Download Free Medical Peptic Ulcer Disease PowerPoint Presentation

Peptic Ulcer Disease PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : An ulcer is a discontinuity or break in a bodily membrane that impedes the organ of which the membrane is apart of continuing its normal functions

Tags : pud,Peptic Ulcer Disease,Peptic Ulcer,Ulcer,Disease

Published on : Mar 06, 2023 | Views : 2135 | Downloads : 6

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

By: Yussif Osei
Slide 2-

INTRODUCTION ULLCER An ulcer is a discontinuity or break in a bodily membrane that impedes the organ of which the membrane is apart of continuing its normal functions,
Slide 3-

Peptic Ulcer Also known as “peptic ulcer disease” {PUD} Peptic ulcer is a break in the lining of the stomach, first part of the small intestine, or occasionally the lower esophagus.
Slide 4-

Site of Peptic Ulcer Ulcer development Duodenum (80%) Stomach (19%) Duodenum and stomach (4%) Esophagus, gastroenterostomy, stoma, jejunum, Meckel's diverticulum (1%)
Slide 5-

Type of Peptic Ulcer Acute peptic ulcer Cushing ulcer Curling ulcer Chronic peptic ulcer Duodenal ulcer Gastric ulcer Esophageal ulcer Bleeding ulcer Refractory ulcer
Slide 6-

ppt slide no 6 content not found
Slide 7-

Difference Between DU & GU
Slide 8-

ETIOLOGY OF PEPTIC ULCER
Slide 9-

What causes Ulcer No single cause End results of an imbalance between digestive fluids in stomach Most common cause of ulcer is infection with a type of bacteria call Helicobacter pylori (H. pylori)
Slide 10-

Predisposing factors for ulceration includes: Helicobacter pylori Smoking and alcohol Drugs: NSAIDS and corticosteroid-both affect mucosal defense Stress: burns, major surgeries Gastric hypersecretion (eg. Zollinger-Ellison syndrome) Serious illness Genetics
Slide 11-

Pathophysiology The upper G.I system consists of Esophagus Stomach Duodenum Stomach Cardia: secretion of mucous Body: Parietal cells Chief cells Antrum: G cells Gastric secretions (about 2.5L HCL daily) Smooth muscle – churning Sub-mucosa – veins and arteries that carries blood to the liver
Slide 12-

Pathophysiology Defensive factors Bicarbonate Mucus layer Mucosal blood flow Prostaglandins Rapid epithelial renewal Aggressive factors Helicobacter pylori HCL NSAIDS Stress Smoking & Alcohol Ageing
Slide 13-

ppt slide no 13 content not found
Slide 14-

Pathophysiology The gastroduodenal mucosal integrity is determined by adequate balance between protective(defensive) and damaging(aggressive) factors When the aggressive factors increase or the defensive factors decrease, mucosal damage will result leading to ulcerations
Slide 15-

Predisposing factors for ulceration includes:
Slide 16-

Helicobacter pylori H. pylori is a gram-negative, spiral & microaerophilic bacterium with multiple flagella at one end Adheres to gastric epithelial lining. Produces various enzymes – urease, heamolysins, fusidase, neuraminidase
Slide 17-

H. Pylori Induced Ulcer Gram negative bacteria produced heat shock proteins Cytokines, histamine, lipopolysaccharides, certain enzymes Phospholipase Urease convert in acidic media urea into ammonia and carbon dioxide. Ammonia itself cause destruction of mucosal lining.
Slide 18-

H. Pylori Induced Ulcer Ammonia cause infection of mucosal lining and ultimately inflammatory mediators release. Cytokines Leukocytes adhesion and inflammatory reactions starts Damage Mucosa of GIT Ulcer occurs
Slide 19-

ppt slide no 19 content not found
Slide 20-

ppt slide no 20 content not found
Slide 21-

NSAIDS
Slide 22-

NSAIDs Induced PUD
Slide 23-

Types of NSAID & Risk of Ulcer
Slide 24-

Steroids Induced Ulcer Steroids acts on cell membrane (phospholipid) Inhibit phospholipase Inhibits arachidonic acid no prostaglandins and damaging of mucosal lining
Slide 25-

