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Premium member Presentation Transcript Acid Peptic Disease: Acid Peptic DiseaseDyspepsia: Dyspepsia Symptoms – Upper GI tractFunctional Anatomy Oesophagus: Functional Anatomy Oesophagus Upper and Lower Sphincter Peristaltic waves 2 major Functions Transport of food Prevention of retrograde flow of GI contents (Upper and Lower Sphincter)Functional Anatomy - Stomach: Functional Anatomy - StomachMucosal Defense System: Mucosal Defense System Mucus – Bicarbonate layer (Pre-epithelial) Mucus HCO 3 - PhospholipidsMucosal Defense System: Mucosal Defense System Surface Epithelial Cells Mucus and HCO 3 - production Intracellular tight junction Restitution Cell ProliferationMucosal Defense System: Mucosal Defense System Sub-epithelial Rich blood supply Provides HCO 3 - Micronutrients and O 2Mucosal Defense System: Mucosal Defense System Prostaglandins plays central role in gastric epithelial defense / repair Regulate mucosal HCO 3 - and mucus secretion Inhibits parietal cell secretion Maintains mucosal blood flow and epithelial cell restitutionGastric Secretion: Gastric Secretion HCL Pepsinogen Mucosal InjuryAcid Secretion: Acid Secretion Basal Acid Secretion Cireadian pattern Highest – Night Lowest - Morning Cholinergic input via vagus Histamenergic inputAcid Secretion: Acid Secretion Stimulate Acid Secretion – 3 Phases Cephalic – Sight, Smell, Taste via Vagus Gastric – When food enters stomach, G cell – Gastrin – Parietal cells IntestinalAcid Secretion: Acid Secretion Somatostatin D cells inhibits Acid Production Direct (Parietal cells) Indirect (Reduced histamine release and gastrin releaseAcid Secretion: Acid Secretion Parietal cells (HCL, IF) Histamine (H 2 ) Gastrin Acetylcholine (Proton pump) Acid secreting pump. H + , K + - AT pase Prostaglandins SomatostatinAcid Secretion: Acid Secretion Chief Cells Gastric fundus Pepsinogen – Pepsin Pepsin role in PUD unclearGERD: GERD Gastro Esophageal Reflux Disease Common GI disorderPathophysiology: Pathophysiology Pressure gradient between Lower Esophageal Sphincter and stomach - lostGERD - Pathophysiology: GERD - Pathophysiology LES tone Without apparent cause Scleroderma Pregnancy Drugs Anticholinergics Smooth muscle relaxantsGERD - Pathophysiology: GERD - Pathophysiology LES tone Surgical damage Esophagitis Smoking Dietary fat, Chocolate, Coffee, C 2 H 3 OH Hiatus Hernia Incompetence of diaphragmatic crural muscleGERD - Pathophysiology: GERD - Pathophysiology Gastric contents likely to reflux Gastric volume increased After meals Pyloric obstruction Gastric stasisGERD - Pathophysiology: GERD - Pathophysiology Gastric contents likely to reflux Gastric contents near GE junction Recumbent Bending down Hiatus HerniaGERD - Pathophysiology: GERD - Pathophysiology Gastric contents likely to reflux Gastric pressure increased Obesity Pregnancy AscitesClinical Features: Clinical Features Heartburn Regurgitation of sour material into mouth Waterbrash Atypical chest pain Dysphagia Extra-esophageal manifestations Chronic cough, Laryngitis, Pharyngitis Morning hoarseness Dental decayComplications: Complications Oesophagitis Barretts Oesophagus Pre-malignant glandular meteplasia of lower esophagus Adaptive response Normal squamous lining replaced by columnar mucosa Oesophageal Adeno Ca Benign Oesophageal StrictureInvestigations: Investigations Indications Alarm symptoms + ElderlyInvestigations: Investigations Endoscopy Normal in 1/3 to ½ patients Abnormal – Erosions / Ulcers / Peptic Stricture Mucosal Biopsy pH monitoring Esophageal motility studies LES