Flashcards in Gastointestinal Pharmacology Deck (53)
What is the pathogenesis of gastroduodenal ulcers?
Excess gastric acid secretion, breakdown of mucosal cytoprotection, Helicobacter pylori infection
What are the goals of ulcer treatment?
reduce ulcerogenic factors, enhance defensive factors, or eradicate any infectious causes
What are pro-ulcerogenic factors?
Acids (HCl, VFA, bile acids), pepsin, infections
What are antiulcerogenic factors?
mucosal cytoprotection, epithelial renewal, external protection
How does one increase the gastric pH to greater than 4 to promote healing?
H2-Histamine receptor blockade, stimulation of gastric PGE receptors, gastric H+-K+-ATPase inhibition (proton pump inhibitors)
H2-Histamine antagonist, decreases acid secretion which decreases pepsin. As treatment continues effectiveness decreases due to an increased secretion of gastrin. Low oral biovalibility and renal clearance
What are examples of H2-histamine antagonists?
famotidine, ranitidine, cimetidine
What are the side effects and indications of H2-histamine antagonist?
Renal disease patients need lower dose, treatment of ulcers due to gastritis, stress, NSAID terapies, gastrinomas
PGE analogue, po administration, needs frequent administration due to rapid hepatic metabolism. Decreases acid secretion stimulated by histamine or gastrin. Less effective than H2-HR antagonists or PPI, increases gastric cytoprotection
How do PGE and PGI promote cytoprotection?
Mucus production (coats surface of the gastric mucosa), bicarb production (neutralizes HCl), intrinsic mucosal barrier (resist back-diffusion of acid), and gastric blood flow (flushes away acid, prevents buildup, maintains tissue pH in normal range)
Indications/side effects/contraindications of misoprostil?
NSAIDs-induced ulcers, increased mast cell influx. Side effects include diarrhea due to prokinetic action. Contraindications include IBD, pregnancy
What is an example of a proton pump inhibitor?
What is the action of proton pump inhibitors?
Irreversibly inactivate H+/K+ ATPase, so effects extend longer than the drug's presence in the body. Reduce acid secretions
Proton pump inhibitor. Oral paste that is a weak base that decreases the release of HCl
Binds to ulcerated tissue to form a seal after oral administration, heals existing ulcers not prevent new ones. Short duration of action. Binds and inactivates bile acids, increases local prostanoid formation.
Either systemic or non-systemic, non-systemic only affects stomach. Maalox and Mylanta examples. Relieve clinical signs, no healing.
Na or Ca carbonate antacids onset
Mg salts (sulfate, hydroxide) onset
intermediate with laxative effect
all hydroxide antacids onset
What is the best type of drug to use to treat an ulcer: PPIs, H2-histamine antagonists, or cytoprotectants?
What are examples of locally-acting emetic agents?
warm water, sodium chloride, 3% hydrogen peroxide, syrup of ipecac (emetine akaloid substance)
centrally acts on D2 dopamine receptors, produces vomiting in 2-10 minutes
simulates alpha2-adrenergic receptors to produce emesis in cats
Indications of anti-emetic drugs
motion sickness, uremia, liver disease, cancer chemo, parvo, trauma
H2-histamine antagonist that lessens irritating effects of acid on the stomach
muscarinic acetylcholine antagonist anti-emetic effects
decrease vagal afferent transmission to vomiting center to decrease vomiting
kaolin-pectin and other coating agents anti-emetic efficacy
not very effective
Simulate gastric motility, block CNS dopamine receptors and 5-HT3 receptors
Action of diphenhydramine, meclizine
may reduce motion sickness by blocking histamine and muscarinic cholinergic receptors