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home - Oesophagus - Gastro Oesophageal Reflux Disease - Oesophagitis Written by Dr Sebastian Zeki
Recognises the typical clinical presentations of gastro-oesophageal
Is aware of the relationships of reflux to pharyngeal, laryngeal and
respiratory symptoms
Knows the range of diagnostic tests
Knows the role of endoscopy and radiology
Understands the role of physiological investigation including
ambulatory pH monitoring
Understands the complications of reflux disease
Recognises the importance of the development of columnar-lined
mucosa; follow-up of such patients and the role of surveillance
Knows the treatment options, both medical and surgical

Can make a clinical assessment, select appropriate
investigations and devise a plan for treatment and follow-up

Explains the condition to the patient and discuss the options for
management with sensitivity and in an understandable manner


ATTACK Before volulus After volvulus Type 1 Hiatus hernia Type 2 Hiatus herna (Paraoesophageal) Mechanism of tLOSRs-Integrated motor response involving not only LOS relaxation-Crural diaphragmatic inhibition-Oesophageal shortening by contraction of its longitudinal muscle-Contraction of the costal diaphragm -tLOSRs are an active, vagally mediated reflex, rather than the result of forceful gastric distentionOne hypothesis is that a primary determinant of reflux disease is not an increased number of tLOSRs, rather an increased proportion of tLOSRs that are associated with acid reflux as opposed to only gas venting. Heartburn in pregnancy is due to both mechanical and intrinsic factors that adversely affect lower esophageal sphincter tone. Written by Dr Sebastian Zeki OE-SOPHA-GE-AL Non-Acid RefluxThis is the reflux of gastric contents with a pH>4.0.Detection of non-acid reflux done by Multichannel intraluminal impedance and pH testing.This may cause symptoms by distention of the oesophagus rather than by acidity."Acid reflux" , "Weakly acid" and "Weakly alkaline" are terms used with ph of <4.0, 4-7 and >7 respectvely.Non-acid reflux usually suspected if less than full response to PPI. Salivary dysfunctionChronic xerostomia is associated with prolonged oesophageal acid exposure and oesophagitis.Smoking causes hyposalivation. Impaired osophageal emptying mechanisms:Peristaltic dysfunction, resulting in either failed or hypotensive (<30 mmHg) peristaltic contractions.Peristaltic dysfunction becoming more common with increasing severity of oesophagitis.“Re-reflux" associated with hiatal hernias also impairs esophageal emptying. Reflux event frequencyThe dominant mechanism varies as a function of disease severity.tLESRs predominate with mild disease.Hiatus hernia and/or a weak sphincter predominate with more severe disease. Anatomy Affects1. Reduces competence of the GOJ in preventing reflux 2. Compromises oesophageal acid clearance.3. Lower threshold for tLER’s HCO3- Blood flow is the main postepithelial defense against acid injury.It increases in response to luminal acid, delivering more bicarbonate to the intercellular space.When the epithelial cells are no longer able to maintain intracellular pH, they lose the ability to volume regulate and cellular edema ensues. Esophageal acid injury also stimulates cell proliferation, which is observed in biopsy specimens as thickening of the basal cell layer of the epithelium. Epithelial Defense: Tight junctions and lipid rich matrix in intercellular space can slow H+ penetration with ion gradients > pH 5.Oesophageal epithelium also extrudes hydrogen ions via a Na/H exchanger; and a Na dependent Cl/HCO3 exchanger. Hydrogen ions are then buffered by extracellular bicarbonate in equilibrium with blood. H+ Oesophageal Defence MechanismsPepsin, bile acids, trypsin, and food hyperosmolality increases susceptibility of esophageal mucosa to acid injury.At pH 2, pepsin disrupts the histologic integrity of the mucosal barrier, increases hydrogen ion permeability, and causes haemorrhage.Pepsin's ability to cause mucosal injury is pH dependent, with maximal enzyme activity below pH 3.Bile acids less important than as acid and pepsin.Preepithelial defenses include surface mucous and bicarbo-nate that maintain a significant pH gradient between lumen and cell surface.Preepithelial defences are poorly developed in the oesopha-gus; as a result, the pH gradient in the mucus layer is minimal or nil. Causes of anatomic disruption of the GOJ:Hiatal hernia and diaphragmatic sphincter in which severity of oesophagi-tis correlates with hiatal hernia size.Hiatus hernia assoc. with a reduced threshold for eliciting tLOSRs in response to gastric distension, hypotensive LOS, and GOJ disruption.BMI and waist circumference which is correlated with intragastric pressure and the gastroesophageal pressure gradient.Obesity which is associated with hiatal hernia/ increased reflux symptoms/ increased frequency of tLOSRs and increased proportion of tLOSRs associated with acid reflux.Pregnancy and exogenous oestrogen which causes heartburn in 30-50 % of pregnancies. Hypotensive lower esophageal sphincter LOS hypotension is as a result of foods, drugs, or habits leading to GORD.Strain-induced reflux occurs when LOS pressure < 4 mmHg.Free reflux is seen when LOS pressure is within 0 to 4 mmHg of intragastric pressure. Transient lower esophageal sphincter relaxations This is the physiological mechanism of belching.The frequency of tLOSRs is greatly increased by distension of the stomach or by assuming an upright posture. Pathophysiology of reflux esophagitis Oesophageal acid Clearance This is defined as following reflux, the period that the oesophageal pH remains < 4.Normally, clearance started by peristalsis and is completed by titration of the residual acid by swallowed saliva (salivary bicarbonate).Prolongation of esophageal acid clearance occurs in 50% with oesophagitis: Operations:Reduction of the herniated stomach into the abdomen.Herniotomy (excision of the hernia sac).Herniorraphy (closure of the hiatal defect).An antireflux procedure- usually a Nissen’s.Gastropexy (attachment of the stomach subdiaphrag-matically to prevent reherniation) if stomach very mobile after repair.Type II paraoesophageal hernia should always be repaired once identified. -Bleeding from Cameron lesions-Respiratory complica-tions from lung compression 50 to 94% of patients with GORD have a type I hiatal hernia compared to 13 to 59% of normals Type III hernias Combine I and II. Type IV hiatus hernia- large defect in the phrenoesophageal membrane, allowing other organs to enter hernia sac. GORD Paraesophageal hernias associated with abnormal laxity gastrosplenic and gastrocolic ligaments. Can develop into gastric volvulus as fixed at the GOJ and stomach rolls up into the thorax- usually organoaxial , occasionally mesenteroaxial volvulus. 5% of hernias 80% of population Transient lower esophageal sphincter relaxationsHypotensive lower esophageal sphincter Anatomy

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