Pharmacology of Gastrointestinal Diseases

Drugs Used in Gastrointestinal Diseases
1

Agents Stimulating the Appetite:
1. Bitters: Wormwood tincture –
Tinctura Absinthii - vial 25 ml PO 15-20 drops
2. Others: Insulin, Vitamins,
Anabolic Steroids: Retabolil, Phenoboline
2

Wormwood tincture contains glycoside Absinthian and Ethereal Oil
composed of Terpenes and a camphor isomer Absenthol.
Bitters stimulate receptors of oral cavity mucous and increase
the excitability of Starvation’s Center located
at Lateral Nucleus Of Hypothalamus.
3

Agents Inhibiting Appetite
Appetite Suppressants – Anorexigenic agents:
1. Centrally acting adrenergic agents – stimulating the CNS:
Phenamine (Amphetamine)
Phepranone (dr. 0.025 g)
2. Centrally acting serotoninergic agonist:
Fluoxetine (Prozac – tab. 0.02 g)
3. Centrally acting agents on both adrenergic and
serotoninergic systems – depressing the CNS:
Sibutramine (caps. 5 and 10 mg)
4

Drugs Used to Treat Peptic Ulcer Disease
I. Inhibitors of Gastric Acid Secretion:
1. Proton Pump Inhibitors:
Omeprazole (caps. 0.02 g)
Lansoprazole (caps. 0.03 g)
Pantoprazole (tab. 0.04 g)
Rabeprazole (tab. 0.01 and 0.02 g)
2. H2-Histamine Receptor Blockers:
Cimetidine (amp. 10%-2 ml, tab. 0.2 g)
Famotidine (tab. 0.02 and 0.04 g)
Ranitidine (tab. 0.15 g)
3. M-Cholinoblockers:
Atropine sulfate (amp. 0.1%-1 ml, tab 0.5 mg)
Platyphyllin hydrotartrate (amp. 0.2%-1 ml, tab. 0.005 g)
Pirenzepine (Gastrozepin – tab. 0.025 and 0.05 g)
5

II. Gastroprotectors:
1. Producing Mechanical Defense of Mucous Coat:
Sucralfate (Venter – tab. 0.5 g)
Bismuth tripotassium dicitrate (De-nol - tab. 0.12 g)
2. Increasing Protective Function of the Mucus Barrier :
● PG analogues:
Misoprostol (PG E – tab. 0.2 mg)
Enprostil (caps. 35 mg), Arbaprostil, Rioprostil
● Others:
Carbenoxolone (Biogastrone – tab. 150 mg)
Dalargin (amp. 0.001 g)
III. Antimicrobial Agents – Suppressing Helicobacter pylori - infection:
Amoxicilline - Tab. 0.25 and 0.5 g
Clarithromycin - Tab. 0.5 g
Metronidazole , Tetracycline 6

IV. ANTACIDS:
Aluminium hydroxide (pulv. 0.25-1.0 g)
Almagel (vial 170 ml)
Maalox
Fosfalugel
Calcium Carbonate (pulv. 0.25-1.0 g)
Magnesium Hydroxide (pulv. 0.25-1.0 g)
Magnesium Trisilicate
Sodium Bicarbonate (Tab. 0.3 and 0.5 g)
8

V. Myogenic Spasmolytics:
No-spa – amp. 2% solution -2 ml,
Tab. 0.04 g (40 mg)
Papaverine hydrochloride –
amp. 2% solution - 2 ml,
Tab. 0.04 g (40 mg)
VI. Others:
Solcoseryl (amp. 2, 5 and 10 ml; vial 250 ml)
9

H2
-antagonists Cimetidine, Ranitidine, Famotidine -
inhibit (by 90%) basal, food-stimulated, and
nocturnal secretion of gastric acid after a single dose.
They block H2
-receptors in the stomach, blood vessels, and
other sites.
They are Competitive Antagonists of Histamine and
are fully reversible.
H2
-antagonists distribute widely throughout the body
(including in breast milk and across the placenta) and are
excreted mainly in the urine.
Clinical Uses: Peptic Ulcers, Zollinger-Ellison Syndrome,
Gastroesophageal Reflux Disease (heartburn)
10

Cimetidine has Endocrine effects and acts as
a Nonsteroidal Antiandrogen
Endocrine effects:
Gynecomastia - abnormal overdevelopment of the breasts in a man
Galactorrhea - continuous release of milk
Impotence, Libido decrease, Reduced sperm count.
Cimetidine inhibits CYP-450 => Slows Metabolism =>
Potentiates the Action of some drugs:
Warfarin
Diazepam
Phenytoin
Quinidine
Carbamazepine
Theophylline
Imipramine 11

