DRUGS THAT AFFECT THE DIGESTIVE SYSTEM

Pharmacology
Prepared by

Nur Athirah Atiqah Binti Azman Abdullah

Nur Aiman Shahira Binti Zakaria
NurFarah Binti Safaruddin
Refella Ronnie
Muhamad Akmal Bin Musa
Muhammad NurHaqim Bin Saidi

Introduction of the drugs

Prescription drugs and medicine for the

gastrointestional organ and diseases relating
to them .
This include any part of digestive track from
mouth to anus, liver , biliary track and
pancreas.

Used of the drugs

Aciphe (rabeprazole sodium)

For treatment of symptomatic
gastroesophageal reflux disease
Afinitor (everolimus)
for the treatment of advanced pancreatic
neuroendocrine tumors
Akynzeo (netupitant and palonosetron)
for the prevention of chemotherapy-induced
nausea and votaming

Alinia (nitazoxanide)
for the treatment diarrhea caused by
cryptosporidium and girdia in children
Aloxi (palonosetron)
for the prevention of nausea and votaming
associated with emetogenic cancer
chemotherapy

Type of the drugs included

Cyramza (ramucirumab)
Eloxatin (oxaliplatin)
Femara (letrozole)
Gastro Mark
Gleevec (imanatib mesylate)
Metozolv ODT ( metoclopramidehydrochloride)

Organs Of The Body That Affected By The

Drugs That Affect The Digestive System

Disease Involved By The Drugs That Affect

The Digestive System

Croup
Acute respiratory illness of young children
characterized by a harsh cough, hoarseness,
and difficult breathing.
Its caused by infection of the upper airway in
the region of the larynx ( voice box), with
infection sometimes spreading into the lower
airway to the trachea ( windpipe ).

 Jaundice
Excess accumulation of bile pigments in the
bloodstream and bodily tissues that cause a
yellow to orange and sometimes even greenish
discoloration of the skin, the whites of the
eyes, and the mucus membranes.
It is best seen in natural daylight and may not
be apparent under artificial lighting.

 Inflammatory Bowel Disease (IBD)

IBD chronic inflammation of the intestines that
results in impaired absorption of nutrients.
IBD encompasses two disorders :
i. Crohn disease( regional ileitis )
ii. Ulcerative colitis
The onset of IBD typically occurs between the
ages of 1 and 35.
Its tends to run in families.

 Dysentery
Infectious disease characterized by
inflammation of the intestine, abdominal pain
and diarrhea with stools that often contain
blood and mucus.
Two(2) major classifications of dysentery:
i. Bacillary ( caused by bacteria )
ii. Amebic ( caused by amoebas )
Bacillary dysentery/shigellosis is caused by
bacilli of the genus Shigella.

Mechanism of actions of the drugs

AcipHex
- Absorption
1. Absolute bioavailability for a 20 mg oral tablet of rabeprazole
more effective(compared to intravenous administration)
2. When ACIPHEX tablets are administered with a high fat meal,
concomitant food intake may delay the absorption up to 4
hours or longer.
3. However, the extent of rabeprazole absorption (AUC) are not
significantly altered.
4. Thus ACIPHEX delayed-release tablets may be taken without
regard to timing of meals.
-Distribution
Rabeprazole is 96.3% bound to human plasma proteins.

 -Metabolism
1. A significant portion of rabeprazole is metabolized via systemic
nonenzymatic reduction to a thioether compound.
2. Rabeprazole is also metabolized to sulphone and desmethyl compounds via
cytochrome in the liver.
3. The thioether and sulphone are the primary metabolites measured in
human plasma. These metabolites were not observed to have significant
antisecretory activity.
4. rabeprazole is metabolized in the liver primarily by to a sulphone metabolite
and cytochrome to desmethyl
5. rabeprazole. exhibits a known genetic polymorphism due to its deficiency in
some sub-populations (e.g., 3 to 5% of Caucasians and 17 to 20% of
Asians). Rabeprazole metabolism is slow in these sub-populations,
therefore, they are referred to as poor metabolizers of the drug.

Excretion
-Following a single 20 mg oral dose of rabeprazole, approximately 90% of the
drug was eliminated in the urine. The remainder of the dose was recovered in
the feces. Total recovery of radioactivity was 99.8%. No unchanged rabeprazole
was recovered in the urine or feces.

Gleevec
Imatinib mesylate

Absorption and Distribution

1. Imatinib is well absorbed after oral administration.
2. Absolute bioavailability is 98%.
3. Mean imatinib AUC increases proportionally with
increasing doses ranging from 25 mg1,000 mg.
4. There is no significant change in the pharmacokinetics of
imatinib on repeated dosing
5. accumulation is fold at steady state when Gleevec is dosed
once-daily.
6. At clinically relevant concentrations of imatinib binding to
plasma proteins in in vitro experiments is approximately
95%, mostly to albumin and acid glycoprotein.

 Metabolism
1. major enzyme responsible for metabolism of imatinib. The main circulating active metabolite
in humans is the N-demethylated piperazine .
2. The plasma AUC for this metabolite is about 15% of the AUC for imatinib.

3. The plasma protein binding of N-demethylated metabolite is similar to that of the parent
compound.

Excretion
Imatinib elimination is predominately in the feces, mostly as metabolites.
Based on the recovery of compound(s) after an oral dose of imatinib,
approximately 81% of the dose was eliminated within 7 days, in feces (68% of dose)
and urine (13% of dose).
Unchanged imatinib accounted for 25% of the dose (5% urine, 20% feces), the
remainder being metabolites.
- Following oral administration , the elimination half-lives of imatinib and its major
active metabolite, the N-demethyl derivative, are approximately 18 and 40 hours,
respectively.
Typically, clearance of imatinib in a 50-year-old patient weighing 50 kg is expected
to be 8 L/h, while for a 50-year-old patient weighing 100 kg the clearance will
increase to 14 L/h.
The inter-patient variability of 40% in clearance does not warrant initial dose
adjustment based on body weight and/or age but indicates the need for close
monitoring for treatment-related toxicity.

Therapeutic uses of the drugs

Aciphex
Healing of erosive or ulcerative in adult.
Healing of duodenal ulcer in adult.

Gleevec
Its can be given by mouth instead of by
injection
Respond relatively quickly

Adverse effects of the drugs

NSAIDs -usually associated with gastric and

duodenal ulsers but are also recognised to
cause:

linchen pinus in the mouth

oesophangeal inflammation

stricturus

small bowel

colonic ulcers

strictures

 COX-2 -selective inhibitors have been

developed and have a more favourable GI
safety profile that standard NSAIDs. Poor
NSAIDs is:

The calcium antagonists, phenytoin and

cyclosporin , induce gum hyperplasia
(particulary in patients with poor oral
hygiene)