” barium enema, which acts to plug the offending diverticulum’. When I mentioned this to my consultant he said he had never heard of this. Could you clarify how this would work and where I could obtain more information?

In children with abdominal pain and fever, does a white cell count help establish a diagnosis of appendicitis?

I have always been taught that ulcerative colitis only affects the large bowel with some associated proctitis. I read in your chapter on gastrointestinal disease that it can cause mouth ulcers and am now confused.

In pseudomembranous colitis, what is the first treatment of choice, metronidazole or vancomycin?

Is Crohn’s disease considered as an autoimmune disease. If it is, are there other predisposing factors to it other than genetics? If it is not, what is its nature?

Why does carcinoma of the ascending colon cause more anaemia than obstruction, and carcinoma of the descending colon more obstruction features and less anaemia?

Can you explain why a patient with colorectal carcinoma might present with diarrhoea and abdominal pain?

What causes the blood to be altered in the presentation of melaena: is it intestinal juice?

What is the differential diagnosis of multiple rectal ulcers in an 18-year-old female?

What is the best surgical technique in a chronic (2–3 years) painful anal fissure that is located sagittally posteriorly?

Can I make a diagnosis of irritable bowel syndrome (IBS) in a 40-year-old female patient without doing gastrointestinal investigations?

What is the cause of abdominal bloating, which is often a symptom in patients with irritable bowel syndrome (IBS)?

1. Where is the Traub’s area situated anatomically?

2. What does it mean if it is dull on percussion?

3. What is the proper way to percuss this area?

In general, it is claimed that only water and some salts are absorbed in the large gut, whereas the small gut is practically free of bacteria (which are present only in the large gut). In a patient on broad-spectrum antibiotics, bleeding can occur as a result of vitamin K deficiency. If the flora synthesizing vitamin K is disturbed, how can vitamin deficiency occur when the large gut is not supposed to absorb? How can this be due to a change in bacterial flora?

Why does colonic cancer more commonly occur on the left rather than the right side of the colon?

How much more likely are patients with reflux oesophagitis to develop cancer of the oesophagus than normal people and does aggressive treatment with H2-blockers or proton pump inhibitors nullify this increased risk?

In Crohn’s disease localized to the ileum there are long-term side effects and pros and cons of drug therapy. Is ileal resection a better option (if Crohn’s disease is localized to the ileum) than long-term medicine therapy which risks complicating lymphoma of the ileum?

Sympathetic fibres are distributed along the entire length of the gut; the stimulation or inhibition of these plays a role in many aspects of gut motility. Increased sympathetic stimulation produces the well-known anxiety symptoms, for example before exams when increased stimulation produces diarrhoea.

The salivary lymph glands are part of the superficial lymphatic drainage of the neck; enlargement occurs in infection and in malignant disease. The submandibular gland is swollen if there is blockage of the duct or if a tumour is present. It can also be affected by the mumps virus, although parotid involvement is more common.

Barrett’s oesophagus is defined as areas of columnar epithelium with intestinal metaplasia extending upwards in the lower oesophagus replacing the normal squamous epithelium. It is due to chronic gastro-oesophageal reflux.

No, it is not recommended to treat asymptomatic reflux oesophagitis. However, many gastroenterologists do treat it in the hope that long-term complications (e.g. stricture, Barrett’s and cancer) can be averted.

No, there is no indication to give long-term PPIs in patients with mild reflux oesophagitis; there is no evidence that this prevents the development of Barrett’s.

Yes, it is safe to give aspirin to a patient already on a PPI, which is – of course – cytoprotective.

No, there are no serious long-term adverse effects. Usually, however, in patients who require long-term treatment, an H₂-receptor antagonist or a proton pump inhibitor is used.

Patients with reflux oesophagitis usually have a low lower oesophageal sphincter pressure, so that reflux is a permanent event. After stopping PPIs, the symptoms return and life-long therapy may be necessary. Some would regard this as an indication for surgery.

No. A highly selective vagotomy will only do the same as the PPIs, that is, reduce the acid output. Try increasing the dose of the PPI to twice daily.

1. Belching is due to swallowing air. It is often picked up as a habit and it is not usually associated with pathology. Occasionally, patients who have upper gastrointestinal symptoms, such as heartburn or abdominal discomfort, swallow air in an attempt to ease their symptoms, and end up belching. Treatment can be difficult; no drugs are effective.

2. Smoking impairs the healing of peptic ulcer disease and also makes gastro-oesophageal reflux worse. It is also associated with relapse in patients with Crohn’s disease (but not in ulcerative colitis) therefore all patients with Crohn’s should be encouraged to stop smoking.

There is no definitive reason why gastric ulcers are more common on the lesser curve. They are usually just distal to the transitional zone between the body (acid-secreting mucosa) and antrum (non-acid-secreting mucosa). Reflux of bile and other duodenal contents into the stomach is thought to play a role.

