Acid-Related Disorders: Gastro-Oesophageal Reflux Disease and Peptic Ulcer Disease

Gastro oesophageal reflux disease and peptic ulcer disease both involve injury linked to stomach contents, but they affect different structures and have different causes. Reflux mainly affects the oesophagus, while peptic ulcers form in the stomach or duodenum. Most symptoms are manageable, but swallowing difficulty, bleeding, weight loss or persistent vomiting need prompt assessment.

What acid related disorders are The stomach produces hydrochloric acid and digestive enzymes to help process food. Its lining normally resists these substances through mucus, bicarbonate, blood flow and rapid cell repair. The oesophagus has less protection because it is designed mainly to transport swallowed material. Disease can develop when stomach contents reflux upwards or when stomach and duodenal protection is disrupted. Two different disease families Gastro oesophageal reflux disease is usually shortened to GORD. GORD involves troublesome reflux of stomach contents into the oesophagus. Peptic ulcer disease involves a deeper break in the lining of the stomach or duodenum. The conditions can coexist, but one does not automatically cause the other. The oesophagus The oesophagus is the muscular tube carrying food and drink from the throat to the stomach. Coordinated muscle contractions move swallowed material downwards. The lining is adapted to brief contact with food rather than repeated exposure to acid and digestive enzymes. The lower oesophageal sphincter The lower oesophageal sphincter is a zone of muscle near the junction between the oesophagus and stomach. It relaxes during swallowing so food can enter the stomach. It then contributes to a pressure barrier that limits movement back into the oesophagus. It is better understood as a functional pressure zone than a perfectly sealed one way valve. How reflux occurs Brief sphincter relaxation occurs normally, particularly after meals. GORD develops when reflux becomes frequent enough to cause troublesome symptoms or complications. Reduced sphincter pressure, transient relaxations and pressure within the abdomen can all contribute. Delayed stomach emptying and impaired oesophageal clearance can also increase exposure. Hiatus hernia The oesophagus passes through an opening in the diaphragm before joining the stomach. A hiatus hernia occurs when part of the stomach moves upwards through this opening. It can weaken the normal pressure barrier and make reflux more likely. Many people with a hiatus hernia have no symptoms, and not everyone with GORD has one. What reflux contains Refluxed material can contain acid, food, pepsin and sometimes bile. Acid is an important cause of irritation, but GORD is not always simply excessive acid production. A person can produce a normal amount of stomach acid yet experience repeated reflux into the wrong place. Heartburn Heartburn is a burning discomfort behind the breastbone that can rise towards the throat. It commonly occurs after meals, when bending or when lying down. The word heartburn does not mean that the heart is burning. Cardiac pain can resemble heartburn, so new or severe chest symptoms require appropriate assessment. Regurgitation Regurgitation is the effortless return of stomach contents into the throat or mouth. It can produce a sour or bitter taste. It differs from vomiting, which usually involves nausea and forceful abdominal contractions. Repeated regurgitation supports a reflux diagnosis but does not establish the cause alone. Other possible GORD symptoms Reflux can cause upper abdominal or lower chest discomfort. Some people report nausea, belching or a sensation of material rising. Chronic cough, throat clearing, hoarseness and dental erosion can be associated with reflux. These throat and respiratory symptoms have many other causes, so reflux should not be assumed automatically. Dyspepsia Dyspepsia is a broad clinical term often translated as indigestion. NICE includes recurrent upper abdominal pain, heartburn or acid regurgitation within uninvestigated dyspepsia. Bloating, nausea and vomiting may accompany it. Dyspepsia describes a symptom pattern rather than one disease. Functional dyspepsia Some people have persistent upper abdominal discomfort without an ulcer or another structural explanation on investigation. This is called functional dyspepsia. Changes in stomach sensitivity, movement and communication with the nervous system may contribute. It is a genuine disorder but is biologically different from peptic ulcer disease. What peptic ulcer disease is A peptic ulcer is a break in the stomach or duodenal lining extending deeper than a superficial erosion. A gastric ulcer forms in the stomach. A duodenal ulcer