tone / Esophageal motor function SurgeryManagement: Management Life Style Weight reduction / Elevation of bed head Avoid large meals / late meals Dietary Avoid fatty foods, coffee, chocolate, alcohol, mint, orange juice Stop smoking Avoid drugsDrugs: Drugs PPI 8 weeks in erosive esophagitis Refractory patients – double dose Long term maintenance therapy often required Does not lead to resolution of Barretts Metaplasia / Ca prevention Side Effects – Vitamin B 12 Calcium absorption may be impairedDrugs: Drugs H 2 receptor antagonist Symptom relief Sucralfate Mucosal protector Anti reflux surgery Fundoplication (Open / Lap)Gastritis: Gastritis Histological diagnosis No typical clinical featuresAcute Gastritis: Acute Gastritis Causes H.Pylori NSAIDs / Aspirin / Iron Alcohol Stress related Bile refluxAcute Gastritis: Acute Gastritis Symptoms No symptoms Dyspepsia Anorexia, Nausea, Vomiting Hematemesis, MalenaAcute Gastritis: Acute Gastritis Investigations Endoscopy / Biopsy Treatment Treat underlying cause Antacids / PPI / Antiemetics – short courseChronic Gastritis: Chronic Gastritis H. Pylori AutoimmuneChronic Gastritis: Chronic Gastritis Type A Gastritis (Autoimmune Gastritis) Body – Predominant form Autoimmune Associated with pernicious anemia Antibodies against parietal cell and IF Other autoimmune diseases Vitiligo, Addisons, ThyroidChronic Gastritis: Chronic Gastritis Type B Gastritis Antral predominant H. Pylori related Increased with age Can lead to gastric Adeno Ca Low grade B cell lymphoma Gastric MALT LymphomaChronic Gastritis: Chronic Gastritis Treatment Aimed at sequelae Pernicious Anemia – parentral B 12 supplementalsPeptic Ulcer: Peptic Ulcer Ulcer in lower esophagus, Stomach, Duodenum, in jejunum after surgical anastomosis to stomach, rarely in ileum adjacent to meckels diverticulumPeptic Ulcer: Peptic Ulcer Pathophysiology Imbalance between aggressive (Acid, Pepsin) and Defensive (Gastric and Duodenal) factorsPeptic Ulcer: Peptic Ulcer Aetiology H. Pylori NSAIDs / aspirin Smoking risk of Gastric Ulcer risk of Duodenal Ulcer More likely to cause complication Less likely to heal Impaired response to therapyPeptic Ulcer: Peptic Ulcer Genetic factors Psychological stress Diet Systemic Disease Chronic Pulmonary Diseases Renal Failure CirrhosisPeptic Ulcer: Peptic Ulcer Clinical features Chronic symptoms Natural history of spontaneous relapse and remissionPeptic Ulcer: Peptic Ulcer Clinical features Abdominal pain Burning / Gnawing Localised to epigastrium Episodic occurrence Relationship to foodPeptic Ulcer: Peptic Ulcer Clinical Features Relationship to food Duodenal Ulcer 90 minute to 3 Hour after food Frequency relieved by antacid / food Gastric Ulcer May be precipitated by food Weight lossPeptic Ulcer: Peptic Ulcer Clinical Features Anorexia / Nausea / Vomiting Silent Anemia due to chronic blood loss Abrupt hematemesis / acute perforation / malenaGastric Ulcer: Gastric Ulcer On Examination Epigastric tenderness Signs of dehydration Tender board like abdomen - perforationGastric Ulcer: Gastric Ulcer Complications GI Bleed Perforation Duodenal ulcer posteriorly into pancreas – Pancreatitis Gastric Ulcer penetrating into Left Hepatic Lobe Gastric outlet obstructionH.Pylori: H.Pylori Gram negative Enzyme urease buffers acidity Produces ammonia from urea Raises pHH. Pylori: H. Pylori Deeper parts of mucous gel / between mucous layer and gastric epithelium Spreads by person to person contact via gastric refluxate or vomitus in developing / in developed Socio Economic StatusH.Pylori: H.Pylori Depletion of Somatostatin from D