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Git Gerd 08.


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Medical college lectures: GIT 4th year.

Medical college lectures: GIT 4th year.

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  • Transcript

    • 1. Gastroesophageal Reflux Disease (GERD)
      • Any symptoms or esophageal mucosal damage,causing discomfort, that results from reflux of gastric acid into the esophagus
      • GERD resulting in heartburn affects 30% of the general population
      • Classic GERD symptoms
        • Heartburn (pyrosis): substernal burning discomfort
        • Regurgitation: bitter, acidic fluid in the mouth when lying down or bending over
    • 2. High Prevalence of Gastroesophageal Reflux Symptoms
    • 3.  
    • 4. Important Reasons to Diagnose and Treat GERD
      • Negative impact on health-related quality of life 1
      • Risk factor for esophageal adenocarcinoma 2
      • Revicki et al. Am J Med 1998;104:252.
      • Lagergren et al. N Engl J Med 1999;340:825.
    • 5. Pathophysiology:
      • Occasional episodes of GERD are common in health.
      • Reflux is normally followed by oesophageal peristaltic waves which efficiently clear the eso, alkaline saliva neutralises residual acid& symptoms do not occur.
      • GERD develops when the oesophageal mucosa is exposed to gastric contents for prolonged periods of time, resulting in symptoms & in a proportion of cases, oesophagitis.
      • Several factors are known to be involved:
    • 6.  
    • 7. 1.AbnormaL LES:
      • In health, LES is tonically contracted, relaxing only during swallowing.
      • Some patients with GERD have reduced LES, permitting reflux when intra-abdominal pressure rises.
      • In others, basal sphincter tone is normal but reflux occurs in response to frequent episodes of inappropriate sphincter relaxation
    • 8. 2.HH:
      • Hiatus hernia causes reflux because:
      • A. The pressure gradient between the abdominal & thoracic cavities, which normally pinches the hiatus, is lost.
      • B. The oblique angle between the cardia& oesophagus disappears.
      • Many patients who have large hiatus hernias develop reflux symptoms, but the relationship between the presence of a HH& symptoms is poor.
      • Hiatus hernia is very common in individuals who have no symptoms& some symptomatic patients have only a very small or no hernia.
      • Nevertheless, almost all patients who develop oesophagitis, Barrett's oesophagus or peptic strictures have a hiatus hernia.
    • 9. 2.HH:
      • Herniation of the stomach through the diaphragm into the chest
      • Occurs in 30% of the population > 50 years
      • Often asymptomatic
      • Heartburn & regurgitation can occur
      • Gastric volvulus may complicate large para-oesophageal hernias
    • 10.  
    • 11. 3.Delayed oesophageal clearance :
      • Defective oesophageal peristaltic activity is commonly found in patients who have oesophagitis.
      • It is a primary abnormality, since it persists after oesophagitis has been healed by PPI.
      • Poor oesophageal clearance leads to increased acid exposure time.
    • 12. 4.Gastric contents
      • Is the most important oesophageal irritant& there is a close relationship between acid exposure time & symptoms.
    • 13. 5. Defective gastric emptying
      • Gastric emptying is delayed in GERD.
      • The reason for this is unknown.
    • 14. 6. Others
      • Recent attention on the importance of duodenogastro-oesophageal reflux, containing bile, pancreatic enzymes&pepsin in addition to acid.
    • 15. 7. Increased inra abd pressure:
      • Pregnancy
      • Obesity: Weight loss may improve symptoms
    • 16. 6. Diet / environmental factors :
      • Dietary fat, chocolate, alcohol , coffee relax LES & provoke symptoms.
      • There is little evidence to incriminate smoking or NSAIDs as a causes.
    • 17. Clinical features
      • The major symptoms are heartburn /regurgitation, often provoked by bending, straining or lying down.
      • 'Waterbrash‘: salivation from reflex salivary gland stimulation as acid enters the eso, is often present.