forms in the first part of the small intestine. The term peptic refers to injury occurring in an environment exposed to acid and digestive activity. Gastric and duodenal ulcers Gastric and duodenal ulcers share major causes but are not identical. Their cancer associations, follow up and surgical anatomy differ. A gastric ulcer may require repeat endoscopy to confirm healing and exclude malignant change. A typical duodenal ulcer is rarely cancerous, but its cause still needs treatment. The two dominant ulcer causes Helicobacter pylori infection and non steroidal anti inflammatory drugs are the two main causes of peptic ulcers. Some ulcers involve both factors. Smoking, severe physiological stress and uncommon acid producing disorders can contribute. Spicy food and ordinary stress do not usually create a true ulcer by themselves. Helicobacter pylori Helicobacter pylori is usually shortened to H. pylori. It is a bacterium adapted to live within the mucus layer of the stomach. The infection often begins in childhood and can persist for decades without treatment. Many infected people never develop symptoms or an ulcer. How H. pylori causes ulcers H. pylori produces chronic inflammation within the stomach lining. It can weaken mucosal protection and alter acid regulation. The exact effect depends on where inflammation is concentrated and how the person responds. This can promote gastric or duodenal ulcer formation. H. pylori and cancer risk Long standing H. pylori infection increases the risk of gastric cancer at population level. Most infected people do not develop cancer. Testing and eradication are important when clinically indicated, particularly in peptic ulcer disease. This association should not turn every positive test into a cancer diagnosis. H. pylori and GORD are different H. pylori infects the stomach lining and is an important cause of peptic ulcer disease. It is not the usual cause of lower oesophageal sphincter dysfunction or GORD. Eradication is prescribed for confirmed infection when indicated rather than as general reflux treatment. Separate reflux symptoms can continue after successful eradication. Non steroidal anti inflammatory drugs Non steroidal anti inflammatory drugs are usually shortened to NSAIDs. Examples include ibuprofen, naproxen and diclofenac. They reduce pain and inflammation by inhibiting cyclo oxygenase enzymes. This also reduces protective prostaglandins within the stomach and duodenum. How NSAIDs injure the lining Protective prostaglandins support mucus, bicarbonate and mucosal blood flow. Reducing them makes the lining more vulnerable to acid and digestive enzymes. An ulcer can develop without much warning pain. NSAIDs also impair platelet function to different degrees, increasing the impact of bleeding. Who has greater NSAID risk Risk increases with previous ulcer or gastrointestinal bleeding. Older age, higher NSAID doses and use of more than one NSAID increase risk. Anticoagulants, antiplatelet medicines, corticosteroids and some antidepressants can add bleeding risk. The individual need for the NSAID and protective treatment should be reviewed. Aspirin Low dose aspirin is an antiplatelet medicine rather than an ordinary pain dose. It can still contribute to ulceration and upper gastrointestinal bleeding. A person taking aspirin for cardiovascular protection should not stop it independently after dyspepsia or suspected bleeding. Urgent clinicians balance bleeding control against heart and stroke risk. Less common ulcer causes Critical illness can produce stress related mucosal injury in hospitalised people. Crohn's disease, cancer and some infections can mimic or cause ulceration. Zollinger Ellison syndrome causes excessive acid production from a gastrin secreting tumour but is rare. An ulcer that does not heal requires review for missed H. pylori, continued NSAID exposure, poor adherence and uncommon causes. Ulcer symptoms Peptic ulcer disease can cause burning, gnawing or aching upper abdominal pain. Nausea, early fullness and bloating can occur. Some people have no recognised symptoms until bleeding or perforation develops. Symptoms cannot reliably identify whether an ulcer is gastric or duodenal. Meal related pain is not a diagnostic rule Traditional descriptions link gastric ulcer pain with eating and duodenal ulcer pain with hunger or night time symptoms. Real presentations overlap considerably. Food response does not confirm ulcer location or distinguish an ulcer from functional dyspepsia. Endoscopy is required when structural diagnosis matters. GORD and ulcer disease can feel similar Both can cause upper abdominal or lower chest discomfort. GORD more characteristically causes heartburn and regurgitation. Ulcer disease more often causes epigastric