Gastrointestinal Drugs

Abraham Degaga (PhD)

1
 Introduction

• Common medical conditions involving the GIT:

– Peptic Ulcer Disease (PUD)
– Gastro-esophageal reflux disease (GERD);
– Nausea and Emesis
– Inflammatory Bowel Disease
– Diarrhea, and constipation.

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 Acid-Related Pathophysiology
The stomach secretes:
• Hydrochloric acid (HCl): aids digestion & barrier to infections
• Bicarbonate: base that is natural mechanism to prevent
hyperacidity
• Pepsinogen: precursor to the enzyme, pepsin
• Intrinsic factor: facilitates absorption of vitamin B12
• Mucus: protects stomach linings from HCl & digestive enzymes
• Prostaglandins: serve a variety of inflammatory & protective
activities

3
 Cells of the Gastric Gland
• Parietal cells
– Produce and secrete HCl
– Primary site of action for many acid-controller drugs
• Chief cells
– Secrete Pepsinogen, a proenzyme to pepsin
– Pepsinogen becomes pepsin when activated by exposure to
acid
– Pepsin breaks down proteins (proteolytic)
• Mucoid cells
– Mucus-secreting cells (surface epithelial cells)
– Provide a protective mucous coat
– Protect against self-digestion by HCl & proteolytic enzymes.
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 Normal GI activity

Factors
Factorsthat
that
Factors
Factorsthat
that Protect
ProtectAgainst
Against
Increase
IncreaseAcidity
Acidity Acidity
Acidity

5
• Factors Increasing
• Factors Decreasing
mucosal damage
mucosal damage
 H. pylori
• Mucus production
 NSAIDs
• Bicarbonate
 Acidic agents production
 Smoking • Blood flow
 Caffeine • Prostaglandins
 Alcohol
 Emotional stress

6
08/31/25 7
 Acid-Related Diseases

• Caused by imbalance of the three cells of the

gastric gland and their secretions
• Most common imbalance is hyperacidity
• Clients report symptoms of overproduction of
HCl by the parietal cells as:
– Indigestion (dyspepsia)
– Sour stomach
– Heartburn
– Ulceration & bleeding

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 Acid-Related Diseases, cont'd

• High & unbalanced acid secretion in the

stomach is associated with;
– Peptic ulcer disease
– Gastroesophageal reflux disease
– Zollinger-Ellison syndrome
– Upper gastrointestinal bleeding
– Erosive esophagitis.

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 Acid-Controlling Agents

• There are three basic categories of

acid controlling agents
– Antacids
– H2 antagonists
– Proton pump inhibitors

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 Antacids
• Are weak bases that react with HCl to form a salt and water.
– reduction of intragastric acidity.
• Because pepsin is inactive at a pH greater than 4,
– antacids also reduce pepsin activity.
• Also promote secretion of:
– Mucus: protective barrier against HCl
– Bicarbonate: helps buffer acidic properties of HCl
– Prostaglandins: increases blood flow to stomach.
• Used alone or in combination with other drugs
• There are different forms of antacids
– Aluminum compounds
– Magnesium compounds
– Calcium compounds
– Sodium compounds
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 Antacids: Aluminum Salts

• Can be found in carbonate or hydroxide forms

• Have constipating effects
– Often used with magnesium to counteract constipating
effects of aluminum compounds
• Examples
– Aluminum carbonate
– Aluminum Hydroxide salt
– Combination products (aluminum and magnesium):
• Peptica gel, Moxal, Mylanta
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 Antacids: Magnesium Salts
• Can be found in carbonate, hydroxide, oxide, trisilicate forms
• Commonly cause diarrhea; so, usually used with other agents to
counteract this effect (usually with aluminum)
• Dangerous when used for patients with renal failure
– failing kidney cannot excrete extra magnesium, resulting in
hypermagnesemia which affects the heart activity.
• Examples
– Magnesium hydroxide, Carbonate salt
– Combination products such as Maalox, Mylanta (are
combinations of aluminum and magnesium)
– Trisilicate: magnesium trisilicate.
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 Antacids: Calcium Salts
 Has many forms but carbonate is most commonly used
calcium preparation.
• Calcium preparations may cause constipation.
• Repeated & excess use may result in kidney stones
• Often advertised as an extra source of dietary calcium
• Calcium preparations also are associated with gas production
– Example: calcium carbonate.