      • A history of weight gain is common.
      • Some patients are woken at night by choking as refluxed fluid irritates the larynx.
      • Others develop odynophagia or dysphagia.
      • A few present with atypical chest pain which may be severe, can mimic angina probably due to reflux-induced oesophageal spasm.
    • 18. Clinical features
      • Classic GERD
      • Extraesophageal/Atypical GERD
      • Complicated GERD
      Clinical Presentations of GERD
    • 19.  
    • 20. Extraesophageal Manifestations of GERD
      • Pulmonary
        • Asthma
        • Aspiration pneumonia
        • Chronic bronchitis
        • Pulmonary fibrosis
      • Other
      • Chest pain
      • Dental erosion
      • ENT
        • Hoarseness
        • Laryngitis
        • Pharyngitis
        • Chronic cough
        • Globus sensation
        • Dysphonia
        • Sinusitis
        • Subglottic stenosis
        • Laryngeal cancer
    • 21. Potential Oral & Laryngopharyngeal Signs Associated with GERD
      • Edema /hyperemia of larynx
      • Vocal cord erythema, polyps, granulomas, ulcers
      • Hyperemia & lymphoid hyperplasia of posterior pharynx
      • Interarytenyoid changes
      • Dental erosion
      • Subglottic stenosis
      • Laryngeal cancer
      Vaezi MF, Hicks DM, Abelson TI, Richter JE. Clin Gastro Hep 2003;1:333-344.
    • 22. Pathophysiology of Extraesophageal GERD
    • 23. Complications: 1. Oesophagitis
      • A range of endoscopic findings, from mild redness to severe. With bleeding, ulceration &stricture formation.
      • There is a poor correlation between symptoms, histological &endoscopic findings.
      • Significant GERD may be present despite normal endoscopy / normal oesophageal histology.
    • 24. Complications: Oesophagitis
    • 25. Complications:2.Barrett's oesophagus
      • ‘ Columnar lined oesophagus'-CLO, is a pre-malignant glandular intestinal metaplasia of the lower oeso, in which the normal squamous lining is replaced by columnar mucosa.
      • Occurs as an adaptive response to chronic GERD,found in 10% undergoing gastroscopy for reflux symptoms.
      • CLO is the major risk factor for oesophageal adenocarcinoma, with a lifetime cancer risk of 10%, more closely related to the severity& duration of reflux rather than the CLO per se.
      • The cancer incidence is estimated at 1/200 patient years (0.5% /year), being low& > 95% with CLO die of causes other than oesophageal cancer.
      • Prevalence is increasing, more in men (especially white) &> 50.
      • It is weakly associated with smoking but not alcohol.
      • E-cadherin polymorphisms, p53 mutations, TGF-β, EGF receptors, COX-2& TNF-α may play roles.
    • 26. Barrett Diagnosis:diagnosis
      • Requires multiple systematic biopsies to maximise the chance of detecting intestinal metaplasia /or dysplasia.
    • 27. Barret:Management
      • Neither PPI nor antireflux surgery will stop progression or induce regression of CLO& treatment is only indicated for symptoms of reflux or complications such as stricture.
      • Endoscopic ablation therapy or photodynamic therapy can induce regression but 'buried islands' of glandular mucosa may persist underneath the squamous epithelium& cancer risk is not eliminated.
      • At present these therapies remain experimental but show promise; they are also used in patients with high-grade dysplasia (HGD) or early malignancy who are not suitable for surgery.
    • 28. Barret: Management
      • Regular endoscopic surveillance can detect dysplasia& malignancy at an early stage & improve 2-year survival but, because most CLO is undetected until cancer develops, surveillance strategies are unlikely to influence the overall mortality rate of oesophageal cancer.
      • Surveillance is expensive &cost-effectiveness conflicting.
      • Surveillance is currently recommended every 2-3 years for those without dysplasia & at 6-12-monthly intervals for those with low-grade dysplasia.
