Gastrointestinal Drugs

Drugs Affecting GI Function

1)
2)
3)

ACh release (Enteric NS)  binds to M1 and M3 receptors
Gastrin release - CNS activation, GI wall distention, chemicals in food
Gastrin activates ECL  Histamine release
-Histamine binds to H2 in parietal cells  stimulate Gs protein  adenylyl cyclase activated  ↑CAMP  protein kinase
activation  proton pump activation  H+/K+/ATPase (resp. for exchange of K+ for H+)  Acid production

4) Gastric mucosa acidified to pH<3  negative feedback  Antral D cells release somatostatin - inhibits gastrin by binding
to ECL and G cell
PGE2 and PGI2  bind to EP3 receptors of parietal & non-parietal mucosal epithelial cells
*cytoprotective action
*stimulates gastric mucus secretion

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Drugs Affecting GI Function
Drugs used to treat Gastric Acidity, PUD and GERD
Physiology of Gastric Acid Secretion
Gastrin

G or
Cholecystoki
nin-B
(CCK-B or
CCK2)

Somatostatin
(SST)

ST2

• HCl and pepsinogen: principal gastric secretory products
capable of inducing mucosal injury
•Basal acid production (circadian rhythm)
*highest in the evening, lowest in the morning
–Cholinergic input via vagus nerve
–Histaminergic input from local gastric sources
•Stimulated conditions
–Cephalic phase: sight, smell, taste of food
-release of Ach (1° stimulant) from CNS
–Gastric phase: food enters stomach  distention of GI
walls  gastrin release from G cells  direct/indirect
promotion of secretion of digestive juices
*direct- parietal cells induced
–Intestinal phase: nutrient assimilation; antral D cells in
gastric mucosa (somatostatin)  inhibits gastric
secretion
Regulatory Mechanisms of Gastric Acid Secretion
•Acetylcholine (neuronal): M3 receptors (basolateral
membrane of parietal cells)
•Histamine (paracrine-“neighboring”): H2 receptors
-Enterochromaffin-like cells adjacent to parietal cells
has H2 receptors
•Gastrin (endocrine) : CCK2 (cholecystokinin)or CCK-B/G
receptors
*Parts of stomach: cardiac, fundus, body, pylorus
Regulatory
Hormones

Acetylcholine

Histamine

Receptors

•M3 on
basolateral
membrane
of parietal
cells
•M1 on ECL
cells

H2 on
parietal cells

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Description

•Released from
postganglionic vagal fibers
•Stimulates "cephalic"
phase of acid secretion
•Indirectly affects parietal
cells by increasing release
of histamine from ECL cells
in the fundus of the
stomach and of gastrin
from G cells in the gastric
antrum
•Released by ECL cells (in
close proximity to parietal

cells)
•Acts as a paracrine
mediator by diffusion
•Most potent inducer of
acid secretion: indirectly by
inducing release of
histamine by ECL cells
•Produced by antral G cells
•Stimulated by CNS
activation, local distention,
& chemical components
of gastric contents
•Produced by antral D cells
•Inhibits gastric acid
secretion
•Stimulated by
acidification of gastric
luminal pH to <3
•Suppresses gastrin
release
by negative feedback

Gastric Defenses Against Acid
•LES (lower
esophageal sphincter)
•Secretion of mucus
layer* stimulated by PG
E2and I2

-Prevents acid reflux
-1° esophageal defense from
gastric acid
-Soluble when secreted but
quickly forms insoluble gel
protecting gastric mucosa
-Slow ion diffusion
-Protects from macromolecules
such as pepsin
-Neutralizes HCl

•Secretion of
bicarbonate ions* by
superficial
gastric epithelial cells
*there should be adequate blood flow
-high metabolic demand and O2 requirement of gastric
mucosa
Drug Classes
•Proton pump inhibitors (PPIs)
•H2 receptor antagonists or blockers
•Agents that enhance mucosal defense
–Prostaglandin analogs (Misoprostol)
–Sucralfate
–Antacids
•Other acid suppressants and cytoprotectants

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Drugs Affecting GI Function
Proton Pump Inhibitors
DRUG
OMEPRAZOLE

Prilosec
Losec
Hovizol
Omepron
Protonix
Risek

ESOMEPRAZOLE

Nexium

LANSOPRAZOLE

Prevacid
Prevacid
FDT

DEXLANSOPRAZOLE

Dexilant

RABEPRAZOLE

Pariet
Aciphex

PANTOPRAZOLE

Entericcoated
contained
inside gelatin
capsules
Entericcoated
granules as
powder for
suspension
Entericcoated
tablets
Powdered
drug
combined
with sodium
bicarbonate
IV
formulations

