Al-Mehdi: Gastric Acid Pharmacology Flashcards
duodenal and gastric ulcer
gastric cancer
(both a consequence of….)
H. pylori infection
H. pylori infection of corpus (body) leads to
gastric cancer
4 steps leading to gastric cancer from H. pylori infection:
- decreased acid secretion (dead parietal cell)
- bacterial proliferation
- nitrite production in antrum
- gastric cancer
H. pylori infection of antrum leads to
peptic ulcer (in duodenum)
5 steps leading to peptic ulcer from H. pylori infection:
- depletion of somatostatin
- increased gastrin
- increased acid secretion
- gastric metaplasia
- H. pylori colonizes and ulcer forms
a2
EP3
SST2
M2
type of G receptor
Gi
H2 type of G receptor
Gs (cAMP)
H1
a1
M1
M3
CCK2
type of G receptor
Gq (Ca2+)
5-HT3 receptor
Ca2+ influx
how is H+ brought into lumen from parietal cell
H+/K+ ATPase
how is Cl- brought into lumen to form acid (HCl) from parietal cell
HCO3/Cl exchanger
membrane H+, K+ ATPase abundance is ______ by Vagus (Ach,M3:Gq)
increased
membrane H+, K+ ATPase abundance is _____ by PGE2 (EP3:Gi)
decreased
membrane H+, K+ ATPase abundance is _____ by G cell gastrin (CCK2:Gq)
increased
where does gastrin travel when it is released by G cell
into blood then to parietal cell
membrane H+, K+ ATPase abundance is ____ by D cell somatostatin (SST2:Gi)
decreased
membrane H+, K+ ATPase abundance is ____ by ECL cell histamine (H2:Gs)
increased
gastrin (CCK2:Gq) also _____histamine secretion by ECL cell
increases
vagus (M1:Gq) also _____ histamine secretion by the ECL cell
stimulates
somatostatin blocks ____ and ___ secretion
gastrin and histamine
vagus (M2:Gi) blocks _____ secretion
somatostatin
Vagus releases GRP to ____ gastrin secretion via bombesin (BB2:Gq)
increase
cells specific to body (corpus) of gut
parietal
chief
cell specific to antrum of gut
G cell