PEPTIC ULCER DISEASE Dr RAMBABU POPURI MD MD Asst. Professor Dept of General medicine Dept of...
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Transcript of PEPTIC ULCER DISEASE Dr RAMBABU POPURI MD MD Asst. Professor Dept of General medicine Dept of...
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PEPTIC ULCERPEPTIC ULCER DISEASEDISEASE
Dr RAMBABU POPURIDr RAMBABU POPURI MDMD
Asst. Professor Asst. Professor Dept of General medicineDept of General medicine
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DefinitionDefinition
A circumscribed ulceration of the A circumscribed ulceration of the gastrointestinal mucosa occurring in areas gastrointestinal mucosa occurring in areas exposed to acid and pepsin and most often exposed to acid and pepsin and most often caused by Helicobacter pylori infection.caused by Helicobacter pylori infection.
More than 5mm in sizeMore than 5mm in size Depth to the sub mucosa.Depth to the sub mucosa.
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Peptic Ulcers: Peptic Ulcers: Gastric & DudodenalGastric & Dudodenal
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Comparing Duodenal Comparing Duodenal and Gastric Ulcersand Gastric Ulcers
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Pathogenesis of UlcersPathogenesis of Ulcers
Aggressive FactorsAggressive Factors H. pyloriH. pylori Drugs (NSAIDs)Drugs (NSAIDs) acid, pepsinacid, pepsin Bile saltsBile salts
Defensive FactorsDefensive Factors Mucus, bicarbonate layerMucus, bicarbonate layer Blood flow, cell renewalBlood flow, cell renewal ProstaglandinsProstaglandins PhospholipidPhospholipid
Therapy is directed at enhancing host defense or eliminating aggressive factors; i.e., H. pylori.
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Risk factors for PUDRisk factors for PUD
High dose of NSAIDsHigh dose of NSAIDs Multiple NSAIDsMultiple NSAIDs Concomitant use of glucocorticoids Concomitant use of glucocorticoids
&anticoagulants&anticoagulants Cigarette smokingCigarette smoking Alcohol consumptionAlcohol consumption
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Genetic predispositionGenetic predisposition
Blood group O –for DUBlood group O –for DU Blood group A –for GUBlood group A –for GU Psychological stress contribute to Psychological stress contribute to
PUDPUD
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Chronic disorders asso with PUDChronic disorders asso with PUD
Systemic mastocytosisSystemic mastocytosis Chronic pulmonary diseaseChronic pulmonary disease Chronic renal diseaseChronic renal disease CirrhosisCirrhosis NephrolithiasisNephrolithiasis HyperparathyroidismHyperparathyroidism CADCAD Polycythemia veraPolycythemia vera Chronic pancreatitisChronic pancreatitis
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Helicobacter pyloriHelicobacter pylori and peptic ulcer disease. and peptic ulcer disease.
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Helicobacter pyloriHelicobacter pylori and peptic ulcer disease. and peptic ulcer disease.
It has been more than 20 years since H Pylori first isolated from human stomach.
More than the half of worlds population are infected (60% - 70%).
Only 15% of H Pylori infected patients will develop symptomatic PUD.
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Helicobacter pyloriHelicobacter pylori and peptic ulcer disease. and peptic ulcer disease.
H Pylori is now recognized as a major etiological factor of PUD:
90% of duodenal ulcers (DU) and 70% of gastric ulcers (GU) are associated with H Pylori. NSAIDs/ aspirin remain the second etiology of PUD.
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Helicobacter pyloriHelicobacter pylori and peptic ulcer disease. and peptic ulcer disease.
The description of H.pylori was a major breakthrough in Gastroenterology.
The recognition of H.pylori as a major pathogen changed the common beliefs about peptic ulcer disease
Schwarz’s dictum: NO ACID NO ULCER
has become: NO H.pylori NO ULCER.
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Helicobacter pylori and peptic ulcer disease.Helicobacter pylori and peptic ulcer disease.
H.pylori induced effects are related to H.pylori induced effects are related to distribution of gastritis distribution of gastritis
H.pylori associated H.pylori associated antral gastritisantral gastritis induces induces increased acid secretion.increased acid secretion.
H.pylori associated H.pylori associated corpus gastritiscorpus gastritis induces induces reduced or even absent acid secretion.reduced or even absent acid secretion.
PangastritisPangastritis induces no overall change in acid induces no overall change in acid production.production.
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Helicobacter pyloriHelicobacter pylori and peptic ulcer disease. and peptic ulcer disease.
