GERD Flashcards
1
Q
NSAIDS
- inhibit function of
A
- cause gastric ulcers
- inhibit function of prostaglandin PGE2
2
Q
GERD Alarming Symptoms
A
- dysphagia
- odynophagia (painful swallowing)
- bleeding
- weight loss
- anemia
- long duration
- no response to treatment
3
Q
Patient-directed Therapy
A
- OTC Antacids
- OTC H2 Receptor Antagonists
- OTC PPI
4
Q
Antacids
A
- react with gastric HCl to form salt and water
- keep pH >4.0
- if CO3 = gas
- if OH = no gas
- Mg2+ = diarrhea
- Al3+ = constipation
5
Q
Gastric Antisecretory Drugs
A
- inhibit activities of histamine, acetylcholine, and the proton pump
6
Q
Gastric Secretory Pathway
A
- ECL cells -> histamine
- histamine binds H2 receptor on parietal cells -> activates H|K ATPase
- – also activated by gastrin and acetylcholine
7
Q
3 principle agents for gastric acid secretion
A
- histamine
- acetylcholine
- gastrin
8
Q
H2 Histamine Receptor Blockers
A
- analog of histamine
- inhibit binding of histamine to H2 histamine receptor on parietal cells -> decreases acid production
- eliminates symptoms in up to 50% of patients
9
Q
Cimetidine
A
H2 Blocker
- first commercial H2 receptor antagonist
- CNS side effects
- – access to CNS, dizziness, drowsiness
- breast development in males (gynecomastia)
10
Q
Ranitidine
A
H2 Blocker
- 10x more active than Cimetidine
- no CNS side effects, no Gynecomastia
11
Q
Famotidine
A
H2 Blocker
(aka pepcid)
- his suggestion
- 30x more active than cimetidine
12
Q
PPIs
A
- provide complete endoscopic mucosal healing of esophagitis at 6-8 weeks in 75%-100% of cases
- more expensive than H2 blockers
- exist in inactive form (prodrug)
- – becomes active when interacts with acid
- – bind irreversibly (covalently) to H|K ATPase, the terminal source of acid in parietal cells
- much slower*
13
Q
What NOT to use with PPI
A
antacid: decrease in H+ will make PPI never active
14
Q
Nizatidine
A
H2 Antagonist
15
Q
H2 Antagonists ending
A
end in -TIDINE
