peptic ulcer disease cengiz pata,md dept. gastroenterology, yeditepe university, medical center
DESCRIPTION
Case Pain: What type of pain? How often? Awakes at night? Relation to food? Complications: Vomiting? (obstruction?) Stools? (melena?) Common deferential diagnosis: Pnacreatobiliary disease Dyspepsia TumorsTRANSCRIPT
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Peptic Ulcer Disease
Cengiz Pata,MDDept. Gastroenterology,
Yeditepe University, Medical center
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Case
• 30 year old male• Epigatsric pain radiating to the back
Questions?
Possible diagnosis
Deferential diagnosis
Possible complications
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Case • Pain: • What type of pain?
How often?Awakes at night? Relation to food?
• Complications:• Vomiting? (obstruction?)
Stools? (melena?)• Common deferential diagnosis:• Pnacreatobiliary disease
DyspepsiaTumors
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Case
• Next diagnostic step? • Endoscopy
Abdominal USUGI?
• DU Ulcer detected- next step? • Test for H. pylori
Exclude NSAID use Rare – assess gastrin, mainly in unusual cases
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Benign gastric ulcer (B)
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Peptic Ulcer
• A defect in the gastrointestinal mucosa extending through the muscularis mucosa.
• Two main forms:1) Helicobacter associated 2) NSAID associated ( Steroids alone – no additional risk, Increased risk when combined with NSAIDS)
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Peptic Ulceration : Additional Causes
• Acid hypersecretion:Gastrinoma ( ZE)Systemic mastocytosisBasophilia in myeloproliferative disorders
• ViralHerpes simplex CMV ( mainly in immune compromised)
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Peptic Ulceration : Additional Causes• Vascular Insufficiency
( including due to crack cocaine)
• Radiation induced
• Chemotherapy induced
• Stress ulceration
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Electron micrograph of H. pylori
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Prevalence of Helicobacter pylori in peptic ulcer
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Seroprevalence of H. pylori with increasing age in developed and developing countries
Developing countries Developed countries100
0
25
50
75
<20 40-50 <20 40-50
10-75%
64-96%
6-39%7-54%
Age range (years)
Prev
alen
ce (%
)
Adapted with permission from Heatley-Helicobacter pylori and Gastrointestinal Disease; Oxford, UK: Blackwell Scientific Publications
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Risk factors for H. pylori infection
• Age
• Country of origin
• Socio-economic status poor housing
bed sharing
overcrowding
large families
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Modes of transmission of H. pylori infection
• Zoonosis unlikely
• Environment unlikely
• Person-to-person oral-oral likely
gastro-oral likely
faecal-oral likely
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H. pylori infection and disease associations
•Chronic gastritis
• Duodenal ulcer
• Benign gastric ulcer
• Gastric carcinoma
• Gastric MALT and non-Hodgkin‘s lymphoma
• Ménétrier‘s disease
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Pattern of gastritis
Duodenal ulcer Gastric ulcer
*H. pylori colonizes areas of gastric metaplasia, leading to chronic duodenitis and eventually duodenal ulcer.
Antralgastritis
*
Corpusitis
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NSAIDS
• In the USA 30 bil OTC 20 mil prescriptions• 3-4% ulcerations• 20,000 die of NSAID complications• 80% have no preceding dyspepsia• Important to identify at risk populations
Previous gastritisElderly
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PD & Systemic Diseases
• COPD
• Renal Failure
• Cirrhosis
• Mastocytosis
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Clinical Presentation
• Abdominal Pain: Epigastric dull “hunger pain”DU- 11/2 –3 hrs postprandial relived by foodMay awake at night GU – May occur with meals
• nausea weight loss more frequent in GU• Sudden pain – perforation?• Vomiting – obstruction?
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Clinical Presentation
• Physical examination:• Poor predictive value, not specific• Pain may occur in RUQ ~ 20%• Detect complications:
Tachycardia, orthostasis- bleeding?Radiation to the back- perforation?Succussion splash – outlet obstruction?