Stress Induced Ulcer In stress energy consumption increase, so increases glycolysis which is usually done by cortisol hormone This hormone inhibit phospholipase A2 No arachidonic acid formation no prostaglandin Increase gastric juice secretions Cause ulcer
Slide 26-

Ulcer Due To Genetic Defect Rare genetics occurs sometime having blood group “O” positive the size of parietal cell is increase Increase cell demand as HCL secretions increase Cause destruction of mucosal lining leading to ulcer
Slide 27-

ZES (Zollinger-Ellison Syndrome_) In this syndrome tumor of goblet cell occurs Abnormal mucus secretions (gastrin acts on parietal cells) Increase secretions of gastric juice Mucosal lining damage
Slide 28-

ppt slide no 28 content not found
Slide 29-

ppt slide no 29 content not found
Slide 30-

PUD complications FI bleeding Perforation Gastric / duodenal obstruction(presents with projectile vomiting, pyloric stenosis) Hemorrhage –may lead to Chronic anemia Recurrence Malignacy0 gastric ulcers
Slide 31-

ppt slide no 31 content not found
Slide 32-

ppt slide no 32 content not found
Slide 33-

Management of peptic ulcer disease
Slide 34-

How are Peptic ulcers treated? If not properly treated, they can lead to serous health problems Ulcers can be treated by: Lifestyle changes Medication Surgery
Slide 35-

Diagnosis Involves 3 criteria Patient history takin Risk factors Symptoms Clinical signs Inspection: Pale, weigh loss, coating of tongue… Palpation: Epigastric tenderness, Pain radiation Vasilenko sign Percussion: Mendel's sign Investigations Non-invasive CBC: Anemic signs, Inflammatory sign +_ H. pylori IgG titer (serology) Stool antigen text C13 or C14 Urea Breath test Invasive: Endoscopy for ulcer detection Gastric mucosal biopsy with histology Rapid Urease test (CLO test)
Slide 36-

Interventions Surgical interventions may be required in certain cases Malignant ulcers Pyloric stenosis Chronic ulcerations Perforations 3 main surgical procedures Vagotomy Anterctomy pyloroplasty
Slide 37-

Non pharmacological treatment Avoid smoking/smoke cessation Avoid foods that aggravate the pain Allay anxiety and stress; reduced if possible Regular small meals Moderation of coffee and tea Avoid late night snacks as they stimulate nocturnal gastric acid secretion Avoid alcohol Have enough rest Avoid NSAID’s when necessary
Slide 38-

Goals of treatment Pharmacological treatment To relieve pain and reduce gastric acid secretions To promote healing of the ulcer To eradicate H. pylori if present To prevent recurrence of ulcer To avoid complications
Slide 39-

Peptic ulcer drugs Proton pump inhibitors (PPI) H2 – receptor antagonist Prostaglandin analogues Sucralfate Antacids Bismuth Chelates ( no longer used; neurotoxic) Selective anti- muscarinic (pirenzepine)
Slide 40-

Proton pump inhibitors (PPI) PPI’s are weak bases and hence need enteric coating to protect it from the acidic state of the stomach PPI’s bind irreversibly to the proton pump, hence have more sustained duration of acid inhibition Should be taken 30minutes before meals It should not be given before endoscopy as they may mask serious underlying pathology. Examples Omeprazole/Esomeprazole Lansoprazole Pantoprazole
Slide 41-

PPI’s contd Mechanism of action: Inhibits the production of gastric acid by blocking the hydrogen-potassium adenosine triphosphate enzyme system (h+k+=atpase) of the gastric parietal cells in the gastric mucosa Thus the exchange of hydrogen and potassium across the membrane to maintain gastric acidity is inhibited
Slide 42-

PPI’s Adverse effects: usually mild and reversible Diarrhea Headache Nausea Abdominal pain Constipation and dizziness Prolonged use of PPI’s is associated with hypomagnesemia
Slide 43-

H2 RECEPTOR ANTAGONIST – H2RA’S Mechanism of action By blocking histamine type two receptors in gastric parietal cells Thus, preventing acid secretion to reduce gastric output H2 RECEPTOR ANTAGONIST combination with PPI at bedtime may enhance gastric PH control at night
Slide 44-