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 Antacids and Antiflatulents
• Antiflatulents: used to relieve the painful symptoms
associated with gas.
• Several agents are used to bind or alter intestinal gas and are
often added to antacid combination products.
OTC antiflatulents
• Activated charcoal
• Simethicone
– Surfactant, alters elasticity of mucus-coated bubbles,
causing them to break.

15
 Antacids: Side Effects
Minimal, and depend on the compound used
• Aluminum and calcium
– Constipation,
– Calcium can also cause kidney stones, gas production
• Magnesium
– Diarrhea
• Calcium carbonate
– Produces gas and belching
• often combined with Simethicone.

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 Antacids: Drug Interactions
• Chelation
– Chemical binding, or inactivation, of another drug
– Produces insoluble complexes
– Result: reduced drug absorption
• E.g. TTCs, fluoroquinolones
• By reducing Gastric acidity, reduce absorption of
– ketoconazole, itraconazole

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Histamine-2 (H2) Antagonists

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 Histamine H2-receptor antagonists
• Reduce acid secretion by reversibly blocking H2 receptors.
• Potently inhibit (70-90%) basal, food-stimulated, and nocturnal
secretion of gastric acid after a single dose.
• Are less potent than the proton pump inhibitors.
• 4 commonly used H2 blockers exist;
– Cimetidine, Ranitidine, Famotidine, Nizatidine
• Are available in oral & Parenteral dosage forms
• Readily absorbed after oral administration
• Have small plasma protein binding capacity.

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 H2-receptor antagonists, cont’d
• Only small amount metabolized in the liver
– No need of dose adjustment in liver malfunction
• Are excreted in the kidney
– Dose adjustment is usually necessary in renal failure.
• All H2 Antagonists are classified as FDA pregnancy category B.
• Cimetidine inhibits CYP450 (CYP1A2, CYP2C9, CYP2D6, and
CYP3A4) and can slow metabolism of several drugs;
– (e.g., warfarin, diazepam, phenytoin, quinidine, carbamazepine,
theophylline, imipramine).
• Ranitidine can also inhibit the CYP450 enzymes
– But it inhibit only small amount
• Famotidine & nizatidine do not inhibit the CYP450 enzymes. 20
 H2 Antagonists: Indications
• GERD, Erosive esophagitis
• PUD
• Adjunct therapy in control of upper GI bleeding
• Zollinger-Ellison syndrome,
– gastrin-producing tumor causes hypersecretion of HCl
• PPIs are now used preferentially.

21
 H2 Antagonists: Side effects
• are usually well tolerated.
• Common SE:
– diarrhea, headache, drowsiness, fatigue, muscular pain,
constipation
• Less common CNS SE:
– confusion, delirium, hallucinations
• Cimetidine when used chronically, can:
– inhibits binding of dihydrotestosterone to androgen receptors,
– inhibits metabolism of estradiol, and
– increases serum prolactin levels.
• Galactorrhea in women
• Gynecomastia, Reduced sperm count, Impotence in men.
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 Proton Pump inhibitors (PPIs)
• Inhibitors of the H+/K+-ATPase (proton pump)
• The most potent suppressors of gastric acid secretion.
• Can inhibit up to 95% of acid secretion
– Blocks the final step in the secretion of gastric acid.
• Omeprazole is the first, Five additional PPIs are now available:
– Dexlansoprazole, Esomeprazole, Lansoprazole,
Pantoprazole, and Rabeprazole.
• Omeprazole & Lansoprazole are racemic mixtures of R– and S-
isomers.
• Esomeprazole is the S-isomer of omeprazole and dexlansoprazole
the R-isomer of lansoprazole.
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 Proton Pump inhibitors, cont’d
• All are available in oral formulations.
• Esomeprazole, Pantoprazole & Lansoprazole:
• approved for IV use.
• For maximum effect, PPIs should be taken 30 to 60 minutes
before breakfast or the largest meal of the day.
• If an H2-receptor antagonist is also needed, it should be taken
well after the PPI for best effect;
– b/c the H2 antagonists will reduce the activity of the proton
pump, and PPIs require active pumps to be effective.