Protonix
Pantoloc

Omeprazole
Esomeprazol
e
Lansoprazole
Lansoprazole

Pantoprazole
Rabeprazole
Omeprazole
Omeprazole

Pantoprazole
Lansoprazole

PROPERTIES AND
INDICATIONS
•Most potent
suppressors of
gastric acid
secretion
•All have
equivalent
efficacy at
comparable
doses
•Promote
healing of gastric
and duodenal
ulcers
•Treat GERD,
including erosive
esophagitis
(either
complicated or
unresponsive to
tx w/
H2-receptor
antagonists)
•Mainstay in the
treatment of
pathological
hypersecretory
conditions,
including the
ZollingerEllison syndrome
(tumors in
pancreas or SI
gastrinoma)

PHARMACOLOGIC
EFFECT/MOA
•Prodrugs that
require activation in
an acid
environment
•Effective in acid
suppression
regardless of other
stimulating factors
(targets final step)
*80-95% diminished
daily gastric acid
secretion
SULFENAMIDE
-active metabolite
-targets secretory
canaliculi inside
parietal cells
-site of
accumulation of
prodrug (cannot
escape cell)
-binds to –SH groups
of Cys of protein
pump (covalent) 
inactivate PP
*irreversible
inhibition causes
prolonged action
bec. it takes time
before new PP are
synthesized

PHARMACOKINETICS

SIDE EFFECTS/CI/DI

•Should be given ~30
to 60 minutes before
breakfast or the
largest meal of the
day

• Nausea, diarrhea,
headache, GI
disturbance, bone
fractures (increased
w/ long-term use:
hip, wrist, spine)
•Decreased
effectiveness of
clopidogrel with
omeprazole
•Low vitamin B12
levels
*Vit B12 + intrinsic
factor complex
requires acid pH for
absorption

•Small intestine:
rapidly absorbed,
highly protein
bound, and
extensively
metabolized by
hepatic
CYP2C19 and CYP3A4
•Maximal
suppression of acid
secretion requires
several doses of PPIs
-not all PP are
simultaneously
activated

•Incomplete
absorption of CaCO3
products
*alternative: Ca
citrate

•Provide a prolonged
(up to 24-to 48-hour)
suppression of acid
secretion, despite the
much shorter plasma
half-lives (0.5 to 2
hours) of
parent compounds

•FDA approved
for reducing risk
of duodenal ulcer
recurrence
associated with
H. pylori
infections
(↓ D cells  low
somatostatin↑acid)
•Lansoprazole:
FDA approved for
treatment and
prevention of
recurrence of

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Drugs Affecting GI Function
NSAID-associated
gastric
ulcers in patients
who continue
NSAID use

H2-Receptor Antagonists
CIMETIDINE

Tagamet

RANITIDINE

Zantac

FAMOTIDINE

Pepcid
H2 Bloc

NIZATIDINE

Axid
(no
longer
marketed
)

•Promote
healing of gastric
and duodenal
ulcers
•Treat
uncomplicated
GERD
•Prevent
occurrence of
stress ulcers
*less potent that
PPIs (70%)
-usually given at
night
-PPI (morning)

• Inhibit acid
production by
reversibly
competing with
histamine for
binding
selectively to H2receptors on the
basolateral
membrane of
parietal cells, BVs,
and other sites
•Predominantly
inhibit basal acid
secretion,
which accounts for
their efficacy in
suppressing
nocturnal acid
secretion

• Rapidly absorbed
after oral
administration
• Peak serum
concentrations within
1 to 3 hours
• Absorption may be
enhanced by food or
decreased by antacids
• Only small % is
protein-bound

•Diarrhea,
headache,
drowsiness, fatigue,
muscular pain, and
constipation
•Confusion,
delirium,
hallucinations,
slurred
speech, and
headaches

• Cimetidine
–Short serum half-life;
inhibits CYP450
(enzyme inhibitor) 
resp for many side
effects

• Cimetidine (longterm, high doses):
Women:
galactorrhea
-inhibits CYP
enzymes that
hydroxylates
estradiol)
Men: gynecomastia,
reduced sperm
count, and
impotence (due to
reduction of
testosterone binding
to androgen
receptor)

