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Back to Basics: Digestive Diseases for the Family Physician

Dr. Jarrod Lee
Gastroenterologist and Advanced Endoscopist
gutCARE Singapore
Dr. Reuben Wong
Gastroenterologist
gutCARE Singapore
Dr. Chia Chung King
Dr. Mark Fernandes
Gastroenterologist and Hepatologist
gutCARE Singapore
20 Mar 2019
Consultants from the private gastroenterology group practice gutCARE, in its 3rd annual symposium in 2018, led GPs into back-to-back lectures, discussions, and interactive sessions on the basics of common digestive diseases in primary care, including pharmacological management and latest updates in gastroenterology.

Acid disorders
Acid secretion in the stomach depends on local (changes in pH, chemical stimuli), hormonal, and neural (parasympathetic and local reflexes) factors. Acetylcholine, gastrin, and histamine work synergistically to stimulate gastric acid secretion while somatostatin inhibits acid secretion.

The integrity of the upper GI tract depends on the balance between “hostile” factors (gastric acid, H. pylori, NSAIDs, and pepsin) and “protective” factors (prostaglandins, mucus, bicarbonate, and mucosal blood flow). A disruption in this balance results in acid disorders and predisposes patients to gastritis and peptic ulcer disease (PUD). Up to 25% of chronic NSAID users will develop PUD, of which 2-4% will bleed or perforate. The risk increases in older patients (>65 years), those with previous PUD, H. pylori infection, and those on concurrent steroid, aspirin, or anticoagulant use.

Antacids, histamine-2 receptor antagonists (H2RAs), and proton pump inhibitors (PPIs), neutralize or reduce gastric acid.  Antacids start to work in seconds, with effects lasting only 20–40 minutes, and do not stop acid production. H2RAs reduce gastric acid production by blocking the H2 receptors on the parietal cell. These drugs work in 15 minutes and are best used “on-demand”. Tolerance to H2RAs develops after 2 weeks.

PPIs are more potent acid suppressors than H2RAs and are currently the gold standard treatment for PUD. PPIs work by blocking acid pumps, the final pathway of acid secretion. PPIs should be taken 30–60 minutes before meals and usually take 5–7 days to take full effect.

Potassium competitive acid blockers (PCABs) are a new class of acid suppressants. Compared with PPIs, PCABs have faster onset of action, longer duration, and dosing is independent of meals. Vonoprazan, a PCAB, has been shown to be superior to PPIs for treatment of H. pylori and GERD.1,2

A good understanding of pharmacology will guide clinical decisions on the most suitable anti-acid medication for each patient.

Understanding Common
Small bowel diseases include gluten enteropathies (coeliac disease and non-coeliac gluten sensitivity (NCGS), and microbiota and malabsorption disorders. Patients with gluten disorders may have intestinal (unexplained chronic diarrhoea, bloating, abdominal distention, malabsorption) and extra-intestinal (iron and vitamin deficiency) manifestations.

Coeliac disease is triggered by ingestion of wheat, rye, and barley-derived gluten in genetically susceptible individuals. Diagnosis is made by antibody test. Genetic testing based on HLA alleles is available but not easily accessible in Singapore. Patients suspected of having coeliac disease can also be confirmed on gastroscopy, where there is scalloping of the small bowel lining. Biopsies are taken and scored using the Marsh score for severity. If positive, management includes life-long gluten-free diet, identifying nutritional deficiencies, access to support groups, and management by a medical team.

There’s also a significant population of patients with NCGS. Their antibody tests are negative, and there is no damage under a microscope, but they feel better on a gluten-free diet. It is important for GPs to make a correct diagnosis.