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 Proton Pump Inhibitors: Mechanism of
Action
• PPIs are prodrugs with an acid-resistant enteric coating to protect
them from premature degradation by gastric acid.
• Coating is removed in the alkaline duodenum,
– the prodrug, weak base, is absorbed and transported to parietal
cells.
• There, it is converted to the active form, which reacts with a
cysteine residue of the H+/K+-ATPase, forming a stable covalent
bond.
• PPIs irreversibly bind to H+/K+-ATPase and inactivate it.
– Acid secretion will resume after a new pump is synthesized.
– New pump synthesis needs 24-48 hours
• Explains why dosed QD or BID, despite short t1/2 (0.5-2hrs).
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 PPIs: PK
• Once absorbed into systemic circulation
– they accumulate inside the parietal cells (protonated,
concentrated more than 1000 times)
• changed to the active form in the acidic environment.
• Rapidly absorbed, highly plasma bound & extensively metabolized
in the liver by the CYP2C19 & CYP3A4.
– Reduce dose with severe liver impairment
• Metabolites excreted in urine and feces.
• Bioavailability of all agents is decreased 50% by food;
– taken on an empty stomach, 30 minutes before meals.

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 PPIs: PK, cont’d
• From a PK perspective, PPIs are ideal drugs: have a short serum
t1/2, concentrated and activated near their site of action, and have
a long duration of action.

Table: pharmacokinetics of Proton pump inhibitors

27
 PPIs: Indications
• Their superiority over the H2 antagonists for suppressing acid
production and healing peptic ulcers has made them the
preferred drugs for;
– Promote healing of gastric & duodenal ulcers.
– GERD
– Zollinger-Ellison syndrome
– NSAIDs induced ulcers bleeding.
– they are also successfully used with antimicrobial regimens
to eradicate H. pylori.

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 PPIs: Side effects
• PPIs are extremely safe.
• Common side effects
– N,V, abdominal pain, constipation, flatulence.
• Less common side effects
– Myopathy, arthralgia, headaches, skin rashes
– Respiratory and Enteric Infections as HCl has protective
effect against infection.

– Decreased absorption of iron, calcium, vit. B12

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 PPIs: Drug interactions
• Because, PPIs have short half-lives;
– Clinically significant drug interactions are rare.
• ↓ in gastric acidity affects drug bioavailability,
– E.g., ketoconazole, itraconazole, digoxin, and atazanavir
• Omeprazole may inhibit the metabolism of warfarin, diazepam,
phenytoin, and cyclosporine.
• Lansoprazole may induce CYP1A2
– increase the excretion of Imipramine, theophylline

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 Mucosal protective agents:
Sucralfate
Sucralfate
•Is a complex salt of aluminum hydroxide and sulfated sucrose.
•is a cytoprotective agent which inhibits hydrolysis of mucosal
proteins by pepsin.
•In acidic environment, it undergoes extensive cross-linking and to
produce a viscous, sticky polymer.
– Attracted to and form a protective barrier over ulcers &
erosions.
•also stimulate Prostaglandin secretion.

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Therapeutic use: Sucralfate
•administered in a dosage of 1 g QID on an empty stomach (at least 1
hr before meals).
•At present, its clinical uses are limited.
•sucralfate is used to treat
– Stress induced ulcers
– Rectal ulcers
• less effective than IV H2 blockers.
Side effects
•Constipation, nausea & dry mouth
•May impair absorption of other drugs such as tetracycline, digoxin,
phenytoin, ketoconazole & fluoroquinolones.
•So should be given at least two hrs after other drugs.
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 Mucosal protective agents: Bismuth
Compounds
• Two bismuth compounds are available:
– Bismuth subsalicylate, and
– Bismuth subcitrate potassium.
• Over 99% of the bismuth appears in the stool.
• Although minimal (< 1%), bismuth is absorbed; it is stored in
many tissues and has slow renal excretion.
• Precise MOA of bismuth are unknown.
• Bismuth coats ulcers and erosions,
– creating a protective layer against acid and pepsin.

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 Bismuth Compounds, cont’d
• It may also stimulate prostaglandin, mucus, and bicarbonate
secretion.
• Bismuth subsalicylate reduces stool frequency and liquidity in
acute infectious diarrhea,
– due to salicylate inhibition of chloride secretion.
• Bismuth has direct antimicrobial effects and binds enterotoxins,
– accounting for its benefit in preventing and treating traveler’s
diarrhea.
• Bismuth compounds have direct antimicrobial activity against
H. pylori.