      • Oesophagectomy is widely recommended for those with HGD as the resected specimen harbours cancer in up to 40%.
      • Recent data suggest that HGD often remains stable & may not progress to cancer, at least in the medium term.
      • Close follow-up with biopsies every 3 months is an alternative strategy for those with HGD.
    • 29. Complications:3. IDA
      • Occurs as a consequence of chronic, insidious blood loss from long-standing oesophagitis.
      • Almost all such patients have a large hiatus hernia& bleeding can occur from subtle erosions in the neck of the sac ('Cameron lesions
    • 30. Complications: 4.Benign oesophageal stricture
      • Develop as a consequence of long-standing oesophagitis.
      • Most elderly & have poor oesophageal peristaltic activity.
      • Present with dysphagia which is worse for solids than liquids.
      • Bolus obstruction following ingestion of meat causes absolute dysphagia.
      • A history of heartburn is common but not invariable;as in many elderly patients.
      • Diagnosis is made by endoscopy, with biopsies to exclude Cancer.
      • Endoscopic balloon dilatation or bouginage is helpful.
      • Subsequently, long-term therapy with a PPI at full dose should be started to reduce the risk of recurrent oesophagitis & stricture formation.
    • 31. GERD:Investigations
      • Young patients with typical symptoms, without worrying features such as dysphagia, weight loss or anaemia, can be treated empirically without investigation.
      • Investigation is advisable if patients present in middle or late age, if symptoms are atypical or if a complication is suspected.
      • Endoscopy is the investigation of choice, performed to exclude other upper GI diseases & identify complications.
      • A normal endoscopy in a patient with compatible symptoms should not preclude treatment for GERD.
      • Twenty-four-hour pH monitoring is indicated if, despite endoscopy, the diagnosis is not clear.
      • A pH of < 4 for > 6-7% of the study time is diagnostic of GERD.
    • 32.  
    • 33. When to Perform Diagnostic Tests
      • Uncertain diagnosis
      • Atypical symptoms
      • Symptoms associated with complications
      • Inadequate response to therapy
      • Recurrent symptoms
      • Prior to anti-reflux surgery
    • 34. Diagnostic Tests for GERD
      • Barium swallow
      • Endoscopy
      • Ambulatory pH monitoring
      • Esophageal manometry
    • 35. Barium Swallow
      • Useful first diagnostic test for patients with dysphagia
        • Stricture (location, length)
        • Mass (location, length)
        • Bird’s beak
        • Hiatal hernia (size, type)
      • Limitations
        • Detailed mucosal exam for erosive esophagitis, Barrett’s esophagus
    • 36. Endoscopy
      • Indications for endoscopy
        • Alarm symptoms
        • Empiric therapy failure
        • Preoperative evaluation
        • Detection of Barrett’s esophagus
        • Detect grade: LA grading classification system for GERD.
    • 37. The LA Classification system – Grade A reflux esophagitis Stomach Grade A : One (or more) mucosal break, no longer than 5 mm, that does not extend between the tops of two mucosal folds.
    • 38. The LA Classification system – Grade B reflux esophagitis Stomach Grade B : One (or more) mucosal break, more than 5 mm long, that does not extend between the tops of two mucosal folds.
    • 39. The LA Classification system – Grade C reflux esophagitis Stomach Grade C : One (or more) mucosal break that is continuous between the tops of two or more mucosal folds, but which involves less than 75% of the circumference.
    • 40. The LA Classification system – Grade D reflux esophagitis Stomach Grade D : One (or more) mucosal break that involves at least 75% of the esophageal circumference.
    • 41. Ambulatory 24 hr. pH Monitoring
      • Physiologic study
      • Quantify reflux in proximal/distal esophagus
        • % time pH < 4
        • DeMeester score
      • Symptom correlation
    • 42. Ambulatory 24 hr. pH Monitoring Normal GERD
    • 43. Wireless, Catheter-Free Esophageal pH Monitoring
      • Improved patient comfort / acceptance
      • Continued normal work, activities&diet study
      • Longer reporting periods possible (48 hours)
      • Maintain constant probe position .
