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PEPTIC ULCER AND NON ULCER DYSPEPSIA

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PEPTIC ULCER AND NON ULCER DYSPEPSIA. DR BANU NISA ABDUL HAMID MASTER IN FAMILY MEDICINE 1 ST YEAR POSTGRADUATE , UKM. Objective. most likely causes of dyspepsia risk factors of recurrent peptic ulcer disease role of Helicobacter pylori in the pathogenesis of peptic ulcer - PowerPoint PPT Presentation

Text of PEPTIC ULCER AND NON ULCER DYSPEPSIA

  • PEPTIC ULCER AND NON ULCER DYSPEPSIADR BANU NISA ABDUL HAMIDMASTER IN FAMILY MEDICINE1ST YEAR POSTGRADUATE , UKM

  • Objective most likely causes of dyspepsiarisk factors of recurrent peptic ulcer diseaserole of Helicobacter pylori in the pathogenesis of peptic ulcer disease and its relationship to ulcer relapsesmanage patients presented with dyspepsiarole of available drugs for the treatment of dyspepsiarecognise the indications for long-term maintenance therapymanage patients with PUD and concomitant high CVD risk needing antiplatelet therapy

  • DYSPEPSIADefination:having one or more symptoms of epigastric pain, burning, post-prandial fullness, or early satiation.

  • 5 MAJOR CAUSE

    Gastro-esophageal reflux (GERD)MedicationsFunctional dyspepsia (FD) non ulcer dyspepsiaPeptic ulcer disease (PUD)Malignancy

  • Some medications that commonly cause dyspepsiaNSAIDSCox-2 inhibitorsBisphosphonatesErythromycinTetracyclinesIronPotassium supplements

    AcarboseDigitalisTheophyllineOrlistatAspirin

  • FUNCTIONAL DYSPEPSIA

  • FUNCTIONAL DYSPEPSIARome III working group defined FD presence of symptoms thought to originate in gastro-duodenal region, in the absence of any organic, systemic ,or metabolic disease that is likely to explain them.[Tack et al. 2006].

  • FUNCTIONAL DYSPEPSIA

  • Rome III diagnostic criteria for functional dyspepsiaAt least 3 months of one or more of thefollowing: bothersome postprandial fullness early satiation epigastric pain epigastric burningAND no evidence of structural disease (including upper endoscopy) that is likely to explain the symptoms.

  • Pathophysiological mechanismDelayed gastric emptyingImpaired gastric accommodation to a mealhypersensitivity to gastric distentionH. pylori infectionaltered duodenal response to lipids or acid abnormal duodenojejunal motility central nervous system dysfunction[Tack et al. 2004].

  • Pathophysiologic mechanisms in functional dyspepsia. H+, acid exposure.CNS modulation stress,illnessVisceral hypersensitivity (fat, ,wall distension)Acid hypersensitivityDecrease fundic accommodationDuodenal hypersensitivityAbnormal distribution ofIgastric contentsGastric dysarrhytmiasOverdistended antrumSmall bowel dysmotilityVagal neuropathyDelayed gastric emaptying/Antral hypomotilityInflammation gastric contents[bacteria (H. pylori), viruses, etc.]

  • Diagnostic criteria: PDS 1. Bothersome postprandial fullness, occurring after ordinary sized meals, at least several times per week AND/OR 2. Early satiation that prevents finishing a regular mealSupportive criteria 1. Upper abdominal bloating, postprandial nausea or excessive belching can be present 2. Epigastric Pain Syndrome may coexist

  • Diagnostic criteria: EPS1. Pain or burning localized to the epigastrium of at least moderate severity at least once per week AND2. The pain is intermittent AND3. Not generalized or localized to other abdominal or chest regions AND4. Not relieved by defecation or passage of flatus AND5. Not fulfilling criteria for gallbladder and sphincter of Oddi

  • Diagnostic criteria: EPSSupportive criteria1. Upper abdominal bloating, postprandial nausea or excessive belching can be present2. The pain is commonly induced or relieved by ingestion of a meal but may occur while fasting3. Postprandial distress syndrome may coexist

  • Management of functional dyspepsia. FDPPIH.pylori eradiacationPromotility agentsNonrespondersAlternative therapiesTricyclics SSRIPromotilityagents

  • PEPTIC ULCER DISEASE

  • PEPTIC ULCERDefination: mucosal lesions that penetrate the muscularis mucosae layer and form a cavity surrounded by acute and chronic inflammation.

