Acid peptic disease 1

2,244 views

Published on

hhh

Published in: Health & Medicine, Business
1 Comment
2 Likes
Statistics
Notes
No Downloads
Views
Total views
2,244
On SlideShare
0
From Embeds
0
Number of Embeds
2
Actions
Shares
0
Downloads
0
Comments
1
Likes
2
Embeds 0
No embeds

No notes for slide

Acid peptic disease 1

  1. 1. DRUG TREATMENT OF ACID PEPTIC DISEASE DR ANEELA KHALID
  2. 2. <ul><li>Dyspepsia </li></ul><ul><li>Feeling of pain in upper abdomen or </li></ul><ul><li>epigastrium. Early satiety, belching, retching, </li></ul><ul><li>nausea and vomiting. </li></ul><ul><li>Non Ulcer dyspepsia </li></ul><ul><li>Patient not suffering from ulcer but has same </li></ul><ul><li>feelings of dyspepsia with unknown </li></ul><ul><li>Pathology . </li></ul><ul><li>10-20% of patients respond to </li></ul><ul><li>treatment of Peptic ulcer. </li></ul>
  3. 3. <ul><li>Heartburn </li></ul><ul><li>Burning sensation, or feeling retrosternally usually is a symptom of GERD. </li></ul><ul><li>Gastritis: </li></ul><ul><li>Small erosions in the endothelium or </li></ul><ul><li>epithelium of gastric mucosa along with </li></ul><ul><li>inflammation. </li></ul>
  4. 4. <ul><li>GERD </li></ul><ul><li>Reflux of acid in the stomach. Mostly tone </li></ul><ul><li>of lower esophageal sphicter is decreased </li></ul><ul><li>due to certain food, drugs or hiatus hernia. </li></ul><ul><li>The acid has caustic effect on esophagus </li></ul><ul><li>which leads to such complications. </li></ul><ul><li>1 Stricture formation </li></ul><ul><li>2 Barret oesophagus </li></ul>
  5. 5. <ul><li>Peptic Ulcer </li></ul><ul><li>Break in the mucosa of Gut usually more </li></ul><ul><li>then 5 mm in diameter. Muscular mucosa is </li></ul><ul><li>always involved in this damage. </li></ul><ul><li>Gastric ulcer in people above 55yrs </li></ul><ul><li>Duodenal ulcer in younger people </li></ul><ul><li>Stress ulcer </li></ul><ul><li>Seen in individuals chronically ill, may be </li></ul><ul><li>bedridden, or hospitalized. These ulcers may </li></ul><ul><li>bleed profusly. </li></ul>
  6. 6. <ul><li>Iatrogenic ulcers. </li></ul><ul><li>NSAIDs inhibit cycloxygenase 1 which is constitutive in nature in stomach. </li></ul><ul><li>Aspirin causes erosive damage to the mucosa </li></ul><ul><li>Corticosteroids decreases immunity </li></ul><ul><li>H pylori is causative organism of Peptic ulcer </li></ul>
  7. 7. Pathogenesis of Acid peptic disease <ul><li>Due to disturbance of the balance between Protective mechanisms of gut and ulcer promoting influences which may be intrinsic or extrinsic. </li></ul>
  8. 8. Classification of Drugs used for Acid Peptic disease <ul><li>1- Agents that decrease Acid pepsin activity </li></ul><ul><li>a-Proton Pump inhibitors </li></ul><ul><li>Omeprazole </li></ul><ul><li>Lansoprazole </li></ul><ul><li>Rabeprazole </li></ul><ul><li>Pentoprazole </li></ul><ul><li>Esomeprazole </li></ul>
  9. 9. <ul><li>b- H 2 receptor blockers. </li></ul><ul><li>Cimetidine </li></ul><ul><li>Ranitidine </li></ul><ul><li>Famotidine </li></ul><ul><li>Nizatidine </li></ul><ul><li>2- Antacids </li></ul><ul><li>Sodium bicarbonate </li></ul><ul><li>Aluminium hydroxide </li></ul><ul><li>Aluminium Phospahate </li></ul><ul><li>Magnesium trisilicate </li></ul>
  10. 10. <ul><li>Megaltride </li></ul><ul><li>Megnisium hydroxide </li></ul><ul><li>Calcium carbonate </li></ul><ul><li>3- Anti Muscarinic </li></ul><ul><li>Pirenzipine </li></ul><ul><li>Telenzepine </li></ul>
  11. 11. <ul><li>4- Mucosal Protectants. </li></ul><ul><li>Sulfated sucrose derivative </li></ul><ul><li>Sucralfate </li></ul><ul><li>Colloidal Bismuth compounds </li></ul><ul><li>Bismuth subsalicylates </li></ul><ul><li>Bismuth subcitrate </li></ul><ul><li>bismuth dinitrate </li></ul>
  12. 12. <ul><li>Prostaglandin analogs </li></ul><ul><li>Misoprostol </li></ul><ul><li>Liqurice derivative </li></ul><ul><li>Carbenoxolone </li></ul>
