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Gastrointestinal Tract


Pe tic Ulcer Disease

Peptic ulcer disease arises from the imbalance between defensive factors (mucus, bicarbonate
and mucosal blood flow) and aggressive factors (acid, pepsin, NSAIDs and Helicobacter pylori).
Hydrochloric acid is secreted by gastric parietal cells due to stimulation of H+ K+
ATPase (proton pump). Histamine (through H2 receptors), acetylcholine (through M1 and M3
receptors) and gastrin (through CCK receptors) are important stimulators of proton pump.
ACh and gastrin exert their action directly as well as through release of histamine.

Antral G-cells produce gastrin on stimulation by dietary peptides. Gastrin mainly

stimulates release of histamine from entero-chromaffin like (ECL) cell and weakly stimulates
proton pump itself. Parietal cells secrete H+ in the lumen through H+ - K+ - ATPase (proton
pump). Vagus nerve (via ACh) help in increasing acid by three mechanisms:
Direct stimulation of proton pump
Stimulation of ECL-cells to release histamine
Direct release of gastrin (by action of G-cells) and inhibition of somatostatin by
action on D-cells (later inhibits release of gastrin).
The main strategies employed for the treatment of peptic ulcer disease and gastritis
are to:


Neutralize gastric acid by antacids.

Decrease secretion of acid in stomach.
Increase protective factors like mucus and bicarbonate.
Protect the ulcer by forming a layer over it.
Stimulate the healing of ulcer.
Kill H. pylori associated with peptic ulcer disease.

Proton pump is stimulated by

Histamine (H1 receptors)
Acetylcholine (M1 and M3
Gastrin (CCK receptors)

Review of Pharmacology

These drugs are weak bases that neutralize gastric acid (do not decrease the volume of
acid secreted). Their major role in peptic ulcer is to provide prompt relief from ulcer pain.
Antacids may be systemic (absorbed from the GIT) or local (poorly absorbed). Sodium
bicarbonate is rapidly acting systemic antacid. It is not indicated for long term use because:

Drugs Decreasing cid ecretion

Recent studies have suggested

an increase in risk of hip fracture
in patients taking PPI on long

Long-term use of PPI is associated with:

Subnormal vitamin B12 levels (reduced absorption)
Increase in risk of hip fractures (reduced Ca2+ absorption)

PPIs are drugs of choice for

Peptic ulcer disease (PUD)
due to any etiology (even
NSAID induced).
disease (GERD)
Zollinger Ellison Syndrome

These are prodrugs (active moiety is sulfenamide) and act by irreversibly inhibiting
H+ K+ ATPase in gastric parietal cells. The drugs in this group include omeprazole,
pantoprazole, esomeprazole, lansoprazole and rabeprazole. These drugs are
weak bases and can be destroyed by gastric acid. To protect them from gastric acid,
these are given as enteric coated tablets. This coating dissolves in alkaline medium
(intestinal juice) and prodrugs are absorbed. On reaching parietal cells, active moiety
(sulfenamide) is formed and gets trapped. These can inhibit both basal acid output
(nocturnal acid secretion) as well as meal stimulated acid output (maximal acid output).
PPIs are given orally in early morning empty stomach (just before breakfast).
Pantoprazole, esomeprazole and lansoprazole can be given i.v. These drugs have
short t1/2 but can inhibit acid secretion for more than 24 hours (hit and run drugs,
inhibit proton pump irreversibly).
PPIs are the drugs of choice for peptic ulcer disease (PUD) due to any etiology
(even NSAID induced). These are also the agents of choice for gastroesophageal
reflux disease (GERD) and Zollinger Ellison Syndrome (ZES). For prevention of stress
induced gastric bleeding, H2 blockers (i.v. infusion) are preferred over PPIs. In patients with
nasoenteric tube, immediate release omeprazole (by nasogastric tube) is currently
PPIs are quite safe drugs and have diarrhea, headache and abdominal pain as
adverse effects. These have been shown to be carcinogenic in rodents but no such
case has been reported in humans.

m inhibitors (PP s)


Gastrointestinal Tract

Proton pump inhibitors have

short t1/2 but can inhibit acid
secretion for more than 24 hours
due to irreversible inhibition of
proton pump.

It releases CO2 that can cause belching and gastric distension (ulcer perforation
can occur).
Sodium chloride formed in the neutralization reaction can be absorbed that
can exacerbate fluid retention in patients of CHF and hypertension.
Systemic and urinary alkalosis may occur.
Rebound hyperacidity can occur.