  • Two types:

  • In MalaysiaFew reports on the pattern of peptic ulcer in Malaysia.Male are more prone than female In both sexes, GU older age grp compare to DUOf the 3 main Malaysian ethnic grp, Chinese of both sexes had the highest frequency of peptic ulcer.Chinese female had the highest frequency of DU. (Source: Profile of PUD in Malaysia,M V Kudva)

  • Risk factorMajor risk factor:Helicobacter pylori infectionNSAIDSASA

  • Etiology and risk factors for peptic ulcer diseaseOdds Ratio

    Nonsteroidal anti-inflammatory drugs 3.7Helicobacter pylori 3.3Chronic obstructive pulmonary disease Chronic renal insufficiency 2.34 2.29Current tobacco use1.993 or more doctor visits in a year1.49Coronary heart disease1.46Former alcohol use1.29obesity1.18

  • Clinical ManifestationNight time awakening /episodic epigastric pain relieved following food intake (most specific clinical sign)Epigastric pain describe as episodic , dull, burning (dyspepsia) pain.46% of patients had reflux symp (heartburn, acid regurgitation) ~ GERD

  • Clinical manifestation

  • Clinical manifestationMost common symp of PUD (> 80 yo) :Epigastric pain (74%)Nausea (23%)Vomiting ( 20%)Less common features:IndigestionBelchingVomitingAssociated with gastric/pyloric stenosisLOAIntolerance to fatty foodsPositive FHX

  • Definitive diagnosisdirect visualization of the ulcer via radiography (upper GI barium swallow, double contrast) or upper GI endoscopy (EGD).Referral to EGD should be considered in all patients:50 years of age or older, with persistent symptoms, anorexia, weight loss, vomiting, and in the presence of signs of GI bleeding.

  • Differential diagnosis of peptic ulcer disease

    CONDITIONTEST(s)FINDINGSGastritisUpper gastrointestinal endoscopy Gastric inflammationGastroesophagealreflux diseaseSymptoms Dyspepsia worse with eatingand upon lying down

    Gastroparesis HistoryHistory of diabetesCholelithiasisExaminationAbdominal ultrasoundRight upper quadranttendernessGallstonesPancreatitisAmylase/lipase ElevatedGastric cancer Upper gastrointestinal endoscopyAbdominal CT scanBiopsy

    Abdominal aorticaneurysmAbdominal ultrasoundAbdominal CT scanSize of aorta

    HepatitisLiver function testsElevatedMyocardial ischemia Cardiac enzymesElectrocardiogramElevated CPKMBElevated troponinST segment changesDeep symmetric T waveinversionMesenteric ischemia SymptomsAbdominal CTPain after mealsMesenteric edema; boweldilatation; bowel wallthickening; intramuralgas; mesenteric stranding

  • ConditionTest(s)FindingsMyocardial ischemia Cardiac enzymesElectrocardiogramElevated CPKMBElevated troponinST segment changesDeep symmetric T waveinversion

    Mesenteric ischemia SymptomsAbdominal CTPain after mealsMesenteric edema; boweldilatation; bowel wallthickening; intramuralgas; mesenteric stranding

  • Common Complication

  • GI Bleeding80 % stop spontaneously- only supportive Rx requiredAsymptomatic/hemate-mesis,coffee ground emesis,malena, tachycardia,shock.Urgent OGDS detect cause of bleeding, start on appropriate therapy.Shock present- aggressive resuscitation & blood transfusion needed.Surgery remains a definate indication and best Rx OGDS/interventional radiology fails.

  • PerforationLifetime prevelance of perforation in PUD pts ~5%.Cause: NSAIDS, H.pyloriBleeding, sudden onset of sudden severe, sharp abdominal pain/ epigastric painAbd : generalized tenderness, guarding, rigidity, rebound tendernessS/S of septic shock tacycardia,hypotension,lethargy,anuria,cyanosisSimple surgical closures, intensive medical treatment, H pylori eradication, NSAID withdrawal have been reported to result in very low recurrence rates.

