GI Pharm Flashcards
What cell in the stomach produces HCl? In what ways can it be controlled/targeted?
- Parietal Cells - proton pump releases H+ (H+ / K+ ATPase).
1. Stimulation of proton pump (GPCR, increases cAMP) - Muscurinic receptor
- Histamine receptor
- Gastrin receptor
- Inhibition of proton pump
* Prostaglandin receptor - Proton pump itself can be targeted
What are some methods in the treatment of ulcers?
- Antacids
- H2 receptor antagonists
- Proton Pump inhibitors
- PGE2 analogues
- Sucralfate
What is the mechanism of action of antacids? What are some side effects?
- Chemically neutralize gastric HCl, and inhibit pepsin secretion
- Side effects include rebound acid secretion, constipation or diarrhea (combo of the two drugs - one causes constipation, the other diarrhea can be given together :) ), and may impair the absorption of other drugs.
What are H2 receptor antagonists used for?
What is their mech of action?
What are some possible side effects?
- Treatment of gastritis, gastric ulcers, esophagitis
- Block the action of the histamine receptor, reducing HCl secretion and decreasing acidity in
- Not many side effects.
What is sucralfate used for?
What is its mech of action?
- Treatment of gastric and duodenal ulcers
- It polymerizes to viscous gel at ph<4 and binds to protein in ulcerated tissue (a bandaid to protect exposed stomach lining)
What are some uses for Proton Pump inhibitors?
What are their mech of action?
- Gastritis, gastric ulcers, esophagitis, prevention and treatment of ulcers caused by NSAIDS/steroids
- Inhibits H+ / K+ ATPase in parietal cells. The binding is irreversible so the cells must synthesize a new pump. This makes these drugs easy to use as they can be given once a day.
- They are only active in acidic environments, which is important because PP are in other areas of the body as well.
What is the use of PGE2 analogues?
What are their mech of action?
What are some possible side effects?
- Prevention and treatment of ulcers caused by NSAIDS
- Agonist at PG receptor of parietal cells, decreasing the release of H+. Increases mucosal blood flow and secretion of mucous also.
- Diarrhea can be a side effect, as well as pregnancy as it can cause uterine contractions
Why is control of emesis difficult?
Why should we not try to stimulate vomiting in horses, ruminants, rodents, or rabbits?
- There are many pathways leading to emesis, so it is hard to control all of them.
- These animals don’t have a vomiting reflex.
What are the main pathways involved in vomiting? How are they connected?
- Chemoreceptor Trigger Zone - located in the medulla. Main site of action for many antiemetics. The BBB around this area is relatively permeable, allowing circulating mediators to act directly.
- Input from Vestibular nuclei (motion sickness)
- Input from Visceral afferents (pharynx, stomach)
- Input from circulating toxins through BBB
- Vomiting Center - located in the medulla. Controls and integrates the visceral and somatic functions involved in vomiting.
- Input from CTZ
- Input from higher centers (these recieve sensory afferents like pain, sight, smells)
- Input from Nucleus of the solitary tract
What are some methods to control vomiting?
- Dopamine and seretonin antagonists in the CTZ (also alpha 2 receptors here…xylazine to induce vomiting)
- Muscurinic and Neurokinin antagonists at the vomiting center
- Seretonin antagonists at the visceral afferents (pharynx, stomach)
- Histamine and muscurinic antagonists at the vestibular nuclei and nucleus of the solitary tract.
Name some methods to induce vomiting.
What are their mech of actions?
- Hydrogen Peroxide - mild gastric irritant
- Syrup of Ipecac - mild gastric irritant, direct activation of receptors in CTZ
- Xylazine - direct activation of receptors in CTZ. Sedation a side effect. Choice for cats.
- Apomorphine - dopamine agonist, acts in the CTZ. Doesn’t activate opioid receptors. Choice for dogs.
- Injectables (xylazine, apomorphine) are beneficial in that you can give them via injection.
