Gastro-oesophageal reflux disease and dyspepsia

GORD and dyspepsia: heartburn, reflux and indigestion in AU practice

GORD — gastro-oesophageal reflux disease — is symptomatic reflux of stomach acid into the oesophagus. Functional dyspepsia (epigastric discomfort, early satiety, bloating) affects roughly one-in-four Australians. Most cases improve with lifestyle change and a short course of a proton-pump inhibitor taken correctly: 30 minutes before breakfast.

Alarm features — unintentional weight loss, difficulty swallowing, iron-deficiency anaemia, persistent vomiting, or new symptoms in anyone over 55 — require urgent investigation rather than a trial of treatment.

Gastro-oesophageal reflux disease (GORD) and dyspepsia are among the most common reasons Australians visit their GP. Approximately 15% of Australian adults experience heartburn at least weekly, and up to one-in-four report significant upper abdominal discomfort each year. Most cases are manageable with straightforward treatment; a smaller number carry symptoms that need prompt investigation.

Understanding the difference between mechanical reflux, functional dyspepsia, and rarer but serious causes helps people make sense of their symptoms and work effectively with their general practitioner.

A. Core clinical — the AU general-practice framework

What drives GORD

The lower oesophageal sphincter (LOS) is a muscular valve between the food pipe and the stomach. When it relaxes inappropriately — or when increased abdominal pressure overwhelms it — stomach acid and digestive contents splash back into the oesophagus. This causes the burning sensation (heartburn) rising from the stomach into the chest, and the bitter or sour taste of regurgitation.

Common contributors include: excess body weight, a hiatus hernia (part of the stomach slides above the diaphragm), large or late meals, lying flat soon after eating, alcohol, smoking, and certain medications. NSAIDs, bisphosphonates, calcium-channel blockers, nitrates, theophylline, and some antidepressants can worsen reflux directly. Pregnancy causes GORD in up to 80% of women during the third trimester, through progesterone relaxing the LOS and physical pressure from the growing uterus.

How dyspepsia fits in

Dyspepsia means upper abdominal symptoms — epigastric pain, bloating, postprandial fullness, early satiety, nausea — without necessarily involving acid reflux. Therapeutic Guidelines (eTG) classifies it as:

  • Functional dyspepsia (Rome IV criteria) — symptoms present for at least three months with no structural explanation found on investigation. This accounts for roughly 70% of dyspepsia cases seen in general practice.
  • Organic dyspepsia — caused by peptic ulcer disease, H. pylori gastritis, NSAID injury, upper GI malignancy, or biliary and pancreatic disease.

GORD and functional dyspepsia frequently co-exist. A structured history and targeted investigation separates them in most cases.

The history your GP takes

A careful account of symptoms shapes every management decision. Key areas to cover include:

  • Character — heartburn (retrosternal burning), regurgitation (acid taste rising into the mouth), versus upper abdominal pain or bloating centred below the breastbone
  • Timing — after meals, nocturnal, worsened lying flat or bending
  • Duration — recent onset versus months to years of symptoms
  • Triggers — specific foods, alcohol, stress, posture changes
  • Alarm features — any of the ALARM criteria (listed in the escalation section below)
  • Medication review — NSAIDs, aspirin, bisphosphonates, and many other common drugs can cause or worsen both conditions
  • Smoking and alcohol history — both directly impair LOS function
  • Weight change — relevant both as a GORD contributor and as a red flag if loss is unintentional

Investigations — when and what

For straightforward GORD or dyspepsia in a person under 55 without alarm features, RACGP guidelines support a clinical diagnosis and trial of treatment without upfront endoscopy.

Recommended tests in general practice:

  • H. pylori testing — urea breath test (Medicare-rebatable) or stool antigen test; indicated in dyspepsia under 55 without alarm features, or when peptic ulcer disease is suspected. Stop PPI at least two weeks, and antibiotics at least four weeks, before testing — otherwise results can be falsely negative.
  • Full blood count and iron studies — to screen for iron-deficiency anaemia, which may indicate occult upper GI bleeding.
  • Liver function tests — when biliary or pancreatic disease is part of the clinical picture.

Second-line investigations when symptoms are refractory or alarm features are present:

  • Gastroscopy — direct visualisation of the oesophageal and gastric lining, allowing biopsy and rapid urease testing for H. pylori.
  • 24-hour oesophageal pH-impedance monitoring — for refractory non-erosive reflux where the diagnosis remains uncertain.
  • Oesophageal manometry — when dysphagia or a suspected motility disorder needs characterisation.
  • Abdominal ultrasound — for suspected biliary or pancreatic pathology.