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Complications
• Bleeding ~ 15% ( More in >60 yrs –NSAID)20% - no warning sign
• Perforation 6-7% FreePenetration: DU posterior to pancreas
GU into Lt hepatic lobe Gastrocolic fistula
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Complications
• Outlet obstruction 1-2%Inflammatory – reversible by TxScar tissue – balloon dilatation, Surgery
• Presentation : Gradual onsetSudden
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Clinical manifestations of ulcer disease
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Differential Diagnosis
• Non ulcer dyspepsia• Tumors of the UGIT• Biliary disease• Reflux disease• Vascular diseases• Pancreatitis • Coronary heart disease
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Diagnosis
• Radiology:Single contrast 80% sensitivity Double 90%(worse for ulcers<0.5 cm, scar tissue)
• Endoscopy: examination of choice good for small ulcersbiopsy samples for HP and malignancytherapeutic
• Assay for HP infection
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Diagnostic methods for H. pylori
Diagnostic method
Histology
Main indication
Diagnosis
Sensitivity (%)
90
Specificity (%)
90
Culture H. pylori antibiotic sensitivities
80-90 95
Rapid urease test
Endoscopy room diagnosis
90 90
Serology Screening and diagnosis
90 90
Urea breath test
To confirm eradication
95 100
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The principle of the urease test
NH2
C
NH2
O + 2H2O + H+
2NH4+
+ HCO3-
Urease
Urea CLOtest
pH change
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The principle of the 13C- or 14C-urea breath test
Reproduced with permission from Mr Phil Johnson, Bureau of Stable Isotope Analysis, Brentford, UK.
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Therapy• Treat H. pylori
• Healing by inhibition of acid secretion:H2 receptor antagonists (H2RA)Proton Pump inhibitors ( PPI)Anti Acid
• CytoprotectionSucralfateAnti AcidBismuth-BasedProstaglandin Analogs
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Therapy of DU
• H2RA – Cure in 80% at 4 wks~95% at 8 wks Split and once daily equally effective
• PPI- Cure in 60-93% at 2 wks 80- 100 % at 4 wks
• Omeprazole Vs ranitidine 14% advantage at 2 wks 9% advantage 4 wks
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Therapy of GU
• Suppress acid by H2RA or PPI• Advantage of PPI less apparent• Sucralfate comparable to H2RA
• Prepyloric ulcers may resemble more DU in terms of response to acid suppression
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Risk stratification of Ulcer Pts
• Low risk:
Intermittent symptomsNonsmokerDiscontinued NSAIDUncomplicatedEasy healing
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Risk stratification of Ulcer Pts• High risk:
Frequent recurrenceRefractory to TxSmokingContinued NSAIDGiant Ulcer ( DU >2 cm GU > 3 cm)AnticoagulationDeformity & scarringElderlyAcid hypersecretion
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General Scheme• HP positive – Eradicate • If Non complicated – No further Tx• If high risk: • Follow by acid suppression for 4-6 wks• Withdraw –
NSAIDSmoking Excess Alcohol
• In GU – Biopsy? Cost and effect- Most CAs detected in first round of endoscopy
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Refractory Ulcers
• Consider refractory after 8-12 wks of Tx• Ensure that refractory symptoms
= refractory ulcer ( endoscopy) • If no ulcer - investigate pain• Consider “silent” refractory ulcer in high risk
pts ( ~25% of refractory ulcers)
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Refractory Ulcers - causes
• Persistent HP infection• Persistent NSAID use • Poor pt compliance• Giant ulcers ( healing at 3 mm/wk)• Smoking• Under laying pathology ( ZE, bands,
crohn’s,infections I.e. TB syphilis, Ly, scarcoidosis )• Impaired response to PPI ( 5% of population)
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Refractory Ulcers - Approach
• Seek causes:DU- HP, NSAIDS, r/o ZE ( gastrin levels)
GU- main concern CARepeat multiple BxEvidence for malignancy: CT, EUS
No explanation - surgery
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Surgery - DU
• Refractory bleeding (~5% of transfused Pts)• Perforation (2-3%)• Outlet obstruction
• Vagotomy + antrectomy Rec. (1%) Comp Vagotomy + pyloroplasty intermediate (10%)Highly selective vagotomy Rec. Comp
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Zollinger Ellison Syndrome
• Severe peptic ulcer diathesis + gastric acid hypersecretion due to -cell endocrine tumor
• 0.1-1% of PUD patients
• Sporadic, or associated with MEN type I (25%)
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Zollinger Ellison Syndrome
• >80% Localized to gastrinoma triangle:cystic & common bile ducts, duodenum, junction head and body of pancreas.