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 Clinical Uses: Bismuth
• dyspepsia and acute diarrhea.
• Bismuth subsalicylate also is used for the prevention of traveler’s
diarrhea (30 mL or 2 tabs QID).
• Used in 4-drug regimens for eradication of H. pylori infection.
• The regimen consists of
– a PPI BID, combined with bismuth subsalicylate (2 tablets;
262 mg each), tetracycline (250–500 mg), and metronidazole
(500 mg) QID/10–14 days.
• Standard “triple therapy” regimens (i.e., PPI, clarithromycin, and
amoxicillin or metronidazole twice daily for 14 days)
– generally preferred.
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 Adverse Effects: Bismuth
• All bismuth formulations have excellent safety profiles.
• Bismuth causes harmless blackening of the stool,
– which may be confused with GI bleeding.
• Liquid formulations may cause harmless darkening of the
tongue.
• used for short periods only and should be avoided in patients
with renal insufficiency.
• Prolonged usage may rarely lead to bismuth toxicity, resulting in
encephalopathy (ataxia, headaches, confusion, seizures).
• High dosages of bismuth subsalicylate may lead to salicylate
toxicity.
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 Prostaglandins: Misoprostol
• Synthetic prostaglandin E1 analog
• Prostaglandins have cytoprotective activity
– Protect gastric mucosa from injury by enhancing local production
of mucus or bicarbonate
– Promote local cell regeneration by ↑ing [growth factors].
– Help to maintain mucosal blood flow.
• Rapidly absorbed from oral administration.
• A single dose can inhibit acid production with in 30 minutes
• Used for prevention of NSAID-induced gastric ulcers
Side effects: Diarrhea, Abdominal cramps
• Contraindicated during pregnancy
– Because it causes uterine contraction.
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Antidiarrheal drugs

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 Diarrhea
•There is no any agreeable definition for diarrhea.
•Abnormal passage of stools with increased frequency, fluidity,
and weight.
•Or excessive fluid weight within 200gm per day stool which
represents the upper limit of normal daily stool in the western
world.
•It is defined as ≥ 3 loose watery stools in a 24 hour period.
•Knowledge about the underlying cause of diarrhea facilitates
effective treatment.

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 Acute diarrhea
– Sudden onset in a previously healthy person
– Lasts from 3 days to 2 weeks
– May be self-limiting
– Resolves without sequelae.
 Chronic diarrhea
– Lasts for more than 3 weeks
– Associated with recurring passage of diarrheal stools,
fever, loss of appetite, nausea, vomiting, weight loss, and
chronic weakness.
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 Causes of Diarrhea
Acute Diarrhea Chronic Diarrhea
Bacterial Tumors
Viral Diabetes
Drug induced Hyperthyroidism
Nutritional Irritable bowel syndrome
Protozoal

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• Diarrhea can be caused by:
• An increased osmotic load within the intestine;
• Resulting in retention of water with in the lumen
• Sorbitol is not absorbed by the body but draws water from
the body into the bowel, resulting in diarrhoea.
• Excessive secretion of electrolytes & water in to the GI lumen
• Usually caused by bacterial toxins (cholera, E. Coli), excess
vasoactive intestinal peptide (VIP) from pancreatic tumors,
laxatives, etc.
• Exudation of proteins, blood & mucus from the mucosal cells.
• Can result from inflammatory diseases of the GIT (IBD)
• Altered intestinal motility
• Results in rapid transient time in the GIT which then reduces
fluid reabsorption from the GIT.
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 Treatment of diarrhea
Non specific antidiarrheals
– Do not address the underlying pathology, provide only
symptomatic relief in mild cases of acute diarrhea.
Oral rehydration salts
– Dehydration & electrolyte imbalances are the principal risks
particularly in infants & children.
– Are cornerstones for pts with acute diarrhea.
– Exploits the fact that nutrient linked cotransport of water &
electrolytes remains intact in most cases of diarrhea.
– Na+ & Cl- absorption is linked to glucose uptake by
enterocytes,
• followed by movement of water in the same direction.
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 Bile acid sequestrants
• Includes: Cholestyramine, colestipol, and colesevelam
• Binds bile salts & some bacterial toxins.
• Useful in the treatment of bile-salt induced diarrhea
 Bismuth subsalicylate
 An OTC drug, used to treat many GI disorders
 Mechanism of action not well known, but known to
 Have anti-secretion, anti-inflammatory & antimicrobial
effects
 Used extensively for prevention & treatment of traveler's
diarrhea.
 Nausea & cramps are also relieved by bismuth
 SE: impaction, dark stools, black staining of the tongue 44
 Opioids
 Are widely used in the treatment of diarrhea
 Act by several mechanisms
• Reduce intestinal motility
• Reduce intestinal secretions & increase intestinal reabsorption of
water.
 Commonly used opioid antidiarrheals includes:
• Diphenoxylate, difenoxin & Loperamide
 Loperamide
• Orally active antidiarrheal agent
• Penetrates the CNS poorly, so have less CNS effects
• Diphenoxylate & difenoxin
o Both can cause CNS effects, when used in higher doses: have
potential for abuse/addiction
o Are available in preparations containing small dose of atropine
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o To discourage abuse & deliberate overdose.
 Side effects
Opioids
• Drowsiness, sedation, dizziness, lethargy
• Nausea, vomiting, anorexia, constipation
• Respiratory depression.
• Bradycardia, palpitations, hypotension
• Urinary retention
• Flushing, rash, urticaria