B. First-line management — lifestyle, PPIs, and H. pylori

Lifestyle changes

The lifestyle measures with the strongest evidence per eTG and Ness-Jensen et al. (2013) are:

  • Weight loss in those who are overweight — even 5–10% body weight reduction reduces reflux frequency by lowering intra-abdominal pressure
  • Avoiding large or late meals — eat at least three hours before lying down
  • Elevating the head of the bed by 15–20 cm — using a block or wedge under the bedhead, not extra pillows (which bend the neck rather than tilt the torso and do not reduce reflux)
  • Stopping smoking — nicotine relaxes the LOS and impairs oesophageal clearance
  • Moderating alcohol — alcohol relaxes the LOS, delays gastric emptying, and directly irritates the oesophageal lining
  • Individual trigger avoidance — common offenders include fatty or spicy food, coffee, mint, chocolate, and carbonated drinks, but these vary between individuals; a food and symptom diary is more useful than blanket exclusion

Left-side sleeping reduces nocturnal reflux more effectively than right-side sleeping, because stomach anatomy keeps acid away from the lower oesophageal junction in this position.

Proton-pump inhibitors (PPIs)

PPIs — omeprazole, esomeprazole, pantoprazole, rabeprazole, lansoprazole — are the most effective acid-suppressing medications available. They work by irreversibly blocking the hydrogen-potassium ATPase pump in parietal cells. To work properly they must be taken 30 minutes before the first meal of the day, when parietal cells are activated by food and ready to be inhibited.

Per Australian Medicines Handbook (AMH), standard dosing is four to eight weeks at the approved dose. After symptom resolution, the aim is to step down to the lowest effective dose — including on-demand use — and discontinue if symptoms do not return.

Long-term PPI use is appropriate in Barrett’s oesophagus, severe erosive oesophagitis (Los Angeles grade C or D confirmed on gastroscopy), or when NSAIDs must be continued long-term in patients at high risk of upper GI bleeding. For everyone else, an annual review of the ongoing need and dose is recommended by the Gastroenterological Society of Australia (GESA).

Monitoring on long-term PPI use should include:

  • Annual vitamin B12 — long-term acid suppression impairs B12 absorption from food
  • Magnesium level — hypomagnesaemia can occur with long-term use, causing cramps, tremor, or seizures
  • Bone density awareness — a modest fracture signal exists, relevant when other osteoporosis risk factors are present
  • Drug interactions — clopidogrel interaction is relevant; pantoprazole or lansoprazole are preferred when clopidogrel is co-prescribed

H2 receptor antagonists

Famotidine (20–40 mg twice daily or at night) is the main H2RA available in Australia following the withdrawal of ranitidine. The TGA withdrew ranitidine from the Australian market in 2020 due to NDMA contamination and it is no longer available. Famotidine is less effective than PPIs for erosive disease but is safe in pregnancy and useful as step-down therapy or for breakthrough nocturnal symptoms added to a morning PPI.

Alginate preparations (for example, Gaviscon) form a physical raft over gastric contents, providing symptomatic relief. They are safe in pregnancy and useful as needed alongside other medications.

H. pylori eradication

Testing and treating H. pylori in dyspepsia under 55 without alarm features is an eTG-endorsed strategy: eradication resolves H. pylori-associated peptic ulcer disease and provides modest reduction in functional dyspepsia symptoms. Standard eradication is a seven-day triple-therapy course: PPI plus amoxicillin plus clarithromycin (available as the combination PBS-listed pack Klacid HP7). A test-of-cure urea breath test is performed at least four weeks after completing the antibiotic course, with PPI stopped at least two weeks beforehand to avoid a false-negative result.

C. Beyond heartburn — atypical presentations and Barrett’s oesophagus

Extra-oesophageal GORD

Acid reflux does not always present as heartburn. Up to 40% of people with GORD have extra-oesophageal manifestations that may be the dominant feature:

  • Chronic cough — especially nocturnal, worse when lying flat; often misattributed to post-nasal drip or asthma
  • Hoarse voice (laryngopharyngeal reflux) — morning hoarseness, frequent throat-clearing, globus (persistent lump-in-throat sensation)
  • Asthma exacerbation — acid micro-aspiration triggers bronchospasm in susceptible individuals
  • Dental erosion — acid exposure creates a characteristic pattern of erosion on the palatal surfaces of upper teeth

When reflux is suspected as the driver of chronic cough that has not responded to standard treatment, a 24-hour pH-impedance study or an empirical high-dose PPI trial (twice daily for eight to twelve weeks) can confirm or exclude the diagnosis before further investigation.

Functional dyspepsia

When gastroscopy, H. pylori testing, and basic bloods are normal, the diagnosis is functional dyspepsia per Rome IV criteria. The Rome IV framework distinguishes two subtypes:

  • Postprandial distress syndrome (PDS) — meal-induced early satiety and postprandial fullness occurring most days
  • Epigastric pain syndrome (EPS) — epigastric burning or pain unrelated to meals

Treatment options with evidence include: low-dose tricyclic antidepressant (amitriptyline 10–25 mg at night) for visceral hypersensitivity; buspirone or mirtazapine for early satiety driven by impaired gastric accommodation; and psychological therapies — cognitive behavioural therapy and gut-directed hypnotherapy — accessed through a Mental Health Treatment Plan.