Aluminium hydroxide [Al(OH)3], magnesium trisilicate, megaldrate and

magnesium hydroxide [Mg(OH)2] are non systemic antacids. These are slower but
longer acting drugs. Rebound acidity does not occur. Al (OH)3 causes constipation
whereas magnesium salts are responsible for diarrhea. Most of the market
preparations contain these agents in combination to minimize the impact on bowel
Simethicone is a water repellant, pharmacologically inert anti-foaming agent. It
reduces flatulence and can also be used to prevent bed sores.
Antacids decrease the absorption of acidic drugs (acidic drugs are ionized in alkaline
medium) and tetracyclines (by forming complexes).
Milk alkali syndrome (hypercalcemia, renal insufficiency and metabolic alkalosis) may
be caused by excessive doses of Na2CO3 or CaCO3 with calcium containing foods
(like milk).


Al (OH)3 causes constipation

whereas magnesium salts are
responsible for diarrhea.

Major role of antacids in peptic

ulcer is to provide prompt relief
from ulcer pain.




Gastrointestinal Tract

Increased risk of enteric bacterial infections

- C. difficile infections
- Bacterial gastroenteritis

rece tor antagonists



Non-selective anti-muscarinic drugs like propantheline and oxyphenonium

can be used for decreasing gastric acid secretion. However, by increasing gastric
emptying time, these drugs prolong the exposure of ulcer bed to gastric acid. Further
anticholinergic adverse effects like dry mouth, blurred vision, constipation and
urinary retention are commonly seen with these drugs. Pirenzepine and telenzepine
are selective M1 blockers that are preferred antimuscarinic agents for peptic ulcer
disease as these are devoid of anticholinergic adverse effects.


Famotidine is most potent H2 blacker.

All H2 blockers except famotidine inhibits the gastric first pass metabolism of ethanol

Loxatidine is a non-competitive blocker of H2 receptors.

Nizatidine also possess anti-AChE activity and can cause bradycardia and enhanced gastric

Nizatidine is having negligible first pass metabolism (~100% bioavailability)

Anti-histaminics (H2 blockers)

are more effective for reducing
basal (nocturnal) acid secretion
(stimulated by gastrin, ACh, as
well as histamine).


These drugs competitively inhibit H2 receptors in parietal cells, thus inhibiting

the acid secretion. ACh and gastrin act partly by causing the release of histamine,
therefore acid secreting capacity of these agents also is decreased by H2 blockers.
Drugs in this group are cimetidine, ranitidine, famotidine, roxatidine, nizatidine
and loxatidine.
These drugs are more effective for reducing basal (nocturnal) acid secretion (histamine
mediated) than stimulated acid secretion (stimulated by gastrin, ACh, as well as
histamine). These drugs can be used for GERD, PUD, ZES and prevention of stress
induced ulcers. Cimetidine is not used routinely because:
It can cross blood brain barrier and result in mental state changes.
It inhibits binding of dihydrotestosterone to androgen receptors that can
manifest as impotence in males.
It inhibits metabolism of estradiol and increases serum prolactin levels on
long term use, thus can cause gynaecomastia (in males) and galactorrhoea (in
It is a potent inhibitor of CYP enzymes and can increase plasma concentration
of warfarin, theophylline and many other drugs.
It is the least potent H2 blocker.


Lanoprazole is most potent PPI

Lansoprazole is safest PPI in pregnancy.

Esomeprazole, lansoprazole and pantoprazole can be given by i.v. route.

Omeprazole and esomeprazole are microsomal enzyme inhibitors. These may decrease the
metabolism of diazepam.

Lansoprazole enhances the metabolism of theophylline


Acid suppressing agents (like PPIs, H2 blockers etc.) can result in tolerance and rebound hyperacidity due to secondary hypergastrinemia.

Drugs ncreasing Protective Factors

PGE1, PGE2 and PGI2 act as anti-ulcer drugs by increasing the release of mucus and bicarbonate


Review of Pharmacology

Ulcer Protective gents


Misoprostol (PGE1 analogue)

is the MOST SPECIFIC drug
for treatment and prevention
of NSAID induced peptic ulcer
whereas drug of choice is proton
pump inhibitor.

and by increasing the mucosal blood flow. PGs also inhibit H+ K+ ATPase and decrease the
acid production. Misoprostol (PGE1 analogue) is the MOST SPECIFIC drug for treatment
and prevention of NSAID induced peptic ulcer (DOC is PPI). Enprostil and rioprostil (PGE2
analogue) are other drugs in this group. Commonest side effect of PG analogues is diarrhea
and colicky abdominal pain.

