Git Gerd Rcp 2009.
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This document discusses GERD (gastroesophageal reflux disease), including its prevalence, definitions, pathophysiology, clinical features, diagnosis, and treatment approaches. It notes that GERD is a common condition resulting in impaired quality of life. Diagnosis involves consideration of symptoms, endoscopy, pH studies, and impedance testing. Treatment follows a stepped approach starting with lifestyle changes and antacids, then H2 blockers or PPIs, and potentially surgery if medical management fails.
Git Gerd Rcp 2009.
- 1. CME Gastroenterology GERD: modern investigation / management Prepared by: Dr. Mohammad Shaikhani, CABM/FRCP.
- 3. Introduction: It is a very common under-diagnosed condition resulting in a significant impairment in quality of life. 24-44% experiencing symptoms for 2 days or more/ week, oesophagiti; 12%, Barrett’s ;1.3%, irrespective of symptoms. 33% with oesophagitis & 46% with Barrett’s were asymptomatic. Severe form can lead to potentially avoidable complications including severe oesophagitis with scarring/stricture formation, Barrett’s& adenoca.
- 4. Definitions: The Montreal classification: ‘ A condition that develops when the reflux of stomach contents causes troublesome symptoms/or complications’. The acid component of the gastric refluxate is responsible for most of the symptoms & pathology, but other components, as bile, may also contribute (nonacid reflux). Quantification of reflux can be achieved either by measuring acid exposure to the distal oesophagus (pH studies) or movement of liquid in the distal oesophagus (impedance studies). Combined impedance&pH measurement characterises all acid & non-acid reflux episodes.
- 5. Non-erosive reflux disease : 70% of patients with heartburn do not have evidence of erosive changes on endoscopy. Of these, a proportion have increased acid reflux on 24-hour pH monitoring, classified as having non-erosive reflux disease (NERD) .
- 6. Functional heartburn : A proportion of patients describe typical reflux symptoms without evidence of reflux. The Rome II definition ‘an episodic burning in the absence of pathologic GER, motility disorders& any structural explanations’. The pathophysiology remains obscure
- 7. R eflux oesophagitis Reflux oesophagitis is reflux causing inflammation or ulceration of the oesophagus Los Angeles classification is now the most commonly used to quantify GERD damage.
- 8. Pathophysiology Results from disruption of the anti-reflux barrier, comprised of: The internal (LOS), a 3–4 cm region of circular muscle in the distal oesophagus. External, the crural diaphragm. Oesophageal clearance by eso peristalsis. Neutralisation mechanisms by saliva. Abnormal TLOSRs not initiated by a swallow, result in the reflux of gastric fluid & gas, account for 90% of reflux episodes, usually mild-moderate GERD. The TLOSR reflex is initiated by tension receptors in the stomach mediated by a vagovagal pathway via the brainstem leading to simultaneous relaxation of crura, LOS & inhibition of peristalsis, inhibited by (GABA-B) receptor . Hiatus hernias increase the magnitude of reflux during TLOSRs.
- 9. Pathophysiology Hypotensive LOS, is responsible for more severe oesophagitis. Reflux occurs more frequently when the pressure in the LOS is from 4-10 mm Hg. Factors which relax the LOS, as caffeine, fat, smoking, drugs (CCB &nitrates)& gastric distention, will increase reflux. The association of increased BMI& GORD remains unclear. Acid in the distal oesophagus is neutralised by saliva& any processes reducing saliva production results in a delay in acid neutralisation& nocturnal reflux episodes are prolonged due to depressed salivation. Impaired distal oesophageal peristalsis results in prolonged acid exposure to acid reflux episodes,apparent in hiatus hernias &ulcerative oesophagitis due to severe GERD, systemic sclerosis& achalasia, where there is peristaltic dysfunction.
- 10. Pathogenic factors in GERD: LES& crural function (hiatus hernia) TLESR. Oesophageal clearance mechanisms (oesophageal motility, saliva) Refluxate (gastric acid, bile, enzymes) Mucosal response to refluxate Drugs affecting anti-reflux barrier (nitrates, calcium antagonists) Diet (fat, caffeine).
- 11. Clinical features of GERD: The most common symptom;s heartburn, regurgitation, belching, epigastric pain, chest pain, dysphagia& acid brash. Less frequent symptoms include odynophagia, globus, nausea & pharyngeal symptoms. Symptoms of GORD, can be highly variable. Diagnosis of GORD can be difficult. For example the presence of heartburn is not entirely predictive of acid reflux. Only 5–10% of episodes of acid reflux produce heartburn. The positive predictive value of heartburn for endoscopic oesophagitis is poor, although the negative predictive value is slightly better.
- 12. Diagnosis of GERD:emprical Most patients with typical symptoms of GORD do not require investigation and will respond to a trial of (PPI). High dose PPI 40 mgm Omeprazole twice daily for 1 week) has a sensitivity of 80% as a diagnostic test for GORD.
