Test 2: lecture 29 +30 GI part 2 Flashcards
sucralfate (sucramal) causes what things
- forms paste to protect gastic epithelial cells
- binds and inactivates bile salts and pepsin
- Stimulates prostaglandin synthesis
- increases Mucosal blood flow
chemical diffusion barriers:
sucralfate (sucramal)
Bismuth subsalicylate (pepto-bismol)
montmorillonite (diarsanyl)
montmorillonite (diarsanyl)
smectite clay forms protective layer in stomach
absorbs toxins, bacteria, viruses, enzymes and free radicals
used for diarrhea in dogs and cats by coating intestinal mucosa
chemical diffusion barriers:
sucralfate (sucramal)
Bismuth subsalicylate (pepto-bismol)
montmorillonite (diarsanyl)
— is a chemical diffusion barrier drug that is used to treat diarrhea in dogs
montmorillonite (diarsanyl)
smectite clay forms protective layer
absorb toxins, bacteria, viruses, enzymes and free radicals
chemical diffusion barriers:
sucralfate (sucramal)
Bismuth subsalicylate (pepto-bismol)
montmorillonite (diarsanyl)
how does bismuth subsalicylate (Pepto-Bismol) work
Bismuth:
* Coats ulcerated mucosal surfaces
* Absorbs toxins
* Mild antibacterial action (H pylori)
Salicylate (aspirin)
* Anti-inflammatory action
can’t be metabolized by cat
chemical diffusion barriers:
sucralfate (sucramal)
Bismuth subsalicylate (pepto-bismol)
montmorillonite (diarsanyl)
GI is under — control what happens when you give atropine?
PARA
blocks ACh (muscarinic) receptors
cause dry, mouth, tachycardia, decrease secretions, bronchioconstriction, large pupils ect.
pirenzepine
M1-selective blocker
but causes decreased gastric acid somehow even though there are M3 receptors on parietal cells?
H1 receptors
Located on smooth muscle and endothelium and in CNS and promotes vasodilation, bronchoconstriction, smooth muscle activation, and CNS activation
make you sleepy
H2 receptors are found where and cause what?
Located on parietal cells and regulates histamine-mediated gastric acid secretion
what are the H2 receptor blockers
cimetidine (Tagamet)
ranitidine (Zantac)
famotidine (Pepcid)
Pepcid Complete (Life cycle management)
nizatidine (Axid)
cimetidine (Tagamet)
1st gen H2 blocker
decreases gastric acid without causing sleepiness (H1 blockage)
- inhibits CYP → toxic levels of drugs from decreased metabolism
- many drug interactions
- decreases liver blood flow→ decreased clearance of propranolol and lidocaine
H2 receptor blockers:
cimetidine (Tagamet)
ranitidine (Zantac)
famotidine (Pepcid)
Pepcid Complete (Life cycle management)
nizatidine (Axid)
ranitidine (Zantac)
2nd gen H2 blocker
fewer side effects that cimetidine → less drug interactions, less CYP inhibition
longer lasting
10x more potent
H2 receptor blockers:
cimetidine (Tagamet)
ranitidine (Zantac)
famotidine (Pepcid)
Pepcid Complete (Life cycle management)
nizatidine (Axid)
famotidine (Pepcid)
3rd gen H2 receptor blocker
poor bioavilability
30x more potent than cimetidine
no CYP inhibition
increases motility of stomach
H2 receptor blockers:
cimetidine (Tagamet)
ranitidine (Zantac)
famotidine (Pepcid)
Pepcid Complete (Life cycle management)
nizatidine (Axid)
Pepcid Complete (Life cycle management) is a combo of what drugs
famotidine H2 antagonist (10 mg)
calcium carbonate antacid (800 mg) (constipation)
magnesium hydroxide antacid (165 mg) (diarrhea)
Ca and Mg balance each other out
Antacids act quickly and H2 blocker act slowly
H2 receptor blockers:
cimetidine (Tagamet)
ranitidine (Zantac)
famotidine (Pepcid)
Pepcid Complete (Life cycle management)
nizatidine (Axid)
nizatidine (Axid)
H2 receptor blocker
no CYP inhibition
excreted unchanged in urine
increases motility of stomach
H2 receptor blockers:
cimetidine (Tagamet)
ranitidine (Zantac)
famotidine (Pepcid)
Pepcid Complete (Life cycle management)
nizatidine (Axid)
which H2 blockers do not cause CYP inhibition
famotidine (pepcid)
nizatidine (axid)
H2 receptor blockers:
cimetidine (Tagamet)
ranitidine (Zantac)
famotidine (Pepcid)
Pepcid Complete (Life cycle management)
nizatidine (Axid)
— is an experimental gastrin blocker
netazepide (YF476)
CCKB receptor blocker
— are proton pump inhibitors
omeprazole (Prilosec)
lansoprazole (Prevacid)
esomeprazole (Nexium)
rabeprazole (Aciphex)
how does omeprazole (Prilosec) work
weak base that is absorbed and then protonated
will irreversibly covalently bind and inhibit proton pump inhibitors
lasts 2-3 days
proton pump inhibitors:
omeprazole (Prilosec)
lansoprazole (Prevacid)
esomeprazole (Nexium)
rabeprazole (Aciphex)
— covalently and irreversibly binds and blocks proton pumps
omeprazole (prilosec)
lasts 2-3 days
proton pump inhibitors:
omeprazole (Prilosec)
lansoprazole (Prevacid)
esomeprazole (Nexium)
rabeprazole (Aciphex)
what happens with prolonged use of omeprazole (prilosec)
Prolonged decrease in gastric acid production will cause increase in stomach pH
this can cause bacterial overgrowth → pneumonia
stomach will try to bring pH back to 4 by increasing acid → increased gastrin levels and parietal cell hyperplasia
omeprazole: irreversibly and covalently bind to proton pump
proton pump inhibitors:
omeprazole (Prilosec)
lansoprazole (Prevacid)
esomeprazole (Nexium)
rabeprazole (Aciphex)
how does prostaglandin help with gastric mucosal integrity
(1) Inhibit gastric acid secretion
(2) Stimulate bicarb secretion
(3) Stimulate mucous secretion
(4) Increase mucosal blood flow
(5) anti-inflammatory
how does misoprostol (Cytotec) work
prostaglandin
Binds to Prostaglandin receptor on parietal cell and ↓ intracellular cAMP levels leading to a ↓ in proton pump activity
(1) Increase mucous production in gastric ulcers
(2) Co-administered with NSAIDs to prevent ulceration
off label uses of misoprostol (Cytotec)
prostaglandin
Primary Indications:
* Increase mucous production in gastric ulcers
* Co-administered with NSAIDs to prevent ulceration
Off label Uses:
* induce labor by causing smooth muscle contraction
* Abortion in conjunction with RU-486
* Erectile dysfunction
the — plexus of the ENS controls gut motility
myenteric
the — plexus of the ENS controls secretions and absorption
Submucosal plexus
Promote elimination of soft formed stools
laxatives