Presentation on theme: "Gastroesophageal Reflux Disease (GERD)"— Presentation transcript:
1 Gastroesophageal Reflux Disease (GERD) Dr. Maha Arafah
2 Objectives Understand the Pathophysiology of reflux esophagitis. Upon completion of this lecture the students will :Understand the Pathophysiology of reflux esophagitis.Know clinical features of reflux esophagitisDescribe the pathology (gross and microscopic features) of reflux esophagitisKnow the complications of reflux esophagitis
3 Anatomic radiographic landmarks of the lower esophageal sphincter (LES).
4 Gastroesophageal Reflux Disease (GERD) Gastroesophageal reflux is a normal physiologic phenomenon experienced intermittently by most people, particularly after a meal.Gastroesophageal reflux disease (GERD) occurs when the amount of gastric juice that refluxes into the esophagus exceeds the normal limit, causing symptoms with or without associated esophageal mucosal injury.
6 Definition American College of Gastroenterology (ACG) Symptoms OR mucosal damage produced by the abnormal reflux of gastric contents into the esophagusOften chronic and relapsingMay see complications of GERD in patients who lack typical symptoms
7 Physiologic vs Pathologic Physiologic GERPostprandialShort livedAsymptomaticNo nocturnal sxPathologic GERDSymptomsMucosal injuryNocturnal sx--distinction between normal and GERD is blurred because some degree of reflux is physiologic is all folksPhysiologic—postprandially, short lived, asymptomatic, not during sleepPathologic—symptoms or mucosal injury and often with nocturnal symptoms
9 GERD Pathophysiology Abnormal lower esophageal sphincter Functional (frequent transient LES relaxation)Mechanical (hypotensive LES)Foods (eg, coffee, alcohol),Medications (eg, calcium channel blockers),Location hiatal herniaorB. Increase abdominal pressureThe most common cause of (GERD).decrease the pressure of the LES.obesityPregnancyincreased gastric volume
10 PathophysiologyPrimary barrier to gastroesophageal reflux is the lower esophageal sphincterLES normally works in conjunction with the diaphragmIf barrier disrupted, acid goes from stomach to esophagus--At level of diaphragmatic hiatus—main deterrant to reflux--disruption due to –review slide--multifactorial
11 Summary of Pathogenesis of GERD impaired lower esophageal sphincter-low pressures or frequent transient lower esophageal sphincter relaxationhypersecretion of aciddecreased acid clearance resulting from impaired peristalsis or abnormal saliva productiondelayed gastric emptying or duodenogastric reflux of bilesalts and pancreatic enzymes.
12 Clinical Manisfestations Most common symptomsHeartburn—retrosternal burning discomfortRegurgitation—effortless return of gastric contents into the pharynx without nausea, retching, or abdominal contractions--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%Atypical symptoms….coughing, chest pain, and wheezing.
13 Extraesophageal manifestations of GERD Otolaryngeal:hoarsness/laryngitisCh. Sore throatOther:Noncardial chest pain
14 Diagnostic Evaluation If classic symptoms of heartburn and regurgitation exist in the absence of “alarm symptoms” the diagnosis of GERD can be made clinically and treatment can be initiated--heartburn +/- regurgitation high specificity, low sensitivity
15 Esophagogastrodudenoscopy Endoscopy (with biopsy if needed)In patients with alarm signs/symptomsThose who fail a medication trialThose who require long-term txThe procedure lacks sensitivity for identifying pathologic refluxAbsence of endoscopic features does not exclude a GERD diagnosisAllows for detection, and management of esophageal injury or complications of GERD--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% of patient’s with gerd will have a neg egd.
16 pH24-hour pH monitoringAccepted standard for establishing or excluding presence of GERD for those patients who do not have mucosal changesTrans-nasal catheter or a wireless, capsule shaped device--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.
17 Complications Erosive esophagitis Stricture Barrett’s esophagus --dysphagia, odynophagia, early satiety, gi bleed, anemia, vomit, wt loss
18 Complications Erosive esophagitis Responsible for 40-60% of GERD symptomsSeverity of symptoms often fail to match severity of erosive esophagitis--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%
19 Esophagitis Elongation of lamina propria papillae Eosinophils and neutrophilsElongation of lamina propria papillaebasal zone hyperplasia,
20 Complications Esophageal stricture Result of healing of erosive esophagitisMay need dilation4-20% of patients
21 Complications Barrett’s Esophagus 8-15%Barrett’s EsophagusIntestinal metaplasia of the esophagusAssociated with the development of adenocarcinoma--1950—Norman Barrett%--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
22 Pathophysiology of Barrett’s Esophagus Acid damages lining of esophagus and causes chronic esophagitisDamaged area tries to heal in a metaplastic process and damaged squamous cells are replaced by metaplastic columnar cells defined by the presence of goblet cells (intestinal metaplasia)This specialized intestinal metaplasia can progress to dysplasia and adenocarcinomaMany patients with Barrett’s are asymptomaticAdenoca with barretts 0.5%/yr without barretts 0.07%/yr
24 The risk of cancer in Barrett's esophagus is estimated to be 40 to 100 times Endoscopic surveillance is recommended for all patients with Barrett's esophagus. Endoscopy is performed every 2 years, and biopsies are taken from the area of abnormal mucosa.If the biopsies reveal low-grade dysplasia, then the frequency of endoscopies is increased.
25 If high-grade dysplastic changes are seen and confirmed by a second pathologist, then the risk of subsequent adenocarcinoma is greater than 25%, and surgical resection should be considered.