pain, bleeding or anaemia. These are tendencies rather than reliable diagnostic boundaries. Symptoms do not show severity reliably Severe heartburn can occur without visible oesophagitis. Severe oesophagitis can occasionally cause modest symptoms. A large ulcer may be painless until it bleeds. Clinical decisions therefore consider warning features, medicines, tests and response to treatment. Clinical assessment The clinician asks where discomfort occurs, what it feels like and how long it lasts. They ask about swallowing, vomiting, bleeding, weight change and anaemia symptoms. Medicines are reviewed carefully, including prescribed and over the counter NSAIDs and aspirin. The assessment also considers cardiac, biliary and pancreatic disease. Routine reflux often does not need immediate endoscopy Typical heartburn and regurgitation without alarm features can usually begin with clinical management. NICE does not recommend endoscopy for every person with reflux or dyspepsia. Routine camera testing would expose many people to inconvenience and procedural risk without changing treatment. Endoscopy becomes more important when symptoms, age related criteria or treatment response increase concern. Dysphagia is an alarm symptom Dysphagia means difficulty swallowing or a sensation that food sticks after swallowing. NICE recommends a suspected cancer pathway referral for dysphagia at any adult age. Benign causes such as reflux stricture and motility disorders remain possible. The urgent pathway is used because oesophageal or stomach cancer must be excluded promptly. Weight loss and age related referral NICE recommends a suspected cancer pathway referral for people aged 55 or over with weight loss plus upper abdominal pain, reflux or dyspepsia. Weight loss means unintentional loss rather than a planned dietary change. The age and symptom combination guides professional referral and does not diagnose cancer. Treatment resistant dyspepsia at age 55 or over NICE advises considering non urgent direct access upper gastrointestinal endoscopy for people aged 55 or over with treatment resistant dyspepsia. Treatment resistant means symptoms persist despite appropriate initial care. The word non urgent does not mean unimportant, and worsening symptoms require reassessment. Anaemia and other age related criteria For people aged 55 or over, upper abdominal pain with low haemoglobin can justify direct access endoscopy. Raised platelets with nausea, vomiting, weight loss, reflux, dyspepsia or upper abdominal pain can also meet NICE criteria. Nausea or vomiting combined with weight loss, reflux, dyspepsia or upper abdominal pain is another endoscopy pattern in this age group. Clinicians apply the full guideline rather than asking patients to self score these combinations. Persistent vomiting Persistent or recurrent vomiting requires assessment because it can cause dehydration and electrolyte disturbance. It can reflect gastric outlet obstruction, severe inflammation, medicine effects or another abdominal disease. Vomiting with weight loss or other alarm features increases the need for investigation. Anaemia Slow gastrointestinal bleeding can cause iron deficiency anaemia. Possible features include fatigue, pallor, breathlessness and reduced exercise tolerance. A blood count identifies the anaemia pattern but does not show the bleeding source. Unexplained low haemoglobin with upper gastrointestinal symptoms requires further assessment. Acute gastrointestinal bleeding Vomiting fresh blood or dark coffee ground material can indicate upper gastrointestinal bleeding. Black, sticky, tar like stool is called melaena and can result from digested blood. Dizziness, fainting, clammy skin or confusion can indicate substantial blood loss. Significant acute bleeding requires same day emergency specialist care. Ulcer perforation An ulcer can rarely erode through the full thickness of the stomach or duodenal wall. Digestive contents then leak into the abdominal cavity. This can cause sudden severe pain, a rigid abdomen, shock and life threatening infection. Perforation requires immediate emergency surgery assessment. Gastric outlet obstruction Inflammation or scarring near the stomach outlet can block food passage. Possible features include persistent vomiting, early fullness, weight loss and dehydration. Cancer and other diseases can cause a similar presentation. Urgent investigation is required. Endoscopy Upper gastrointestinal endoscopy is also called gastroscopy. A flexible camera passes through the mouth to examine the oesophagus, stomach and duodenum. It can identify oesophagitis, ulcers, strictures, bleeding and suspicious lesions. Biopsies can be taken for microscopic examination or H. pylori testing. What endoscopy