Pathophysiology of peptic ulcer

This ppt is suitable for b.pharma students. This ppt is prepared according to b.pharma IInd semester syallbus. In this ppt we provide all topics related to pathophysiology of peptic ulcer. In this ppt we covered introduction, types, sign & symptoms, pathophysiology, diagnosis, complications and treatments.

1. Pathophysiology of Peptic ulcer Rajat Srivastava Assistant Professor ARK College of Pharmacy, Kaushambi , UP

2. Introduction Peptic ulcer also known as peptic ulcer disease. A condition in which there is a discontinuity in the entire thickness of the gastric or duodenal mucosa that persists as a result of acid and pepsin in the gastric juice. The term peptic ulcer applies to mucosal ulceration near the acid bearing regions of GIT.

3. A condition in which wounds appear in the lining of stomach or duodenum, along with a burning stomach pain is termed peptic ulcer. In this case, a low pH peptic juice (acid) secreted by the walls of stomach or duodenum starts eroding the mucosa. Peptic ulcer disease (PUD) = Mucosal defect in the GIT (gastric or duodenal) exposed to acid and pepsin secretion.

4. Sites of peptic ulcer Duodenum…………………….80% Stomach………………………..19% Duodenum & Stomach………..4%

5. Peptic Ulcer

6. Types: Peptic ulcer are mainly of following of two types- Gastric ulcers: This ulcer type affect the stomach lining and may be acute or chronic. It is characterized by pain while the food is still in the stomach. Duodenum ulcers: This ulcer type affect the upper part of small intestine and may acute or chronic. It is characterized by pain when stomach is empty, or may result after several hours of food consumption.

7. Epigastric pain occurring 30 minutes to 1 hour after meals Aggravated by eating (because acid secretion increase at meal time) leads to weight loss. Relieved by vomiting (because acid is expelled out). No pain at hours of sleep (HCL production decrease at hours of sleep). More common in person older than age 50. Epigastric pain occurring 2-3 hours after meals. Relieved by food (because the pyloric sphincter, at the junction of stomach and duodenum, closes upon eating to concentrate food in the stomach) causes weight gain. Not relived. Pain at hours of sleep (because gastric emptying continuous at hours of sleep). More common between age 25 and 50. Gastric ulcer Duodenum ulcer

8. Etiology/Causes of peptic ulcer Helicobacter pylori, Gram – ve microaerophillic bacterium found in gastric antrum of human stomach . 95% duodenum ulcer & 80% gastric ulcer associated with H.Pylori . NSAID’S like aspirin, ibuprofen, etc. used frequently. Alcoholism Smoking Radiotherapy Cancer of stomach

9. Pathophysiology Pepsinogen is activated to pepsin in presence of HCl and a pH of 2 to 3. Secretion of HCl by parietal cells has a pH of 0.8. pH reaches 2 to 3 after mixing with stomach contents. Surface mucosa of stomach is renewed about every 3 days. Mucosa can continually repair itself except in extreme instances.

10. Mu c o s al b a r r i e r p r e v e n ts b a ck d i f fu s i on of acid from gastric lumen through mucosal layers to underlying tissue. Mucosal barrier can be impaired and back diffusion can occur. H C L fr e ely en t ers muc o sa when ba r ri e r is broken Result: Injury to tissue occurs cellular destruction and inflammation

11. BACK DIFFUSION OF ACID

12. H.Pylori Induced Ulcer Gram negative bacteria produced heat shock proteins Cytokines, histamine, lipopolysaccharides , certain enzymes Phospholipase Urease , protease, etc. Urease convert in acidic media urea into ammonia and carbon dioxide. Ammonia itself cause destruction of mucosal lining.

13. Ammonia cause infection of mucosal lining and ultimately inflammatory mediators release. Cytokines, leukocytes adhesion and inflammatory reactions starts Damage mucosa of GIT Ulcer occurs

14. Drug Induced Ulcer Approximately 15% of patients on long-term NSAID develop PUD. NSAIDs - ↓prostaglandin (PG) by inhibiting the cyclooxygenase (COX) enzymes. Three iso -enzymes COX-1, COX-2, COX-3 COX-1 → PG production in gastric mucosa.

15. COX-1 & COX-2

16. Stress Induced Ulcer

17. Steroids Induced Ulcer

18. Signs & Symptoms Abdominal pain Nausea Vomiting Weight loss Fatigue Heartburn Indigestion Chest pain Blood in vomiting Bloody or dark tarry stools Loss of appetite

19. Complications 1. Hemorrhage Blood vessels damaged as ulcer erodes into the muscles of stomach or duodenal wall Coffee ground vomits or occult blood in tarry stools 2. Perforation An ulcer can erode through the entire wall. Bacteria and partially digested food spill into peritoneum, resulting in acute peritonitis. 3. Narrowing & Obstruction Swelling and scarring can cause obstruction of food leaving stomach, resulting repeated vomiting.

20. Diagnosis Endoscopy X-ray studies- performed after drinking a thick barium solutions. Other test- Blood test for haemoglobin - for detecting presence of anaemia . Stool occult blood test- for detecting blood in stool. Bacterial culturing for H.Pylori

21. Treatment Ulcer can be treated by following ways- Lifestyle changes Medications Surgery

22. Lifestyle changes Eliminate substrate that can causing ulcers Stop drinking and/or smoking Stop using NSAID’s

23. Medications Proton pump inhibitors (PPIs) Reduce acid level and allow ulcer to heal These include- Esomeprazole Lansoprazole Omeprazole Pantoprazole Rabeprazole

24. Medication (Cont.) Antibiotics Used for H.Pylori induced ulcer Multiple combinations of antibiotics Taken for 2-3 weeks along with PPIs

25. Medications (Cont.) Antacids- Neutralise the gastric acidity and reduce pepsin activity Cytoprotective agents- protect the tissues lining the stomach and small intestine