The herbal preparation Iberogast (STW-5) has some evidence for functional dyspepsia symptom relief, but the GESA notes hepatotoxicity reports in the literature and advises discussing use with your GP before starting.

Barrett’s oesophagus and surveillance

Barrett’s oesophagus — intestinal metaplasia replacing the lower oesophageal squamous lining — occurs in about 1–2% of adults and is the main precursor to oesophageal adenocarcinoma. Per GESA Barrett’s surveillance guidelines, surveillance gastroscopy intervals are:

  • Non-dysplastic short-segment Barrett’s (under 3 cm): every three to five years
  • Non-dysplastic long-segment Barrett’s (3 cm or more): every two to three years
  • Low-grade dysplasia: six-monthly surveillance or consideration of endoscopic ablation
  • High-grade dysplasia: referral for endoscopic mucosal resection or radiofrequency ablation at a specialist centre

Long-term PPI use is standard care for Barrett’s, as sustained acid suppression reduces the rate of dysplastic change over time.

D. Australian operations

Medications and access

All five PBS-listed PPIs (omeprazole, esomeprazole, pantoprazole, rabeprazole, lansoprazole) are available at standard PBS co-payment for GORD and peptic ulcer disease without Authority. H2 receptor antagonists (famotidine) are also PBS-listed. The Klacid HP7 H. pylori eradication combination pack is PBS Authority Required (Streamlined) for confirmed peptic ulcer or test-positive dyspepsia. All subsidised medications are listed and searchable on the PBS website.

H. pylori urea breath testing (Medicare) and stool antigen testing are both Medicare-rebatable. Full blood count, iron studies, and liver function tests are bulk-billed under standard Medicare pathology items.

Alginate products and antacid combinations are available without prescription from pharmacies and are not PBS-listed.

GP care planning

Chronic GORD with significant comorbidities — such as obesity with reflux, co-existing obstructive sleep apnoea, or asthma worsened by reflux — may qualify for a GP Chronic Condition Management Plan (GPCCMP, MBS items 965 and 967), enabling referrals to dietitians and exercise physiologists with Medicare subsidy.

Australian consumer resources

E. Special populations

Pregnancy. Lifestyle measures and alginate (Gaviscon) are first-line in pregnancy — both are safe for the developing baby. Famotidine has well-established safety data in pregnancy. If a PPI is needed, omeprazole has the most accumulated safety data of the PPIs during pregnancy and is the usual choice.

Older adults. The risk of Clostridioides difficile infection, osteoporosis, and hypomagnesaemia associated with long-term PPI use is more clinically significant in older adults. In those also taking clopidogrel, pantoprazole or lansoprazole are preferred to reduce a potential CYP2C19 interaction. The TGA has withdrawn ranitidine; famotidine is the preferred H2RA.

People on NSAIDs or aspirin. Anyone taking regular NSAIDs or low-dose aspirin with additional upper GI risk factors — age over 70, prior peptic ulcer, co-prescription of corticosteroids or anticoagulants — should have a co-prescribed PPI. This is a well-supported safety practice, and prescribing software often flags it automatically.

Eosinophilic oesophagitis. This increasingly recognised condition — characterised by eosinophil infiltration of the oesophageal lining — presents with food bolus impaction or progressive dysphagia, particularly in younger atopic people, and does not respond to PPIs alone. Diagnosis requires biopsies taken at gastroscopy showing eosinophils ≥15 per high-power field. Treatment involves swallowed topical corticosteroids (budesonide or fluticasone), dietary modification, and in severe or refractory cases, dupilumab via specialist referral.

When to escalate

Seek same-day assessment (or present to your nearest emergency department) if you have:

  • Blood in vomit or vomit that looks like coffee grounds (haematemesis)
  • Black, tarry, foul-smelling stools (melaena — indicates upper GI bleeding)
  • Severe chest pain that could be cardiac in origin
  • Complete inability to swallow (possible food bolus impaction requiring emergency gastroscopy)

See your GP within one to two weeks if you have any ALARM features:

  • Anaemia — iron-deficiency anaemia not explained by menstrual loss
  • Loss of weight — unintentional
  • Anorexia — persistent loss of appetite
  • Recent onset of progressive symptoms in anyone aged 55 or over
  • Melaena or haematemesis
  • Dysphagia — difficulty swallowing food, or pain on swallowing

Other reasons to arrange prompt review include persistent vomiting, a palpable abdominal mass or enlarged lymph node, and a strong family history of gastric or oesophageal cancer.