• Ranitidine
–Longer-acting and 510x more potent vs.
cimetidine
• Famotidine
–20-50x more potent
vs. cimetidine, 3-20x
vs.
ranitidine
• Nizatidine
–Similar potency to
ranitidine; eliminated
principally by kidneys
(bioavailability ~100%)

Agents that Enhance Mucosal Defense:
Prostaglandin Analogs
•Prostaglandin E2 (PGE2) and prostacyclin (PGI2)
–Major PGs synthesized by the gastric mucosa
–Bind to EP3 receptor on parietal cells and stimulate the Gi pathway  decreased intracellular cAMP and gastric acid secretion
•PGE2: cytoprotective effects (stimulation of mucin and bicarbonate secretion; increased mucosal blood flow)
DRUG
PROPERTIES AND
PHARMACOLOGIC
PHARMACOKINETICS
SIDE EFFECTS/CI/DI
INDICATIONS
EFFECT/MOA
MISOPROSTOL
•Synthetic analog of PG
• Degree of inhibition of •Rapidly absorbed after •Diarrhea, with or
Cytotec
E1
gastric acid secretion
oral administration
without abdominal
•FDA approved to
is directly related to dose •Rapidly and extensively pain and cramps

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Drugs Affecting GI Function

SUCRALFATE
Iselpin, Carafate

prevent NSAID-induced
mucosal injury

de-esterified to form
misoprostol acid

• Complex of aluminum
hydroxide and sulfated
sucrose

•Inhibits pepsinmediated hydrolysis of
mucosal proteins

•Single dose inhibits
acid production within
30
minutes
•Therapeutic effect
peaks at 60-90 minutes
and
lasts for up to 3 hours
•Food and antacids
decrease the rate of
absorption
•Free acid is excreted
mainly in the urine
•Elimination half-life of
~20 to 40 minutes
• Should be taken on an
empty stomach 1 hour
before meals

• Epidermal growth
factor (EGF)

•pH <4: undergoes
extensive cross-linking
to produce a viscous,
sticky polymer that
adheres to epithelial
cells and ulcer craters for
up to 6 hours
after a single dose

• Effectively heals
duodenal ulcers and is
used in long-term
maintenance therapy to
prevent their recurrence

BISMUTH
SUBSALICYLATE
Pepto-Bismol

• Antimicrobial in H.pylori
associated PUD

ANTACIDS

•Acid-neutralizing ability
depends on capacity to
neutralize gastric HCl and
on whether the
stomach is full or empty

Sodium

Very water-soluble

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(30%)
*dose-related,
begins w/in first 2
wks after initiation
of therapy & often
resolves
spontaneously w/in a
week
•CI: IBD-misoprostol
exacerbates IBD
-Pregnancy: ↑uterine
contractility
-taken 4x daily: limits
its use

•AE: constipation
(2%)
•CI: renal failure
with risk for Al
overload
•DI: taken at least 2
h after
administration of
phenytoin, digoxin,
cimetidine,
ketoconazole and
fluoroquinolones
(sucralfate
decreases
absorption of these
drugs)

•Additional
cytoprotective effects
(stimulation of local
production of PGs and
EGF)
•Effectively heal peptic
ulcers by:
–Inhibiting pepsin
activity
–Increasing mucus
secretion
–Interacting with
glycoproteins in necrotic
mucosal tissue and
protect the ulcer crater
• Weak bases that react
with gastric acid to
form water and a salt to
diminish gastric
acidity
• Also reduce pepsin
activity
Rapidly absorbed from

• Alkali and sodium

Page 5

Drugs Affecting GI Function
bicarbonate

the
stomach

loads may pose a risk
for patients with
cardiac or renal
failure
•Systemic alkalosis,
belching and
flatulence
(NaHCO3)

Calcium carbonate
Tums, Calsan,
Calci-Aid

–Also used as calcium
supplements for
treatment
of osteoporosis

Calcium may induce
rebound acid secretion,
necessitating more
frequent administration

Combination of
Mg2+ and Al3+
hydroxides
Magaldrate,
Maalox

–Symptomatic relief of
peptic ulcer disease and
GERD
–Promote healing of
duodenal ulcers
–Used as last-line therapy
for acute gastric ulcers

Magaldrate:
hydroxymagnesium
aluminate complex
converted rapidly in
gastric acid to
Mg(OH)2 and Al(OH)3

Simethicone
Disflatyl
+ CaCO3+ Vit D
(Esvicalforte)
+ Al and Mg
hydroxides
(Mylanta, Maalox
plus, Kremil-S)

