Lax, Antidiarrheals, IBS Tx Flashcards
Fluoxetine Paroxetine Sertaline MOA TU
MOA: SSRI, increases afferent activity
TU: constipation
Dietary fiber Methylcellulose Polycarbophil Psyllium MOA TU Tox
MOA: bulk laxatives, attract water and increase stool mass–distention causes increased 5-HT release
TU: diarrhea and constipation (normalizes both)
Tox: allergies, flatulance, worsen obstruction
Cascara sagrada
MOA
PK
Tox
MOA: anthraquinone, acts only on large intestine as laxative
PK: slow
Tox: dependence and myenteric plexus damage (longterm), pigmentation of mucosa
Danthoron
MOA
PK
Tox
MOA: anthraquinone, acts only on large intestine as laxative
PK: slow
Tox: dependence and myenteric plexus damage (longterm), pigmentation of mucosa
Senna
MOA
PK
Tox
MOA: anthraquinone, acts only on large intestine as laxative
PK: slow
Tox: dependence and myenteric plexus damage (longterm), pigmentation of mucosa
Bisacodyl
MOA
PK
Tox
MOA: acts only on large intestine as laxative
PK: slow, prodrug (6 hr to activation)
Tox: dependence and myenteric plexus damage (longterm), pigmentation of mucosa
Caster oil
MOA
PK
Tox
MOA: prokinetic on entire GI
PK: fast, acts as prokinetic
Tox: dependence and myenteric plexus damage (longterm), pigmentation of mucosa, dehydration and electrolyte imbalances, uterine contractions (abortifacent)
Toxicity of contact cathartics
dependency and myenteric nerve damage (long term) pigmentation of mucosa uterine contractions (caster oil)
Alosetron MOA PK TU Tox
alesetron
MOA: 5-HT3 antagonist, block afferent stimulation, decrease peristalsis
PK: longer duration than anti-emetics
TU: diarrhea-predominant IBS–last resort
Tox: excessive hospitalizations, ischemical colitis (may be fatal)–incidence increaes w/ CYP4A2 inhibitor use
Cisapride MOA PK TU Tox
cisapride
MOA: 5-HT4 agonist on presynaptic, increase NT release, increase peristalsis
PK: tegaserod is more specific
TU: diabetic gastroparesis
Tox: long QT, more w/ comorbids and CYP3A4 inhibitors
Tagaserod MOA PK TU Tox
tagaserod
MOA: 5-HT4 agonsist, increase NT release, increase peristalsis
PK: more specific than cisapride
TU: constipation-predominant IBS
Tox: long QT, more w/ comorbids and CYP4A4 inhibitors
Diphenoxylate MOA PK TU Tox
diphenoxylate
MOA: enkephalins, inhibit motility and secretions
PK: co-Tx w/ atropine, so not dependent
TU: anti-diarrheal
Tox: cramps, megacolon if pt has ulcerative colitis, if high levels –> euphoria like opiates
Loperamide MOA PK TU Tox
loperamide
MOA: enkephalins, inhibit motility and secretions
PK: does not cross BBB
TU: anti-diarrheal
Tox: cramps, megacolon if pt has ulcerative colitis
Alvimopan
MOA
TU
Tox
alvimopan
MOA: selective µ-receptor antagonist
TU: constipation 2˚ to opiate Tx in hospital
Tox: increased risk of MI
Methylnaloxone
MOA
TU
Tox
methylnaloxone
MOA: selective µ-receptor antagonist
TU: constipation 2˚ to opiate Tx on hospice
Tox: none
Domperidone
MOA
TU
Tox
domperidone
MOA: inhibition of inhibitory dopamine interneurons, increasing motility
TU: impaired gastric emptying (vagotomy, gastroparesis)
Tox: somnolence, nervousness, aggitation, tardative dyskinesia (irreversible)
Metoclopramide
MOA
TU
Tox
Metoclopramide
MOA: inhibition of inhibitory dopamine interneurons, increasing motility
TU: impaired gastric emptying (vagotomy, gastroparesis)
Tox: somnolence, nervousness, aggitation, tardative dyskinesia (irreversible)
TCAs
MOA
TCAs
MOA: decrease NE reuptake –> increased activation of alpha-2 on cholinergic parasympathetics –> decreased ACh release, decreased motility
Lubiprostone MOA PK TU Tox
lubiprostone
MOA: activates CIC2, increases Cl- secretion
PK: poor absorption, low systemic effects
TU: chronic constipation, constipation IBS
Tox: diarrhea, nausea, headache, fetal loss
Linaclotide MOA PK TU Tox
linaclotide
MOA: activates cGMP –> CFTR
PK: poor absorption, low systemic effects
TU: constipation
Tox: diarrhea, maternal death, peds lethal
Octreotide MOA PK TU Tox
octreotide
MOA: somatostatin analog, decrease fluid secretion, high dose decreases motility (low increases motility)
PK: long t1/2
TU: severe diarrhea (dumping, vagotomy, short gut, AIDS)
Tox: impaired pancreatic secretion, decreased fat absorption –> KADE deficiencies, decrease in gallbladder motility –> stones, insulin/glucagon imbalance, hypothyroidism and bradycardia
Bismuth subsalicylate in secretions MOA PK TU Tox
bismuth subsalicylate
MOA: subsalicylate decreases PG and Cl secretion in large intestine, antimicrobial–binds enterotoxin
TU: prevention of traveller’s diarrhea, opiates better when diarrhea starts
Tox: black stool and tongue, salicylate tox
Lactulose, Magnesium hydroxide, Sodium phosphate, Polyethylene glycol
MOA
TU
Tox
MOA: osmotic cathartics
TU: constipation when nerves disrupted
Lactulose special TU
decease plasma ammonia (portal systemic encephalopathy)
Sodium phosphate tox
if in blood
deplete intravascular volume, hypokalemia
Magnesium hydroxide toxo
if in blood
hypermagnesemia in renal failure
Lactulose tox
if in blood
metabolized by gut bacteria –> lots of gas and cramps
Cholestyramine, colestipol
MOA
TU
Tox
MOA: binds bile acids, prevents osmotic diarrhea 2˚ to bile acid loss
TU: Crohn’s, terminal ileal resection
Tox: constipation, fecal impaction, KADE and drug loss
Docusate Mineral oil MOA TU Tox
MOA: ducusate = surfactant, mineral oil lubricates
TU: widespread
Tox: mineral oil–lipid pneumonitis if aspirated, KADE loss
