In this presentation slide my main concern is the pharmacology of GIT MUCOUS MEMBRANE but you will also know briefly about the anatomy,physiology and pathology of it.

1. BY
ABU BAKAR TARIQ
UNIVERSITY OF SARGHODHA

3. 1
• Mucous Membrane & Organs.
• Anatomy, Physiology & Pathology
2
• Pharmacology of Oral Mucosa
• Pharmacology of Esophageal Mucosa
3
• Pharmacology of Gastric Mucosa.
• Pharmacology of Intestinal Mucosa.

4. ‘‘Mucous Memberane’’
Mucous Memberane is:
 The Linning of certain organs.
 Passages that communicate with the Surface of
organ.

5. “Anatomy of Mucosa Membrane’’
 What is Composition of Mucous Memberane?
Consists of:
• Epithelium-layer of epithelial cells.
• Lamina Propria-Loose Connective Tissue.

6. ‘‘Epithelium’’
 A single or stratified layer of cells underlines:
• Cavities
• Blood vessels
• Organs
GIT
Oral
Ear
Lungs
Urinary Tract

7. ‘‘Lamina Propria’’
 Underlines Epithelium.
 Provide Nutrition to it.
 Contains:
o Lymphocytes
o Plasma cells
o Mast Cells
o Glands(Mucus)
o Leucocytes etc.

8. “Some Examples of Mucous Membrane”
Oral Mucosa(mouth)
Esophageal Mucosa(esophagus)
Gastric Mucosa(Stomach)
Intestinal Mucosa(Intestine)

9. “Physiology of GIT ”
Mucous Membrane Involve in:
Protection:
Physical Barrier
(Mucus)
Immune Barrier
(Lymph nodes)

10. ‘‘Physiology’’
 Secretions:
 HCL
 Enzymes
 Mucous
 Serotonin
 Histamine

11. ‘‘Physiology’’
Absorption:
• Proteins
• Carbohydrates
• Fats
• Vitamins
• Water
• Electrolytes
• DRUGS

12. “Physiology’’
Regulation:

13. “Pathology”
 Oral Mucosa:
 Candidiasis
 Amphthous ulcer
 Mouth Cancer
 Smoker’s palate
 Smoker’s Melanosis

14. ‘‘Pathology’’
Esophageal Mucosa:
 Esophagitis(Inflammation of Esophagus)
 GERD
 Tumors

15. ‘‘Pathology’’
Gastric Mucosa:
 Acute Gastritis
 Chronic gastritis
 Gastric Ulcer
 Gastric Cancer etc.

16. ‘‘Pathology’’
 Intestinal Mucosa:
 Duodenal Ulcer
 Enterocolitis
 Diarrhea
 Constipation
 IBD
 Celiac Sprue etc.

17. “Pharmacology of Oral Mucosa”
Fungal Infection:
 Candidiasis
(Oral Thrush)
 Agent:
Candida albicans
 Appearance:
White plague

18. “Drugs Used”
AZOLES:
 Fluconazole
(Fungicure)
 Miconazole
 Itraconazole
 Ketoconazole
 Clotrimazole

19. “Mechanism of Action”
 Fluconazole acts by inhibiting the synthesis of
Ergosterol, a major component of the cell membrane
of yeast and fungi.
 Inhibition of Ergosterol synthesis leads to some
structural and functional impairment of cytoplasmic
membrane.
Side Effects:
Nausea
Abdominal Discomfort
Diarrhea

20. “Aphthous Ulcer”
 Also Known as Canker Sores.
 Appeared as:
Small, Shallow
lesions.
 Drug used:
Amlexanox
(Apthasol)

21. “Mechanism of Action”
Amlexanox :
Inhibit inflammation by inhibiting
release of histamine and leukotrienes.
 Side effects:
 Nausea
 Diarrhea

22. “Squamous cell carcinoma”
 Also known as Oral Cancer.
 Agent:
1. Smoking
2. Tobacco
3. Alcohol
 Appeared as:
1. Erythroplakia
2. Leukoplakia

23. “Leukoplakia & Treatment”
 NO DRUG IS AVAILABLE
 Chemotherapy

24. “Smokers palate ”
 Also known as ‘‘Stomatitis nicotinia’’.
 Agent:
 Cigar
 Cigarette
 Appeared as:
White opaque dots on
Palate
 Treatment:
Stop Smoking

25. “Smokers Melanosis”
 Agents:
Smoking
 Appeared as:
Melanin
Pigmentation in gums
 Treatment:
Quit smoking

26. “Duodenal Ulcer”
 Gasrtic Acid cause
Errosive damage to
Duodenal part of
Small intestine if
The mucous barrier
is damaged.
 Agents:
 H.pylori.
 Anti-Inflammatory Drugs.

