Drugs acts on GIT with their pharmacological parameters. By Dr. Yousuf Ali Sarker DVM, MS, FVS, BAU

2. DRUG ACTING ON ALIMENTARY CANAL
Dr. YOUSUF ALI SARKER
Department of Pharmacology
Faculty of Veterinary Science, BAU

3. TALK PLAN
 Introduction
 Drug acting on mouth and pharynx
 Drug acting on esophagus
 Drug acting on stomach
 Drug acting on intestine
 References

4. INTRODUCTION
 The digestive system process food/drugs into molecules
that can be absorbed and utilized by the cells of the body and
elimination
 A long continuous tube that extends from the mouth to the
anus.
Epithelial layer:
1. Mucosa
2. Submucosa
3. Muscular layer
4. Adventatia or serosa
Site of drug interaction

5.  Salivary stimulant or Sialogogue
Direct sialogogue
 Carbamoylcholine, arecoline, pilocarpine
Indirect sialogogue or reflex sialogogue
Simple bitter
Alkaloid bitter
Aromatic bitter
 Antisialogogue
Atropine, hyoscine, hyosciamine, kaolin
 Appetizing and stomachic
DRUG ACTING ON MOUTH AND PHARYNX

6. Salivary stimulant or Sialogogue
Mechanism of action
 Incase of reflex sialogogue salivation causes by stimulating taste bud
of tongue
Salivary aciner cell
Activation of cAMP or Ca2+ dependent pathway
Intracellular increases Ca2+Regulate secretory granules
Depolarization occursActivation of receptors (M3)
cAMP pathway Ca2+ pathway
Secretion occurs (Melvin, 2005)

7. Antisialogogue
Mechanism of action
 Competitive antagonist for the receptors which are
responsible for salivation
e.g.: Muscarinic (M1. M2, M3, M4), adrenergic receptors
 Reduce flow and fluidity of saliva
 Used to limit the flow of excess saliva, which often
occurs secondary to anesthetic drug use
 Atropine, hyoscine etc

8. Appetizing and Stomachic
 Appetite is primarily controlled by ventral and lateral
nuclei of hypothalamus.
 Several neuro-transmitter, glucocorticoids and B-
vitamins can non-specifically stimulate/ control appetite
Ammonium bicarbonate
Sodium bicarbonate
Pulv. nux vomica
Pulv. ginger
Pulv. gentian

9. DRUG ACTING ON ESOPHAGUS
 Parasympathomymetics drugs: (arecoline or pilocarpine)
 Stimulate salivation and increase esophageal peristalsis for the relief
of choke in animals
 Phenothiazine derivative tranquilizers relief choke by relaxing
esophagus
 Metoclopramide
 Increases esophageal motility
 Improve gastrooesophageal sphincter function
 Accelerate gastric emptying
 H2-antagonists
 For gastroesophagel reflex disease(GERD)
 Proton-pump inhibitors

10.  Emetics
 Antiemetics
 Antacids
 Proton Pump Inhibitors (PPI)
 H2 blockers
 Demulcents
 Carminatives and
 Antizymotics
DRUG ACTING ON STOMACH

11.  Drugs are those causes emesis or vomition
 Changes in GI muscle; rapid oral or rectal expulsion of GI contents
 Treatment of toxic ingestion, acute indigestion
 Morphine, Apomorphine, NaCl solution, Ipecacuanha
Emetics
(Stewart, 2010)
Classification
Centrally acting Peripherally acting Both
 Morphine
 Apomorphine
 Nikethamide
 Mustard
 Antimony and K+ tartrate
 Hypertonic NaCl solution
Salts of heavy metals
Ipecacuanha
(emetine &
cephaeline)
(Hornby, 2001)

12. Emetics(cntd)
Mechanism of vomition
 Gastric irritation
 Mucosal injury (GERD)
(PPW, Gut)
 Drugs(Morphine)
 Metabolic causes
 Bacterial toxin
(CTZ)
 Motion
 Labyrinth disorder
(VS)
 Meningeal irritation
 Hypornatremia
 Fear/anxiety
(Crebral cortex)
Vomiting
Centre
Vomotion
(Riviere & Papich, n.d.)
(Stewart, 2010)

