Drug Therapy for Peptic Ulcer Disease Flashcards
Peptic Ulcer Disease (PUD) (Patho)
Group of gastrointestinal disorders
Differentiated by degree of erosion of gut wall
Caused by:
Imbalance between aggressive and defensive factors
Pepsin
Proteolytic enzyme the promotes protein breakdown
Pepsin activity is pH dependent
As pH increases so does pepsin activation
pH of > 5 is needed to prevent pepsin activation
Goal of drug therapy should be to raise gastric pH above 5
Most Common Causes of PUD
Helicobater pylori (H. pylori) #1 cause Additional aggressive factors must also be present
Non-steroidal anti-inflammatory drugs (NSAIDs) #2 cause
H. pylori
Gram (-) bacillus
Colonizes stomach and duodenum
NSAIDs
Prevent synthesis of prostaglandins (group of lipids made at sites of tissue damage or infection that are involved in dealing with injury and illness)
Pepsin
Proteolytic enzyme (enzymes that break protein)
Smoking
Delays ulcer healing
↑ risk of recurrence
Mucus
Protective barrier over the underlying epithelial cells
Bicarbonate
Base secreted by epithelial cells; neutralize acid
Blood flow
Maintains healthy cells and prevents ischemia
Prostaglandins
Molecules that promote mucus and bicarbonate production
GERD
Occurs when stomach acid or bile reflux back into the esophagus
Primary cause:
Incompetent lower esophageal sphincter (LES)
Factors contributing to impaired LES function
Foods Alcohol Caffeine Medications Smoking Recumbent position
Histamine2 Receptor Antagonists (H2RA)
Drugs Cimetidine Ranitidine Famotidine Nizatidine
Histamine2 Receptor Antagonists (H2RA)
Cimetidine
Ranitidine
Famotidine
Nizatidine
A first-line treatment for PUD and GERD
Promote gastric healing by preventing acid secretion
All 4 agents equally effective
Serious adverse reactions uncommon
Cimetidine (difference)
Adverse effects:
CNS
Increased risk of Pneumonia
DDI:Inhibitoy of CYP450
Antacids
Proton Pump Inhibitors (PPI)
Omeprazole
Esmoeprazole
Lansoprazole
Dexlansoprazole
Rabeprazole
Pantoprazole
Proton Pump Inhibitors (PPI)
Most effective drugs for inhibiting acid secretion
All agents equally efficacious
Well tolerated
Selection based on cost, preference, DDIs
Mechanism of Action PPI
Irreversible inhibition of proton pump
- -Short half-life
- -Long PD effects
- -New proton pumps must be created to overcome affects of drugs
- -EXCEPTION rabeprazole
Sucralfate MOA AND PHARMACOKINETICS
Mechanism of action
Undergoes polymerization and cross-linking in the stomach → sticky gel
Binds to ulcer
Blocks acid and pepsin from reaching tissue
Pharmacokinetics
Minimal systemic absorption
Duration of action ~6 hour
Sucralfate (Indications, AE, DDI’s, Implications)
Indication
Treatment and maintenance of PUD
Adverse effects
Constipation
DDIs
Minimal
May ↓ absorption of some medications
Nursing implications:
Give 1 hour before meals
Separate from other medications by ~2 hours
Misoprostol (MOA and Indications)
Mechanism of action
Analog of prostaglandin E1 (PGE)
Promotes PGE synthesis
Indication
Prevent ulcers in patients on chronic NSAID therapy
Misoprostol (AE, Contraindications)
Adverse effects: Diarrhea Abdominal pain Contraindications Pregnancy – category X drug Precautions MUST be taken in women of child-bearing age
Antacids
Alkaline products that neutralize stomach acid
- -If pH raised > 5, may also inhibit action of pepsin
- -May increase production of PGE
Poorly absorbed systemically
Exception sodium bicarbonate