Flashcards in GI1 Deck (26)
In the stomach, parietal cells release:
Why would you give a GERD/ulcer patient an anticholinergic at bedtime?
prolonged reduction in acid secretion beyond the duration of a simple antacid
Which receptors is blocked by substituted benzimidazoles?
Remember these are the PPIs, so it is the H-K-ATPase on the lumenal surface of the parietal cell
Which drug is given as an ulcer treatment in RA patients? What is the rationale?
Misoprostol; since RA pts and others are on NSAIDs, ulcer risk is high, so replace prostaglandins with PGE2 analog
Which drug class is the only to primarily effect the lumenal rather than the basolateral surface of parietal cells?
PPIs: substituted benzimidazoles
Which class of antireflux/acid medications has rebound acidity after cessation of treatment?
What?s the worst thing about treating ulcers?
They come back!
What two layers overlay and are secreted by the superficial epithelial cells of the stomach lumen?
Mucus and bicarbonate layers
What three signaling molecules stimulate secretory activity by a parietal cell, and what drugs counteract them?
Histamine: H2 receptor antagonists
What solution uses sucrose as a complexing agent with an antacid to bind ulcerated tissue at a healing rate comparable to H2 blockers? What is the antacid?
Sucralfate; aluminum hydroxide
What non-FDA approved treatment has a lower ulcer recurrence rate than H2 blockers?
Pepto Bismol (Bismuth) - crystals deposit in ulcers' acidic environment
What is the role of prostaglandins in parietal cell function? How is this altered by NSAIDs?
On H2 or ACH signaling, ATP generates active cAMP in the parietal cell. Prostaglandins block this process. Since NSAIDs (broadly) block prostaglandin activity, they allow unimpeded/unregulated signaling effects resulting in hypersecretion
What is the relationship between ulcer healing and acid suppression during the day?
The higher the percentage of the day in which you can suppress acid production, the shorter the time that an ulcer needs to heal
What is the preferred therapy for H pylori and associated ulcers?
BID PPI/Ranitidine with 2 of [amoxicillin/ clarithromycin/ metronidazole]
BID PPI with TID/4ID tetracycline, bismuth, metronidazole
What is the pH goal of antacid therapy?
a pH of 5, reducing the proteolytic activity of pepsin
What is the MOA of an antacid?
Direct neutralization of hydrochloric acid in the stomach
What is the major direct effect of overtreating an over-secreting stomach with antacids?
Elevated absorption of the antacid:
Calcium bicarb - hypercalcemia
Al Hydroxide - excess Al, etc.
What is the 3-pronged approach to increasing the stomach's mucosal resistance?
Coat the ulcer (mechanical), increase mucous/bicarb secretions, and eradicate H pylori
What happens to bicarbonate production in a patient with gastric/duodenal ulcers?
What drugs are ineffective to prevent ulcers if NSAIDs are on board?
H2 blockers and sucralfate; misoprostol is the only one approved
What are the 4 criteria to be met by ulcer treament, and in what 3 ways can it be accomplished?
1) Relieve symptoms (pain)
2) Promote healing
3) Prevent complications
4) Prevent recurrence
A) Neutralize acid
B) Decrease acid production
C) Increase mucosal resistance
What are the 2 anticholinergics used in GERD/Ulcers?
Atropine and Probantheline/Probanthine
List the PPIs in order of greatest CYP450 interaction to least. What is the practical result of this?
Greatest: Omeprazole, Lansoprazole, Rabeprazole, and Pantoprazole=Least (Dexlansoprazole is the odd one out, not sure why)
If a patient is on complex drug regimens, use pantoprazole
In the stomach, gastrin cells release ___ based on signals from the ___ nerve. The released hormone activates ___ cells.
Disruption of the mucosal blood flow (left gastric artery, submucous plexus, etc) is thought to have what effect?
Loss of the protective mucus layer overlying the region of impaired blood flow