  • Gastric outlet obstructionmore commonly due to malignancy than PUD. nausea, vomiting, bloating, indigestion, epigastric pain, and weight loss.endoscopy has the advantage of being diagnostic and can rule out possible malignancy. Malignant obstruction is reported in 66% of patients.Outcomes may be improved with effective ulcer therapy with acid reduction and eradication of H pylori.Surgery is associated with significant morbidity and mortality and should be reserved for endoscopic treatment failures. Surgical palliation for malignant disease has poor results and high rates of morbidity and mortality.

  • HELICOBACTER PYLORI

  • HELICOBACTER PYLORI (HP)Gram negetive spiral bacteriaTransmitted: fecal-oral ,oral-oral, mother to child routes, iatrogenic.Highly prevalent in developing country & lower socioeconomic .HP +ve subjects have 10-20% lifetime risk of developing PUD.

  • PIC of halicobacter

  • Common Treatment Regimn

    RegimenCommentTrile therapy PPI; amoxicillin 1 g BID; clarithromycin500mg BID for 10 -14 days First line treatment

    Sequential therapyPPI and amoxicillin 1 g BID for 5 days followed by PPI,clarithromycin 500mg BID, tinidazole 500mg BID for 5 daysMay be first line where macrolideresistance is common

    Quadruple therapyPPI; bismuth 525mg QID; metronidazole 500mg QID;and tetracycline 500mg QID for 14 daysTreatment for failure

  • Overall ,triple therapy for 14 days has been shown to be more effective at eradication of H pylori than dual therapy. A recent meta-analysis did not find a difference in H pylori eradication rate between quadruple (PPI +bismuth +metronidazole + tetracycline for 1014 days) and triple therapy (PPI+clarithromycin +azithromicin for 714 days).

  • H. pylori has been found more frequently in dyspeptic patients than in controls and has been shown to affect acid secretion and, to a lesser extent, gastric motility .Test and treat strategy(< 50YO, no alarming symp)In areas of low H. pylori prevalence (< 20%), the empirical use of PPIs alone is considered to be an equal option for symptom relief .

  • NICE guidelines recommend initiation of a 4 week trial of full dose PPI therapy in patients with uninvestigated dyspepsia.

  • Test available for H.pylori:Blood antibody test (enzyme-linked immunosorbent assay [ELISA]). This test detects exposure to H pylori but cannot be used to confirm successful treatment.Urea breath test. This test is adequate for screening and for confirming cure following treatment. The use of PPIs within 2 weeks of testing can interfere with the results.Stool antigen test. This test is adequate for screening and for confirming cure following treatment.Stomach biopsy. Gold standard. It is adequate for screening and for confirming cure. Results depend on the number of biopsies and the experience of the pathologist.

  • RELATIONSHIP WITH ULCER RELAPSESStudies showed that the rate of Helicobacter pylori "reappearance" and of duodenal ulcer relapse up to 6 years after eradication of H. pylori. (Archimandritis A, Balatsos V. 'Bacteriology and epidemiology of Helicobacter pylori infection. J Clin Gastroenterol. 1999;28(4):345.)

    Recent studies have suggested that the eradication of H. pylori affects the natural history of duodenal ulcer disease such that the rate of relapse decreases markedly. (Asaka M,Ohtaki T,Kato M. Causal role of Helicobacter pylori in peptic ulcer relapse. Gastroenterol.1994 Jul;29 Suppl 7:134-8.)

  • Chronic PUD was almost exclusively due to H. pylori infection with up to 90% of duodenal ulcers and 70% of gastric ulcers attributed to this bacterium.However, NSAIDs and aspirin are now responsible for most ulcer disease in developed countries. (d2- advances in public health, effective H.pylori eradication therapy).