H2RA’S Example Ranitidine Cimetidine Fomatidine Nizadine Adverse effects Diarrhea Headache Dizziness Rash Tiredness Gynecomastia and impotence occur occasionally with cimetidine Effectively heal ulcer when NSAID therapy is stopped Main role of H2RA is the empirical management of dyspepsia symptoms
Slide 45-

Prostaglandin Analogues Mechanism of action: Has anti secretory and protective properties promoting peptic ulcer healing Can be used as prophylaxis against NSAIs induced ulcers Example: Misoprostol (cytotec) Adverse effect Diarrhea (it may be sever and require withdrawal) Nausea & vomiting Abnormal vagina bleeding with menorrhagia Flatulence Abortifacient
Slide 46-

SUCRALFATE Aluminum salt of sucrose octasulphate Weak antacid Has mucosal protective effects by stimulating bicarbonates and mucosa secretion and stimulation of mucosal prostanoids. Main side effect is constipation
Slide 47-

ANTACIDS ACTS BY Neutralizing gastric acid However only effective for a short period Alginates are added to antacids to relive reflux symptoms Antacids are best given when symptoms occur or are expected
Slide 48-

ANTACIDS Side effects of antacid are considered in choosing type of antacid Aluminum salt antacids may cause constipation While magnesium salts may cause diarrhea Hence a combination of these are preferred to produce neutral effect on intestinal transit Also regular intake may cause hypercalcemia Antacids containing sodium bicarbonate should not be given to patient on restricted salt diet Magnesium trisilicate has very high sodium bicarbonate content Liquid antacids are usually preferred over tablets Antacid dosing: 10-15mL 8 or 6 hourly; of liquid Mf-Al antacids promote ulcer healing, but less than anti secretary drugs
Slide 49-

Examples of antacids Magnesium sulfate Aluminum salts Calcium carbonate Sodium bicarbonate Nugel Aludrox Maalox Maalox plus Ducon Adverse effect Constipation(Aluminium) Diarrhea (magnesium) Flatulence ( Carbonate & bicarbonates)0 Nausea & vomiting
Slide 50-

Management – H. Pylori Eradiction Most patients with DU are infected with H. pylori Eradicate with 7 day course of PPI plus combination of antibiotics classes of antibiotics used include Macrolide (clarithromycin) Penicillin(amoxycillin) Metronidazole For initial therapy against H. pylori a 7-10 day triple therapy comprising of a PPI or H2RA, Clarithromycin, and either amoxicillin or metronidazole For a quadruple therapy, bismuth chelate is added these regimen eradicate H. pylori 85% of cases Dual therapy of PPI and one antibiotic can be used, but produces low rates of eradication PPI regimen is continued for -8 weeks to ensure wound healing
Slide 51-

Amoxicillin Active against H. pylori Shown to be 90% active against H.pylori Should not be given to patients with true penicillin allergy Erythematous rash Maculopapular rash GI adverse effects do not constitute allergy (nausea, vomiting, diarrhea) Urticarial rash does not constitute true penicillin allergy
Slide 52-

Clarithromycin Very active against H. pylori Generally well tolerated May cause GI adverse effects such as: Nausea Diarrhea Vomiting Not given to pregnant and lactating women, excreted in milk
Slide 53-

Metronidazole Active against gram negative bacteria including H. pylori Causes disulfiram-like reactions with alcohol Side effect: Metallic taste in mouth GI irritations including nausea and vomiting Metronidazole is not the 1st line antibiotic in H. pylori eradication But it can be given when there’s treatment failure, symptoms do not resolve Tinidazole can be given in place of Metronidazole
Slide 54-

Current Drug Regimen- H. Pylori Eradication
Slide 55-

Unhealed Ulcer/ Continued Symptoms/ Recurrence In people with an unhealed ulcer, rule out Non-adherence, Malignancy Failure to detect H. pylori Inadvertent NSAID use or other ulcer-inducing medication And rare causes such as Zollinger-Ellison syndrome or Crohn’s disease/ If symptoms recur after initial treatment, offer a PPI to be taken at the lowest dose possible to control symptoms. Discuss using the treatment on an ‘as-needed’ bias with people to manage their own symptoms.
Slide 56-

ppt slide no 56 content not found