OMEPRAZOLE is the prototype of substituted benzimidazoles,
which inhibit the final step in gastric acid secretion and
have overtaken H2
blockers for acid-peptic disorders.
Mechanism of Action: Irreversible Inhibition of
the H+
/K+
-ATPase (the Proton Pump)
A singly daily dose Inhibits 100% of Gastric Acid secretion
12

PROSTAGLANDINS E2
and I2
:
HCL and Gastric Acid Secretion
↑Secretion of MUCUS and BICARBONATE
- CYTOPROTECTIVE EFFECT
MISOPROSTOL – a stable analog of PG E1
- is approved for prevention of gastric ulcers
induced by NSAIDs
13

ANTACIDS are weak bases that react with gastric acid to
form water and a salt, thereby diminishing gastric
acidity.
Since PEPSIN is inactive at pH > 4.0,
Antacids also PEPTIC ACTIVITY.
They ⇓ H Pylori Colonization and ⇑ PGs synthesis.
Bismuth subnitrate [Tab «Vicairum», «Vicalinum»
De-nol [Bismuth tripotassium dicitrate - Tab 0.12]
Aluminum hydroxide [pulv 0.25-1.0 g]
Magnesium hydroxide [ pulv 0.25-1.0 g]
Almagel, Maalox
Sodium bicarbonate [Tab 0.3 and 0.5]
Calcium carbonate [pulv 0.25-1.0 g]
14

Emetic Agents - are the drugs that produce vomiting.
They may be classified as:
1. Centrally acting, by stimulation of the CTZ:
Apomorphine hydrochloride (amp. 1%-1 ml) -
a semisynthetic derivative of Morphine.
It stimulates D2-receptors of the trigger zone.
Injected SC, it causes vomiting within 5 minutes
2. Peripherally acting: stimulate the vomiting center reflexively:
Preparations from Thermopsis and Ipecacuanha
Copper Sulfate and Zinc Sulfate have peripheral action
through irritation of stomach mucosa.
Emesis has a reflexive character after their introduction,
however they are not used to produce vomiting. 15

Antiemetic Agents
Metoclopramide – Tab. 5 mg, amp. 0.5%-2 ml
inhibits D2
receptors in the brain’s CTZ and
in high dose blocks 5-HT3
-receptors to inhibit or reduce
nausea and vomiting.
Domperidone (Motilium) – Tab. 10 mg
- inhibits D2
receptors.
Advantage of Domperidone is its no penetrating blood-brain
barrier and no-inducing Extrapyramidal Effects.
Clinical Uses:
Functional disorders of the GIT,
Stomach hypotonia, Reflux-esophagitis.
16

Corticosteroids: Dexamethasone
Methylprednisolone
are effective against Emetogenic Chemotherapy.
Their antiemetic mechanism may involve blockade of PGs.
The antagonists of the Serotonin Receptors:
Ondansetron (amp. 0.2%- 2 and 4 ml, tab. 4 and 8 mg)
Tropisetron -
selectively block 5-HT3
receptors:
 In the periphery (visceral afferent fibers) and
 In the brain (CTZ).
Ondansetron is approved for prevention of postoperative
nausea and/or vomiting.
17

ANTIDIARRHEALS
Loperamide - is widely used to control acute and chronic
diarrhea.
It is phenylpiperidine derivative and has Opioid-like actions
on the gut:
Activates Presynaptic Opioid Receptors
in the enteric NS to inhibit Acetylcholine Release and
decrease peristalsis.
Side effects: drowsiness, abdominal cramps, dizziness,
Toxic Megacolon => they should not be used in young
children or patients with severe colitis.
18

Classification of Cholagogic Agents
I. Agents Stimulating Bile Formation:
1. Agents Containing Bile Acids: Allochol, Cholenzyme
2. Synthetic agents: Oxaphenamide (tab. 0.25 g)
3. Plant drugs: Cholosas (vial 300 ml)
II. Agents Stimulating Bile Migration:
1. Cholekinetic agents (increasing the Bile Tone):
Magnesium Sulfate, Sorbitol, Berberis
2. Cholespasmolytic agents –
Decreasing the Biliary Tract and Sphincter Oddi tone:
• Spasmolytics: Papaverine, No-spa, Euphyllin, Magnesium sulfate
• M-cholinoblockers: Platyphyllin hydrotartrate
All cholagogic agents increase bile production by hepatic cells.
19