• 60 % malignant, up to 50% with metastasis
• Clinical: PUD >90% (recurrent, multiple, refractory, complicated)
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Zollinger Ellison Syndrome
• Esophageal complaints ~60%
• Diarrhea ~50% (fluid overload, pancreatic enzyme dysfunction, epithelial dysfunction)
• Combination should raise clinical suspicion
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Clinical features of Zollinger-Ellison syndrome
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MEN I • Autosomal Dominant:
Parathyroid (~90%), Pancreas (40-80%)Pituitary (30-60%)
• Contributory effect of hyperparathyroidism, hypercalcemia hypergastrinemia acid secretion
• Higher incidence of carcinoids
• Smaller and multiple duodenal gastrinomas
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Diagnosis of Gastrinoma
• Combination of clinical signs • Fasting gastrin levels (> 150 pg/ml) • Avoid confounding factors
(hypochlorhydria, PPIs, outlet obstruction, renal failure)
• Assess acid secretion (if low- excludes)• Provocative tests (calcium, secretin)
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Treatment
• Localization (EUS, Oct scan, MRI, CT)
• Exclusion of metastasis
• If positive – symptomatic cure
• If negative attempt surgical resection ( less likely in MEN I ~ 6%)
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Case -2
• 70 year old lady , RA
• Dizziness and weakness for the last week.
• Mild abdominal pain
• Questions?
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Case-2
• Stools? • Melena • Drugs? • NSAIDS• Next action? • Gastroscopy
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Gastric Ulcer with Stigma
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Treatment
• H2RA
• Oral PPI
• Oral PPI + H2RA
• IV PPI
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H2 RA
• Very safe drugs
• Tolerance after 48 hrs IV treatment
• Less effective than PPIs in suppressing acid secretion (block only histamin)
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Treatment
• Heavy consumption of NSAID
• Should H. pylori be tested for? Treated?
• YES
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Drugs for treatment of acid disorders and H. pylori infection• H2 Receptor antagonists
• PPI
• Anti H. pylori regimens
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Overall Control of Acid Secretion
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The parietal cell
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The proton pump
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Biologic mechanism of action of substituted benzimidazoles (proton pump inhibitors)
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Kinetics of PPI Effect
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Summary of PPI effects • Inhibit ~70% of acid secretion
• Need to coordinate pump activation & PPI availability (t/2~60-90 min)
• Pump re-synthesis (half life ~ 50 hours 25% synthesis between single day doses)
• Cysteins accessible to reducing activity of glutathione
• Spontaneous pump recycle every 60-120 min (Potential to block)
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Optimization of acid control
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Guidelines for use of antibiotic therapy in patients with Helicobacter pylori infection
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Treatment regimens for eradication of Helicobacter pylori
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Therapeutic options
clarithromycin2 x 250 - 500mg
metronidazole2 x 400 - 500mg
amoxycillin2 x 1000mg
PPI X 2eradic
ation
rate
90%
eradication rate
90%
eradication rate >80%
_<
_<
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Choice between treatments
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Treatment failures
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