FODMAPs (fructans, oligosaccharides, disaccharides, monosaccharides, polyols) are sugars in food that are poorly digested, which are then acted upon by the local microflora to create symptoms like gas, bloating, stomach pain, diarrhoea, and constipation. At gutCARe, we do hydrogen-methane breath testing to confirm FODMAP malabsorption. Evidence showed a diet low in FODMAPs effectively reduced functional GI symptoms in IBS patients.3

Small intestinal bacterial overgrowth (SIBO) occurs when there is altered anatomy in the gut,  an underlying GI motility disorder (gastroparesis), or systemic disorders (systemic sclerosis, hypothyroidism), and commonly, chronic narcotic or PPI use which suppresses the gastric acid.4 Testing for SIBO includes the traditional small bowel aspiration and culture, and now the hydrogen methane breath testing which GPs can do and with reproducible results. Treatment usually involves the use of rifaximin, a minimally absorbed antibiotic with high luminal activity.

Constipation Haemorrhoids
Constipation can be classified as primary (functional) or secondary. Sometimes, functional constipation is also classified based on colon transit. Colon transit study is a useful investigation for constipation.

Treatment for constipation includes fibre (except in those with slow-transit constipation) which is cheap and easily accessible. Polyethylene glycol, given once daily, is effective in improving stool frequency and consistency; it may be combined with a stimulant laxative and is superior to lactulose. Lactulose is a synthetic disaccharide that requires 24–48 hours to take full effect. Senna, a stimulant laxative, is more natural and its long-term use does not cause structural or functional alteration of the intestinal muscle. Bisacodyl, another stimulant laxative, exerts motor effect through the mucosal afferent nerves. Prucalopride is a highly selective 5HT4 agonist that is useful for slow-transit constipation. Lubiprostone, a chloride channel agonist, accelerates intestinal transit, softens stools, and increases stool frequency. The guanylate cyclase-C receptor agonist, linaclotide, also stimulates intestinal fluid secretion and transit and is used for chronic idiopathic constipation and irritable bowel syndrome with constipation (IBS-C).

Treatment strategies for haemorrhoid include increased fibre and water intake, refraining from toilet straining, exercise, avoidance of medications that cause constipation or diarrhoea, and limiting intake of fatty food and alcohol. For inflammation or pruritus, warm sitz baths can be used, along with hydrocortisone suppositories and analgaesic cream, but not very often. Haemorrhoidectomy works for external haemorrhoid. Thrombosed haemorrhoids require conservative treatment unless pain is severe.  For those with larger haemorrhoids or haemorrhoids that are closed to the dentate line, the HET Bipolar System which uses gentle heat to occlude the blood supply, may be an option. When there is suspicion of upper GI bleed, there is definitive change of bowel habit, or if there are symptoms suggestive of colorectal cancer, the patient should be referred for colonoscopy.

Infectious Diarrhoea
Diarrhoea is the passage of >3 unformed stools in 24 hours.5 It can be acute (lasting ≤14 days), persistent (15–30 days), or chronic (>30 days). Acute diarrhoea of infectious aetiology can be secretory, osmotic, or inflammatory (dysentery), typified by blood in the stool.

Salmonella and Campylobacter are the most common bacterial pathogens identified in Singapore. Norovirus is the main cause of viral gastroenteritis and there is an increasing incidence of Clostridium difficile associated with prolonged use of antibiotics and hospitalization.

Secretory diarrhoea involves the movement of water and ions (ion-channel mediated) into the bowel lumen, resulting in watery diarrhoea that continues independent of food intake. Stool volume is >1 litre/day. Osmotic/malabsorptive diarrhoea is associated with fluid and food intake and the osmotic content of the intestinal lumen drawing fluid into the lumen. Inflammatory diarrhoea arises as a result of inflammation and necrosis of the intestinal mucosa.

The advent of molecular diagnostic tests has enabled greater sensitivity in determining the cause of diarrhoea in cases of dysentery, moderate-to-severe disease, and symptoms lasting >7 days.

Oral rehydration therapy (ORT) is the primary treatment for acute diarrhoeal infections. Patients can receive adjunctive loperamide or bismuth salicylates to control stool passage. Empiric antimicrobial therapy is not indicated for routine acute community-acquired diarrhoeal illness as the majority are likely to be viral.  However, antibiotics (either a quinolone or azithromycin) can be considered in cases of traveller’s diarrhoea.5
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