Acid Peptic Disease

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Acid Peptic Disease:

Acid Peptic Disease

Dyspepsia:

Dyspepsia Symptoms – Upper GI tract

Functional 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 - Stomach

Mucosal Defense System:

Mucosal Defense System Mucus – Bicarbonate layer (Pre-epithelial) Mucus HCO 3 - Phospholipids

Mucosal Defense System:

Mucosal Defense System Surface Epithelial Cells Mucus and HCO 3 - production Intracellular tight junction Restitution Cell Proliferation

Mucosal Defense System:

Mucosal Defense System Sub-epithelial Rich blood supply Provides HCO 3 - Micronutrients and O 2

Mucosal 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 restitution

Gastric Secretion:

Gastric Secretion HCL Pepsinogen Mucosal Injury

Acid Secretion:

Acid Secretion Basal Acid Secretion Cireadian pattern Highest – Night Lowest - Morning Cholinergic input via vagus Histamenergic input

Acid Secretion:

Acid Secretion Stimulate Acid Secretion – 3 Phases Cephalic – Sight, Smell, Taste via Vagus Gastric – When food enters stomach, G cell – Gastrin – Parietal cells Intestinal

Acid Secretion:

Acid Secretion Somatostatin D cells inhibits Acid Production Direct (Parietal cells) Indirect (Reduced histamine release and gastrin release

Acid Secretion:

Acid Secretion Parietal cells (HCL, IF) Histamine (H 2 ) Gastrin Acetylcholine  (Proton pump) Acid secreting pump. H + , K + - AT pase Prostaglandins Somatostatin

Acid Secretion:

Acid Secretion Chief Cells Gastric fundus Pepsinogen – Pepsin Pepsin role in PUD unclear

GERD:

GERD Gastro Esophageal Reflux Disease Common GI disorder

Pathophysiology:

Pathophysiology Pressure gradient between Lower Esophageal Sphincter and stomach - lost

GERD - Pathophysiology:

GERD - Pathophysiology  LES tone Without apparent cause Scleroderma Pregnancy Drugs Anticholinergics Smooth muscle relaxants

GERD - Pathophysiology:

GERD - Pathophysiology  LES tone Surgical damage Esophagitis Smoking Dietary fat, Chocolate, Coffee, C 2 H 3 OH Hiatus Hernia Incompetence of diaphragmatic crural muscle

GERD - Pathophysiology:

GERD - Pathophysiology Gastric contents likely to reflux Gastric volume increased After meals Pyloric obstruction Gastric stasis

GERD - Pathophysiology:

GERD - Pathophysiology Gastric contents likely to reflux Gastric contents near GE junction Recumbent Bending down Hiatus Hernia

GERD - Pathophysiology:

GERD - Pathophysiology Gastric contents likely to reflux Gastric pressure increased Obesity Pregnancy Ascites

Clinical 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 decay

Complications:

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 Stricture

Investigations:

Investigations Indications Alarm symptoms + Elderly

Investigations:

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 Surgery

Management:

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 drugs

Drugs:

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 impaired

Drugs:

Drugs H 2 receptor antagonist Symptom relief Sucralfate Mucosal protector Anti reflux surgery Fundoplication (Open / Lap)

Gastritis:

Gastritis Histological diagnosis No typical clinical features

Acute Gastritis:

Acute Gastritis Causes H.Pylori NSAIDs / Aspirin / Iron Alcohol Stress related Bile reflux

Acute Gastritis:

Acute Gastritis Symptoms No symptoms Dyspepsia Anorexia, Nausea, Vomiting Hematemesis, Malena

Acute Gastritis:

Acute Gastritis Investigations Endoscopy / Biopsy Treatment Treat underlying cause Antacids / PPI / Antiemetics – short course

Chronic Gastritis:

Chronic Gastritis H. Pylori Autoimmune

Chronic 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, Thyroid

Chronic 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 Lymphoma

Chronic Gastritis:

Chronic Gastritis Treatment Aimed at sequelae Pernicious Anemia – parentral B 12 supplementals

Peptic Ulcer:

Peptic Ulcer Ulcer in lower esophagus, Stomach, Duodenum, in jejunum after surgical anastomosis to stomach, rarely in ileum adjacent to meckels diverticulum

Peptic Ulcer:

Peptic Ulcer Pathophysiology Imbalance between aggressive (Acid, Pepsin) and Defensive (Gastric and Duodenal) factors