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 α2 receptor agonists
 Clonidine
• Have special roles in
• Diabetics with chronic diarrhea
• Diarrhea caused by opiate withdrawal
• Works by stimulating absorption & inhibit secretion of fluid
& electrolytes.
• Can also inhibit GIT motor activity by presynaptically
inhibiting Ach release from nerves in the myenteric plexus.
 Octreotide
o Is a Somatostatin analogue
o Is effective in inhibiting severe secretory diarrhea due to
hormone tumors of the pancreas & GIT.
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 Octreotide, cont’d
o MOA
o inhibits secretion of hormones such as gastrin, vasoactive
intestinal peptide (VIP), insulin, secretin, motilin, etc
o Octreotide has been used with varying success in other
forms of secretory diarrhea, such as:
o Chemotherapy induced diarrhea
o HIV associated diarrhea.
o Diabetes mellitus associated diarrhea.

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Laxatives

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• Constipation
– Defined as infrequent passage of stool
– Usually described as:
• Decreased frequency of stool (<3 times per week)
• Difficulty in initiation or passage of stool
• Passage of firm stool or small volume of faces
• Feeling of incomplete evacuation
– Cause could be:
• Lack of dietary fibers
• Hormonal disturbances
• Neurogenic disorders
• Systemic illness, Drugs
– In most cases of chronic constipation no specific cause is
found.
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Management of constipation
•Non pharmacological options
– Can be used for many cases of constipation
– Includes:
• Using high fiber diet (20-30g/day)
• Adequate fluid intake
• Avoiding constipating drugs
•Pharmacological options
– Are reserved to pts in whom the non pharmacological
options failed.
– Involves the uses of a group of drugs called
laxatives/cathartics.
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• Laxatives based on their mechanism of action can
be classified into different groups
– Bulk forming agents
– Osmotic laxatives
• Saline laxatives
• Non digestible sugars & alcohols

– Stool softeners (emollients)

– Stimulant (irritant) laxatives
– Prokinetic agents

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 Bulk forming laxatives
 Includes: natural plant products (psyllium,
methylcellulose) and synthetic fibers (Ca
polycarbophil)
 All act by increasing the bulk (mass) of the faces
 attract water & form a hydrogel
 Then the hydrogel increases the fecal mass & stretches the
walls of the GIT which stimulates peristalsis.
 This action may need 2-3 days after administration.
 Side effects:
 Impaction
 Fluid overload.
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 Osmotic: Saline laxatives
• Refers to laxatives which contain magnesium ions &
phosphate compounds.
• Poorly absorbable.
• Includes: magnesium sulfate, magnesium hydroxide,
magnesium citrate & sodium phosphate.
• MOA: Their laxative action results from osmotically
mediated water retention.
• Phosphate salts are better absorbed than magnesium based
preparations.
• So phosphate salts need larger dose administration.
• Should be used cautiously or avoided in patients with:
• Renal insufficiency, cardiac disease, electrolyte imbalance
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 Osmotic: Non digestible sugars &
alcohol
o Includes: lactulose, mannitol & Sorbitol
o Work by similar mechanism with the saline laxatives
o Can be used in the treatment of constipation:
o Caused by opioids & vincristine
o Of the elderly
o Of idiopathic chronic constipation

o Abdominal bloating & rectal irritations are the SEs

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Stool softeners (emollients)
 Includes the docusate salts: docusate sodium & docusate
calcium, Glycerin suppository.
 Have wide spread use
• Docusate salts
– Are surfactants which lower the surface tension of the stool
to allow mixing of fatty substances.
• Results in softening of stool & permits easier defecation
– also stimulate intestinal fluid & electrolyte secretions
– SEs: skin rashes, decreased absorption of vitamins.