If GORD or dyspepsia does not respond to two adequate trials of PPI at the correct dose and timing, refractory symptoms warrant specialist assessment — to confirm the diagnosis, check for eosinophilic oesophagitis, and review the treatment approach.

What this article is and is not

This article draws on current Australian general practice guidelines — Therapeutic Guidelines (eTG), Australian Medicines Handbook, RACGP resources, and Gastroenterological Society of Australia recommendations — to provide general health information about GORD and dyspepsia. It is not personal medical advice and does not create a doctor–patient relationship.

The decision about which medications are appropriate, how long to take them, and when further investigation is needed is made with your own GP or treating clinician based on your individual circumstances.

For consumer-friendly information: HealthDirect — reflux, Better Health Channel — heartburn, GESA patient resources.


Sources cited

  1. Therapeutic Guidelines (eTG) — Gastrointestinal: GORD and dyspepsia
  2. RACGP — GORD clinical resources
  3. Australian Medicines Handbook
  4. Gastroenterological Society of Australia (GESA)
  5. TGA — Ranitidine recall 2020
  6. PBS — Medicines subsidised in Australia
  7. HealthDirect — Reflux and GORD
  8. Better Health Channel — Heartburn
  9. Ness-Jensen E et al. — Lifestyle interventions in GORD (Aliment Pharmacol Ther 2013)

Frequently asked questions

  • How is GORD different from functional dyspepsia?

    GORD is reflux of stomach contents causing heartburn or regurgitation — acid moving up into the oesophagus. Functional dyspepsia is discomfort centred on the upper abdomen (epigastric pain, bloating, early satiety, nausea) with normal investigations. The two conditions overlap frequently, and many people have both. About 70% of dyspepsia is functional while the remaining 30% has an organic cause such as peptic ulcer disease, H. pylori gastritis, or upper GI malignancy. Your GP can usually distinguish them from the history and decide whether further testing is needed.

  • How long should I take a PPI?

    For an initial episode of GORD or dyspepsia, a four-to-eight-week course is standard. If symptoms settle, your GP will try stepping down to the lowest effective dose — sometimes switching to on-demand use (taking the tablet only on symptomatic days). Long-term PPI use is appropriate in specific situations: Barrett's oesophagus, severe erosive oesophagitis confirmed on gastroscopy, or ongoing NSAID use in those at high risk of upper GI bleeding. Indefinite use without review is worth discussing with your GP, as lower doses often suffice over time.

  • What lifestyle changes actually make a difference for reflux?

    The lifestyle measures with the strongest evidence for GORD are: weight loss if you are overweight, avoiding large or late meals (at least three hours before lying down), and elevating the head of the bed by 15–20 cm using a block or wedge under the bedhead — not extra pillows, which bend the neck rather than tilt the torso. Stopping smoking and moderating alcohol benefit reflux significantly. Trigger avoidance (fatty food, coffee, alcohol, mint, chocolate) is individual — a food and symptom diary is more useful than blanket exclusion lists.

  • What is H. pylori and do I need to be tested?

    Helicobacter pylori is a bacterium that colonises the stomach lining in about one-in-four Australians and causes chronic gastritis, peptic ulcers, and — rarely — gastric cancer or MALT lymphoma. Testing is recommended when you have dyspepsia and are under 55 without alarm features, when a peptic ulcer is confirmed, or when you have iron-deficiency anaemia without another clear cause. Testing is by urea breath test or stool antigen — both are accurate and Medicare-rebatable. You must stop your PPI for at least two weeks before the test. If positive, a one-week antibiotic course can eradicate the infection and resolve most ulcers.

  • When do I need a gastroscopy?

    A gastroscopy (camera into the oesophagus and stomach) is indicated when alarm features are present, when symptoms do not respond to an adequate PPI trial, or for surveillance of Barrett's oesophagus. Alarm features requiring prompt gastroscopy include: unintentional weight loss, progressive difficulty swallowing, vomiting blood or passing black tarry stools, iron-deficiency anaemia, and new persistent symptoms in anyone over 55. A routine gastroscopy for straightforward GORD without alarm features in a younger person has low diagnostic yield and is not recommended before a proper trial of lifestyle changes plus PPI.

  • What is Barrett's oesophagus and should I be worried?

    Barrett's oesophagus is a change in the lining of the lower oesophagus — normal squamous cells replaced by intestinal-type columnar cells — caused by long-term acid exposure. It is found in about 1–2% of adults. Barrett's itself is not cancer, but it carries a small lifetime risk (roughly 5%) of developing into oesophageal adenocarcinoma. For this reason, people with Barrett's have periodic surveillance gastroscopies — how often depends on the length of Barrett's tissue and whether precancerous changes (dysplasia) are present. Long-term PPI use and not smoking are the main strategies to reduce progression risk.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.