Peptic 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 therapy

Peptic Ulcer:

Peptic Ulcer Genetic factors Psychological stress Diet Systemic Disease Chronic Pulmonary Diseases Renal Failure Cirrhosis

Peptic Ulcer:

Peptic Ulcer Clinical features Chronic symptoms Natural history of spontaneous relapse and remission

Peptic Ulcer:

Peptic Ulcer Clinical features Abdominal pain Burning / Gnawing Localised to epigastrium Episodic occurrence Relationship to food

Peptic 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 loss

Peptic Ulcer:

Peptic Ulcer Clinical Features Anorexia / Nausea / Vomiting Silent Anemia due to chronic blood loss Abrupt hematemesis / acute perforation / malena

Gastric Ulcer:

Gastric Ulcer On Examination Epigastric tenderness Signs of dehydration Tender board like abdomen - perforation

Gastric Ulcer:

Gastric Ulcer Complications GI Bleed Perforation Duodenal ulcer posteriorly into pancreas – Pancreatitis Gastric Ulcer penetrating into Left Hepatic Lobe Gastric outlet obstruction

H.Pylori:

H.Pylori Gram negative Enzyme urease buffers acidity  Produces ammonia from urea Raises pH

H. 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 Status

H.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 Asymptomatic

H.Pylori:

H.Pylori Diagnosis Non Invasive Serology Urea Breath Test Fecal Antigen Test Invasive (Antral Biopsy) Histology Rapid Urease Test (CLO) Culture – GOLD Standard

H.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 Hourly

H.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 Hourly

H.Pylori:

H.Pylori Side Effects Diarrhoea Flushing and vomiting when taken with C 2 H 5 OH Nausea, Vomiting Abdominal cramps Headache, Rash

NSAIDs:

NSAIDs Established Risk Factors Advanced age History of Ulcer Concomittent use of Glucocorticoids, Anticoagulants High dose NSAIDs Serious, Multisystem Disease

NSAIDs:

NSAIDs Epithelial effect (due to PG depletion) Direct toxicity “Ion Trapping” Endothelial Effect – Stasis, Ischemic

Peptic Ulcer:

Peptic Ulcer Diagnosis Endoscopy Biopsy

Peptic Ulcer:

Peptic Ulcer Treatment 1. General measures Avoid Aspirin NSAIDs Smoking Alcohol 2. Treatment of H.Pylori infection 3. Drugs 4. Surgery

Peptic Ulcer:

Peptic Ulcer Treatment with Drugs (Medical) Antacids Aluminium and Magnesium containing Avoid in Renal Failure Hypermagnesemia Chronic Neurotoxicity Symptomatic

Peptic Ulcer:

Peptic Ulcer Treatment with Drugs (Medical) H 2 Receptor Antagonist Less potent than PPI May develop tolerance Once daily at bed time Cimetidine - Gynecomastia

PPI:

PPI Omeprazole, Esomeprazole, Lanzoprazole, Rabeprazole, Pantoprozole Irreversibly inhibit H + , K + -AT Pase Most potent Inhibit all phases of gastric secretion Rapid onset Before meals

Mucosal 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 neurotoxicity

Mucosal Protective Agents:

Mucosal Protective Agents Prostaglandin Analogues Misoprostol – 200 mg Q 6 Hourly Diarrhoea, Uterine bleeding and Contractions Contraindicated in pregnant women

Stress 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 Bleed

Stress Related Mucosal Injury:

Cushings Ulcer – Trauma Curlings Ulcer – Severe Burns PPI – 1 st choice for Prophylaxis Sucralfate Stress Related Mucosal Injury

Non Ulcer Dyspepsia:

Non Ulcer Dyspepsia Chronic dyspepsia (Pain / Upper Abdominal Discomfort) in the absence of organic disease

Non Ulcer Dyspepsia:

Clinical Features Usually in young < 40 years Females 2 : 1 Abdominal pain Dyspepsia Morning symptoms characteristic Non Ulcer Dyspepsia

Non 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 causes

Non Ulcer Dyspepsia:

Treatment Counselling Fat restriction may help Antacids / Prokinetics Low dose Amitryptilline Non Ulcer Dyspepsia

Gastroparesis:

Gastroparesis Defective gastric emptying Diabetes Mellitus Systemic Sclerosis / Amyloidosis Early satiety, recurrent vomiting Treatment Metaclopramide / Domperidone

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