13.  Drugs which assist in suppressing emesis
 Several neurotransmitters are responsible for stimulating
the vomiting center
 Successful therapy involves blocking one or more
receptor for these neurotransmitter.
Antiemetics
Antiemetic drugs based on receptor antagonism
5-HT1, HT3 M1, M3 D2 H1 NK1
 Apomorphine HCl
Dolasetron
Scopolamine Chlorpromazin
 Metclorpromide
Promethazine
Doxylamine
Aprepitant
Fosaprepitant
(Riviere & Papich, n.d.)

14. Antiemetic (cntd)
Mechanism of action (Metclorpromide)
Increases peristalsis of the jejunum and duodenum
Inhibit the action of dopamine (D2 receptor)
Increases tone and amplitude of gastric contractions
Relaxes the pyloric sphincter and duodenal bulb
 Pre- anesthetic medication
 Motion sickness
 Drug induced vomition
 Morning sickness
 Radiation sickness
Drowsiness
Dry mouth
Blurred vision
Constipation
Euphoria
Therapeutic Uses Adverse Effects

15. Acid secretion mechanism of parietal cell

16. Effect of Helicobacter pylori in gut wall

17. Antacid
 Used to relief of peptic ulcer pain associated with
hyperchlorhydria
 Hyperacidity, Peptic ulcer diseases, Gastritis, Reflux
esophagus
Classification
Systemic Non- systemic
NaHCO3
NaCO3
Al(OH)3 gel
CaCO3
MgCO3
Mg(OH)2

18. Antacid
↓
Neutralize acid
↓
Raise of pH (>3.5)
↓
Inactivation of pepsin
↓
Protection of gastric mucosa
Mechanism of action of Antacid
Antacid (cntd)

19. Proton Pump Inhibitor
 Strong inhibitors of gastric acid secretion
 Irreversible inhibition (H+-K+ -ATPase) of proton pump
 Faster relief and healing than H2 receptor blockers
 Indicated in PUD, Gastritis, GERD
 e.g.: Omeprazole, Lansoprazole, Esomiprazole,
Pantoprazole

20. Proton Pump Inhibitor (cntd)
Mechanism of action
H+-K+ -ATPase

21. Histamine H2 receptor blockers
 Inhibit secretion of gastric acid through competitive inhibition of
Histamine H2 receptors
 Prevention & treatment of PUD, Esophagitis, GI bleeding,
stress ulcers
 May alter the effects of other drugs through interactions with
CYP450 (especially cimetidine)
 e.g.: Ranitidine, Cimetadine, Famotadine, Nizatidine,
Roxitidine

22. Histamine H2 receptor blockers (cntd)
Mechanism of action
Fomatidine /Ranitidine
Competitively block H2 receptor
Histamine cannot act
Decrease cAMP formation
Reduction of acid secretion
Healing of ulcer
(Abdel-Aziz, Windeck, Ploch, & Verspohl, 2006)

23.  Coat, protect, lubricate and sooth gastric mucosa of GIT
 Liquid paraffin, Vegetable oil, glycerol, Sugar
Demulcents
Agents
Mechanism of action
Coat lining of GIT
Inhibit irritation to lining
Protection & soothing

24. Expulsion of gases from the stomach (eruction)
Volatile oil, NaHCO3, MgCO3,Fennel, Peppermint
Carminatives
Correct dosage
Mechanism of action
Mild irritation to gastrointestinal mucosa
Release gas from stomach
Vasodilatation
Relaxation of gastro-intestinal musculature
(cardiac sphincter)

25.  Prevent or decrease bacterial or enzymatic fermentation
 Prevent further gas production during bloat or tympany
 Volatile oil (liq. paraffin), chloroform, chloral hydrate, ethyl
alcohol
Antizymotics
 Methyl group can increase surface tension of fluid/foam
 Decrease foam stability
Mechanism of action

