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GASTROESOPHAGEAL REFLUX DISEASE
 

GASTROESOPHAGEAL REFLUX DISEASE

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GASTROESOPHAGEAL REFLUX DISEASE

GASTROESOPHAGEAL REFLUX DISEASE

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  • --distinction between normal and GERD is blurred because some degree of reflux is physiologic is all folks Physiologic—postprandially, short lived, asymptomatic, not during sleep Pathologic—symptoms or mucosal injury and often with nocturnal symptoms
  • --At level of diaphragmatic hiatus—main deterrant to reflux --disruption due to –review slide--multifactorial
  • --black arrow squamo-columnar jxn—Z-line --Z-line has undulating smooth contours --green arrow—gastric columnar epithelium above round black sphincter --red arow—pink white esophageal squamous epithelium --ulcerations in 2-7%
  • 4-20% of patients
  • --1950—Norman Barrett --10-15% --black arrow squamo-columnar jxn—Z-line --Z-line has undulating smooth contours --green arrow—gastric columnar epithelium above round black sphincter --red arow—pink white esophageal squamous epithelium --RFs—male, smoker, age, obese
  • Adenoca with barretts 0.5%/yr--------without barretts 0.07%/yr
  • --gerd related chest pain may mimic angina—squeezing/burning, substernal, radiates to back, neck, jaw, arms. Minutes to hours. After meals, awakens patient from sleep, exacerbated by emotional stress --water brash—hypersalivation—heartburn and regurg of sour fluid or tasteless saliva into mouth --globus—lump in throat irrespective of swallowing --odynophagia—esophageal ulcer --nausea—infrequent --hrt burn 70-85%//regurg 60%//dysphagi 15-20%//angina 33%//asthma 15-20%
  • --need further eval if any present—egd--
  • --heartburn +/- regurgitation high specificity, low sensitivity
  • Once established h&p dx and no alarm symptoms can proceed with dx/therapeutic trial of tx.
  • --if trial of med did not work or if alarm symptoms or long term 5yrs need egd 1a evidence—dysphagia/early satiety/gi bleed/odynophagia/vomiting/wt loss/anemia --50-70% of patient’s with gerd will have a neg egd.
  • --Transnasal catheter or a wireless capsule shaped device affixed to distal esophagus --cather positioned 5cm above manometrically defined upper limit of les --capsul attached 6cm proximal to endoscopically defined squamocolumnar jxn --if mucosal changes—have dx and do not need 24hph.
  • --Tums, rolaids, maalox --$1 billion in yearly expenditures --aluminum/calcium—constipation Mag--diarrhea
  • --otc dose uniformly half of standard lowest prescription dose --similar clinical efficacy
  • --no significant differences in symptomatic tx of GERD or healing of erosive esophagitis 1a evidence --works only on active pumps—take 30-60min prior to meals --long-term tx generally benefits outweigh risks
  • candidacy --esophagitis—by egd --need normal manometry/motility --partial response to acid suppression --reduce hh, repair diaphragm, strengthen ge jxn—antireflux barrier --75-90% effective at alleviating hrtburn/regurg --better at helping with hrtburn/regurg than atypical sx

GASTROESOPHAGEAL REFLUX DISEASE GASTROESOPHAGEAL REFLUX DISEASE Presentation Transcript