cannot establish alone A normal endoscopy does not exclude all reflux disease. Endoscopy negative reflux can still cause troublesome symptoms. A visual ulcer appearance cannot always exclude cancer without biopsy and follow up. Clinical context and pathology remain important. Testing for H. pylori NICE recommends a carbon 13 urea breath test or stool antigen test for non invasive testing. Laboratory serology may be used only where local performance has been validated. Office based rapid blood antibody tests are not recommended because their accuracy is inadequate. Preparing for an H. pylori test Proton pump inhibitors can suppress H. pylori and cause a false negative result. NICE requires a two week PPI washout before breath or stool testing. Antibiotics should not have been taken during the preceding four weeks. The clinician advises how symptoms can be managed safely during the washout. Antibody testing limitations H. pylori antibodies can remain positive after an infection has been eradicated. Serology therefore cannot reliably confirm cure. A breath test is the NICE recommended retest method after eradication when retesting is required. Test and treat NICE offers H. pylori test and treat for uninvestigated dyspepsia without alarm features. A positive result leads to eradication therapy. A negative result directs attention towards acid suppression, functional dyspepsia and other diagnoses. Testing does not replace urgent referral when alarm features are present. H. pylori eradication therapy Current NICE CG184 uses a seven day course containing a PPI and two antibiotics. The exact combination depends on penicillin allergy and previous exposure to clarithromycin or metronidazole. Local antimicrobial guidance and resistance patterns can affect selection. Completing the full regimen matters because partial treatment encourages failure and resistance. Eradication adverse effects The antibiotic combination can cause nausea, diarrhoea, altered taste and abdominal discomfort. Severe allergy, significant antibiotic associated diarrhoea or another serious reaction requires urgent advice. Medicine interactions must be checked before treatment begins. Confirming eradication NICE recommends retesting after H. pylori associated gastric or duodenal ulcer treatment. Timing is usually six to eight weeks after treatment begins, depending on the ulcer and care plan. The person again needs an adequate PPI and antibiotic washout for accurate non invasive testing. Routine retesting after every uncomplicated functional dyspepsia treatment is not required by CG184, although individual circumstances differ. Gastric ulcer follow up NICE recommends repeat endoscopy six to eight weeks after treatment begins for a gastric ulcer with H. pylori, depending on the lesion size. The purpose is to confirm healing and ensure that a malignant ulcer has not been missed. A typical duodenal ulcer does not automatically require the same endoscopic follow up. Treating GORD with a proton pump inhibitor A proton pump inhibitor is usually shortened to PPI. It blocks the final acid secretion pump within stomach parietal cells. NICE offers a full dose PPI for four or eight weeks for GORD. The aim is symptom control and healing when acid has injured the oesophagus. Treating uninvestigated dyspepsia NICE offers empirical full dose PPI treatment for four weeks as one initial strategy. H. pylori test and treat is another initial strategy. The order can depend on symptoms, medicine use, previous testing and local care pathways. Severe oesophagitis NICE recommends a full dose PPI for eight weeks to heal severe oesophagitis. Long term full dose maintenance is offered because relapse and complications are more likely. Failure to heal or persistent symptoms prompts review, dose adjustment or specialist advice. Treating H. pylori negative ulcer disease A person with an ulcer who tests negative for H. pylori and is not taking NSAIDs receives full dose PPI or an H2 receptor antagonist for four to eight weeks. A non healing ulcer requires reassessment for missed causes, medicine exposure and malignancy. Treating an NSAID associated ulcer The NSAID is stopped where possible. NICE recommends full dose PPI or an H2 receptor antagonist for eight weeks for a diagnosed ulcer. If H. pylori is also present, eradication therapy is given. When an NSAID must continue, the need, dose and protective strategy require regular review. Gastroprotection Some people at increased ulcer or bleeding risk need a PPI while taking an NSAID or antiplatelet medicine. This is called gastroprotection. The benefit can outweigh long term medicine risks in a person with a strong indication. Stopping gastroprotection without reviewing the original risk can cause preventable