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
surface mucosal cell (foveolar cell) hyperplasia
Menetrier Disease
increase in _____ causes HER1 activation (human EGFR1)—hyperplasia
increase in TGF-alpha
hypoproteinemia
parietal cell loss (achlorhydria)
giant gastric rugae
Menetrier Disease
to Rx Menetrier disease
Cetuximab
Trastuzumab
2 main causes of peptic ulcer disease
H. pylori and NSAID use
gastrin producing tumor’s primary location
duodenum
gastrin producing tumor
gastrinoma
to dx peptic ulcer disease
H pylori test (stool, urea); endoscopy
to Rx peptic ulcer disease
PPI
H2 blockers
Ab’s (for H. pylori)
-prazoles
PPIs
PGE2 analog used for peptic ulcer disease
Misoprostol
PPI that inhibits CYP2C19
Omeprazole
PPIs can lead to what -emia
hypergastrinemia
best treatment for GERD
PPI
are PPIs safe during pregnancy
yes
K+ competitive acid blocker used for peptic ulcer disease
VONOPRAZAN
H2-blockers
-TIDINEs
reduces acid secretion and binds to EP3 (Gi)
PGE2
these 2 H2 blockers have no significant avidity for CYP450 enzymes
FAMOTIDINE
NIZATIDINE
agonist for EP3 (Gi)
MISOPROSTOL
mucosal defense agent CI in pregnancy
MISOPROSTOL
SE of SUCRALFATE
bezoar formation
side effect of Mg(OH)2 (magnesium dihydroxide) antacid
diarrhea
SE of CaCO3 (calcium carbonate) antacid
constipation
CaCO3 can lead to ______ in CKD
hypercalcemia
triple therapy for H. pylori infection without macrolide resistance
PPI
clarithromycin
amoxicillin
if patient with H. pylori infection is allergic to penicillin, what can you substitute amoxicillin with
Metronidazole
quadruple therapy for H. pylori infection
PPI
tetracycline
metronidazole
bismuth
chronic NSAID users can present with ___ or ____ without prior ulcer symptoms
ulcer bleeding or perforation
pathogenesis of peptic ulcers w/ NSAIDs
PGE2 depletion (barrier loss)
direct toxicity
ischemia
what parts of the gut does H. pylori affect
corpus
antrum
what part of the gut do NSAIDs affect
the whole gut
Rx NSAID ulcer
stop NSAIDs
PPI
in patients with gastritis/ulcer/ or asthma, what drugs to use for pain
Celecoxib
acetominophen
______ is tolerable in patients w/ peptic ulcers or asthma
acetaminophen
inhibits COX 3 in brain
acetaminophen
