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
somatostatinacid)
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

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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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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

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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 receptor 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 (receptors),
intestinal secretion
(dreceptors), or
absorption ( 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)

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