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Git Gerd Rcp 2009.

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GIT: GERD from clinical medicine 2009.

GIT: GERD from clinical medicine 2009.

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Git Gerd Rcp 2009. Presentation Transcript

  • 1. CME Gastroenterology GERD: modern investigation / management Prepared by: Dr. Mohammad Shaikhani, CABM/FRCP.
  • 2.  
  • 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.
  • 15.  
  • 16.  
  • 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.
  • 25.  
  • 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.
  • 28.  
  • 29.