PUD Flashcards
What is PUD?
ulceration of the mucosa anywhere in the GI tract exposed to acid and pepsin
Which PUD form is most common?
Duodenal > Gastric
What is PUD caused by?
- Helicobacter pylori (HP)
- Chronic NSAID use
- Stress-related mucosal damage
Does smoking improve or worsen PUD?
worsen
What is the mechanism of stress-related mucosal damage?
- decreased mucosal defense mechanisms
- emotional stress –> increased smoking/ NSAID use –> increased risk of PUD
What is the pathogenesis of PUD?
Imbalance between aggressive factors and mechanisms that maintain mucosal integrity
What is the most common cause of duodenal (~95%) and gastric ulcers (~80%)?
H. pylori
How is H.pylori spread?
- fecal to oral route
- oral to oral route
What are possible mechanisms for H.pylori induced mucosal damage?
- catalyzes urea–> ammonia–> erodes mucosal barrier and epithelial damage
- production of cytotoxins
- production of mucolytic enzymes
How likely are ulcers caused by chronic NSAID use?
Duodenal (2-5%) and gastric (10-20%)
What are mechanisms for NSAID induced ulcers?
- inhibit cyclooxygenase activity–> decrease prostaglandin production
- decrease gastric and mucosal blood flow
- decreased mucus and bicarbonate secretion
- decreased cellular replication and repair
Who is more likely to experience major complications due to NSAIDs?
- > 60 y/o
- Hx of PUD
- High dose/ multiple NSAIDs or low dose ASA daily,
What medications administered with NSAIDs will increase risk of PUD?
- corticosteroids
- anticoagulants
- oral bisphosphonates
- antiplatelet agents
- SSRIs
What NSAID is the most ulcerogenic?
Aspirin
What is the first presentation of NSAID-induced ulcers?
bleeding/ perforation
What are common presentations of gastric ulcers?
- pain is not predictable
- food can cause pain
- weight loss
What are common presentations of gastric ulcers?
- pain more likely to follow consistent pattern
- food often eases pain and returns in 1-3 hours
- noctural epigastric pain
- nonspecific dyspepsia
What are the major complications of PUD?
- bleeding
- perforation
- death from acute bleeding
What lab tests are used to determine H.pylori-induced ulcers?
- Rapid Urease Test (CLO test)
- serologic antibody test
- Urea Breath Test (UBT)
- Fecal Antigen Test (FAT)
How is the Rapid Urease test done?
Mucosal biopsy–> urea rich medium with pH sensitive dye–> HP urease will produce NH3, increase the pH and cause a color change
How does a serologic test determine HP infection?
Detects IgG to HP in serum
What are problems with the serologic test?
Can’t distinguish active infection from past exposure because antibodies persist for up to 5 years
How does the Urea Breath Test (UBT) work?
Patient ingests molecule with C 13/14–> H. pylori urease produces CO2 13/14–> CO2 13/14 is in blood and can be detected in breath
How does the Fecal Antigen Test (FAT) work?
polyclonal antibody test detects presence of HP in the stool
Patients recently taking antibiotics & bismuth compounds (~4 weeks), or anti-secratory agents (~2weeks) can cause false positives in what test?
UBT
What tests are used for initial screening for infection?
serologic, UBT, FAT
What tests are used to determine eradication?
UBT and FAT
How long after treatment is completed do you need to wait before confirming eradication?
4 weeks
What are 1st line therapies for HP eradication?
- Bismuth-based quadruple therapy
- Standard Triple Therapy
- Concomitant therapy
What is used for Standard Triple Therapy?
Amoxicillin + Clarithromycin + PPI
Penicillin allergy: Metronidazole
When is Standard Triple Therapy 1st line?
Clarithromycin resistance rates <15% and patient has NEVER taken a macrolide antibiotic
What is used for Bismuth-based Quadruple Therapy?
Tetracycline + Metronidazole + Bismuth subsalicylate + PPI
What can be used for Bismuth-based Quadruple therapy if there is a salicylate allergy?
Bismuth subcitrate (Pylera)
When is Bismuth-based quadruple therapy
1st line?
Clarithromycin resistance rates > 15% and/ or patient has taken a macrolide antibiotic
What agents are used for concomitant therapy?
Clarithromycin + Amoxicillin + Metronidazole/ Tinidazole + PPI
What are 2nd line “salvage therapies”?
- Levofloxacin-based Triple Therapy
- Rifabutin-based Triple Therapy
What agents are used for Levofloxacin-based Triple Therapy?
Amoxicillin + Levofloxacin + PPI
What agents are used for Rifabutin-based Triple Therapy?
Omeprazole + Amoxicillin + Rifabutin
When would Rifabutin- based triple therapy be used?
persistent HP infection; preferred if patient received clarithromycin therapy prior
How long after eradication is a PPI continued for?
2 weeks
What is used to treat H. pylori negative ulcers?
H2 antagonists
Sucralfate
PPI
How long does it take for H2 antagonists and Sucralfate to heal ulcers?
6-8 weeks
How long does it take for PPIs to heal ulcers?
4 weeks
Which kind of ulcers are more difficult to treat?
gastric ulcers
What are treatment options for NSAID induced ulcers?
- D/c NSAID
- Stardard healing dose of H2RA, sucralfate, or PPI
What are treatment options for NSAID induced ulcers when NSAIDs cannot be discontinued?
- Decrease dose
- APAP, non-aceylated agent, selective COX-2 inhibitor
- Use PPI
What patients should receive long term maintenance therapy with a PPI or H2RA?
- HP positive ulcers with failed eradication attempts
- refractory ulcers
- heavy smokers
What agents are best for chronic NSAID users to prevent recurrence of ulcers?
- PPIs
- Misoprostol
What are important counseling points for patients with PUD?
- communicate cause
- address risk factors
- rationale of multi-drug regimens and importance of adherence + completion of therapy
- make patient aware of GI bleeding
What are signs of GI bleeding?
- tarry stools
- abdominal pain
- vomiting with blood