27. “Symptoms”
1. Pain Upper tummy
2. Bloating
3. Retching
4. Sickness
5. Vomiting
6. Burning

28. “Drugs for Duodenal Ulcer”
 Bismuth Salts
 Cimetidine (HCl)
 Omeperazole
 Pirenzepine (di HCl)
 Propantheline (Br)
 Ranitidine
 Omeprazole
 Sucralfate

29. “Mechanism of Bismuth Salt”
 Bismuth Salts are antimicrobial agents,Antacid and
used to treat Duodenal ulcer.
 Bismuth salt(Bismuth
Salicylate) retards the
Expulsion of fluids
into the GIT system by
Coating them.
 Its anti-inflammatory action
by Prostaglandin Inhibition.

30. “Celiac Disease”
 Auto-immune disorder occurs due to indigestion of
Gluten.
 Low Absorptive surface of Small Intestine.

31. “Symptoms”
 Anemia.
 Chronic Diarrhea.
 Weight Loss.
 Fatigue.
 Cramps.
 Bloating.
 Irritability.
 Burning.

32. “Drugs For celiac Disease”
 Celecoxib(NSAIDS)
 Celiprolol (HCL)
 Gluten Free Diet.
 Vitamins & Mineral Supplements.

33. “Mechanism of Celecobix”
 COX-II Inhibitor.

34. “Mucosal Abnormalities in AIDS”
 In Acute Phase HIV induce cell lysis and killing of
infected cell by cytotoxic T-Cells accounts for CD4
T-cell depletion in Small Intestinal Mucosa.

35. “Agents”
 Human Immuno-deficiency Virus(HIV)
 Pro-inflammatory cytokinins

36. “Symptoms”
 Diarrhea
 Waitloss
 Dysphagia
 Abdominal Pain
 Gastro-intestinal Bleeding
 Lymphoma
 Bilary Tract Disorders

37. “Drugs”
 NTRI’s(Nucleotide Reverse Transcriptase Inhibitors)
 Anti-retro viral Therapy
 CCR-5 Receptor Antagonists
 Integrase Inhibitor

38. “Mechanism of NTRI’s”

39. “Adverse Effects of Stavudine”
 Numbness
 Rash
 Diarrhea
 Headache
 Hand Pain
 Feet Pain

40. “Large Intestinal Mucosa”
Introduction:
 Large intestine Absorbs mainly Nutrients, Water,
Electrolytes and vitamins.
Role of microbiota:
 Microflora reduce the capability of pathogenic species
to cause damage to mucosa of colon.
 The increased use of antibiotics reduce the normal
population of the microflora that lead to the damage
of intestine and cause high risk of pathogenicity.

41. “Forms of IBD”
Two forms of IBD:
Ulcerative Colitis:
(localized)
Crohn’s Disease:
(Transmural)

42. “Inflammatory Bowel Disease(IBD)”
MECHANISM OF ACTION

43. “Drugs Used in IBD”
1. Glucocorticoids(Prednisolone & Budesonide)
2. Aminosalycilates(Salfasalazine,Balsalazide)
3. Immunosuppressant(Thiopurine)
4. Antibiotics(Ciprofloxacin)

44. “Glucocorticoids”
 Drugs:
 Prednisolone(Prelone).
 Budesonide(Pulmicort).
 Mechanism of action:
Prednisolone act by Inhibiting nuclear factor (NF- Kb)
 Adverse Effects:
 Acne
 Constipation
 Nausea.

45. “Mechanism of Prednisolone”

46. “Amino-Salicylates”
Mechanism of action:
 Reduce inflammation by scavenging of free radical.
 By inhibition of the production of interleukin-1
andTumor Necrosis Factor(TNF)
 And Also by inhibition of NF-kb
Drugs:
 Sulfasalazine(Azulfidine)
 Olsalazine(Dipentum)
 Balsazide(Colazide)

47. “ADVERSE EFFECTS”
 Headache
 Fatigue
 Rash
 Diarrhea

48. “Immunosuppressants”
Mechanism of Action:
 Thiopurine impair purine biosynthesis.
 Hinders DNA synthesis and thus inhibit the
proliferation of cells.
 So the two types of lymphocytes(T & B) affected by the
inhibition of purine synthesis

49. “DRUGS & Adverse Effects”
Drugs:
 Thiopurine derivatives
 Azothiopurine(Immuran)
 6-Mercaptopurine(Purinethol)
Adverse Effects:
 Vomiting
 Bone marrow Suppression
 Elevation in liver Function.

50. “Anti-TNF Therapy”
Mechanism of Action:
 Drugs caused the lysis of TNF alpha cells by cell
mediated cytotoxicity.
 Drugs:
 Infliximab(Remicade)
 Adalimumab