Emetic/Antiemetics/Gastroprotectants Flashcards
Apomorphine
Acts as a D1 and D2 dopaminergic agonist, stimulating the chemoreceptor trigger zone to induce emesis as a non-selective dopamine agonist
Side effects: Failure to produce emesis, refractory vomiting, nausea, sedation
Adverse sedative effects can be reversed with an opioid agonist such as naloxone
Alpha-2 Adrenergic Agonist
Induces emesis
Thought to occur through the stimulation of the chemoreceptor trigger zone at least in part through the area of postrema of the medulla oblongata
Concerns include sedation, hyperglycemia, bradycardia, increased systemic vascular resistance, and increased cardiac afterload. Drug: dexmeditomidine
Xylazine
Alpha-2 adrenergic agonist
Dexmeditomidine
Alpha-2 adrenergic agonist
Peripheral acting emetics
most common include hydrogen peroxide, syrup of ipecac, and salt paste
syrup of ipecac no longer used due to potential for abuse and fatal cardiac arrhythmia.
Salt paste no longer clinically used due to risk of hypernatremia and questionable efficacy
Hydrogen peroxides: irritate oral, esophageal and gastric mucosa
Phenothiazine Derivatives
Acepromazine, chlorpromazine and prochlorperazine
Reduce emesis through blockade of dopamine receptors in CRTZ and emetic centers
No longer used because of potential side effects and availability of more effective agents
Produce an alpha-1 adrenergic antagonist which causes systemic vascular resistance and vasodilation; can result in hypotension
Metoclopramide
Prokinetic
Dopamine and serotonin antagonist and cholinergic agonist
Increases lower esophageal sphincter tone, facilitates gastric emptying
short half-life, thus usually prescribed as a CRI
contraindication: mechanical obstructions in the GI tract and intussusceptions
Ondansetron
Serotonin (5-HT3) Antagonist
Block serotonin receptors in the CRTZ and peripherally
Appear to be more effective than phenothiazine and metoclopramide
Side effects are rare
Maropitant
Neurokinin-1 (NK) antagonist
Blocks substance P at vomiting center in the brain
Proton Pump Inhibitors
Omeprazole, pantoprazole, esomeprazole
Inhibits Na/K ATPase pump activity
Recommended treatment for acid suppression; controls proton deposition in the gastric lumen and hydrochloric acid secretion
H2 Histageneric Antagonist
Famotidine, ranitidine, cimetidine
H2 blockers
Specific antihistamines that reduce the action of histamine at histamine receptors on gastric parietal cells; reduce stomach acid
Sucralfate
Sucrose sulfate-aluminum complex
Binds to locally injured GI lining and creates a physical barrier
Promotes bicarb production and may increase production of prostaglandin E2
Commonly used to treat GI or duodenal ulcers
Can also be beneficial in esophageal strictures
Misoprostol
Synthetic prostaglandin E1 analogue
It improves gastric blood flow, decreases gastric acid production, increases mucus production and bicarb secretion, and promotes cell turnover.
Specifically used to help prevent NSAID-induced GI injury and ulceration
Also has effects on myometrial contraction
Wear gloves when handling
cholestyramine
bile acid sequestrant.
binds to bile in GIT to prevent its reabsorption.
Strong ion exchange resin - exchanges chloride anions and anionic bile acids in GIT and bind them to resin matrix for elimination.
Intravenous lipid therapy
The theory for MOA is that because it is lipophilic, it sequesters lipophilic toxins, reducing the concentration and toxicity until the compound is metabolized and excreted.
Other theories: ILE provides myocytes with energy and augments cardiac performance, restoring myocardial function, and increasing intracellular calcium.
Side effects: hypersensitivity reactions, phlebitis, fat embolism, fat overload syndrome, pancreatitis, worsening of ARDS, hemolysis, coagulopathy