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Stimulant (irritant) laxatives
 Contain a variety of drugs whose exact mechanism of
action is not known.
 But they are thought to act on the GI mucosal cells of the
intestine to stimulate peristalsis and stimulate colonic
electrolyte and fluid secretion.
• Contains

– Diphenylmethane derivatives

– Anthraquinones

– Ricinoleic acid 57
 Stimulant (irritant) laxatives, cont’d
Diphenylmethane derivatives
• Includes: Bisacodyl, sodium picosulfate
• Bisacodyl
•Marketed as enteric coated preparations & suppositories
–It induces a bowel movement within 6–10 hours when given orally
and 30–60 minutes when taken rectally.
•Needs hydrolysis by endogenous esterases in the bowel for
activation.
• taken at bed time (coated tab) & will produce effect in the
morning.
• It has minimal systemic absorption and appears to be safe for acute
and long-term use.
• Overdose can lead to fluid & electrolyte deficits. 58
• Anthraquinones
– Includes: cascara, aloe, senna
– They mainly act on the colon than the ileum
– Produce their laxative effects with in 8-10 hours after
oral administration
• Makes them suitable for dosage overnight
• Castor oil
– Is a bland oil that is hydrolyzed in the gut to yield the
active metabolite, ricinoleic acid
– Acts on ileum & colon to induce an increased fluid
secretion & colonic contraction.
– Due to adverse consequences to the colon, shouldn’t
be used for long period of time. 59
• Stimulants can cause:
– Nutrient malabsorption
– Skin rashes
– Gastric irritation
– Rectal irritation

60
Antiemetic and Antinausea
Agents

61
 Antiemetic & Antinausea agents
• Nausea – Unpleasant feeling that often precedes Vomiting
• Emesis (vomiting) – Forcible emptying of gastric, & occasionally,
intestinal contents
• Antiemetic agents – Used to relieve N & V
• Vomiting center (VC) & Chemoreceptor trigger zone (CTZ)
– Both located in the brain
– Once stimulated, cause the vomiting reflex
• Several types of receptors are involved in the emetic response,
– Important among these are receptors for serotonin,
dopamine, acetylcholine, histamine
62
 Antiemetic & Antinausea agents (Cont…)

a) Anticholinergic agents (E.g. Hyoscine)

– Benefits derive from suppressing nerve traffic in the
neuronal pathway that connects the vestibular
apparatus of the inner ear to the vomiting center.
– Most effective drug for prevention & treatment of
motion sickness
– The most common side effects are dry mouth,
blurred vision, & drowsiness.

63
 Antiemetic & Antinausea agents (Cont…)

b) Antihistamine agents (H1 receptor blockers)

– E.g. dimenhydrinate, diphenhydramine, meclizine,
promethazine
– Inhibit ACh & H1 receptors

• Prevent cholinergic stimulation in vestibular & reticular

areas, thus preventing N &V
– They are also used for nonproductive cough, allergy
symptoms, sedation.

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 Antiemetic & Antinausea agents (Cont…)

c) Neuroleptic agents
– E.g. chlorpromazine, perphenazine,
triflupromazine
– Block dopamine receptors on the CTZ

– Also used for psychotic disorders, intractable

hiccups

65
 Antiemetic & Antinausea agents (Cont…)
d) Prokinetic agents
– E.g. metoclopramide, cisapride
– Block dopamine (D2 receptor) in the CTZ
• Cause CTZ to be desensitized to impulses it receives
from the GIT.
– Also stimulate peristalsis in GIT (by blocking peripheral D2
receptors), enhancing emptying of stomach contents
• Dopamine (D2) in GIT inhibits Ach release,
– Prokinetic effect is due to this blockade effect.
– Also used for GERD, delayed gastric emptying
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 Antiemetic & Antinausea agents (Cont…)

e) Serotonin (5HT3) blockers

– Block serotonin receptors in the GIT, CTZ, & Vomiting
Centre.
– E.g. dolasetron, granisetron, ondansetron
– They are the most effective drugs available for suppressing
N & V caused by highly emetogenic anticancer drugs.
– These agents are also used to suppress N & V associated
with radiation therapy & anesthesia.
– The most common side effects are headache, diarrhea, &
dizziness.
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