Either morning or evening. It has a prolonged action so that the effect lasts over 24 hours.

Neither drug is recommended in pregnancy, but ranitidine is probably safe. No drug should be used in pregnancy unless absolutely essential.

Yes; the inhibition of gastric mucosal cyclo-oxygenase (COX) activity is a systemic effect.

A patient with a bleeding peptic ulcer, which is usually due to Helicobacter pylori, should have eradication therapy. In the case of a bleeding ulcer, eradication must be checked with a ¹³C urea breath test or a stool antigen test. When eradication has been shown to be successful, it is safe to use low-dose aspirin. (Note: patients with and without a history of ulcers can bleed even with low-dose aspirin.)

Sulpiride is not used. It does have an antimuscarinic action, which would reduce acid production, but in GORD this is offset by a reduction in lower oesophageal sphincter tone. It is therefore not useful in peptic ulcer or GORD.

Clopidogrel does cause dyspepsia and abdominal pain, and it can lead to gastrointestinal bleeding. So, is it ‘gentle’? The answer must be ‘No’.

There is no drug interaction. Indeed, PPIs are used as mucosal cytoprotective agents in patients on NSAIDs.

If, by antacids, you mean aluminium hydroxide or magnesium trisilicate the answer is ‘Yes’, but only in very large doses. They work by neutralizing acid, which in turn makes the mucosa more resistant to damage. A proton pump inhibitor is more practical.

No, but there is little point in using both except for immediate symptom relief, e.g. with an alginate containing antacid in gastro-oesophageal reflux disease (GORD).

Omeprazole is formulated as enteric-coated granules and is absorbed in the small intestine. Antacids therefore have no effect on its absorption.

Yes, it increases the Q-Tc interval.

1. Endoscopy is used in:

• Gastric ulcer: for diagnosis and to take biopsies to exclude malignancy; it is also used for follow-up of gastric ulcers.

• Duodenal ulcer: for diagnosis, although in young patients with Helicobacter pylori antibodies and typical history endoscopy is not necessary.

2. Good double-contrast barium meals are comparable to endoscopy but as biopsies cannot be taken (e.g. for H. pylori and malignancy), their use is becoming less frequent.

Telithromycin is a newly introduced macrolide and should be effective in H. pylori eradication regimens, 800mg × 2 daily. However, you are always better to stick to the tried and tested – in this case the macrolide clarithromycin – until the evidence changes.

The problem is metronidazole resistance, which runs at 50% at least and is probably higher in some areas. The other problem is the cost, as you say. It might be reasonable in your country to try omeprazole, metronidazole, amoxicillin and use clarithromycin instead of metronidazole for treatment failures. Tetracycline has been used in combination regimens it is also cheap and is a possible alternative to clarithromycin.

Most duodenal ulcers and 80% of gastric ulcers are due to Helicobacter pylori infection. Eradication therapy of the organism is the same. It is usual to check that a gastric ulcer has healed (thereby excluding a malignant ulcer) by doing repeat gastroscopy; this is not necessary for duodenal ulcers.

In vitro, omeprazole inhibits the growth of H. pylori below pH 7. Clinically, it is thought that omeprazole enhances the local immune response by increasing intragastric pH. It also reduces the washout of antibiotics from the mucosa and lowers the inhibitory concentrations of pH-sensitive antibiotics.

Rebound increased acid secretion lasting about 2 months occurs after 40mg a day of omeprazole for 2 days. Yes, rebound hyperacidity also occurs after withdrawing histamine H₂-receptor antagonists.

The LOS is tonically closed at rest. This resting tone is maintained by both myogenic properties and active tonic neural excitation. The reduction in tone and reduction of the LOS that occurs with swallowing is under the control of cholinergic and NANC neurones. As you say, NO acts on the NANC inhibitory neurones, which inhibit the excitatory cholinergic neurones, thus reducing acetylcholine release.

In achalasia there is a selective loss of the inhibitory neurones in the myenteric plexus. This leads to excitation of the smooth muscle at the LOS by mediators such as acetylcholine. Sildenafil increases NO production. It is the NO-containing neurones that are particularly affected in achalasia so that relaxation of the sphincter is impaired.

In practice, outside the emergency room or postoperatively (looking for ileus), bowel sounds are not helpful. A succussion splash can indicate gastric obstruction but is seldom helpful in practice.

Any patient who has bled from a peptic ulcer – and who is therefore presumably Helicobacter pylori (HP) positive – should have eradication therapy. Successful eradication of HP following a bleed must be checked with either an HP breath test or a stool test. After eradication, the same risks of aspirin therapy apply as to the normal population.

There are no reliable ways of distinguishing lower from upper gastrointestinal bleeding by faecal analysis. Obviously bright red blood suggests lower GI bleeding – except when blood loss is huge, when blood loss from higher up can be bright red blood. Altered blood, e.g. a melaena stool, is from lesions proximal to the caecum.