  •  Definition of GERD  Epidemiology of GERD  Pathophysiology of GERD  Clinical Manisfestations  Diagnostic Evaluation  Treatment  Complications
  •  Symptoms OR mucosal damage produced by the abnormal reflux of gastric contents into the esophagus  Often chronic and relapsing  May see complications of GERD in patients who lack typical symptoms
  •  Physiologic GERD Postprandial Short lived Asymptomatic No nocturnal sx  Pathologic GERD Symptoms Mucosal injury Nocturnal sx
  •  GERD occurs in all ages but, most common in those older than 40 years of age.  About 10-20% of people in western countries suffer from GERD symptoms on a weekly basis  About 7% have symptoms daily.  Except for NERD and pregnancy , no much difference in incidence between men and women.  But for Barrett’s esophagus, prevalence is more in males particularly white adult males.
  •  Primary barrier to gastro esophageal reflux is the lower esophageal sphincter  LES normally works in conjunction with the diaphragm  If barrier disrupted, acid goes from stomach to esophagus May be due to  Spontaneous transient LES relaxations  Transient increase in intra abdominal pressure  An atonic LES
  •  Drugs that reduce LES tone include calcium channel antagonists (e.g., nifedipine, verapamil, diltiazem), nitrates, anticholinergic agents(e.g.,tricyclic antidepressants , antihistamines), and oral contraceptives and estrogen.  Foods that reduce LES tone include chocolate, fatty foods , onions, peppermint, and garlic  Smoking(nicotine) reduces LES tone.
  • 2)DISRUPTION OF ANATOMICAL BARRIERS  Associated with hiatal hernia  The size of hiatal hernia is proportional to the frequency of LES relaxations  Hypotensive LES pressures and large hiatal hernia- more chance of GERD following abrupt increase in intra abdominal pressure 3) ESOPHAGEAL CLEARANCE  The GI acid produced spent too much time in contact with the esophageal mucosa  Normally swallowing contributes to esophageal clearance by increasing salivary flow  Saliva decreases with increasing age, so more often seen with elderly.
  • 4)MUCOSAL RESISTANCE  The mucus secreated by the mucus secreting glands involves in the protection of esophagus  The bicarbonate s moving from the blood to the lumen can neutralize acidic refluxate in the esophagus. On repeated exposure to the refluxate or due to some defect in normal mucosal defenses hydrogen ions diffuse into the mucosa, leading to cellular acidification and necrosis leading to esophagitis. 5)DELAYED GASTRIC EMPTYING  An increase in gastric volume may increase both the frequency of reflux and the amount of gastric fluid available to be refluxed  Physiologic Postprandial Gastro esophageal reflux occurs
  • 6)COMPOSITION OF REFLUXATE  If the pH of the refluxate is less than 2, esophagitis may develop secondary to protein denaturation  Also pepsinogen activated to pepsin at this pH may cause esophagitis.
  •  Erosive esophagitis  Responsible for 40-60% of GERD symptoms  Severity of symptoms often fail to match severity of erosive esophagitis
  •  Esophageal stricture  Result of healing of erosive esophagitis  May need dilation  Common in the distal esophagus and are generally 1 to 2 cm in length.
  •  Barrett’s Esophagus  Columnar metaplasia of the esophagus,i.e replacement of the squamous epithelial lining of the esophagus by specialized columnar- type epithelium  Associated with the development of adenocarcinoma  Have a greater chance (30%) of developing esophageal stricture
  •  Barrett’s Esophagus  Acid damages lining of esophagus and causes chronic esophagitis  Damaged area heals in a metaplastic process and abnormal columnar cells replace squamous cells  This specialized intestinal metaplasia can progress to dysplasia and adenocarcinoma
  •  3 CLASSES OF SYMPTOMS  TYPICAL SYMPTOMS May be aggravated by activities that worsen gastroesophageal reflux such as recumbent position, bending over, or eating a meal high in fat.  Heartburn—retrosternal burning discomfort  Regurgitation—effortless return of gastric contents into the pharynx without nausea, retching, or abdominal contractions  Water brash (hyper salivation)  Belching
  • ATYPICAL SYMPTOMS In some cases, these extra esophageal symptoms may be the only symptoms present, making it more difficult to recognize GERD as the cause, especially when endoscopic studies are normal.  Nonallergic asthma  Hoarseness  Pharyngitis  Chest pain  Dental erosions
  • ALARM SIGNS/SYMPTOMS These symptoms may be indicative of complications of GERD such as Barrett’s esophagus, esophageal strictures, or esophageal cancer  Dysphagia  Early satiety  GI bleeding  Odynophagia  Vomiting  Unexplained Weight loss  Iron deficiency anemia  Choking  Continual pain