Bismuth subcitrate is used for

peptic ulcer whereas another
salt, bismuth subsalicylate is
used in Travellers diarrhea. It
reduces stool frequency by inhibiting PG synthesis and chloride secretion apart from having
antimicrobial and gastroprotective effects.

Sucralfate should not be given

with antacids as it polymerises
only in acidic medium.

These drugs form a covering over the ulcer bed that prevents its exposure to gastric acid.
Sucralfate and colloidal bismuth subcitrate are two important ulcer protective drugs.
Sucralfate: It is aluminium salt of sulfated sucrose. At pH below 4, its molecules
polymerize to form a sticky layer that covers the ulcer base and acts as a physical
barrier to prevent acid exposure. It can bind phosphates also and can result in
hypophosphatemia. It should not be given with antacids because it acts only in
acidic medium (antacids raise the pH by neutralizing the gastric acid). Most common
side effect of sucralfate is constipation.
Colloidal bismuth subcitrate: It also forms an acid resistant coating over the ulcer.
It also dislodges H. pylori from the surface of gastric mucosa and kills it. Adverse
effects include blackening of tongue and bismuth toxicity (osteodystrophy and
Rebamipide and Ecabet are cytoprotective drugs acting by increase in PG generation
and by scavenging reactive oxygen species.

Carbenoloxone is obtained from the roots of licorice. It causes epithelisation of ulcer without
decreasing acid production. It can displace aldosterone from plasma protein binding sites
and result in hypertension, sodium and water retention and hypokalemia.
Triple drug therapy for H. Pylori
PProton pump inhibitor

nti elicobacter Pylori Drugs


Gastrointestinal Tract

Ulcer ealing Drugs

H. pylori infection can be detected by urea breath test. It is responsible for relapse of PUD.
Drugs used for the treatment of H.pylori include:

Colloidal bismuth subcitrate


nti metic Dr gs

Gastrointestinal Tract

Vomiting (emesis) occurs due to stimulation of vomiting centre (VC) in lateral medullary
reticular formation. It receives input from GI mucosa, chemoreceptor trigger zone (CTZ) and
vestibular apparatus.
Irritation of GI mucosa by drugs or irritants leads to release of serotonin that
stimulates VC via 5HT3 receptors.
CTZ is rich in dopamine (D2) and serotonin (5HT3) and neurokinin (NK1) receptor.
Motion sickness occurs due to stimulation of vestibular apparatus and cerebellum.
These structures result in stimulation of VC by activating M1 and H1 receptors.
By stimulation of H1 receptors, histamine plays a permissive role in all types of

orning ickness

Drugs for

otion ickness

Hyoscine is used as i.m. injection or transdermal patch (applied behind pinna) for
prophylaxis of motion sickness. It has no role in treatment, once the vomiting
Antihistaminics like promethazine, diphenhydramine, cyclizine or meclizine can
also be used for prophylaxis.
Cinnarizine (antihistaminic with anticholinergic and antiserotonergic properties) is
used for treatment of vertigo.

Combination of doxylamine (antihistaminic) with pyridoxine (Vit B6) in high dose

is safest anti-emetic drug in pregnancy
D2 blockers although effective should not be used due to their teratogenic potential

Drugs for hemotherapy and adiation therapy nduced Vomiting


Drugs For

5 HT3 blockers like ondansetron, granisetron, dolasetron, palonosetron and

ramosetron are DOC for this condition.
Palonosetron is most potent 5 HT3 blocker. Dolasetron may prolong QT interval.
Palonosetron has longest t1/2 whereas ondansetron has shortest t1/2.
Efficacy of these drugs increases if used along with antihistaminics, D2 blockers or
These drugs are also effective in hyperemesis of pregnancy and post operative nausea.
D2 blockers like metoclopramide and domperidone can also be used
Vomiting due to cisplatin (most emetogenic anti cancer drug) can occur within 24
hours or it may be delayed (after 2 days). DOC for the former condition is 5HT3
blocker whereas for the latter condition, DOC is aprepitant (substance P antagonist).
Palonosetron may also be effective in delayed emesis.
Aprepitant is a highly selective NK1 receptor antagonist, orally active, and enter the

Combination of doxylamine (antihistaminic) with pyridoxine (Vit

B6) in high dose is safest antiemetic drug in pregnancy

5 HT3 blockers like ondansetron,

granisetron, dolasetron, palonosetron and ramosetron are DOC
for chemotherapy induced vomiting.


