Recommended
More Related Content
What's hot
What's hot (20)
Similar to Physiology of Peptic Ulcer Disease
Similar to Physiology of Peptic Ulcer Disease (20)
Recently uploaded
Recently uploaded (20)
Physiology of Peptic Ulcer Disease
- 1. PHYSIOLOGY OF PEPTIC ULCER DISEASE Prepared by Jacktan Josephat Facilitator: Dr. D. Ngarashi © June, 2020
- 2. Objectives • To discuss gastro duodenal mucosal barrier • To discuss pathophysiology of peptic ulcer disease • To discuss physiology of peptic ulcer disease treament
- 3. Introduction • Mucosa lining excoriation extending to muscularis mucosae • Disruption of balance between aggressive and protective factors • 1,576 (0.42%) deaths in Tanzania in 2017 (WHO) Picture Source: dr. michael koeplin
- 4. Gastro-duodenal Mucosal Barrier • Properties of mucosa – Prevents acid-peptic damage • Pre-epithelial protection – Mucus gel, bicarbonates • Epithelia protection – Tight junctions, secretin, surfactant, PGs, scavengers, turnover, restitution • Sub epithelial protection – Blood flow, acid-base balance Picture source: wikipedia
- 5. Clinical Presentation and Classification Duodenal Gastric more associated with acid hyper secretion more associated with acid mucosa protection damage pain felt later following meal 2-3 hours pain felt earlier following meal ½-1 hours pain often felt in the night or early morning often relieved by eating or anti- acids not relieved by eating ( may exacerbate) or anti-acids may lead to weight gain may lead to weight loss less associated with vomiting often associated with vomiting common in lower ages common in advanced ages relatively common esp. in men relatively les common (3:1)
- 6. Pathophysiology of PUD Pictures sources: hopkinsmedicine.org & the New England Journal of Medicine Risk factors Alcohol
- 9. • Gastric hyper secretion: due to either i. Imbalance between D (secreting Somatostatin) and G (secreting gastrin) cells function – Zollinger-Ellison Syndrome: gastrin secreting tumor – Impaired inhibitory mechanisms ii. Physiological stress – Enhanced stimulation and response to vagal stimulation: e.g. Head injury, brain tumor, infections: Cushing’s ulcer – Severe burn: Curling’s ulcer
- 11. source: international journal of medical and applied sciences
- 12. Physiology of Treatment Source: basicmedicalkey.com/drugs-for-gastrointestinal-tract-disorders/
- 13. Source: Journal of the American Medical Association
- 14. Peptic Ulcer Complications • Intractable pain • Obstruction – Especially at the pylorus: healing with fibrosis • Malignancy: rarely
- 15. References 1. Despopoulos (2003) Color Atlas of Physiology Thieme 2. Fox, Stuart Ira Human Physiology, 12th ed 3. Guyton and Hall Text of Medical Physiology 11th ed 4. https://michaelkoeplinmd.com/peptic-ulcer-disease-causes-symptoms-and-treatment/ 5. https://emedicine.medscape.com/article/181753-overview#a6 6. https://en.wikipedia.org/wiki/File:Stomach_mucosal_layer_english_labels.svg 7. https://www.nejm.org/doi/full/10.1056/NEJM199003293221307 8. hopkinsmedicine.org/gastroenterology_hepatology/_pdfs/esophagus_stomach/peptic_ulcer_disease.pd f 9. Kumar, pavan & narayan, naveen & Mahajan, vikrant. (2013). A clinico-pathological study of duodenal ulcer perforation and its management in a rural area in karnataka. International journal of medical and applied sciences. 2. 47. 10.https://www.medscape.com/answers/181753-13856/does-smoking-alcohol-or-caffeine-increase-the- risk-of-peptic-ulcer-disease-pud
Editor's Notes
- Tight junctions: prevents backflow of H+ and pepsin The surfactant molecules of the gastric epithelium have each two hydrophobic hydrocarbon chains that are orientated out at the exterior surface. These surfactants may prevent water-soluble agents in the gastric lumen from reaching and damaging the epithelial cells. Salicylate and sodium deoxycholate result in a rapid decrease in the hydrophobicity of the mucosa Prostaglandins are found in high concentration in the gastric mucosa and gastric juice. Exogenous prostaglandins inhibit acid secretion, stimulate mucus and bicarbonate secretion, alter mucosal blood flow, and provide dramatic protection against a wide variety of agents which cause acute mucosal damage. There is now strong evidence that endogenous prostaglandins modulate acid secretion by blocking the histamine-stimulated increase in cyclic AMP within the parietal cell
- Other factors: balance btn D (Somatostatin) and G (gastrin) cells,
- Urease: immune reaction Endotoxins: lipopolysaccharide and PLP Ammonium hydroxide Elevated gastrin secretion: alkaline by ammonium, reduced D cells Elevated acid secretion: proliferation of parietal ells
- Brain tumors, traumatic head injury, and other intracranial processes including infections, can cause increased intracranial pressure and lead to overstimulation of the vagus nerve.Efferent fibers of the vagus nerve then release acetylcholine onto gastric parietal cell M3 receptors, causing insertion of hydrogen potassium ATPase vesicles into the apical plasma membrane Curling's ulcer is an acute gastric erosion resulting as a complication from severe burns when reduced plasma volume leads to ischemia and cell necrosis (sloughing) of the gastric mucosa
- Alcohol dissolves alkaline surfactant, promotes gastric emptying, irritation Nicotine causes mucosa vasoconstriction
- Alcohol dissolves alkaline surfactant, promotes gastric emptying, irritation Nicotine causes mucosa vasoconstriction
- Healing by fibrosis causing obstruction Rarely, malignancy