  13. 14. H 2 ANTAGONISTS <ul><ul><ul><li>CIMETIDINE </li></ul></ul></ul><ul><ul><ul><li>RANITIDINE </li></ul></ul></ul><ul><ul><ul><li>FAMOTIDINE </li></ul></ul></ul><ul><ul><ul><li>NIZATIDINE </li></ul></ul></ul>p
  14. 15. CIMETIDINE <ul><li>     CHEMICAL STRUCTURE </li></ul><ul><li> </li></ul>
  15. 16. MOA <ul><li> </li></ul>
  16. 17. <ul><li>Pharmacokinetics of H 2 receptors blockers </li></ul><ul><li>Absorbed rapidly from intestine </li></ul><ul><li>Cimetidine, Ranitidine and famotidine undergo first pass metabolism and has 50% bioavailability. </li></ul><ul><li>Nizatidine has little first pass effect </li></ul><ul><li>Half life ranges from 1.1 to 4hrs, whereas </li></ul><ul><li>duration of action follows the dose given </li></ul><ul><li>Eliminated from body by hepatic metabolism, glomerular filtration, and renal excretion. </li></ul>
  17. 18. <ul><li>Pharmacodynamics of H 2 receptors blockers </li></ul><ul><li>H 2 receptor blockers competitively inhibits parietal cell H 2 receptors and suppress basal and meal stimulated acid secretion in a linear dose dependant manner. </li></ul><ul><li>Volume of gastrin secretion and pepsin concentration are also reduced. </li></ul><ul><li>They reduce acid secretion stimulated by histamine as well as by gastrin and cholinomimetic agents through two mechanism </li></ul>
  18. 19. <ul><li>1-Histamine released from ECL cells is blocked from binding to the parietal cells H 2 receptors. </li></ul><ul><li>Direct stimulation of parietal cell by gastrin or acetylcholine has a diminished effect on acid secretion in the presence of H 2 receptor blockade. </li></ul><ul><li>H 2 blockers inhibits 60 to 70 % of acid secretion in 24 hrs time . </li></ul><ul><li>More effective in reducing nocturnal acid secretion and modest impact on meal stimulated acid secretion. </li></ul><ul><li>Recommended doses reduces more then 50% acid inhibition for 10hrs hense prescribed twice daily. </li></ul>
  19. 20. THERAPEUTIC USES <ul><li>        DUODENAL ULCER. </li></ul><ul><li>         GASTRIC ULCER. </li></ul><ul><li>        GASTRO OESOPHAGEAL REFLUX DISEASE. </li></ul><ul><li>        ZOLLINGER – ELLISON SYNDROME. </li></ul><ul><li>         UPPER GASTROINTESTINAL BLEEDING. </li></ul><ul><li>        STRESS ULCERS. </li></ul><ul><li>        PREANAESTHETIC USE (MENDELSON’S SYNDROME, ACID ASPIRATION SYNDROME). </li></ul><ul><li>         NON ULCER DYSPEPSIA </li></ul><ul><li>   </li></ul>
  20. 21. PREPARATIONS AND DOSES <ul><li>  </li></ul><ul><ul><ul><li>CIMETIDINE 400-800mg </li></ul></ul></ul><ul><ul><ul><li>RANITIDINE 150 mg </li></ul></ul></ul><ul><ul><ul><li>FAMOTIDINE 20 mg </li></ul></ul></ul><ul><ul><ul><li>NIZATIDINE 15 0 mg </li></ul></ul></ul>
  21. 22. ADVERSE EFFECTS <ul><li> eadache, myalgia, fatigue, diarrhea or constipation </li></ul><ul><li>    CNS (Confusion, agitation ,hallucination) </li></ul><ul><li>     ANTI – ANDROGEN (inhibits binding of dihydrotestosterone to androgen receptors, increases serum prolactin level) </li></ul><ul><li>    Blood dyscrasias </li></ul><ul><li>    Enzyme inhibitor </li></ul><ul><li>    Cardio toxicity on i/v administration </li></ul><ul><li> Reversible abnormalities in liver chemistry </li></ul>
  22. 23. <ul><li>RANITIDINE </li></ul>
  23. 24. RANITIDINE <ul><li>COMPARISON BETWEEN </li></ul><ul><li>CIMETIDINE & RANITIDINE </li></ul>
  24. 25. COMPARISON     CIMETIDINE   RANITIDINE CHEMISTRY IMIDAZOLE DERIVATIVE FURAN DERIVATIVE BIO – AVAILABLILITY 80 % 52 % PLASMA PROTEIN BINDING 20 % 15 % T ½ 2 HRS 2 HRS CROSSING OF B B B POOR VERY POOR DURATION OF ACTION SHORT LONG
  25. 26. POTENCY LESS 5 TIMES MORE THAN CIMETIDINE DOSE 800 mg 300 mg BINDING WITH CYT – P 450 PRESENT NEGLIGIBLE DRUG – INTERACTION INTERFERES WITH HEPATIC METABOLISM OF DRUGS NEGLIGIBLE TOXICITY CNS ENDOCRINOL-OGICAL HEPATIC NOT SEEN

×