- 13. Diagnosis of GERD:OGD Patients of any age presenting with typical reflux symptoms with the following alarm symptoms should have an urgent endoscopy: Dysphagia Unintentional weight loss GIB Anaemia Persistent vomiting. Endoscopy should also be performed before oesol pH studies. A negative endoscopy does not exclude NERD. Screening endoscopy for the diagnosis of Barrett’s in patients of any age with a history of chronic heartburn cannot be recommended, as the absolute risk of adenocarcinoma is < 1:1,000&40% of who develop adenocarcinoma in association with Barrett’s oesophagus do not have a history of heartburn.
- 14. Diagnosis of GERD:Ph studies Acid exposure of the distal oesophagus can be measured either by placing a nasooesophageal probe 5 cm above the physiological LOS or by placing a wireless capsule probe endoscopically. Measurements of pH can be taken for either 24 or 48 hours. PPI or (H2A) should bes topped one week before the procedure. Patients who have oesophagitis demonstrated on endoscopy do not need pH studies for diagnostic purposes. Patients who have refractory symptoms to a trial of PPI may have inadequate acid suppression. This can be demonstrated by pH studies obtained while the patient is taking PPIs. It is reasonable as an alternative, however, to escalate PPI dose in these patients.
- 17. Diagnosis of GERD: Eso manometry Does not influence the management except in a few circumstances: Where oes motility abnormalities are suspected as achalasia. To correctly place the pH probe 5 cm above the LOS. Prior to anti-reflux surgery, although studies suggest this very rarely changes outcome or helps tailor surgery.
- 18. Diagnosis of GERD: MC Intraluminal impedance. Useful for the investigation of PPI-resistant reflux symptoms although its role has not yet been completely defined.
- 19. Treatment: The is to effectively control symptoms&prevent associated complications by adopting a stepped approach. The effects of drugs on either the healing and/or symptom relief of oesophagitis or NERD is generally greater in patients with endoscopy proven oesophagitis .
- 20. Treatment: Life style Simple manoeuvres outlined below may have a marked effect on symptoms: Dietary changes: avoiding fat, caffeine& alcohol Avoiding late meals: Nocturnal reflux can be minimised by consuming small meals long before slee.p Although the association of obesity is unclea,rbut there is association with oesophageal adenocarcinoma& many other well-known diseases, so weight loss is suggested as part of management.
- 21. Treatment: antacids/alginates Antacids consist of calcium carbonate, magnesium& aluminum salts in various compounds or combinations. The effect of antacids is due to partial neutralisation of gastric HCL & inhibition of the proteolytic enzyme, pepsin. Alginate mechanism of action is due to the formation of a gel in the presence of gastric acid. Alginate-based raftforming usually contain sodium or potassium bicarbonate; in the presence of gastric acid,converted to carbon dioxide, which becomes entrapped within the gel precipitate, converting it into a foam which floats on the surface of the gastric contents, much like a raft on water& providing a relatively pH-neutral barrier. They improve reflux symptoms, but do not heal oesophagitis. They are indicated for very mild symptoms. No role for antacids/ alginates in the maintenance of GORD .
- 22. Treatment: Acid inhibition H2As / PPIs should be prescribed for patients with symptoms not well controlled on lifestyle changes or antacids/alginates. PPI are prodrugs, which are activated in the acidic canalicular space of the parietal cell, inhibiting the final pathway of acid secretion and suppress acid production for several days. (H2A) reversibly bind H2 gastric parietal cell receptors. Both H2As&PPIs effectively heal and prevent relapse of oesophagitis, but PPIs are superior to both H2As/ prokinetics. The efficacy of PPIs is dose dependant& mucosal healing is dependent upon the proportion of time the intra-gastric pH is 4 . The dose effect of H2As , is constant. At equivalent doses, all the PPIs appear to be equally efficacious. PPI should be taken 30 minutes before meals.
- 23. Treatment: Non-repons to PPI Patients with typical reflux symptoms, who do not respond to initial courses of PPIs fall into one of the following groups: Patients with an alternative diagnosis. Patients with inadequate acid suppression Patients with functional heartburn .
- 24. Treatment: Non-repons to PPI If symptom control is not achieved after four weeks, we suggest extending PPI therapy to two months as healing improve from 68- 84% A proportion of patients fail to adequately increase the gastric pH 4 with standard-dose PPIs. Doubling the PPI dose does appear to have an additional effect specially in patients with more severe oesophagitis (LA grade C and D. A proportion of patients experience nocturnal acid breakthrough, even with twice daily PPI,so addition of an H2A before sleep may reduce nocturnal symptoms, however, the benefit may be limited by tachyphylaxis.
- 26. Treatment: Prokinetic agents Existing drugs have not shown promise Little data exist for domperidone. GABA-B agonists may be potential targets for future developments.
- 27. Treatment: Surgery There is no statistical difference between outcomes of medical therapy (PPI or H2A)&surgery. Given the recognised postoperative mortality associated with surgery of up to 0.4%, this is only recommended if patients with provenwho do not respond to medical therapy, do not wish to take medication or have associated respiratory symptoms not responding to PPI. The most common complications of Nissen fundoplication include dysphagia & gas-bloat syndrome in up to 50% of patients. Furthermore, after a median of five years, up to 50% of patients after surgery require medication to control symptoms.