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GI drugs- antiulcer drugs - Coggle Diagram
GI drugs- antiulcer drugs
Gastric ulceration and erosion (GUE) in small animals
gastric ULCERS= FULL-thickness loss of gastric mucosa
gastric EROSIONS= PARTIAL loss of mucosa with preservation of muscularis mucosae
clinical signs
"coffee ground" vomitus
bleed into stomach, blood acted upon by gastric acid
melaena
black tarry faeces, doesn't necessarily mean bleeding in GIT--> could just be swallowed blood
causes
primary GID
foreign body
neoplasia
severe inflammation
RARELY dietary indiscretion
gastritis caused by dietary indiscretion DOES NOT = GUE
secondary GID
drugs (NSAID
liver dz
uraemia
hypoadrenocorticism
tumours outside GIT--> gastrinoma, mast cell tumours
Gastric acid production
gastric acid
parietal cells
PROTON PUMPS
histamine
enterochromagin cells
H2 RECEPTORS
gastrin
G cells
Indications for antiulcer drugs
diseases causing GUE
NSAID toxicity
management of diseases where gastric ulceration is a risk e.g. renal dz + liver dz
prevent secondary oesophagitis in severe vomiting
where reflux is a concern
post BOAS surgery
brachycephalic anaesthetics
refluxing brachys
NOT anti-emetics
H2 receptor antagonists
Cimetidine (Zitac)
the only vet product
give every 6-8hrs
only suppresses acid production for 3-5hrs
Ranitidine (Zantac)
give every 8-12hrs
prokinetic activity
increases gut motility in upper GIT and to a lesser extend in lower GIT
no longer marketed for humans due to concerns about being carcinogenic
Famotidine (Pepcid)
give every 12-24hrs
IV bolus, IV infusion, oral
consider: cost, client convenience, concurrent drug therapy, justification of prescribing off label
continuous use results in pharmacological tolerance
Sucralfate
ulcer "bandaid"--> protects from gastric acid + pepsin
symptomatic treatment
Proton pump inhibitors
omeprazole (Gastroguard)
equine
clinical signs of GI ulcers in horses
unexplained weight loss +/- reduced appetite/altered eating patterns
changes in behaviour
mild recurrent colic
cutaneous sensitivity manifest as biting of flanks or resentment of girthing, grooming, leg aids or rugging
teeth grinding
stereotypic behavious
poor performance + changes in rideability--> reduced willingness to work and reluctance to go forward
pantoprazole
esomeprazole
lansoprazole
target final common pathway of gastric acid production
inactivate H+-K+-ATPases in acid environment of pariettal cells
max inhibitory effect between 2-4 days after start of therapy
off label
no evidence to support prophylactic use of gastroprotectant therapy in dogs and cats with nonerosive gastritis e.g. acute gastritis due to dietary indiscretion
most effective when administered just before a meal
efficacy reduced if administered with histamine receptor antagonists
2x daily
dose needs to be tapered if administered for longer than 3-4weeks to avoid rebound hyperacidity
Misoprostol (Cytotec)
synthetic PGE1
manage/prevent NSAID toxicity
causes abortion