Dyspepsia & Peptic Ulcer Disease Flashcards
Peptic Ulcer Disease
defintiion
• Group of ulcerative disorders “ dependent on acid & pepsin
• Primarily refers to gastric (GU) & duodenal ulcer (DU)
• Presentation: Dyspeptic symptoms, (e.g., episodic upper abdominal pain, bloating, abdominal
fullness, nausea, early satiety), Asymptomatic (70%)1, Complicated (hemorrhage, perforation)
• Natural HX: Healing w/o intervention, Upper GI bleeding, Perforation,
Obstruction. (severe)
• Two major causes: H. pylori infection; NSAID use
• Diagnosis: Visualization via endoscopy.
Typically episodic upper abdominal pain
Ulcers
Many pt are asymptomatic, usually heal on its own
Peptic Ulcer Disease
normal defenses
vs aggressive factors
normal:
Mucus
HCO3
Prostaglandins
aggressive:
H. pylori, NSAIDs
Smoking, EtOH
Acid, Pepsin
Dyspepsia
• Definition
– Symptom complex of epigastric pain or discomfort originating in the upper GI (epigastric)
tract (e.g., Nausea, bloating, fullness, early satiety, slow digestion, excessive burping,
heartburn, acid regurgitation)
• Canadian prevalence: 29% 7% of visits to family physicians • Etiology – Organic (40%) • GERD most common (30%) • Peptic Ulcer Disease (20%) • Cancer (<1%) – Functional Dyspepsia (60%) • Non ulcer dyspepsia (NUD) • Non erosive reflux disease (NERD)
Approach to Undiagnosed Dyspepsia
• Research definitions of dyspepsia (Rome Criteria)
attempt to $ inclusion of GERD
– (i.e., exclude pts with heartburn or acid
regurgitation as primary symptom)
• In practice, there is considerable overlap in
symptom presentation & it can be difficult
to distinguish b/w dyspepsia & GERD.
• Clinically relevant definition of dyspepsia:
Predominant epigastric pain lasting at least
1 month.
Approach to Undiagnosed Dyspepsia
flowchart
see slide 7 for more
- check for other causes: cardiac, hepatobiliary, medication
- red flags: >50, vomiting bleeding/anemia, abdominal mass, weight loss, dysphagia –> endoscopy rec
- NSAID and regular ASA use?
- Is dom symptom heartburn regurgitation?
if yes, treat as reflux - do H. pylori test
history - q’s to ask
History
• Exclude non GI sources of pain
• Identify those with predominant reflux like Sx
• Medication History for causes/aggravators of
dyspepsia (e.g., ASA, NSAIDS, antiplatelet,
bisphosphonates, CCB, iron, etc.)
Etiology of PUD
most common
less common
risk factors (4)
• Most common: H. pylori, NSAIDs
• Less common
– Stress ulcers
– Acid hypersecretory states (e.g. Zollinger-Ellison Syndrome)
– Other drugs: clopidogrel, sirolimus, bisphosphonates
– Viral (Herpes simplex, Cytomegalovirus)
– Vascular insufficiency/Crack cocaine
– Chemotherapy/Radiation
– Idiopathic
• Risk Factors
– Smoking, Alcohol, Genetic Factors, Psychological stress,
– Uncertain: Dietary factors
Definitions Peptic Ulcer Gastric ulcer (GU) Duodenal ulcer (DU) Gastritis:
Peptic Ulcer: A mucosal break in the stomach or duodenum ≥5mm.
Gastric ulcer (GU) Most commonly in the antrum & lesser curvature.
Duodenal ulcer (DU) Most commonly in the Duodenal bulb
Gastritis: Inflammation associated with gastric mucosal injury.
Peptic Ulcer Disease
Epidemiology
• Lifetime prevalence in North America ~ 10%1
• ~2,500 cases/year in Alberta2
• PUD Trends
– Incidence increases with age
– Similar incidence in men & women
– $ Peptic ulcer & GI cancer rates (upper GI malignancy more common
after 55 years of age)3
– # Peptic ulcer hemorrhage & perforation in older individuals
Helicobacter pylori
• Gram negative bacteria: lives b/w mucous layer & surface epithelial cells
• Causally linked to:
– Gastritis, Peptic ulcer disease
– Gastric cancer (2.8 – 6x risk), (MALT) lymphomas
– Lack of causal evidence for GERD
• Mechanism of injury
– Direct mucosal damage
– Alterations in the immune/inflammatory response
– Hypergastrinemia leads to hypersecretion of gastric acid
• Eradication thought to decrease gastric cancer risk, but unproven
• Of patients with H. pylori infection
– 20% get symptomatic PUD
– < 1% develop stomach cancer
H. pylori Epidemiology
risk factors (3)
transmission
• Prevalence in Canada: 35-40%1
– ~30% of Canadians with dyspepsia have active H. pylori infection.4
– $ Prevalence over time
• Risk Factors: – Population density
– Lower socioeconomic status
– Ethnicity (e.g. up to 95% on a reserve)2 & recent immigrants3
- No association with gender & smoking status
- Transmission: Gastro-oral, Fecal-oral, maternal colonization
- Percent of ulcers that are H. pylori positive
H. pylori Diagnosis
Non-invasive Methods (3)
• Urea breath test (UBT)
– Makes use of H. pylori’s urease enzyme
– Collect breath samples before & after oral ingestion of radiolabeled substrate with a test tube or balloon
– If H. pylori is present, radiolabeled urea is hydrolyzed to ammonia & radiolabeled CO2 “ positive test
– 2 different UBT 13C = Helikit
• Stool antigen test (HpSAT)
– First line test for diagnosis in Alberta
– Also useful for evaluating treatment success
• Serology
– IgG antibodies to H. pylori
– Remains positive after successful eradication
– Higher False Positive rate (~20%)
H. pylori Diagnosis
Invasive (i.e. Endoscopic) Methods (3)
- Biopsy rapid urease:
- H. pylori urease generates ammonia
- Culture:
- Gold standard
- Histology:
- Allows direct identification, look under microscope
H. pylori Diagnosis
Rely on amount of bac present
Affected by current PPI therapy or recent antibiotic ues
False Negative Results are Common
Important with tests that depend on bacterial load
– UBT Prep Stool antigen testPrep Culture, rapid urease, & histology,
• Common after use of antibiotics, proton pump
inhibitors, & bismuth
– To minimize false negatives, when checking H. pylori status
patient should be off (if possible)1
• Antibiotics, bismuth: 4 weeks
• PPI: 1-2 weeks
Goals of Therapy
• Overall goals
– Relieve ulcer pain, Heal ulcer, Prevent ulcer recurrence
– Prevent ulcer complications & A/E from drug therapies
• H. pylori positive: Eradicate H. pylori “ Cure the disease
– Want to use regimens that have ITT cure rates of > 80%
– Successful eradication increase ulcer healing & decrease recurrence
“Need to treat 2 patients with Hp eradication instead of placebo to prevent 1 duodenal ulcer relapse.”