Review of Pharmacology
brain. It is metabolized by CYP3A4 enzymes and can also inhibit the metabolism of
drugs metabolized by this enzyme e.g. warfarin.
Fosaprepitant is an intravenous prodrug of aprepitant.
Netupitant is a newer NK1 antagonist approved for chemotherapy induced vomiting
(both acute and delayed in combination with palonosetron)

Drugs for Post perative Vomiting

5 HT3 antagonists are preferred over other drugs.

ther Drugs for Vomiting
Steroids like dexamethasone can be used as anti-emetic agents in chemotherapy
induced vomiting.
Benzodiazepines like lorazepam and alprazolam may be useful for anticipatory
component of nausea and vomiting before surgery.
Dronabinol (a cannabinoid) possesses anti-emetic properties and acts by stimulating
CB1 receptors. It can also stimulate appetite (used for AIDS with anorexia). Central
sympathomimetic (tachycardia, palpitations etc.) effects, paranoid reactions and thinking
abnormalities may appear as adverse effects.

metic Dr gs

astroeso hageal e l x Disease ( er )


It is a condition in which acid in the stomach reaches the esophagus and causes mucosal
inflammation. Two strategies for the management of this condition are either to decrease the acid
production (by PPIs) or to increase the forward movement of GIT (so that the contents do not reflux
upwards). The drugs used for increasing the GI motility are known as prokinetic drugs.
These drugs can also be used for the treatment of gastroparesis, post operative paralytic ileus
and constipation.
Prokinetic Drugs
ACh is the main excitatory neurotransmitter in the GIT. Cholinergic neurons contain
excitatory (5-HT4) as well as inhibitory (5HT3, D2) presynaptic receptors.
Thus D2 and 5HT3 antagonists and 5 HT4 agonists will increase the release of ACh and
stimulate the GI motility.

etoclo rami e

Gastrointestinal Tract

Apomorphine and ipecacuanha can be used to produce vomiting for treatment of poisonings.
Emetics should not be used for kerosene and corrosive (acid and alkali) poisonings.

It possesses central as well as peripheral D2 blocking action. Central D2 blocking action is

responsible for its antiemetic effects.

It is also a prokinetic drug due to agonistic action at 5HT4 receptors (main

mechanism) and antagonistic action at 5HT3 receptors.
Prokinetic action is due to release of ACh and thus can be antagonized by atropine.
It increases gastric peristalsis (enhances gastric emptying) and LES tone but has no
effect on colonic motility.
Metoclopramide is mainly used as an antiemetic agent. It can also be used in
GERD and for the treatment of gastroparesis (in diabetic patients). Another
indication of this drug is to enhance gastric emptying for emergency general
anaesthesia (if the patient has taken food within 4 hrs.)
D2 blocking action can result in extrapyramidal side effects (muscle dystonia,
Parkinsonism etc.) and hyperprolactinemia (leading to galactorrhoea).


Gastrointestinal Tract

Dom eri one

It is a D2 receptor antagonist and cannot cross blood brain barrier. It is mainly used as an
antiemetic (less efficacious than metoclopramide) drug and is devoid of extrapyramidal and
hyperprolactinemic adverse effects. It decreases l-dopa induced vomiting without interfering with
its efficacy.


Domperidone decreases l-dopa

interfering with its efficacy.

Cisapride has been withdrawn

in some countries due to its
QT prolonging action whereas
Tegaserod has been withdrawn
from India due to increased
infarction and stroke.

ther Prokinetic Dr gs

rritable owel yn rome (


Levosulpiride (l-isomer of sulpiride; an antipsychotic drug) is a newer D2 blocker having

prokinetic activity.
Loxiglumide is a CCK1 receptor antagonist indicated for constipation dominant IBS.
Macrolides (like erythromycin) are motilin agonists. Erythromycin is indicated in
diabetic gastroparesis. Rapid development of tolerance limits this use.