Approximately 50% of cases of GI bleeding are from peptic ulcer disease, and a PPI (e.g. omeprazole) reduces the rate of recurrent bleeding and the need for surgery. In many patients it is initially unclear where the bleeding is coming from, so PPIs tend to be given to everybody even though they have never been shown to be of value in, for example, variceal bleeding.

The answer is that we have better serological screening tests, e.g. tissue transglutaminase and endomysial antibodies, which are now being used extensively. The general awareness of coeliac disease has also increased.

Theoretically, yes! However, even a gluten-free diet has very tiny amounts of gluten and probably these small amounts are not overtly harmful in most patients. A few patients might be very sensitive.

This is anecdotal data and is probably incorrect; often the bleeding stops spontaneously. We have decided to remove this anecdotal piece of advice from future editions.

Between 70 and 90% of patients with appendicitis have a raised white cell count > 15000. This has a sensitivity of 20–60%, with a specificity of 85–100% in children with appendicitis. Imaging (e.g. ultrasound and computed tomography) should now be used to make a diagnosis of appendicitis.

You have been correctly taught. Ulcerative colitis (UC) only affects the large bowel, i.e. the colon and rectum, with a small number of patients having some inflammation of the very distal part of the ileum (called backwash ileitis). This distinguishes UC from Crohn’s disease, which affects anywhere from the mouth to the anus, most commonly the small and large bowel. Both diseases are, however, associated with ‘non-specific’ mouth ulcers, which also occur in a number of gastrointestinal diseases (e.g. coeliac disease) and other conditions (e.g. Behçet’s disease).

Metronidazole is the first choice, largely due to the cost of oral vancomycin.

Crohn’s disease is not usually considered to be an autoimmune disease, although the immune system is very involved in the pathological process. We do not know the exact cause of Crohn’s disease but it is felt by most that some aetiological agent (perhaps a bacterium?) stimulates the immune system to over-respond in a genetically susceptible person. CARD 15 gene mutations contribute to disease susceptibility.

Further reading

Podolsky D (2002) Inflammatory bowel disease. New England Journal of Medicine347: 417–429.

Carcinoma of the caecum and ascending colon tend to bleed and cause anaemia but not obstruction because of the large size and ‘give’ in the right side of the colon. The reverse is true of the descending colon; a carcinoma is more likely to obstruct the smaller, more rigid left colon.

Very often, the symptoms are not related and the colorectal cancer is found incidentally when a patient is investigated for pain or diarrhoea. Right-sided colonic lesions do not usually produce gut symptoms. Lesions in the sigmoid do, probably by partial obstruction.

No; it is bacteria.

Multiple rectal ulcers are common in inflammatory bowel disease. They also occur in infective proctitis (e.g. due to amoebae) or in sexually transmitted infections (e.g. herpes viral infections). Rectal spread occurs in gonococcal infection and can produce ulcers. The answer is to take samples for cultures and biopsies for histological diagnosis.

A lateral internal sphincterotomy is the best surgical procedure. This is the advice of the American Gastroenterological Association (AGA) in its Medical Position Statement 2002.

You must first make sure that there are no ‘alarm’ symptoms (Box 6.1). Take a very careful history because most patients of this age with IBS will have a preceding history of IBS. Simple blood tests and a follow-up of the patient are also very helpful in the diagnosis.

Box 6.1 Alarm symptoms: indications for upper gastrointestinal endoscopy

• Weight loss

• Protracted vomiting

• Haematemesis or malaena

This is difficult to answer! We agree this is a very common symptom. It is not due to air/wind, which most patients think.

Traub’s space is an area of resonance overlying the gas bubble in the left lateral hemithorax. Its size and localization depend on the contents and position of the stomach. Percuss with the patient on his or her right side.

Small amounts of menaquinones (a form of vitamin K), which are synthesized by bacteria, are absorbed in the colon.

It is true that 55–60% of colonic tumours occur on the left side; this figure includes rectal cancers (20%). There is no convincing reason for this; suggestions include faecal stasis on the left side and mucosal deficiencies at a cellular level.

Patients with weekly reflux symptoms are nearly eight times more likely to develop adenocarcinoma compared with those without symptoms. The greater the frequency, severity and duration of reflux symptoms, the greater the risk (Lagergren et al. 1999). The risk is unaffected by drug therapy as far as we know, but proton pump inhibitors (PPIs) are usually given.

Lagergren J et al. (1999) Symptomatic gastroesophageal reflux as a risk factor for esophageal adenocarcinoma. New England Journal of Medicine340: 825–831.

Not necessarily better as, of course, Crohn’s disease often recurs after surgery. It is, however, a useful treatment particularly if localized pain in the right iliac fossa (due to partial obstruction) is a prominent symptom.

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