Pharmacology Of Drugs: Stomach Acid And H. Pylori Flashcards
How to differentiate cardiac issues from GERD chest pain?
GERD = heartburn, belching, taste acidic, symptoms don’t worsen with physical activity
- often will say the symptoms are worse at night also
Heart attack/CAD = nausea, dyspnea, diaphoresis, radiating pain that gets worse with exertion
How to confirm GERD?
Patient history
Endoscopy Or pH 24 hr tests
What is first line in GERD?
PPI’s
Peptic ulcer vs duodenal ulcer differentiate
Gastric:
- pain occurs at any time during the day
- eating food immediately precipitates pain
- causes weight loss, nausea, vomiting, diffuse epigastric pain
Duodenal:
- pain occurs at night only and often causes them to wake up
- pain occurs 1-3 hrs after a meal and is relieved immediately by food
- will cause weight gain and pinpoint epigastric pain
both are seen in PUD and both cause some type of epigastric pain and usually hemoptysis
How does NSADIs cause damage to stomach mucosal barriers
1) inhibits COX-1 enzymes
2) decreases PGE2-synthesis
3) decreases mucus secretion, bicarbonate secretion and blood flow tot he gastric region
4) decreased bicarbonate and mucus = increased acidic damage/vulnerability to gastric acid
What two endogenous materials can be used to inhibit gastric acid secretion directly
Prostaglandins (PGE2/PGI2)
- binds to own receptors on parietal cells
Somatostatin
- binds to own receptors on parietal cells
How does H. Pylori cause peptic ulcers?
Presence of H. Pylori and its virulence enzyme urease = increase pH in the stomach
Increased pH in stomach -> stimulates G cells to release gastrin (this chronically occurs)
Release in gastrin -> increases parietal cell proliferation and secretion of HCl
also H. Pylori inflammatory modulators -> inhibts D cell stimulation -> decreased somatostatin -> releases inhbition of G cels that somatostatin tonically has -> increases gastrin release
Ways to test for H. Pylori infection
Histology with biopsy
- gold standard with highest sensitivity
Culture biopsy or use rapid urease tests
Antibody detection (takes longer)
Urea breath test
- not very sensitive and has rates of false (-)
Drug regiments to kill H. Pylori
1st line = PPI based triple therapy
- PPI + clarithromycin + amoxicillin
1st line = bismuth-based quadruple therapy
- PPI or H2 antagonist + bismuth sub-salicylate + metronidazole + tetracycline
2nd line = 7 therapy (only for refractory or failed both 1st line)
- H2 antagonist + bismuth sub-salicylate + metronidazole + tetracycline + amoxicillin + PPI + levofloxacin
how does Gastrin work to increase stomach acid in tissues
1) H+/K+ ATPase works by taking one K+ from lumen and into cell for one H+ ion into lumen
2) Histamine released from Enterochoffmin-like cells (ECL) activated H2 receptors on parietal cells and hyperstimulates #1 production
gastrin works primarily by stimulating ECL cells and releasing excess histamine, but does also act directly on H+/K+ ATPase on parietal cells slightly
Other than histamine and gastrin, how else is stomach acid production increased?
Vagal stimulation
- either ACh directly binding to M3 receptors on parietal cells to induce more acid secretion
- OR indirectly by release Gastrin releasing peptides (GRP) to G-cells to release more gastrin
what is Zollinger-Ellison syndrome
Tumors in pancreas/duodenum or pylorus of stomach that are made in G-cells (gastromas)
- produces mass gastrin and almost always LEDs to PUD
Need PPIs to treat (can also use H2 but not as affective)
- also need surgery
Symptoms:
- abdominal pain
- Durham
- GERD
- N/V
- bleeding for PUD
- weight loss
**associated with multiple endocrine neoplasia type 1 (MEN1)
What is the ultimate endogenous acid production inhibitor?
Somatostatin
- inhibits H2 receptors on ECL cells
- inhibits Gastrin release from G-cells
*also stops SST receptors found on gastromas