Cisapride, mosapride, renzapride, prucalopride and tegaserod are 5-HT4 agonistic drugs
with no action on D2 receptors (no antiemetic property). These drugs increase whole GI motility
including colon.
Cisapride was previously used for the treatment of GERD but it has been withdrawn
in some countries due to its QT prolonging action. It is metabolized by CYP 3A4
and therefore should not be administered with microsomal enzyme inhibitors
like ketoconazole and erythromycin (increased chances of torsades de pointes,
an arrhythmia with QT prolongation). Mosapride and renzapride do not prolong QT
interval. Tegaserod can be used for constipation dominant irritable bowel syndrome.
However, recently it has also been withdrawn from India due to increased incidence
of myocardial infarction and stroke.

It is a condition characterized by abdominal pain, bloating and altered bowel habits

(diarrhea or constipation)
For relieving pain, the drugs used are TCAs (fluoxetine is less effective) and
anticholinergics like dicyclomine and hyoscine.
Treatment of IBS
5-HT4 agonist
- Tegaserod
- Prucalopride

- Dicyclomine
- Hyoscine

Kappa agonist
- Fedotozine


Reserpine analog
- Mebeverine

Chloride channel
- Lubipristone

5HT3 antagonist
- Alosetron

Guanylate cyclase

Constipation dominant

- Loperamide
- Diphenoxylate

Diarrhea dominant

Tricyclic antidepressants
- Impiramine
- Desipramine
- Nortriptyline

For pain relief

Linaclotide is a guanylate
cyclase agonist indicated for
oral treatment of idiopathic
constipation and IBS with

onsti ation


High fibre diet, adequate fluid intake and regular exercise are best measures to prevent
constipation. Patients not responding to these measures may require laxatives. These can be
classified as


Review of Pharmacology

Bulk-forming agents are contraindicated in presence of megacolon

Saline purgatives should not be given in chronic renal failure
Stimulant purgatives are contra-indicated in presence of intestinal obstruction.
Chronic use of anthraquinone derivatives (like senna and cascara) may lead to melanosis coli
(brown pigmentation of colon)
Phenolphthalein is not used now due to risk of potential carcinogenicity
Lubiprostone and Linaclotide: These stimulate Cl channel opening in the intestine,
increase liquid secretion in gut and decrease transit time, therefore used for chronic
Methylnaltrexone and alvimopan are used for opioid induced constipation.

Lubiprostone is used for

chronic constipation. It acts by
opening in the intestine,
Increasing liquid secretion in
Decreasing transit time.

Diarrhea can be treated by antibiotics effective against the causative organism. In noninfective diarrhea, drugs useful are

Loperamide is a non-addictive over the counter anti-diarrheal drug. Diphenoxylate is

another opioid but has addictive potential if used for prolonged periods. It is always given in
combination with atropine to prevent the abuse (atropine will produce dry mouth and other
anticholinergic side effects). These drugs are contraindicated in infective diarrhea.

Racecadrotil is enkephalinase inhibitor (inhibits breakdown of enkephalins; endoge

nous opioids) having antidiarrheal effect.
Clonidine is indicated for diabetics with chronic diarrhea.


ther Dr gs

Crofelemer is a new drug approved for relieving symptoms of

diarrhea in AIDS patients taking
anti-retroviral therapy. It acts by
blocking two chloride channels;
CFTR and anoctamin-1.

This long acting somatostatin analog can be used to decrease secretory diarrhea and other
symptoms of carcinoid syndrome and VIPoma. In low doses (50 g, s.c.), it stimulates motility,
whereas at high doses (100-250 g, s.c.), it inhibits motility. In higher doses, it is also useful for
the treatment of diarrhea due to vagotomy, short bowel syndrome and AIDS. It can also be
used for treatment and prophylaxis of acute pancreatitis.

ctreoti e

Atropine is added to lopermide to

decrease its addictive potential.

ioi s


Gastrointestinal Tract

New Formula WHO-ORS


3.5 g

2.6 g


1.5 g

1.5 g

Trisodium citrate

2.9 g

2.9 g


20 g

13.5 g





90 mmol/L

75 mmol/L

20 mmol/L

20 mmol/L


80 mmol/L

65 mmol/L


10 mmol/L

10 mmol/L


111 mmol/L

75 mmol/L

Total osmolality

311 mosm/L

245 mosm/L

In new formula WHO-ORS,

concentration of NaCl and
glucose as well as total
osmolarity is decreased.

n lammatory owel Disease


In new formula WHO-ORS, concentration of NaCl and glucose as well as total osmolarity is decreased
WHO standard fomula was based on cholera stools in which loss of Na+ was more. There
is a significant decrease in cholera cases and major cause of diarrhea now-a-days is
rota virus. New composition ORS is based on stool composition of rota virus patients.
Use of standard formula ORS has lead to development of edema (excess of sodium) and
increased stool frequency (unabsorbed glucose acts as laxative) in some patients.