-Provides a relatively
balanced and sustained
neutralizing capacity
Surfactant added in
antacid preparations that
may decrease foaming
and hence esophageal
reflux

-Poorly absorbed
(sustained antacid
effect)

-Mg (fast acting)
-Al (slow acting)

•Na content for
hypertensive or HF
patients
• Release of CO2
from bicarbonateand carbonatecontaining antacids
can cause belching,
nausea, abdominal
distention, and
flatulence
•Constipation (Al
hydroxide)
•Diarrhea (Mg
hydroxide)
•Hypophosphatemia
(Al-containing)
• Accumulation of
cations in renal
insufficiency

Antimicrobial Agents
• Optimal therapy for patients with PUD (both duodenal and gastric ulcers) who are infected with Helicobacter pylori
TRIPLE THERAPY
PPI + Metronidazole/Amoxicillin +
Clarithromycin

QUADRUPLE THERAPY
Bismuth Subsalicylate +
Metronidazole + Tetracycline + PPI

Other Acid Suppressants and Cytoprotectants
DRUG
M1 Muscarinic
Receptor Antagonists
PIRENZEPINE

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PROPERTIES AND INDICATIONS
-40-50% suppression

PHARMACOLOGIC EFFECT/MOA

SIDE EFFECTS/CI/DI
-significant undesirable
anticholinergic effect
-risk of blood disorders
-poor efficacy

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Drugs Affecting GI Function
TELENZEPINE
REBAMIPIDE Mucosta

Used for ulcer therapy (100mg)

ECABET Gastrom

also used for ulcer therapy in
Japan
–Derivative of glycyrrhizic acid
found in licorice root
-Used for ulcer therapy in Europe

CARBENOXOLONE

Appears to exert a
cytoprotective effect both by
increasing PG generation in
gastric mucosa and by
scavenging reactive oxygen
species
Appears to increase the
formation of PGE2and PGI2
–Unclear mechanism; may alter
the composition and
quantity of mucin

Hypokalemia and
hypertension due to
excessive mineralocorticoid
receptor activation

-Inhibits type I isozyme of 11-B
hydroxysteroid dehydrogenase
 protects mineralocorticoid
receptor activation by cortisol in
the distal nephron

DRUGS USED FOR BOWEL MOTILITY DISORDERS
Drug classes:
•Prokinetic agents and antiemetics
•Laxatives
•Antidiarrheals

Dopamine in GIT

Serotonin (5-HT)

•Present in significant amounts in the GIT
•Inhibitory effects on motility: reduction of LES and
intragastric pressures
–Mediated by D2-dopaminergicreceptors
–Result from suppression of Ach release from myenteric
motor neurons

•>90% of total 5-HT in the body exists in GIT
•Produced by ECL cells and rapidly released in response to
chemical and mechanical stimulation
•Triggers the peristaltic reflex
•5-HT1stimulation of the gastric fundus release
of nitric oxide and reduces smooth muscle tone
•5-HT4stimulation of excitatory motor neurons enhanced Ach
release at the NMJ
•5-HT3and 5-HT4receptors facilitate interneuronal signaling

Prokinetic Agents and Antiemetics
•Medications that enhance coordinated GI motility and transit of material in the GI tract
•Appear to enhance the release of excitatory neurotransmitter at the nerve-muscle junction without interfering with the
normal physiological pattern and rhythm of motility
2 TYPES
5-HT3 RECEPTOR BLOCKERS
DOPAMINE RECEPTOR ANTAGONISTS
Ondansetron (Zofran); Granisetron (Kytril); Palonosetron (Aloxi);
Metoclopramide, Domperidone, Phenothiazines,
Butyrophenones
Dolasetron(Anzemet)

Prokinetic Agents and Antiemetics
•Substituted benzamides
•Derivatives of PABA
•Structurally related to procainamide
•Additional advantage of relieving nausea and vomiting by antagonism of dopamine receptors in CTZ (high brain center for
vomiting)

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Drugs Affecting GI Function
DRUG

I. METOCLOPRAMIDE
Reglan, Plasil

Domperidone
Phenothiazines

PROPERTIES AND
INDICATIONS
•Ameliorate nausea and
vomiting that often
accompany GI
dysmotility syndromes
•Improve gastric
emptying in
symptomatic patients
with gastroparesis
(paralysis of GIT)
•IV: adjunctive measure
in medical or
diagnostic procedures
(e.g., intestinal
intubation or contrast
radiography of the GIT)
•Treatment of
chemotherapy-induced
emesis (as well as
prophylaxis of
anticipatory vomiting 
CTZ)
OFF-LABEL USE:
Treatment of persistent
hiccups