26. Emollient Laxative
Liquid Paraffin
Anionic Surfactant
Bulk Laxative
Stimulant Laxative
Osmotic Laxative
DRUG ACTING ON INTESTINE
Classification
Laxative are the agent that evaquate Soft formed
stool without griping and lose of water
Laxative
Di Palma, 2007

27. Mechanism of Action of Laxative
Little amount is absorbed
Increase the bulk of feces
Increase water content of the feces
Promote evacuation of feces
 Polyethylene glycol (PEG3350) is a modern laxative designed to act
without the use of metabolizable or irritating substances
Di Palma, 2007

28. Purgative
 Bulk Purgative
Methyl cellulose
Ispaghula husk
 Osmotic Purgative
MgSO4
Lactulose
 Faecal Softners (Emoliants)
Liquid paraffin
 Stimulant Purgative
Glycerol
Purgative are the agent that promote defaecation as
a result of muscle contraction
Classification

29. Mechanism of Action of Purgative
They absorb water and swell and an emollient gel formation
The increased volume or bulk leads to distention with reflex
contraction producing peristaltic activity
Feces remain soft and hydrate
Defecation occurs

30. Cathertics
Oral administration of MgSO4
↓
Slow and incomplete absorption from GIT
↓
Water retained in the intestinal lumen by peristaltic movement
↓
Indirectly increased peristaltic movement, Semi-fluid and watery
evacuation
 Evacuate More Fluid Feces
Osmotic Cathartics
 Irritant Chathartics
Mechanism of Action
(Toxicologists, 2004)

31. Mechanism of Action
Astringent
↓
Protein precipitation
↓
Covers the surface of the cell or tissue
↓
Tissue remain impermeable to the passage of fluid in
either direction
↓
No water lose
Antidiarrhoeal
Astringent
Antispasmodic

32. Enema
 GIT surgery
 Radiological examination
 Endoscopy
 Before delivery
Rectal suppository
Uterine suppository
Vaginal suppository
Indication

33. REFERENCES
Abdel-Aziz, H., Windeck, T., Ploch, M., & Verspohl, E. J. (2006). Mode of action
of gingerols and shogaols on 5-HT3 receptors: Binding studies, cation uptake by
the receptor channel and contraction of isolated guinea-pig ileum. European
Journal of Pharmacology, 530(1-2), 136–143.
http://doi.org/10.1016/j.ejphar.2005.10.049
Di Palma, J. a, Cleveland, M. V., McGowan, J., & Herrera, J. L. (2007). A
randomized, multicenter comparison of polyethylene glycol laxative and
tegaserod in treatment of patients with chronic constipation. The American
Journal of Gastroenterology, 102(9), 1964–1971. http://doi.org/10.1111/j.1572-
0241.2007.01365.x
Lundell, L. (2015). The physiological background behind and course of
development of the first proton pump inhibitor. Scandinavian Journal of
Gastroenterology, (January), 1–5. http://doi.org/10.3109/00365521.2015.1013981

34. Najm, W. I. (2011). Peptic Ulcer Disease. Primary Care - Clinics in Office
Practice, 38(3), 383–394. http://doi.org/10.1016/j.pop.2011.05.001
Riviere, J. E., & Papich, M. G. (n.d.). Veterinary Pharmacology & Therapeutics
(pp. 1247–1270). WILEY-BLACKWELL.
Scully, C. (2003). Drug effects on salivary glands: dry mouth., 44(10), 165–176.
Retrieved from http://discovery.ucl.ac.uk/157676/
Toxicologists, C. (2004). Position paper: cathartics. Journal of Toxicology.
Clinical Toxicology, 42(3), 243–253. http://doi.org/10.1081/CLT-120039801
REFERENCES (CNTD)

35. Thank You All
Question/s??
yousuf.bau10@gmail.com