bleeding. Stepping down PPI treatment When symptoms have settled and no continuing high risk indication exists, NICE encourages using the lowest effective dose. Some people can use treatment only when symptoms occur. Others can stop and use an antacid or alginate occasionally. Step down is not appropriate for every person with severe oesophagitis, stricture, Barrett's related treatment needs or high risk gastroprotection. Annual review People needing long term treatment should receive at least annual review. The review confirms the indication, dose, symptom control and medicine interactions. It considers a supervised reduction or stopping trial when appropriate. It also prevents unnecessary indefinite repeat prescribing after the original condition has resolved. Rebound acid after stopping Acid secretion can rise temporarily after prolonged PPI treatment stops. This can produce short term rebound heartburn or dyspepsia. A gradual step down, temporary alginate or an H2 receptor antagonist can help selected people. Rebound symptoms do not automatically prove that lifelong high dose treatment is required. H2 receptor antagonists H2 receptor antagonists reduce acid through a different stomach cell receptor. NICE offers them when PPI response is inadequate or a PPI is unsuitable in relevant pathways. They are generally less powerful for healing severe reflux oesophagitis. Antacids and alginates Antacids neutralise acid for short term symptom relief. Alginates form a floating barrier that can reduce reflux after meals. They act quickly but do not heal a significant ulcer or severe oesophagitis alone. Frequent long term self treatment should not delay assessment of persistent symptoms. Lifestyle measures for reflux People can avoid individual food or drink triggers when a consistent link exists. Eating the main evening meal well before lying down can help nocturnal symptoms. Raising the head end of the bed can reduce night time reflux for some people. Weight reduction can improve symptoms when excess weight increases abdominal pressure. Avoid unnecessary dietary restriction No single universal reflux diet works for everyone. Removing many foods without evidence can reduce nutrition and quality of life. A practical approach tests reproducible triggers while maintaining a balanced diet. Smoking and alcohol Smoking can impair the reflux barrier and directly irritate the upper digestive tract. Alcohol can worsen symptoms in some people and adds cancer risk when used heavily. Reducing or stopping is most useful when intake is excessive or clearly triggers symptoms. Oesophagitis Oesophagitis means inflammation and injury of the oesophageal lining. It can cause pain, bleeding or difficulty swallowing. Repeated healing can produce scar tissue and narrowing. PPI treatment reduces acid exposure and supports healing. Oesophageal stricture A stricture is narrowing caused by inflammation and scarring. Food may stick, particularly solid food. Endoscopic dilatation can widen the narrowed segment. NICE recommends long term full dose PPI after reflux related stricture dilatation to reduce recurrence. Barrett's oesophagus Barrett's oesophagus is a change in the cell type lining the lower oesophagus. It is associated with long standing reflux but can occur without recognised heartburn. The diagnosis requires endoscopic assessment and histology. It increases oesophageal adenocarcinoma risk, but most people with Barrett's do not develop cancer. Who is considered for Barrett's investigation NICE does not recommend routine endoscopy for every person with GORD. It can be considered after discussion when individual risk is higher. Relevant factors include long duration or frequency of symptoms, previous oesophagitis, hiatus hernia, stricture, ulceration, male sex and older age. Barrett's surveillance Surveillance uses planned endoscopy and biopsies to look for dysplasia or early cancer. The interval depends on segment length, pathology and individual health factors. NICE is reviewing surveillance recommendations, so specialist care follows the current pathway at the time. Surveillance has potential harms as well as benefits and is not identical for everyone. Ulcer bleeding An ulcer can erode into an artery and cause major haemorrhage. Hospital treatment includes resuscitation, urgent endoscopy and endoscopic haemostasis when required. PPI treatment reduces acid around the treated site. The underlying H. pylori or NSAID cause must also be addressed to reduce recurrence. Ulcer perforation Perforation creates a hole through the stomach or duodenal wall. It can cause peritonitis, sepsis and shock. Antibiotics, resuscitation and urgent surgical care are often required. A PPI taken at home cannot safely treat this complication. PPIs