  •  If classic/typical symptoms like heartburn and regurgitation exist in the absence of “alarm symptoms” the diagnosis of GERD can be made clinically and treatment can be initiated
  •  H2RA or PPI  Expect response in 2-4 weeks  If no response  Change from H2RA to PPI  Maximize dose of PPI  If PPI response inadequate despite maximal dosage  Confirm diagnosis  EGD(Esophagogastrodudenoscopy)  24 hour pH monitor
  •  Endoscopy (with biopsy if needed)  In patients with alarm signs/symptoms  Those who fail a medication trial  Those who require long-term treatment  Important in distinguishing between esophagitis and Barret’s metaplasia  Absence of endoscopic features does not exclude a GERD diagnosis  Confirmation can be achieved by provocative tests such as an acid perfusion test(Bernstein test), standard acid reflux test etc.
  •  24-hour pH monitoring  Helps in establishing the presence of acid above the LES as the cause of symptoms or esophageal damage.  Documents the amount of time the esophageal pH is low.  Useful in patients who have not responded or who have had an incomplete response to empiric therapy, have symptoms with out evidence of mucosal injury, or have atypical symptoms.  Trans-nasal catheter or a wireless, capsule shaped device
  • Patient with heartburn Iniate tx with H2RA or PPI H2RA taken BID Good response Frequent relapses On demand tx PPI taken QD Good response Maintenance therapy with lowest effective dose Symptoms persist Consider EGD if risk factors present (> 45, white, male and > 5 yrs of sx) Increase to max dose QD or BID Good response Confirm diagnosis EGD, ph monitor No Yes Yes No Yes Yes No No
  •  Goals of therapy  Alleviate or eliminate the patients symptoms.  Decrease the frequency or recurrence and duration of gastro esophageal reflux.  Promote healing of the injured mucosa.  Prevent the development of complications.
  •  Lifestyle modifications  Avoid large meals  Avoid acidic foods (citrus/tomato), alcohol, caffiene, chocolate, onions, garlic, peppermint  Decrease fat intake  Avoid lying down within 3-4 hours after a meal  Elevate head of bed 4-8 inches  Avoid meds that may potentiate GERD (CCB, alpha agonists, theophylline, nitrates, sedatives, NSAIDS)  Avoid clothing that is tight around the waist  Lose weight  Stop smoking
  •  Antacids  Over the counter acid suppressants and antacids appropriate initial therapy  Approx 1/3 of patients with heartburn-related symptoms use at least twice weekly  More effective than placebo in relieving GERD symptoms
  •  Histamine H2-Receptor Antagonists  Competitively block the histamine receptors in gastric parietal cells, thereby preventing acid secretion  More effective than antacids for relieving heartburn in patients with GERD  Faster healing of erosive esophagitis  Can use regularly or on-demand
  • AGENT DOSAGE Cimetadine 400-800mg twice daily Cimetidine(tab),Zydus Cadila Famotidine 20-40mg twice daily Famocid(tab), Sun Nizatidine 150mg twice daily Axid Ranitidine 150mg twice daily Aciloc(tab), Cadila
  •  Proton Pump Inhibitors  Effective not only with patients having erosive esophagitis or complications(Barret’s esophagus), but also with non erosive GERD who have moderate to severe symptoms.  Act by decreasing the basal and stimulated gastric acid secretion through inhibition of the final step of acid secretion by the parietal cell- the H+/K+ ATPase proton pump.  Better control of symptoms with PPIs vs H2RAs and better remission rates  Faster healing of erosive esophagitis with PPIs vs H2RAs
  • AGENT DOSAGE Esomeprazole 20-40mg daily Esomac(tab), Cipla Omeprazole 20mg daily Lomac(cap), Cipla Lansoprazole 15mg daily Lan(Cap), Intas Pantoprazole 40mg daily Pan-OD(tab), Burgeon Rabeprazole 20mg daily Rabeloc(tab), Cadila
  •  H2RAs vs PPIs 12 week freedom from symptoms  48% vs 77% 12 week healing rate  52% vs 84% Speed of healing  6%/wk vs 12%/wk
  •  Antireflux surgery  Failed medical management  Patient preference  GERD complications  Medical complications attributable to a large hiatal hernia  Atypical symptoms with reflux documented on 24-hour pH monitoring
  •  Postsurgery  10% have solid food dysphagia  2-3% have permanent symptoms  7-10% have gas, bloating, diarrhea, nausea, early satiety  Within 3-5 years 52% of patients back on antireflux medications
  •  Endoscopic treatment Relatively new No definite indications Select well-informed patients with well- documented GERD responsive to PPI therapy may benefit  Three categories Radiofrequency application to increase LES reflux barrier Endoscopic sewing devices Injection of a nonresorbable polymer into LES area
  •  Definition of GERD  Epidemiology of GERD  Pathophysiology of GERD  Clinical Manisfestations  Diagnostic Evaluation  Treatment  Complications
  • ?QUESTIONS?