Diagnosis:
Invasive methods (require endoscopy): HE stain, modified Giemsa stain,
rapid urease test
Non-invasive methods: serology (ELISA), 13C or 14C urea breath test, stool antigen test.
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Helicobacter pyloriHelicobacter pylori and peptic ulcer disease and peptic ulcer disease..
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Helicobacter pyloriHelicobacter pylori and peptic ulcer disease. and peptic ulcer disease.
H.pyloriH.pylori exerts several effects on gastric acid exerts several effects on gastric acid production production
Increase in basal gastrin levels.Increase in basal gastrin levels. Increase in basal acid output.Increase in basal acid output. Increase in peak acid output.Increase in peak acid output.
All effects are reversed after successful eradication of All effects are reversed after successful eradication of H.pylori.H.pylori.
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Treatment Plan: H. PyloriTreatment Plan: H. Pylori
Medications:Medications: Triple therapyTriple therapy for 14 days is for 14 days is considered the treatment of choice. considered the treatment of choice. Proton Pump Inhibitor + clarithromycin and amoxicillinProton Pump Inhibitor + clarithromycin and amoxicillin
Can substitute Flagyl 500 mg PO bid for 14 d if Can substitute Flagyl 500 mg PO bid for 14 d if allergic to PCNallergic to PCN
Goal: complete elimination of H. Pylori. Once Goal: complete elimination of H. Pylori. Once achieved reinfection rates are low. Complianceachieved reinfection rates are low. Compliance!!
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Signs and Symptoms of PUDSigns and Symptoms of PUD
Can be symptomaticCan be symptomatic anorexia, nausea, vomiting, belching, bloating, anorexia, nausea, vomiting, belching, bloating,
heartburn, epigastric pain (pain in the upper abdomen)heartburn, epigastric pain (pain in the upper abdomen) awakened at night (usu. around 3am)awakened at night (usu. around 3am) duodenal ulcersduodenal ulcers
epigastric pain, tenderness, burning, gnawing, epigastric pain, tenderness, burning, gnawing, aching between xiphoid process and belly buttonaching between xiphoid process and belly button
relieved with food intake or antacidsrelieved with food intake or antacids gastric ulcergastric ulcer
diffuse pain over midepigastrium (midstomach)diffuse pain over midepigastrium (midstomach) worsened by foodworsened by food
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Signs and Symptoms, contSigns and Symptoms, cont..
Can also be asymptomaticCan also be asymptomatic ““silent ulcer”silent ulcer” associated with chronic NSAID useassociated with chronic NSAID use
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Complications of PUDComplications of PUD
BleedingBleeding-15%-15% vomited blood or black material that looks like coffee vomited blood or black material that looks like coffee
groundsgrounds red blood in stool usu. indicates hemorrhoidsred blood in stool usu. indicates hemorrhoids if stool black or tarry, foul smelling, usu. doesn’t if stool black or tarry, foul smelling, usu. doesn’t
involve the rectum area involve the rectum area PUD PUD the elderly can bleed w/o any prior symptomsthe elderly can bleed w/o any prior symptoms
Perforation, penetrationPerforation, penetration -6to7% -6to7% gastric outletgastric outlet obstructionobstruction-2% -2%
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Physical examinationPhysical examination
Epigastric tendernessEpigastric tenderness Tachycardia & orthostatic Tachycardia & orthostatic
hypotentionhypotention Severly tender & board like Severly tender & board like
abdomenabdomen Succusion splash- GOO-2%Succusion splash- GOO-2%
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DiagnosisDiagnosis
Barium meal studyBarium meal study Endoscopy –most sensitive & specificEndoscopy –most sensitive & specific DDDD: :
NUDNUD Proximal GI tumorsProximal GI tumors GERDGERD Biliary colicBiliary colic Chronic pancreatitisChronic pancreatitis
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Treatment of PUDTreatment of PUD
ACID NEUTRALISING AGENTSACID NEUTRALISING AGENTS Mg(OH)2,Al(OH)3,CaCO3,NaHCO3Mg(OH)2,Al(OH)3,CaCO3,NaHCO3
ACID SUPPRESSING DRUGSACID SUPPRESSING DRUGS H2 BlokersH2 Blokers PPIPPI
CYTOPROTECTIVE AGENTSCYTOPROTECTIVE AGENTS SucralfateSucralfate Colloid bismuth subcitrate Colloid bismuth subcitrate PGE1 analogue- misoprostole 200mcg qidPGE1 analogue- misoprostole 200mcg qid
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