Standard formula ORS

Hydration must be maintained in all cases of diarrhea to prevent fluid depletion

and shock. It is mostly accomplished by the institution of oral rehydration solution.
It contains sodium and potassium chloride, trisodium citrate and glucose. Glucose
helps in the absorption of sodium because glucose facilitated sodium reabsorption
remains intact even in severe diarrhea. Trisodium citrate is added to prevent acidosis.
Previously sodium bicarbonate was used for this function but now sodium citrate
is preferred because it imparts a longer shelf life to ORS. Composition of ORS used
previously and now is as follows:


ral ehydration olution (

Gastrointestinal Tract


Ulcerative colitis and Crohns disease are two distinct disorders classified under inflammatory
bowel disease (IBD).
5-aminosalicylic acid (5-ASA) is the main anti-inflammatory compound that acts
locally in the colon. When given alone by oral route, more than 80% is absorbed in
proximal intestine and very little reaches the diseased site i.e. colon. To decrease the
absorption it may be associated with some inert compound. Sulfasalazine (5-ASA +
sulfapyridine), olsalazine (5-ASA+ 5-ASA) and balsalazide (5-ASA + amino benzoyl
alanine) are effective for the treatment of ulcerative colitis. The inert compound
prevents the absorption in proximal GIT and the combination reaches the colon
where the bacteria cleaves the azo bond to free 5-ASA for action. Approximately 85%
sulfapyridine is absorbed from colon leading to adverse effects.
Different formulations (like time release tablets and coating in pH sensitive
resins that dissolve at pH 7) of 5-ASA have been developed to deliver it to colon.
These formulations are known as mesalamine.
5-ASA is the first line treatment for mild to moderate ulcerative colitis. Efficacy
in Crohns disease has not been established. Absorption of sulfapyridine (in
sulfasalazine) lead to nausea, vomiting, GI upset, bone marrow suppression,
hypersensitivity and oligospermia. Olsalazine may result in secretory diarrhea.

5-ASA is the first line treatment

for mild to moderate ulcerative


l cocorticoi s

Review of Pharmacology


It is used for the induction and maintenance of remission of Crohns disease but not
ulcerative colitis.
F-a thera y



Prednisone, prednisolone, hydrocortisone and budesonide are used in the

treatment of moderate to severe ulcerative colitis and Crohns disease.
Purine analogs
Azathioprine and 6-MP are important agents for the induction and maintenance of
remission of ulcerative colitis and Crohns disease.

Infliximab, adalimumab and certolizumab are useful in Crohns disease. Efficacy

in ulcerative colitis is doubtful. Infliximab is given by i.v. route whereas other two
are administered s.c. Certolizumab is a pegylated anti-TNF- indicated for crohns

Gastrointestinal Tract

nti- ntegrin hera y

Natalizumab is recently approved for moderate to severe Crohns disease not
responding to other therapies. It is targeted against 4 subunit of integrins. The
patient on natalizumab therapy should not be on other immunosuppressants due to
risk of progressive multifocal leukoencephalopathy (PML).
Vedolizumab is a new anti-integrin that block 4 b7 in GIT but not in brain. It is,
thus, less likely to cause PML.


Monoclonal Antibodies
Crohns Disease



D u


Gastrointestinal Tract

Drug of choice

Peptic ulcer
Gastric ulcer

Proton pump inhibitors (PPI)

Duodenal ulcer


Stress ulcer




H. pylori associated

Lansoprazole + Amoxycillin + Clarithromycin

Zollinger Ellison syndrome


Gastro Esophageal Reflux



Chemotherapy induced

5-HT3 antagonists like palonosetron

Levo-dopa induced


Migraine associated


Drug or disease associated




Radiation induced


Cisplatin - induced
* Early

5-HT3 antagonists


Prophylaxis of motion sickness


Pregnancy (Morning sickness)

Doxylamine + Pyridoxine

* Delayed

Opioid induced constipation

Methyl naltrexone

Diarrhea in carcinoid syndrome


To prevent dehydration in diarrhea


Crohns disease


Ulcerative colitis

5-ASA derivatives

Hepatic encephalopathy