  • EGD(Esophagogastroduodenoscopy)

  • Alarm symptoms that require prompt EGD in dyspeptic patients.AnemiaEvidence of acute/chronic bleedingPrevious history of peptic ulcerOdynophagiaDysphagiaRecurrent or persistent vomitingUnintentional weight loss

  • Prompt endoscopy is recommended in patients with alarm symptoms or patients over a threshold age (35-55 years).Men , younger age prevalence at diagnosis of upper GI malignancy

    Once failed a 48 week trial of PPI therapy (in an area of low prevalence of H. pylori)/ failed to respond to eradication of H. pylori (in an H. pylori endemic region) upper endoscopy is indicated.

    Performing upper endoscopy during a symptomatic period especially while the patient is off acid-suppressant therapy is important to making a diagnosis of functional dyspepsia by excluding other potential causes of symptoms.

  • Upper GI barium radiography: inferior to upper endoscopy and is generally not recommended as part of the work up for dyspepsia.

  • Management of dyspepsia

  • Full dose PPI trialAge>50 oralarm symptomsEGDAge20%)Trial off medicationor change toan alternate medicationUse of NSAIDsor other probableoffending medicationTypical GERDsymptomsContinued symptoms despiteadequate PPI trialFull dose PPI trialTreat as GERDEmpiric trial of PPI46 weeksTest and treatfor H. pylori(Stool antigen or breathtest off PPI for >2 weeks)SymptomresolutionNoNegetiveYes

  • EGDEmpiric trial of PPI46 weeksTest and treatfor H. pylori(Stool antigen or breathtest off PPI for >2 weeks)Treatment basedon endoscopic findings1. Biopsy for H. pylori (unless negativeH. pylori stool antigen or breath testOFF PPI for greater than 2 weeks)1. Reassurance4. Evaluate and treat for IBS2. Consider alternate causes of abdominal pain3. Consider trial of low dose trycydicantidepressant or antispasmoticNo responseNo respondAbnormal EGDNormal EGDNote: diagnostic algorithm may differ based on regional cancer risk, gender, and age of patient at presentation.

  • Refractory Functional Dyspepsia

  • Patients who do not respond to empiric PPI therapy, have normal upper endoscopy, and who either are negative for H. pylori or have cleared infection following treatment yet continue to have dyspepsia represent a challenging group.

  • First, the diagnosis should be re-evaluated, considering other disorders that may be mistaken for dyspepsia. In the absence of an alternate disease, reassurance and education of the patient with functional dyspepsia becomes important.

  • Although not validated in the functional dyspepsia population, a positive physician-patient interaction including reassurance can reduce health care seeking behavior.Patients are often also educated to eat smaller, more frequent meals to avoid gastric distention and to avoid food that aggravates symptoms.

  • TREATMENT

  • Treatment of PUD consists of healing the ulcer and prevention of complications. All plans should include appropriate management of PUD risk factors. discontinue smoking; offered stress management programs and counseled to avoid NSAIDs, aspirin, and alcohol abuse.Management of patients with PUD requires detection and eradication of H pylori infection and the administration of antisecretory therapy, preferably PPIs, for a minimum of 4 weeks.

    If patients recover after the first course of treatment, they should be observed. If symptoms persist, antisecretory therapy with PPIs / histamine receptor (H2) blockers should be continued for an additional 4 to 8 weeks, and repeat EGD should be considered.re-evaluated for H pylori infection

  • NSAIDSEconomic modeling suggests that Cox-1 NSAIDs + H2 blockers or Cox-1 NSAIDs + PPIs are the most cost-effective strategies for avoiding endoscopic ulcers in patients requiring long-term NSAID therapy. PPIs are more effective than H2-blockers at standard dosages in reducing the risk of gastric and duodenal ulcer, and are superior to misoprostol in preventing duodenal but not gastric lesions.

  • ASPIRINAspirin is commonly recommended to reduce the risk of cardiovascular events.Several factors have been identified to increase the risk of patients to develop aspirin-associated GI bleeding. These include a history of previous GI ulcer, ulcer complications, dyspepsia, H pylori infection, and simultaneous use of aspirin with NSAIDs or clopidogrel.The use of enteric-coated or buffered aspirin does not significantly decrease the risk of ulcer complications due to its systemic effect. PPI + aspirin significantly reduces the risk recurrent ulcer bleeding.