      Potential Advantages
    • 44. Esophageal Manometry
      • Assess LES pressure, location / relaxation
        • Assist placement of 24 hr. pH catheter
      • Assess peristalsis
        • Prior to antireflux surgery
      Limited role in GERD
    • 45. Treatment Goals for GERD
      • Eliminate symptoms
      • Heal esophagitis
      • Manage or prevent complications
      • Maintain remission
    • 46. Management: Life-style
      • Weight loss
      • Avoidance of dietary items that worsen symptoms.
      • Elevation of the bed head in those who experience nocturnal symptoms
      • Avoidance of late meals
      • Modify diet
        • Eat more frequent but smaller meals
        • Avoid fatty/fried food, peppermint, chocolate, alcohol, carbonated beverages, coffee and tea.
      • Avoid eating within 2-3 hours of bedtime.
      • Giving up smoking.
    • 47. Management: antacids
      • Proprietary antacids &alginates also provide symptomatic benefit.
      • H2-receptor antagonist drugs also help symptoms without healing oesophagitis.
      • PPI are the treatment of choice for severe symptoms &for complicated reflux disease
      • PPI are better than H2Bs in healing oesophagitis& relieving symptoms.
      • Symptoms almost invariably resolve& oesophagitis heals in the majority of patients.
      • Recurrence of symptoms is common when therapy is stopped& some require life-long treatment at the lowest acceptable dose.
    • 48. Effectiveness of Medical Therapies for GERD Treatment Response Lifestyle modifications/antacids 20 % H 2 -receptor antagonists 50 % Single-dose PPI 80 % Increased-dose PPI up to 100 %
    • 49. Treatment Modifications for Persistent Symptoms
      • Improve compliance
      • Optimize pharmacokinetics
        • Adjust timing of medication to 15 – 30 minutes before meals (as opposed to bedtime)
        • Allows for high blood level to interact with parietal cell proton pump activated by the meal
      • Consider switching to a different PPI as esmo or rebeprazol.
    • 50. GERD is a Chronic Relapsing Condition
      • Esophagitis relapses quickly after cessation of therapy
        • > 50 % relapse within 2 months
        • > 80 % relapse within 6 months
      • Effective maintenance therapy is imperative
    • 51. GERD IN OLD AGE
      • Prevalence: higher.
      • Severity of symptoms: does not correlate with the degree of mucosal inflammation.
      • Complications: late complications as peptic strictures or bleeding from oesophagitis are more common.
      • Recurrent pneumonia: consider aspiration from occult GERD.
    • 52.  
    • 53. Erosive Esophagitis
    • 54. Peptic Stricture Barium Swallow Endoscopy
    • 55. Esophageal Stricture: Dilating Devices
    • 56. TTS Balloon Dilation of a Peptic Stricture
    • 57. Barrett’s Esophagus
    • 58. Esophageal Cancer Barium Swallow Endoscopy
    • 59.  
    • 60. When to Discuss Anti-Reflux Surgery with Patients
      • Intractable GERD – rare
        • Difficult to manage strictures
        • Severe bleeding from esophagitis
        • Non-healing ulcers
      • GERD requiring long-term PPI-BID in a healthy young patient
      • Persistent regurgitation/aspiration symptoms
      • Not Barrett’s esophagus alone
    • 61. Endoscopic GERD Therapy
      • Endoscopic antireflux therapies
        • Radiofrequency energy delivered to the LES
          • Stretta procedure
        • Suture ligation of the cardia
          • Endoscopic plication
        • Submucosal implantation of inert material in the region of the lower esophageal sphincter
          • Enteryx
    • 62. Time is cruel: