3 - GI Flashcards
Where in the GI tract is PUD most common?
Lesser curvature of the stomach
Duodenum
The defensive factors of the GI mucosa include:
Mucus
Bicarbonate
Blood Flow
Prostaglandins
Why are prostaglandins so helpful to the mucosa?
Stimulate secretion of mucus and bicarbonate
promote vasodilation
suppress gastric acid secretion
Why isn’t H. Pylori destroyed in the stomach?
It resides in between the epithelial cells and the mucus barrier
Why are NSAIDs so harmful to the gut?
Because they inhibit prostaglandin growth
Acid itself is almost never enough to cause PUD. The only disease in which gastric acid consistently causes PUD is:
Zollinger-Ellison Syndrome
(a tumor that secretes gastrin, causing MASSIVE amounts of acid release)
What are the factors that aggressively attack the Mucosa?
H. Pylori
NSAIDs
Gastric Acid
Pepsin
Smoking
If a patient is at risk for a peptic ulcer but has to take NSAIDs, what can be done prophylactically?
You can start them on a PPI (omeprazole). Can also do misoprostol, but it causes diarrhea so it’s not preferred
If NSAIDs can’t be discontinued and the patient has an ulcer, how should treatment proceed?
A PPI is the best choice
How big a role does diet play in PUD?
Actually, very minor role
the ulcer diet really doesn’t accelerate healing and their no evidence that caffeine promotes ulcer formation
BUT frequency can have an effect. Eater smaller more frequent meals can promote healing
Which ABX are most often employed to combat H Pylori?
Clarithromycin
Amoxicillin
Bismuth
Tetracycline
Metronidazole
Tinidazole
Which ABX is used alone to treat H Pylori?
None of them!
H2 RECEPTOR BLOCKERS
MOA AND DRUG LIST
Cimetidine (Tagamet)
H2 receptors cause acid secretion
Suppresses both basal secretion AND secretion stimulated by gastrin and acetylcholine
When should cimetidine and antacids be taken?
At least an hour apart
PROTON PUMP INHIBITORS
MOA AND DRUG LIST
Omeprazole
Prodrug that’s converted to active form in the parietal cells
Causes irreversible inhibition of H,K-ATPase pump, blocking acid formation
Inhibits basal and stimulated gastric acid
Which is more effective: PPIs or H2 blockers?
PPIs!
They also act faster
Why do H2 blockers and PPIs increase the risk of pneumonia?
Anytime you decrease the acidity of the stomach, you allow bacteria to proliferate
This results in a secondary increase in the colonization of the respiratory tract AND impaired WBC function
When are patients at highest risk of developing pneumonia if they take a PPI?
Only within the first few days. After that the risk drops off
How does acid secretion impact osteoporosis?
decreased acid secretion means decreased absorption of calcium
Which electrolyte is most impacted by long term PPI use?
Magnesium (causes hypomagnesemia)
SUCRALFATE
MOA
Promotes healing by creating a protective gel that adheres to the ulcer crater, creating a barrier to the back diffusion of H ions
DOES NOT have any effect on acid secretion
How can the adverse GI effects of antacids be minimized?
Combine an antacid that causes diarrhea (magnesium hydroxide) with one that causes constipation (aluminum hydroxide)
OR give it with sodium
There are four groups of antacids:
Aluminum Compounds
Magnesium Compounds
Calcium Compounds
Sodium Compounds
Why do bulk-forming laxatives work?
They basically cause the poop to swell, softening the stool and stretching the intestinal wall (which stimulates peristalsis)