  • MEDICATION

  • CLASSMedicationTypical dosePrecautionsHistamine -2 Receptor blockerCimetidine (Tagamet)

    Ranitidine (Zantac)

    Famotidine (Pepcid)400 mg BID

    150mg BD

    20 mg BD High incidence of sideeffects and potential fordrug interactions due toinhibition of CYP450

    Proton pump inhibitorsOmeprazole

    Lansoprazole

    Pantoprazole 20-40 mg daily

    15-30 mg daily

    40mg BDAltered metabolism ofmedications throughCYP450

    Prostaglandins Misoprostol200 mg QID Dose-dependent diarrheaand abdominal painAvoid in fertile women andduring pregnancy

    Other medications Sucralfate1 g QID Contains aluminum, shouldbe avoided in patientswith renal failureCan prevent absorption ofother medications

  • INTERACTIONS H2 RECP ANTAGOCimetidine (Tagamet) will inhibit drug metabolizing enzymes and increase plasma concentrations for:

    Benzodiazepines CoumadinTheophyllineCaffeineOral hypoglycemicsDilantinTricyclic antidepressantsFlagylPropranololTegretol

  • PROTON PUMP INHIBITORSOmeprazole (Prilosec)Lansoprazole (Prevacid)

  • In a cost-simulation model, PPI therapy was calculated as the most cost effective strategy in dyspeptic patients at 30 years of age and in areas of low H. pylori prevalence. For 60-year-old patients, H. pylori test and treat was the most cost-effective strategy .Significantly better response rate for omeprazole (31%) than for ranitidine (21%), cisapride (13%) and placebo (14%).

  • MISOPROSTILProstaglandin analog that replaces prostaglandins lost in stomach as result of NSAID therapyOnly indicated for NSAID induced ulcerationSide effects : diarrhea and abdominal pain

  • SULCRALFATE - CARAFATEViscous gelAdheres to ulcerated tissue and protects it from acid / pepsinMinor side effect is constipationNo major side effectsMay impede absorption of some drugs

  • NON-DRUG THERAPYDiet plays only a minor role in ulcer management.No conclusive evidence that caffeine containing beverages promote ulcer formation or interfere with recovery.Thought that alcohol can be harmful to lining of stomachBeneficial to eat 5-6 small meals a day instead of 3 large ones to decrease fluctuations in gastric pH.

  • When to referPatient 55 yo presenting with dyspepsia without red flags, routine endoscopy is unnecessary ( chances of devp GIT cancer is 1 in a million).Older than 55yo with new onset persistant dyspepsia despite lifestyle & drug modification & 4/52 Rx.Younger than 55 & symp unresponsive to full dose PPI ,HP eradication,& lifestyle modification where concern exists about diagnosis.

  • Case Scenario

  • Case scenario:

    A 60 year old man k/o :Diabetes Mellitus and Hypertension for 10 years c/o: epigastric discomfort for 1 month duration. The pain worsened at night and would awaken him from sleep. He denied of other GIT symptoms such as malena, lost of weight or anorexia. He also suffered Left hemiparesis from Ischaemic Stroke since 3 months ago. His current treatment is metformin 1gm bd, perindopril 4mg od, aspirin 150mg od and Simvastatin 20mg ON. Currently, his vital signs are stable and examination including abdomen was unremarkable.Proceed with management

  • This history is typical of dyspepsia.Non-pharmacology :stop aspirinExplain that dyspepsia is a common condition that usually responds well to treatmentOffer lifestyle advice, including smoking cessation, weight loss, reduced alcohol and caffeine intake, and regular exercise.

  • Pharmacological: Aspirin + PPICaspirin + PPITiclid

    Symptoms should be present for a minimum of 3 months;however, symptoms for greater than 6 months are typical.

    2. Heartburn was removed from the symptoms that refer to FD**The H2 antagonists are generally regarded as safe drugs. There are however, some problems when any drugs are considered safe. The abuse and/or misuse in clinical practice which could mask underlying disease and the abuse and/or misuse by the lay population which can also mask underlying disease.**Bind to and irreversibly block the proton pump in gastric mucosal cells.Are most effective and most rapid acting agents in reducing gastric acid**Remember - *prostaglandins inhibit acid secretion, promote mucus and bicarbonate secretion and increase regional blood flow via vasodilation****