Hepatoprotectors
Lipoic Acid [Thioctic acid]: Tab. 12 mg, amp. 0.5% - 2 ml
Legalon (Silymarin): Dr. 70 mg, Caps.140mg
- contains Extract from dry Lady's-milk (Silybum marianum)
and its flavonoids Silymarin and Silybinin.
Hepabene: 1 capsule contains 100 mg of Lady's-milk extract
and 275 mg of Fumitory (Fumaria officinalis) Extract.
=> Cholagogic, Hepatoprotector and Spasmolytic actions.
Methionine (essential amino acid)
PO 0.5 - 1.0 g 3-4 times / day
Clinical Uses:: Dyskinesia of Biliary Tracts, Toxic Liver Lesion,
Alcoholism, Chronic Liver Diseases, Liver Cirrhosis.
20

Agents Used in Disturbances of
the Excretory Function of Pancreas
I. For Substitute Therapy:
PANCREATIN (CREON) contains Pancreatic Enzymes
AMYLASE, PROTEASE, LIPASE –
is extracted from Fresh Hog Pancreas.
Preparations containing PANCREATIN:
DIGESTAL
MEZYM-FORTE
FESTAL
PANZYNORM
21

2. Inhibitors of the Proteolytic Enzymes of Pancreas
- are used mainly for patients with HYPERSECRETION of Pancreas at
Acute Pancreatitis and as Systemic Haemostatic Agents.
CONTRICAL (Trasylol, Aprotinin) – vial 30 000 KIU/ml
naturally occurring protease inhibitor.
• It inhibits Trypsin, Plasmin,
and plasma and tissue Kallikreins.
• Inhibits Fibrinolysis through
inhibition of Plasmin and Kallikreins.
• Inhibits activation of the Intrinsic Clotting System,
a process that initiates coagulation and promotes
fibrinolysis.
22

ORLISTAT is a pancreatic Lipase inhibitor,
preventing the breakdown of dietary fat to
fatty acids and glycerols.
It causes a dose-related increase in fecal fat that
plateaus at 32% of dietary fat.
23

LAXATIVES
I. Irritant Laxatives – Purgatives, Cathartics
1. Small Bowel Irritant Purgative:
Vegetable oils: Castor Oil (Oleum Ricini)
2. Large Bowel Irritant Purgative:
 Drugs containing Antraglycosides:
Radix Rhei, Cortex Frangulae Alni, Folia Sennae
 Synthetic agents:
Phenolphthaleine, Isaphenine, BISACODYL
II. Osmotically Active Laxatives –
Agents acting on all Bowel Sections (Bulk Laxatives):
Salt laxatives: MgSO4 ; Na2SO4
24

CASTOR OIL (Oleum Ricini) is obtained
from the first cold pressing of the seed.
Ricinoleic acid arises as a result of fat digestion:
the duodenal mucosa releases
the enterohormone Cholecystokinin / Pancreozymin
(CK/PZ) into the blood.
The hormone elicits contraction of the gallbladder and
discharge of bile acids via the bile duct, as well as release
of lipase from the pancreas (intestinal peristalsis is also
stimulated).
CASTOR OIL is not indicated after the ingestion of lipophilic toxins
likely to depend on bile acids for their absorption.
25

LARGE BOWEL IRRITANT PURGATIVE
Drugs containing ANTRAGLYCOSIDES are
of plant origin:
Folia Sennae
Ffructus Sennae -
of the Senna plant
Cortex Frangulae – of the bark of Buckthorn
Rhizoma Rhei - the roots of RHUBARB
the Leaf Extract from Aloe Species.
Following ingestion of galenical preparations or of the anthraglycosides,
discharge of soft stool occurs after a latency of 6 - 8 h.
The anthraquinone glycosides themselves are inactive but are converted
by colon bacteria to the active free aglycones.
26

27
Bisacodyl (tab. 5 mg; rectal supp. 10 mg)
is rapidly converted by intestinal enzymes
and gut bacteria into its active metabolite
which directly irritates and stimulates the large bowel.
Given by the enteral route, bisacodyl is subjected to
hydrolysis of acetyl residues, absorption,
conjugation in the liver to Glucuronic Acid (or also to sulfate),
and biliary secretion into the duodenum.
Oral administration is followed by discharge of soft formed
stool after 6-8 hours.
When given in suppository, it produces its effect within 1 h.

Pharmacology of Gastrointestinal Diseases

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Pharmacology of Gastrointestinal Diseases