are effective but not risk free PPIs are among the most effective treatments for acid related disease. Most people tolerate them well, and benefits can clearly outweigh risks. Long term treatment should still have a continuing indication and periodic review. Unnecessary treatment exposes a person to adverse effects without benefit. Low magnesium Long term PPI use can rarely cause significant hypomagnesaemia. Possible symptoms include muscle twitching, weakness, seizures or abnormal heart rhythm. Risk is more important with prolonged use and medicines such as diuretics or digoxin. Clinicians consider magnesium monitoring in higher risk situations. Fracture association Observational studies suggest a modest association between prolonged high dose PPI use and hip, wrist or spine fracture. Other health factors may explain part of the association. People at osteoporosis risk still need ordinary bone health assessment rather than indiscriminate PPI withdrawal. Infection and nutrient considerations Reducing stomach acid can alter the gastrointestinal environment. Long term use has been associated with some enteric infections and with reduced absorption of nutrients such as vitamin B12, iron or magnesium in susceptible people. These effects are uncommon and do not justify stopping an indicated PPI without review. Kidney and other reported associations Kidney inflammation is an uncommon recognised adverse reaction to PPIs. Observational studies have reported other associations, but they do not always prove that the PPI caused the condition. New kidney dysfunction, rash or unexplained systemic symptoms require medicine review. Medicine interactions Omeprazole and esomeprazole can reduce activation of clopidogrel. UK regulatory advice discourages this combination unless it is considered essential. Other PPIs can often be selected when gastroprotection is needed with clopidogrel. The full medicine list should be reviewed rather than treating all PPIs as interchangeable. Do not stop a necessary PPI abruptly without review A person with previous ulcer bleeding, severe oesophagitis or required NSAID gastroprotection may face substantial risk if treatment stops. The correct decision balances the original indication, current symptoms and adverse effect risk. Lowest effective dose does not always mean no treatment. Surgery for confirmed reflux Laparoscopic fundoplication strengthens the mechanical reflux barrier by wrapping part of the stomach around the lower oesophagus. NICE considers it for confirmed acid reflux when symptoms respond to acid suppression but long term treatment is unwanted or not tolerated. Potential effects include swallowing difficulty, bloating and inability to belch or vomit normally. Specialist testing confirms reflux before surgery. When symptoms do not respond Persistent symptoms despite an adequate PPI trial need review of adherence, dose timing and the original diagnosis. Functional heartburn, oesophageal hypersensitivity, eosinophilic oesophagitis and motility disorders can mimic GORD. Cardiac, biliary and pancreatic causes may also need reconsideration. Simply increasing acid suppression indefinitely can delay the correct diagnosis. Taking a PPI correctly Many PPIs work best when taken before food, commonly before breakfast. The exact timing depends on the preparation and prescribed regimen. Missed doses, inconsistent use and taking treatment only after severe symptoms can reduce benefit during a healing course. The pharmacy label and clinical instructions should be followed. Prognosis Most uncomplicated GORD can be controlled with lifestyle measures and appropriate medicine. Peptic ulcers usually heal when H. pylori is eradicated or the ulcer causing medicine is addressed. Recurrence is more likely when the cause persists. Alarm symptoms and complications require investigation rather than repeated empirical treatment. What this lesson should not be used for This lesson cannot distinguish GORD, ulcer disease, functional dyspepsia, cancer or heart disease from symptoms alone. Do not use pain timing or response to antacids as proof of the cause. Do not start or stop aspirin, NSAIDs, antibiotics or long term PPIs without appropriate clinical advice. Do not delay referral for dysphagia, bleeding, weight loss or persistent vomiting. Call 999 for major bleeding, collapse or sudden severe abdominal or chest pain.

GORD results from repeated movement of stomach contents into the oesophagus, while peptic ulcers are deeper defects in the stomach or duodenal lining, usually caused by H. pylori or NSAIDs. Typical uncomplicated reflux can begin with clinical treatment, but dysphagia, bleeding, weight loss, persistent vomiting or relevant NICE age thresholds require investigation.