Pharmaco Flashcards
Increases GI motility
ACh, Substance P, serotonin
Decreases GI motility
VIP/NO/ATP, NE/Epi, Opioids (morphine)
Increase stomach acid
Gastrin, histamine, ACh, NSAIDs, alcohol
Decreases stomach acid
Somatostatin, prostaglandin PGE2
What does CCK do? Where is it released?
Increase gallbladder contraction and bile secretion, increase zymogen secretion from pancreas; released in duodenum
What do incretins like GIP/GLP do? Where is it released?
Increase insulin release; duodenum
Where is secretin released? What does it do?
Duodenum, increases HCO3- release by pancreas
What does dopamine do?
D1 receptors - more cAMP, increases gastric motility, causes receptive relaxation, more ACh release
D2 receptors - less cAMP
How does stomach respond between meals?
Less acid, more mucus
How does stomach respond after meals?
More acid, less mucus - parietal cell cannaliculi emerge, proton pumps are exposed to lumen
What produces the acid and mucus?
Acid - parietal cells
Mucus - Mucous cells/Goblet cells
What does PGE2 do?
Decreases acid and increases mucus release
How can aspirin cause gastric ulcers?
It is a COX inhibitor, which lowers production of PGE2. This means more acid and less mucus are produced. Leads to gastric ulcers.
How can you clinically decrease acid secretion (which drugs?)
-prazoles (proton pump inhibitors) - irreversible inhibitor
-tidines (H2/histamine blockers) - reversible inhibitor
Prostaglandins - used with patients who need NSAIDs
Muscarinic blockers (not very good)
What are antacids? What are the two types?
Bases that neutralize gastric acid, can be bicarbonate or hydroxide salts
Systemic antacids - cause systemic alkalosis
Nonsystemic antacids - stay in GI tract