Cells Gastrin release from G Cells PUD Gastric mucosal associated lymphoid tissue (MALT Lymphoma) Gastric Adeno Carcinoma AsymptomaticH.Pylori: H.Pylori Diagnosis Non Invasive Serology Urea Breath Test Fecal Antigen Test Invasive (Antral Biopsy) Histology Rapid Urease Test (CLO) Culture – GOLD StandardH.Pylori: H.Pylori Treatment Duodenal and Gastric Ulcer with H.Pylori positive 1 st Line Therapy PPI Q 12 Hourly Clarithromycin 500 mg Q 12 Hourly Amoxycilline 1 gm 12 th hourly / Metronidazole 400 mg Q 12 HourlyH.Pylori: H.Pylori Treatment 2 nd Line Therapy PPI Q 12 Hourly Bismuth 120 mg Q 6 Hourly Metronidazole 400 mg Q 12 Hourly Tetracycline 500 mg Q 6 HourlyH.Pylori: H.Pylori Side Effects Diarrhoea Flushing and vomiting when taken with C 2 H 5 OH Nausea, Vomiting Abdominal cramps Headache, RashNSAIDs: NSAIDs Established Risk Factors Advanced age History of Ulcer Concomittent use of Glucocorticoids, Anticoagulants High dose NSAIDs Serious, Multisystem DiseaseNSAIDs: NSAIDs Epithelial effect (due to PG depletion) Direct toxicity “Ion Trapping” Endothelial Effect – Stasis, IschemicPeptic Ulcer: Peptic Ulcer Diagnosis Endoscopy BiopsyPeptic Ulcer: Peptic Ulcer Treatment 1. General measures Avoid Aspirin NSAIDs Smoking Alcohol 2. Treatment of H.Pylori infection 3. Drugs 4. SurgeryPeptic Ulcer: Peptic Ulcer Treatment with Drugs (Medical) Antacids Aluminium and Magnesium containing Avoid in Renal Failure Hypermagnesemia Chronic Neurotoxicity SymptomaticPeptic Ulcer: Peptic Ulcer Treatment with Drugs (Medical) H 2 Receptor Antagonist Less potent than PPI May develop tolerance Once daily at bed time Cimetidine - GynecomastiaPPI: PPI Omeprazole, Esomeprazole, Lanzoprazole, Rabeprazole, Pantoprozole Irreversibly inhibit H + , K + -AT Pase Most potent Inhibit all phases of gastric secretion Rapid onset Before mealsMucosal Protective Agents: Mucosal Protective Agents Sucralfate 1gm Q 6 Hourly Physiochemical barrier Enhancing PG synthesis Enhancing Mucosal defense and repair Positive mucous and HCO 3 secretion Constipation Avoid in Chronic Renal Failure Aluminium induced neurotoxicityMucosal Protective Agents: Mucosal Protective Agents Prostaglandin Analogues Misoprostol – 200 mg Q 6 Hourly Diarrhoea, Uterine bleeding and Contractions Contraindicated in pregnant womenStress Related Mucosal Injury: Stress Related Mucosal Injury Shock Sepsis Severe Burns Severe Trauma Head injury Gastritis / Ulcer Most common in Fundus & Body ( Acid producing regions ) Most common presentation – GI BleedStress Related Mucosal Injury: Cushings Ulcer – Trauma Curlings Ulcer – Severe Burns PPI – 1 st choice for Prophylaxis Sucralfate Stress Related Mucosal InjuryNon Ulcer Dyspepsia: Non Ulcer Dyspepsia Chronic dyspepsia (Pain / Upper Abdominal Discomfort) in the absence of organic diseaseNon Ulcer Dyspepsia: Clinical Features Usually in young < 40 years Females 2 : 1 Abdominal pain Dyspepsia Morning symptoms characteristic Non Ulcer DyspepsiaNon Ulcer Dyspepsia: Non Ulcer Dyspepsia Features of Irritable Bowel Syndrome No weight Loss Anxious No diagnostic Signs (Inappropriate tenderness) Drug history / Alcohol misuse Endoscopy to rule out other causesNon Ulcer Dyspepsia: Treatment Counselling Fat restriction may help Antacids / Prokinetics Low dose Amitryptilline Non Ulcer DyspepsiaGastroparesis: Gastroparesis Defective gastric emptying Diabetes Mellitus Systemic Sclerosis / Amyloidosis Early satiety, recurrent vomiting Treatment Metaclopramide / Domperidone You do not have the permission to view this presentation. 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