Lecture 11 PUD Flashcards
What is dyspepsia and its etiology
Epigastri pain or discomfort originating in the upper GI tract ( eg. Nausea, bloating, fullness, slow digestion, burping, heartburn)
Etiology: Organic (40%)
GERD (30%)
PUD (20%)
Cancer (<1%)
Functional dyspepsia (60%)
Non ulcer dyspepsia (NUD)
Non erosive reflux disease (NERD)
Presentation, natural HX, causes and diagnosis of peptic ulcer disease
Presentation: Dyspeptic symptoms ( upper abdominal pain, bloating, abdominal fullness, early satiety). (Asymptomatic 70%)
Natural hx : healing w/o intervention, upper GI bleeding, perforation, obstruction
Two major causes: H. Pylori, NSAID use
Diagnosis : endoscopy visualization
Clinically relevant definition of dyspepsia is ….
Predominant epigastric pain lasting at least 1 month
See slide 7 in notes
Risk factors for PUD
Smoking, alcohol, genetic factors, psychological stress
Uncertain : Dietary factors
Definition of
Peptic ulcer
Duodenal ulcer
Gastric ulcer
Gastritis
Peptic ulcer: mucosal break in the stomach or duodenum >5mm
Duodenal ulcer: most commonly in the duodenal bulb
Gastric ulcer: most commonly in the antrum and lesser curvature
Gastritis: inflammation associated with gastric mucosal injury
True or false, incidence of PUD increases with age
True
Helicoobacte pylori
Bacteria type
Casually linked to what diseases
Mechanism of injury
Gram negative bacteria : lives between mucosal layer and surface epithelial cells
Causally linked to gastritis, peptic ulcer disease, gastric cancer
Direct mucosal damage, alterations in the immune/inflammatory response, hyper gastronomic leads to hyper secretion of gastric acid
Risk factors of H.pylori and transmission
Population density, lower economic socioeconomic status
No associated with gender
Transmission: gastro-oral, fecal-oral, maternal colonization
H pylor diagnosis ( 3 ways)
Urea breath test (UBT): collect breath sample before and after oral ingestion of radiolabeled substrate with a test tube or balloon, if present radio labeled urea is hydrolyzed to ammonia and radiolabeled co2 -> positive test
Stool antigen test: First line test for diagnosis in Alberta
Serology: rapid point of care test, IgG antibodies of H pylori, remains positive after successful eradication
How to minimize false negative on H pylori test
Patient should be off of antibiotics, bismuth : 4weeks, PPI 1-2 weeks
First line recommendations for treating PUD
PBMT: PPI + bismuth + metronidazole + tetracycline
PAMC : PPI + Amoxicillin+ metronidazole + calrithromycin
PPI triple:
PAC
PMC
PAM
All for 14 days because leads to 10% higher eradication rate
Quick tip ***
Recommended dosing for regimen of H pylori
Use
Omeprazole 20mg po BID
Amoxicillin 1g po BID
Metronidazole 500mg BID
Clartihromycin 500mg po BID
Tetracycline 500mg po QID
Levofloxacin 500mg po daily
Rifabutin 150mg po BID
Pepto bismol 2 caplets po QID
Resistance patterns in Canada and locally in Alberta of
Metronidazole
Clarithromycin
Amoxicillin
Tetracycline
Metrondiazole: 20%
Calrithromycin: 2-8%
Amoxicillin: <1%
Tetracycline : < 3%
Treatment for patients not allergic to penicillin (H pylori
1st line
2nd line
3rd line
4th line
1st line: PAMC, PBMT
2nd line: PMAC, PMBT
3rd line: Levo-amox (PAL)
4th line: rif-amox (PAR) or refer to GI
Main adverse effects of…
Metronidazole
Calrithromycin
Tetracycline
Amoxicillin
Bismuth
- disulfiram reaction, metallic taste
- altered taste, CYP 3A4
- photosensitivity skin reactions
- diarrhea
- darkening of stool, diarrhea
Read page 30 pathway
General principles for 1st line treatment failure
Use different first line therap than that used initially
Ex. PPI BID + amoxi 1g BID + levofloxacin 500mg daily for 14 days
Is maintained acid suppression required after successful H.pyloi eradication
No need for curative course of acid suppression after therapy eradication
May be indicated for, uncomplicated gastric ulcers, patient with frequent ulcer recurrences, heavy smokers
Duration 8 weeks PPI
PUD in pregnancy
Postpone treatment untill after pregnancy
Dyspepsia with a normal endoscopy
Non drug management
Drug therapy
Non drug: reassurance, avoidance of triggers
Drug therapy: empirical PPIx 4-8 weeks, little evidence for long term PPI treatment, tricyclic antidepressants
Clinical characteristics of H.pylori and NSAID induced ulcers
H. Pylori : Chronic, DU> GU, More dependent, usually epigastric, superficial, less severe, single vessel
NSAID induced: Chronic, GU>DU, Less dependent, often asymptomatic, deep, more severe, single vessel
Most and least GI toxic NSAD and COX-2
NSAID
Most: Ketoprofen
Least: Ibuprofen
COX-2
Most: refecoxib
Least: ketorolac
Myth about NSAID induced Ulcers
Low dose ASA dose not cause GI ulcers
Buffered/Coated ASA is better for preventing ulcers
Acute upper GI bleeding (AGIB)
Signs and symptoms
Etiology
Goals
Signs and symptoms: hematemesis, Melena, hematochezia, weakness, dizziness
Etiology: Categorized as Variceal, PUD accounts for 50% of upper GI bleeds
Goals : stabilize patients, relieve ulcer pain, heal ulcer, prevent ulcer recurrence, prevent complications
Overview of treatment of NSAID induced Ulcers
If you can stop the NSAID, then discontinue
If continued NSAID is absoultely necesssary, secondary prevention with PPI or misoprostl co-therapy or COX-2 inhibitor
Quick pointers for PPI, H2RA
PPI superior to H2RA
Misoprostol similar to omeprazole for ulcer healing, but increase adverse effects; omeprazole is better for maintained of remission
All different treatment of NSAID induced ulcers
Pantoprazole, Rabeprazole, omeprazole, esomeprazole, lansoprazole, dexlansoprazole, ranitidine, cimetidine, famotidine, nizatidine
For DU typically 4 weeks for “azoles” but 4-8 for GU
Stress related mucosal bleeding
Majority risk factors and prevention
Majority risk factors: mechanical ventilation, coagulopathy, hypotension, sepsis, hepatic failure etc….
Prevention with
Enteral nutrition
H2RA
PPI
Sucralfate
Look at page 60 deprescribing
Summary for
H pylori PUD
Functional Dyspesia
NSAID PUD
PUD Bleed
PPI de-prescribing
H pylori PUD:
- Typically diagnosed by UBT; eradication if test positive
-trend to treat with more drugs for longer duration
- acid suppression post eradication: NOT for uncomplicated DU; yes GU
Functional Dypepsia:
- moderate quality of life evidence for TCA, very low for pro kinetics and psychotherapy
NSAID PUD:
- assess risk for GI toxicity, routine prev. Not indicated for all ( PPI-Misoprostol>H2RA)
-Treatment: Stop NSAID, PPI x4 weeks DU, 8 wks GU
PUD Bleed:
- IV PPI bolus & 72 hr CIVI lower re-bleed risk, length of stay, & need for transfusion, no mortality benefit
PPI De-prescribing:
- Don’t maintain long term PPI therapy without an attempt to reduce/stop treatment once yearly in appropriate patients