II. DOMPERIDONE
Motilium

PHARMACOLOGIC
EFFECT/MOA
•5-HT4-receptor agonism,
vagal and central 5HT3-antagonism, and
possible sensitization of
muscarinic receptors on
smooth muscle
•Increases LES tone and
stimulates antral and
small intestinal
contractions

PHARMACOKINETICS

SIDE EFFECTS/CI/DI
•Extrapyramidal
effects
–Dystonias
(uncoordinated
movement) and
parkinsonian-like
symptoms (TRAP 
tremor, rigidity,
akinesia, postural
instability)
–Tardive dyskinesia
(slow abnormal
movement; may be
irreversible)
•Galactorrhea

*confined effect in upper
digestive tract; no colonic
effect

Treatment:
Anticholinergics
Antihistamines

•Predominantly
antagonizes the dopamine
D2 receptor without major
involvement of other
Receptors

Does not readily cross
BBB to cause
extrapyramidal side
effects

•No significant effects on
lower GI motility
III. PHENOTHIAZINES
Prochlorperazine
Comprazine

IV.
BUTYROPHENONES
Droperidol Inapsine
Haloperidol Haldol
Serenace

• Treatment of
chemotherapy-induced
emesis (i.e.,
low or moderately
emetogenic
chemotherapeutic
agents
• Moderately effective
antiemetics

–Increasing dose
improves antiemetic
activity

Hypotension,
restlessness, EPS,
sedation

• Droperidol: used for
sedation in endoscopy
and surgery (+ opiates or
BZDs); cause QT
prolongation

5-HT3 Receptor Blockers
DRUG
ONDANSETRON
Zofran

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PROPERTIES AND
INDICATIONS

PHARMACOLOGIC
EFFECT/MOA
Selectively block 5HT3 receptors in the

PHARMACOKINETICS/DOSING
-Can be administered as a
single dose prior to

SIDE EFFECTS/CI/DI
Headache as
common SE

Page 8

Drugs Affecting GI Function
visceral vagal afferent
fibers and CTZ in the
brain

GRANISETRON
Kytril
PALONOSETRON
Aloxi

chemotherapy (IV or PO);
efficacious against all grades
of emetogenic therapy
- Longer duration of action

DOLASETRON
Anzemet

Substance P/neurokinin-1 Receptor Blocker
DRUG
APREPITANT
Emend

PROPERTIES AND INDICATIONS
•Only indicated for highly or
moderately emetogenic
chemotherapy regimens

PHARMACOKINETICS/DOSING
•PO administration with
dexamethasone and
palonosetron

SIDE EFFECTS/CI/DI
•Constipation and fatigue
as major SEs

LAXATIVES
•Commonly used for constipation to accelerate the movement of food through the GIT
•May cause electrolyte imbalances when used chronically
•Increase potential for loss of pharmacologic activity of poorly absorbed, delayed-acting, and ER oral drugs by accelerating
intestinal transit time
•All except lubiprostone have risk of dependency for the user

IRRITANTS and STIMULANTS
DRUG
Senna

PROPERTIES AND INDICATIONS
•Active ingredient is a group of
sennosides
(anthraquinone glycosides)

Bisacodyl

•+ docusate-containing stool
softener: useful in
treating opioid-induced constipation
•Potent stimulant of the colon
available as
suppositories and enteric-coated
tablets

Castor Oil

• Abortifacient

•Hydrophilic colloids from
indigestible parts of fruits and
vegetables

Magnesium
citrate
Magnesium
hydroxide
Sodium
phosphate

• Electrolyte solutions containing
PEG: used as
colonic lavage solutions to prepare
the gut for
radiologic or endoscopic procedures

PHARMACOLOGIC EFFECT/MOA
•Causes evacuation of the bowels
within 8 to 10 hours
•Causes water and electrolyte
secretion into the bowel

•Acts directly on nerve fibers in the
colonic mucosa

•Broken down in the small intestine
to
ricinoleic acid (very irritating to the
stomach and promptly increases
peristalsis)
•Form gels in the large intestine,
causing water
retention and intestinal distension,
thereby
increasing peristaltic activity
•Nonabsorbable salts that hold
water in the
intestine by osmosis, causing bowel
distention which increases intestinal
activity and
produces defecation in a few hours

