Constipation and diarrhea Flashcards
Dioctyl sodium MOA
decrease water tension for easier passage of stool with no effect on intestinal peristalsis
Dioctyl AE and CI
Dont use with abdominal pain, N/V, irritates mucosa and increase intestinal absorption of other drugs. Short term use
What is the most potent class of laxatives?
stimulant laxatives
Bisacodyl MOA
Stimulant laxative that acts predominantly on large bowel, increases mucosal permeability, increase back diffusion, increase propulsive contractility by stimulating myenteric plexus, stimulate PG synthesis. Prodrug converted by enteric bacteria
Bisacodyl AE and CI
overdosing= fluid and electrolyte loss, enterocyte damage, colonic inflammatory response
Lactulose MOA
disaccharide which is not absorbed and produces osmotic effect. Metabolized to formic and acetic acid by bacteria–> fecal acidifier traopping ammonium
What drug is used in C-IBS?
Lubiprostone
MOA of lubiprostone
Activation of Cl channel to increase permeability in an PKA independent fasion. Alleviates symptoms
What does laxative abuse do?
leads to constipation requiring several days to accumulate bulk which people take even more laxatives for. Bowel become unresponsive.
What anti-diarrheal is an absorber of etiological factors in the lumen?
Bismuth subsalicylate- absorb harmful bacteria, viruses, toxins
What drug is used to prevent Traveler’s diarrhea?
bismuth subsalicylate
MOA of opiates
Alter intestinal motility to increase contact time between ingested matter and intestinal epithelium. Decrease secretions, decrease motility, increase muscle tone, increase sphincter tone, anti-spasmodics, decrease cramps
Loperamide MOA
interacts with intestinal opiod receptors and binds to and inhibits Ca binding protein calmodulin
Describe neural control of emesis
Vomiting center is in the area postrema medulla and sends signals vomiting, swallow, and saliva. Receives signals from : limbic system of forebrain, motion via 8th nerve, taste, vagal and visceral afferents, chemoreceptor trigger zone. Limbic system sends signals for nausea
What receptors aid in signal transmission to emetic center?
inner ear motion to cerebellum: M1, H1
Blood born emetics act on 5-HT3, D2, M1, substance P receptors
Scopolamine MOA
anti-cholinergic muscarinic receptor blocker to prevent motion fibers signalling to CTZ. prophylactic only for motion sickness
Scopolamine AE
sedation, extrapyramidal (dry mouth, drowsiness)
Cyclzine MOA
H1 antihistamine to counter motion sickness
Meclizine MOA
H1 antihistamine that exerts a depressant effect on hyperstimulation of labyrinthine function. Used for vestibular disturbances.
Chlorpromazine MOA
centrally acting anticholinergic and anti-dopaminergic (at CTZ), used for N/V and intractable hiccoughs
Droperidol MOA
blocks dopaminergic receptors in the CTZ. used for post-op N/V
Metoclopramide MOA
Dopamine receptor antagonist that blocks chemotherapeutic induced activation of D2 receptors in CTZ. Stimulates gastric emptying. given prophylactically prior to cancer chemo and prevention of post op N/V
Granisetron MOA
Antiemetic serotonin antagonist, potent, blocks receptors in stomach and small intestine, and CTZ
What is the most effective anti-emetic?
serotonin antagonists
Dolasetron MOA
Antiemetic serotonin antagonist with longer half life
Methylprednisolone MOA
Corticosteroids have anti-emetic effect and reduce side effects. Prevent PG production.
Aprepitant MOA
substance P/NK1 receptor antagonist that is used as an adjunct drug for preventing emesis by cytotoxic drugs. It crosses the BBB and inhibits emesis via central actions. Completely metabolized by CYP3A4
Lorazepam MOA
benzodiazepine, used in adjunct to other antiemetic drugs, effective in pt with anticipatory vomiting, give 1 day prior to chemo
Describe use of anti-emetics in cancer chemo
Combination of 5-HT3 + (dexamethasone, benzodiazepine, NK1 antagonist, or D2 antagonists are added)