SIDE EFFECTS/CI/DI

• Abdominal cramps and
potential for atonic colon
with prolonged use
•Food interaction: basic
food, milk
 Causes GI irritation
• CI in pregnancy

•Used cautiously in
immobile patients
-potential to cause intestinal
obstruction

*less abdominal cramps and gas

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Drugs Affecting GI Function
Lactulose
Duphalac

• Semi-synthetic disaccharide sugar
that cannot be hydrolyzed by
intestinal enzymes

Docusate
sodium

•Often used for prophylaxis rather
than acute treatment

• Oral doses are degraded in the
colon by colonic bacteria into lactic,
formic, and acetic acids  increases
osmotic pressure  fluid
accumulation, colon distention, soft
stools, and defecation
•Surface-active agents that become
emulsified with stool, producing
softer feces and ease of passage

•Not to be taken
concomitantly with mineral
oil

Docusate
calcium
Docusate
potassium

Lubricant Laxatives
Mineral oil
Glycerin
suppositories

•Mineral oil to be taken orally in an
upright position to prevent aspiration
and lipid & lipoid pneumonia

•Act by facilitating the passage of
hard stools

Chloride Channel Activators
Lubiprostone

•Used in the treatment of chronic
constipation

•Activates chloride channels to
increase fluid secretion in the
intestinal lumen

• Nausea as common SE

•Metabolism occurs quickly in the
stomach and jejunum

ANTIDIARRHEALS
Causes of diarrhea
•Increased osmotic load within the intestine, resulting in retention of water within the lumen
•Excessive secretion of electrolytes and water into the intestinal lumen
•Exudation of protein and fluid from the mucosa
•Altered intestinal motility resulting in rapid transit and decreased fluid absorption
DRUG
PROPERTIES AND INDICATIONS
PHARMACOLOGIC EFFECT/MOA
Bulk-forming and Hydroscopic Agents
Methylcellulose
•Hydrophilic and poorly
•May work as gels to modify stool texture and viscosity and to
Citrucel
fermentable colloids or polymers produce a perception of decreased stool fluidity
that absorb water and increase
•Adsorb intestinal toxins or microorganisms
Aluminum hydroxide stool
and/or by coating or protecting the intestinal mucosa
Alternagel
Bulk
Bile Acid Sequestrants
Cholestyramine
Colestipol
Colesevalam
•Crystal complex consisting of trivalent
•Low pH of the stomach: drug reacts with HCl to
Bismuth
bismuth and salicylate suspended in a mixture form bismuth oxychloride and salicylic acid
subsalicylate
of
Pepto-Bismol
magnesium aluminum silicate clay
•Antisecretory, anti-inflammatory, and
antimicrobial effects
•Prevention and treatment of traveler's
diarrhea;
other forms of episodic diarrhea and acute
gastroenteritis
Antimotility and Antisecretory Agents

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Drugs Affecting GI Function
•Opioids
•Loperamide
•Diphenoxylate and difenoxin
•Octreotide and somatostatin
Opioids

Loperamide
Lormide
Lomotil
Imodium

•An orally active
antidiarrheal agent with µreceptor activity agent and
penetrates the CNS poorly
•Effective against
traveler's diarrhea, used
either alone or in
combination with
antimicrobial agents
(trimethoprim,
cotrimoxazole,or a
fluoroquinolone)

•Effects on intestinal
motility (µreceptors),
intestinal secretion
(dreceptors), or
absorption (µ and d
receptors)
•Increases small
intestinal and mouth-tocecum transit times
•Increases anal sphincter
tone

•Usual adult dose: 4 mg
initially followed by 2 mg
after each subsequent
loose stool, up to 16 mg
per day

•40 to 50 times more
potent than morphine as
an antidiarrheal

•Must be discontinued if
no clinical improvement in
acute diarrhea within 48 h

•Overdosagecan
result in CNS
depression
(especially in
children) and
paralytic ileus less
movement of
intestines

•Used as adjunct
treatment in almost all
forms of chronic diarrheal
disease

Diphenoxylate

Octreotide &
Somatostatin

•Lacks significant abuse
potential
•Related structurally to
meperidine; more
potent than morphine as
antidiarrheal

•Rapidly deesterified to
difenoxin
•Both can produce CNS
effects when used in
higher doses (40 to 60
mg per day)

*see previous handouts
(hormones)

Abigail Mata | Phar 141

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